01-24-2011, 02:35 PM
USMLE WORLD STEP-3 INTERNAL MEDICINE
Cardiology
CAD
Multiple risk factors increase the risk of acute CAD.
The risk can be significantly reduced by decreasing LDL cholesterol and, to a lesser degree, by adequately controlling the blood pressure (in diabetic patients, as well as in patients with previous CAD, a blood pressure lower than 130/80 mmHg is recommended). The contribution of other interventions such as smoking cessation, diabetes control, exercise, and HDL increase is also beneficial, but not as critical as the first two measures.
♥In patients with hypercholesterolemia and hypertriglyceridemia ► a statin is the best initial drug of choice. The primary target of therapy is normalizing LDL-cholesterol; the secondary target is normalizing non-HDL cholesterol(total cholesterol – HDL cholesterol).
♥If the statin fails to control hypertriglyceridemia► gemfibrozil or niacin can be added.
In prospective studies of healthy patients, those with higher plasma fibrinogen concentrations developed coronary heart disease more frequently. Fibrinogen levels decrease only 20 years after smoking cessation; while certain drugs such as atorvastatin and lovastatin can produce hyperfibrinogenemia. Even though it is uncertain how dangerous hyperfibrinogenemia can be, it is currently recommended to maintain fibrinogen levels as low as possible and to discontinue any medication that can increase them, unless the benefits outweigh the risks.
Exercise electrocardiography should be the initial test of choice for evaluation of suspected CAD in patients with a normal resting EKG and the ability to exercise.
Exercise stress testing is useful for the diagnosis and risk stratification of patients with stable angina. Exercise testing is useful to identify a high-risk group that will benefit from coronary angiography.
♥Patients at high risk have one of the following findings on exercise testing:
1. failure to increase their blood pressure with exercise
2. Inability to complete stage I of Bruce protocols
3. Appearance of horizontal or down sloping ST segment during exercise
♥Pharmacological stress testing is an alternative to exercise stress testing, and is indicated in the setting of CAD, when the patient is unable to exercise due to some underlying medical disorder (amputation), when an exercise stress test is relatively contraindicated (MI, unstable angina), or in patients in whom interpretation of an EKG is difficult because of preexisting changes, such as left bundle branch block, baseline ST/T changes from left ventricular hypertrophy, etc.
♠Both adenosine and dipyridamole scans are contraindicated in patients with COPD because they can induce bronchospasm.
♥The American College of Cardiology/American Heart Association (ACC/AHA) defines a positive exercise stress test as ►1 mm or more of down sloping or flat ST segment depression during exercise or during the recovery period.
♥Exercise echocardiography is more sensitive than the resting echocardiogram or stress EKG, and is also commonly done in patients with stable angina.
♥Resting echocardiography or EKG is useless in stable angina when the patient has no active chest pain.
-Principles and practice of stress testing are based on the relative development of manifestations of myocardial ischemia as the stress to the myocardium is increased. Regional wall motion defects are the first to appear (detected by stress echocardiography). This is followed by significant perfusion defects (detected by perfusion scans), pulmonary capillary wedge elevation, ST segment changes on electrocardiogram, and finally, anginal pain.
-Stress imaging should therefore be pursued if there are no EKG changes during or after the stress test. It is also the modality of choice in patients with bundle branch block, WPW syndrome, paced ventricular rhythm, and baseline ST changes before exercise (ventricular hypertrophy, digitalis therapy, etc.). A positive stress test result in a patient with symptoms warrants further intervention, preferably with a coronary angiogram.
-Nuclear scans should be performed in subsets of patients with baseline ST segment changes.
-It is important to recognize the advantages and limitations of different available testing modalities for the evaluation of myocardial ischemia.
--Adenosine, along with dipyridamole and dobutamine, is one of the most frequently used pharmacologic agents to induce ischemia in patients with poor functional status.
--Sestamibi test is one of the three available technetium-99m labeled tracers used frequently for radionuclide imaging.
-In patients with angina and a prior history of revascularization (PTCA or CABG), technetium-99m (sestamibi) and thallium perfusion imaging are the two types of radionuclide perfusion imaging modalities used for characterizing the ischemia, establishing the functional effects of lesions, and determining the viability of myocardium.
-The two modalities are also used in patients with complete left bundle branch block (LBBB), electronically-paced ventricular rhythm, preexcitation (WPW) syndromes, > 1 mm ST segment depression at rest, LVH with repolarization changes, and in patients who are unable to exercise.
♥Coronary angiography is indicated in the setting of stable angina pectoris when the angina is refractory to medical treatment, or when exercise testing identifies the patient as high-risk.
►Studies have shown that compared to angioplasty, Coronary artery bypass graft (CABG) improves long-term survival in diabetic patients with multivessel disease and recent Q-wave infarction.
-Good, perioperative control of the blood glucose levels is advocated during CABG. An insulin drip achieves better blood glucose control during CABG, and decreases the incidence of sternotomy wound infections.
-According to the ACC/AHA guidelines, patients who are unable or unfit to exercise should undergo adenosine or dipyridamole myocardial perfusion imaging for the diagnosis and risk stratification of CAD. Adenosine, along with dipyridamole and dobutamine, is one of the most frequently used pharmacologic agents to induce ischemia in patients with poor functional status.
►All patients with chronic stable angina should undergo an exercise stress test for prognostic and risk stratification.
►All patients with coronary artery disease and stable angina should be referred for an exercise stress test for further risk stratification.
♥Patients with a low risk treadmill score (able to exercise more with a normal EKG) have less than 1% annual mortality rate.
♥On the other hand, patients who have a high-risk treadmill score (presence of chest pain or EKG changes with minimal exercise) have greater than 3% annual mortality rate and require more aggressive management.
►Metformin use is contraindicated in patients with renal failure, sepsis, hepatic dysfunction, and severe heart failure. It should also be stopped in patients who are at risk to develop renal failure, such as those who will undergo angiography, a procedure that involves infusion of a high load of contrast agent
►In patients whose chest pain may be ischemic in origin, supplemental oxygen and ASA aspirin should be administered immediately, followed by Nitroglycerin, Morphine, and Beta-blockers (presuming no contraindications exist).
►Calcium channel blockers can be harmful in patients with acute MI.
►Beta blockers, ACE inhibitors, and statins have significant effects on the secondary prevention of coronary artery disease, and should be continued indefinitely unless absolutely contraindicated.
►The only indications of calcium channel blockers in the setting of acute myocardial infarction include:
♥Intolerance to beta blockers, post-infarction angina refractory to beta blockers and nitrates, and rapid atrial fibrillation with contraindications to beta-blocker use (COPD, pulm. disease)
♠Peripheral edema is a well-known side effect of calcium antagonist therapy. It is more common with dihydropyridine agents (e.g. nifedipine, amlodipine), but also occurs in 2 to 15% of patients taking diltiazem [cardizem]. The exact mechanism of calcium antagonist-associated edema is not known; arteriolar dilatation seems to be responsible for increased interstitial fluid accumulation in these patients
Acute pericarditis
Acute pericarditis (infarct associated or infarction pericarditis) can occur within one to four days as a direct complication of a transmural myocardial infarction. The recurrence of chest pain three days after a myocardial infarction, which gets worse with position changes and deep inspiration, is suggestive of infarction pericarditis. It is usually a clinical diagnosis, and is supported by the presence of pericardial friction rub and EKG changes of pericarditis (sinus tachycardia, diffuse ST segment elevations with PR segment depression).
-A pericardial rub is usually heard over the left sternal border and can be present during any of the phases of the cardiac cycle. It is heard as a superficial scratchy or grating sound, which gets more pronounced when the patient leans forward.
-The EKG changes of pericarditis are not always seen, but usually resemble that of an acute myocardial infarction.
Infarction pericarditis
-Is seen less frequently in patients with early and complete reperfusion. It is usually a transient episode and does not affect the management of acute myocardial infarction, unless it is complicated by a large pericardial effusion or tamponade.
>>It should be managed with close clinical observation and adequate pain control.
>>Nonsteroidal anti-inflammatory medications (NSAIDs) are effective in alleviating the pain associated with acute pericardial inflammation, although there are some concerns that they may increase the risk of myocardial rupture after a transmural MI.
D/DX:
1. Chordae tendineae or papillary muscle rupture is a life threatening mechanical complication of an acute myocardial infarction. It usually occurs two to seven days after the infarction and causes acute hemodynamic instability. Patients also develop acute pulmonary edema.
2. Dressler’s syndrome, or post-cardiac injury syndrome, occurs in patients with myocardial infarction and after cardiac surgery. It is an autoimmune mediated syndrome, which usually develops weeks to months after an acute MI. It usually presents with fever, leukocytosis, pleuritic chest pain, and a pericardial rub.
3. A left ventricular aneurysm usually occurs as a late complication of a transmural myocardial infarction (usually a large anterior wall MI). It may result in heart failure, ventricular arrhythmias, or peripheral arterial embolization due to the formation of a left ventricular thrombus. It develops over a longer period of time, and is usually not associated with chest pain. Persistent ST elevation can be present in these patients.
►Sinus bradycardia is commonly seen as a complication of an inferior wall myocardial infarction.
-It is usually present transiently, immediately after or within the first six hours, and resolves within 24 to 48 hours of acute myocardial infarction. Most of the episodes are asymptomatic, and resolve without any therapy or intervention.
>>BUT: Active intervention is required in patients with sinus bradycardia after myocardial infarction, if the patient exhibits signs and symptoms of hemodynamic compromise.
>>The definite treatment is by reperfusion of the infarcted myocardium, either with thrombolysis or percutaneous transluminal coronary angioplasty (PTCA).
>>If bradycardia persists after reperfusion, the patients can still respond to the administration of intravenous Atropine.
>>VERY HD UNSTABLE: Temporary transvenous cardiac pacing is usually required in patients with persistent bradycardia and hemodynamic instability after myocardial infarction, despite the above measures.
►Recent myocardial infarction and atrial fibrillation are two most common causes of arterial thromboembolism.
►The single most important step in the early management of the patients with acute arterial occlusion diagnosed by history and physical examination is immediate IV heparin therapy followed by continuous heparin infusion.
►Heparin therapy will prevent further propagation of thrombus, and inhibit thrombosis distally in the arterial and venous systems due to low flow and stasis.
♥An important issue for many patients after a myocardial infarction is when sexual activity can be safely resumed
-Therefore, this should be addressed in all sexually active patients before hospital discharge.
-A consensus panel concluded that patients resuming sexual activity 6 weeks after an uncomplicated myocardial infarction are at low risk for future myocardial events.
On the other hand, those resuming sexual activity within six weeks are at intermediate risk, and those resuming activity within two weeks are at high risk.
•Patients with complications such as post-infarction chest pain, evidence of arrhythmias, or heart failure are also at intermediate or high risk
•Patients at intermediate risk should receive further evaluation and subsequent reclassification into the low-risk or high-risk category, while patients at high risk should be stabilized with appropriate therapy before resuming sexual activity.
•Consultation with a cardiologist prior to resuming sexual activity is recommended in all high-risk patients
Radionuclide ventriculography [RVG]
-The anthracyclines (doxorubicin, daunorubicin, idarubicin, epirubicin, and mitoxantrone) are the most common cause of cardiovascular complications in cancer patients.
-Patients who are about to receive such cardiotoxic chemotherapy are therefore recommended to undergo baseline testing and serial reevaluation of systolic function to identify early signs of cardiotoxicity.
-Noninvasive serial monitoring of cardiac function with radionuclide ventriculography (RVG) has been the most effective way to detect early toxicity and reduce the risk of anthracycline toxicity.
-Radionuclide ventriculography [also known as radionuclide angiography (RNA) or multiple-gated cardiac blood pool imaging (MUGA scan)] is performed by labeling a patient’s red cells with a radioactive tracer and measuring radioactivity over the anterior chest with a gamma camera.
-It is the ideal and most reproducible test for providing longitudinal quantitative assessment of LV systolic function in patients receiving doxorubicin or other anthracyclines. It should be used when detection of slight changes in the ejection fraction are of importance, such as during chemotherapy, before and after cardiac transplantation, and severe CHF
HTN
-According to the new JNC VII guidelines, thiazide diuretics are the initial drugs of choice for the treatment of essential hypertension.
-Approximately 90% of patients with secondary HTN will have an unidentified cause. Of the remaining, around 3% will be due to renovascular HTN. Other less common causes account for less than 1% each, and are comprised of the following: primary hyperaldosteronism, drug-induced HTN, acute stress, and renal parenchymal disease.
-Abdominal or flank bruits are present in 50% of the patients with renovascular HTN. This makes this clinical finding the most common and expected clinical finding in a patient with suspected secondary HTN.
-Almost all guidelines recommend non-pharmacologic measures that can be preventive, adjunctive or sometimes definitive in the treatment of hypertension.
-Weight loss enhances the effect of anti-hypertensive drugs. It is the single most effective non-pharmacologic measure to decrease blood pressure in overweight individuals, and it is believed to reduce the overall cardiovascular risk in such patients.
♥ Note: Smoking cessation is an important component of lifestyle modification that reduces the risk of future cardiovascular events.
CHF
►Ischemic heart disease is the most common cause of congestive heart failure (CHF), especially dilated cardiomyopathy, in the United States. Approximately 50 to 75% of the patients with heart failure (HF) have coronary disease as the etiology.
-Other known etiologies are: hypertension (13%), valvular disease (10-to12%), renovascular disease, and very rare causes, such as obstructive sleep apnea, myocarditis, alcohol or cocaine abuse, etc.
-In a new case of CHF with unknown etiology, efforts must first be made to rule out the presence of coronary lesions which may be corrected by an angioplasty.
-Congestive heart failure is a clinical syndrome that results from impaired or inadequate ventricular emptying (systolic dysfunction) or impaired ventricular relaxation (diastolic dysfunction).
-It is characterized by specific symptoms that are either due to reduced cardiac output (fatigue, weakness) or excessive fluid retention (peripheral or pedal edema, dyspnea).
-All symptoms are exacerbated by exertion, and the degree of these symptoms helps in assessing the severity of heart failure.
♥Heart failure is primarily a clinical diagnosis and is based on a detailed history and physical examination. A detailed history and physical examination can also provide clues to the specific cause of heart failure.
♥CHF: The major criteria include the presence of paroxysmal nocturnal dyspnea, orthopnea, raised jugular venous pressure, pulmonary rales, presence of third heart sound, increased cardiac silhouette, and pulmonary vascular congestion on chest x-ray.
♥CHF: The minor criteria include the presence of bilateral lower extremity edema, nocturnal cough, dyspnea on exertion, tachycardia, presence of pleural effusion, and hepatomegaly.
►The diagnosis of heart failure is based on the presence of two major criteria or one major and two minor criteria, provided the minor criteria cannot be explained by the presence of any concurrent medical illness.
♥Chest radiograph findings suggestive of congestive heart failure include cardiomegaly, pulmonary vascular congestion (especially in the upper lobes), Kerley B lines and bilateral pleural effusions.
-The presence or absence of such findings will help to differentiate heart failure from dyspnea secondary to a primary pulmonary pathology.
-Plasma B type natriuretic peptide levels are useful at times to differentiate between cardiogenic versus non-cardiogenic causes of dyspnea.
♥Rupture of chordae tendineae should be suspected in healthy individuals who develop flash pulmonary edema (heart failure) associated with an acute mitral regurgitation.
-The differential diagnosis of this condition includes infective endocarditis, papillary muscle rupture secondary to ischemia, and mitral valve rupture secondary to trauma.
♥ACE inhibitors are the main therapy for CHF. ]They are indicated even in the asymptomatic phase. Although there is currently insufficient data to show its benefits to the mortality rate of African-Americans and women, their use in CHF is always recommended.
♥The only reasons for not giving ACE inhibitors are=
(1) Poor tolerance to the drugs (presence of severe adverse effects) and
(2) The presence of contraindications, such as renal failure
(Creatinine greater than or equal to 3 mg/dL) or hyperkalemia)
♥ Hydralazine and isosorbide combination is frequently used in the management of congestive heart failure in patients intolerant of ACE inhibitors.
-Patients should be informed regarding the possible adverse reactions that may result from the use of these drugs, and instructed to stop the medication if they develop any of these reactions.
♣The development of drug-induced lupus-like syndrome
-has been associated with the use of hydralazine.
-Other drugs that have been associated with lupus include procainamide, penicillamine, isoniazid, minocycline, diltiazem, methyldopa, chlorpromazine, and interferon-alfa.
-Patients with drug-induced lupus can develop a variety of flu-like symptoms such as fever, malaise, arthralgias, myalgias, and maculopapular facial rash. They can also develop lymphadenopathy, splenomegaly, pleurisy, and pericarditis. An important immunological marker of drug-induced lupus is the presence of antihistone antibodies.
Remember:
All patients with flash pulmonary edema of unknown etiology should be evaluated with an Echocardiogram.
Patients with acute pulmonary edema are initially managed with oxygen, morphine and loop diuretics (IV furosemide).
The two most commonly used antihypertensive agents in the management of hypertensive crisis complicated by acute pulmonary edema are => IV nitroglycerine and IV nitroprusside.
Marfans
Marfan or Ehlers-Danlos syndrome must be suspected in patients with connective tissue abnormalities and an acute mitral regurgitation secondary to chordae tendineae rupture, although a primary, pre-existing mitral valve prolapse (MVP) is the most common cause.
Some cases may be idiopathic (individuals who experience rupture of the chordae tendineae without previous MVP or connective tissue disease), but an etiology can be found in most occasions.
Cardiac risk factors
-Diabetes mellitus is the single most important predictor of adverse cardiovascular outcomes, especially in women. It is considered to be an equivalent of coronary heart disease (CHD).
-The role of glycemic control in the development of macrovascular disease in patients with type-2 diabetes is not firmly established.
=Hypertension is a well-established risk factor.
=The blood pressure should be kept below 130/85 mmHg in diabetics, unlike non-diabetic individuals whose target blood pressure is below 140/90 mmHg.
=Smoking is an important modifiable risk factor. The risk of cardiovascular events declines rapidly after smoking cessation, and approaches that of non-smokers in several years
MAT
Multifocal or multiform atrial tachycardia (MAT) is characterized by the presence of:
3 or more P waves of different morphologies
The QRS complexes are narrow
While the PR segments and the R-R intervals are variable
The heart rate can reach up to 200 beats per minute.
MAT is usually secondary to the following conditions:
1) hypoxia
2) chronic obstructive pulmonary disease (COPD)
3) hypokalemia
4) hypomagnesemia
5) coronary/ hypertensive/ valvular disease
6) medications (i.e., theophylline, aminophylline, isoproterenol)
Treatment M A T:
#1= Correct cause: Do ABGs because Hypoxia and COPD are the most common etiologies that affect mainly elderly patients. -Therapy is aimed at correcting the underlying cause.
#2-If the patient fails to improve >>electrolyte abnormalities (e.g., hypokalemia or hypomagnesemia) should be wanted.
If therapy is not effective and there are no contraindications, beta-blockers can be used successfully. In patients with asthma or COPD, verapamil is the drug of choice.
-SVT and sinus tachycardia are the most frequent types of tachyarrhythmias.
--Narrow and regular QRS complexes, and absent P waves >> suggest supraventricular tachycardia.
--Narrow and regular QRS complexes, and presence of P waves >> Sinus tachycardia
WPW Syndrome can be identified in around 0.2% of the population.
=It is characterized by a short PR interval (less than 0.12sec), a delta wave at the beginning of the QRS complex, QRS duration of 0.12sec or wider, and non-specific ST segments or T wave abnormalities.
=Although WPW Syndrome is not common, its diagnosis is important because it can present as SVT.
=If verapamil or beta-blockers are given, AV nodal conduction will be slow, and the accessory pathway conduction will increase.
=These can lead to ventricular fibrillation (especially if the patients already have atrial fibrillation) and death.
♦ Blocks:
-In comparison to Mobitz I, second-degree AV Block (Wenckebach’s), the PR does not prolong progressively, {PR is fixed] but QRS complexes are suddenly lost periodically
-Mobitz II AV Block can cause dizziness, episodes of syncope, or transient altered mental status, thus explaining the symptoms of the patient. Because Mobitz II can progress to third-degree AV Block, it needs to be managed with a permanent pacemaker. Even if the patient is asymptomatic, the AHA/ACC (American Heart Association/American College of Cardiology) consensus advises the use of a permanent pacemaker inserted through a venous access.
Nonsustained ventricular tachycardia
-Is defined as the presence of three or more consecutive ventricular beats with a heart rate greater than 120 beats/min, and with the episode lasting for less than 30 seconds. It is seen most commonly in patients with some form of structural heart disease, possibly because structural abnormalities lead to ventricular arrhythmia.
-Some structural abnormalities that can lead to nonsustained ventricular tachycardia include scarred myocardium from prior myocardial infarctions (coronary artery disease), ventricular hypertrophy (LVH or hypertrophic obstructive cardiomyopathy), dilated left ventricle (dilated cardiomyopathy), and valvular abnormalities such as mitral valve prolapse.
Although nonsustained ventricular tachycardia can also be seen in patients without any evidence of structural heart disease, it is important to recognize that structural heart disease is the most common cause, and a 2D-echocardiogram and stress test should be obtained to rule out ischemia.
-Patients with multiple risk factors for developing cardiac arrhythmias need proper evaluation for possible implantable cardiac defibrillator placement to prevent sudden cardiac death.
Atrial fibrillation
◘ Treatment of atrial fibrillation in a hemodynamically stable patient is different from one who is unstable.
1-If the patient is hemodynamically unstable (low BP, patient not responding to commands), the treatment of choice is electrical cardioversion.
2-If the patient is hemodynamically stable, the atrial fibrillation has to be categorized first as either an acute or a chronic process.
►If it is an acute process, the patient may undergo either Cardioversion [electrical or pharmacological with anti arrhythmic drugs class III agents (amiodarone, sotalol, ibutilide, etc.).
] or Rate control [B-blocker or CCB] to convert his arrhythmia to sinus rhythm. [If > 48 hrs, cardioversion need 1 month of anticoagulation in high risk pt]
►If it is a chronic process, then the patient should be managed with Rate control and Anticoagulation –heparin/Warfarin
Cardioversion -can be either electrical or chemical.
►Electrical cardioversion is indicated in hemodynamically unstable patients.
►Synchronized cardioversion (electrical shock administered in synchrony with the ‘R’ wave) is the procedure of choice.
-Electrical cardioversion should not be performed without 3-4 weeks of anticoagulation first in chronic atrial fibrillation (> 48 hours), as the risk of embolization is high. -The required joules are about 100-200 joules.
-Atrial fibrillation is generally more resistant to convert to normal sinus rhythm than atrial flutter, and the energy required is much higher.
-If you choose to do chemical cardioversion, the drugs of choice are class III agents (amiodarone, sotalol, ibutilide, etc.).
Lone atrial fibrillation in a patient younger than 60 years of age and without structural or functional cardiac abnormalities [CHF, valvular disease…] does not increase the risk of stroke. However, small studies suggest that there can be some risk, especially if the patient has other risk factors, such as advanced age, diabetes, or hypertension.
For this reason, ASA Aspirin is recommended as prophylactic therapy. The risk of anticoagulation with Coumadin outweighs the benefits in this setting.
♥Amiodarone interacts with Warfarin, prolonging its effect and increasing the risk of bleeding. Its clinical response is predictable; it is known that the Warfarin dose needs to be decreased about 25% in order to avoid over coagulation.
♥ Strokes and Warfarin use:
-The use of FFP or intravenous vitamin K is only necessary if the patient is bleeding or has an INR greater than 20.
-If the INR is supratherapeutic, but not higher than 5, it is enough to hold the Coumadin or decrease its dose.
-All other cases of excessive anticoagulation with Coumadin can be successfully managed with oral vitamin K
TCA toxicity
-TCA overdose is the leading cause of hospitalization and death. The signs of TCA overdose include hypotension, anticholinergic effects, CNS manifestations, and cardiac arrhythmias.
-Cardiotoxic effects are responsible for most of the mortality in patients with TCA overdose.
-TCAs inhibit fast sodium channels, which result to slowing of the phase 0 depolarization in His-Purkinje tissue and the myocardium.
-This may lead to QRS prolongation and reentrant arrhythmias, like ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
►Sodium bicarbonate is the most effective agent for the management of TCA-induced cardiotoxic effects.
►Lidocaine is the antiarrhythmic drug of choice for TCA-induced ventricular dysrhythmias.
Valvular disorders
-Mitral stenosis is a narrowing of the outflow tract from the left atrium to the left ventricle, resulting in increased pressure in the left atrium, pulmonary vasculature, and right side of the heart.
-It is more common in women, and is most commonly linked to a remote episode of rheumatic fever, though congenital mitral stenosis may be found as well.
-On physical examination, mitral stenosis produces a diastolic thrill palpable over the apex and a low-pitched, rumbling diastolic murmur best heard over the apex when the patient is lying in a left lateral decubitus position.
Mitral regurgitation causes an apical holosystolic murmur, and is most often secondary to myocardial infarction, mitral valve prolapse, rheumatic heart disease, or coronary artery disease.
Aortic stenosis causes a crescendo-decrescendo systolic murmur with a normal S1, a diminished A2, and a paradoxical splitting of S2. It is most often secondary to senile degenerative calcification, or congenital malformation.
An aortic valve area of less than 1.0 cm2 is considered severe stenosis. The onset of symptoms markedly affects the prognosis in patients with aortic stenosis; therefore, prompt intervention is recommended in patients who have cardinal symptoms of aortic stenosis (dyspnea of heart failure, anginal pain, and syncope). Aortic valve replacement is associated with marked reduction in symptoms and mortality in patients with symptomatic aortic stenosis, and is considered the treatment of choice.
Critical aortic stenosis and angina at rest >> Highest risk factors for peri-operative cardiac risk
Aortic insufficiency causes a diastolic murmur best heard adjacent to the sternum in the second to fourth intercostal space. It is most often secondary to infective endocarditis, congenital malformation, connective tissue disorders, or rheumatic heart disease.
Pulmonic stenosis causes a systolic crescendo-decrescendo ejection murmur in the left upper sternal border. It is most often secondary to congenital malformation, rheumatic heart disease, or carcinoid.
COA: This is usually associated with a congenital bicuspid aortic wall.
-In a previously undiagnosed patient, the classic presenting sign is hypertension. Most patients are asymptomatic unless severe hypertension is present, which can lead to headaches, epistaxis, heart failure, or dissecting aneurysm. The major clinical manifestation in children and adults with COA is a difference in the systolic blood pressure between the upper and lower extremities. In most cases, the diastolic blood pressures are similar.
-The classic findings are hypertension in the upper extremities, diminished or delayed femoral pulses, and lower unobtainable arterial blood pressures in the lower extremities.
♦ Magnetic resonance imaging (MRI) is the best noninvasive modality to diagnose COA because it can usually clearly define the location of severe coarctation of the aorta. MRI can also detect associated cardiac abnormalities and can be used for serial follow-up after surgical repair or balloon angioplasty.
Delirium
-Acute infections are a common cause of delirium, especially in elderly patients being admitted to the hospital. An important goal of treatment in such patients is to avoid the use of medications that can potentially worsen the acute delirious state.
-Diuretics, ACE inhibitors, spironolactone, beta-blockers, and digoxin are all a part of standard therapy for patients with heart failure or cardiomyopathy due to any cause. ACE inhibitors (lisinopril) have consistently been shown in multiple, large, randomized trials to have a significant beneficial effect on patients with heart failure. They have a very low incidence of central nervous system (CNS) side effects, and do not cause worsening of confusional states or delirium. Lisinopril can be safely started in this patient without the risk of exacerbating his confusion and agitation.
-Digoxin is a cardiac glycoside frequently used in patients with congestive heart failure due to systolic dysfunction and atrial dysrhythmias; however, its use has been associated with significant CNS side effects.
-These include blurred vision, dizziness, confusion, mental disturbances, anxiety, delirium, and hallucinations. Its use should be avoided in patients with ongoing acute mental confusion or delirium.
-Spironolactone is a useful adjunct in the management of patients with congestive heart failure, especially in patients with a low ejection fraction; however, its use can also cause CNS disturbances such as drowsiness, lethargy, and mental confusion.
♥Digoxin toxicity is characterized by nausea, vomiting, anorexia, fatigue, confusion, visual disturbances, and cardiac abnormalities. Verapamil, quinidine, and amiodarone can potentially cause digoxin toxicity.
Syncope
Vasovagal syncope is associated with prodromal symptoms of nausea, lightheadedness, pallor and diaphoresis. It usually occurs when the patient is erect, and recovery occurs in the supine position. Patients are usually young and otherwise healthy. Precipitating events include prolonged standing, exertion, venipuncture, or a painful stimulus.
-Cardiovascular syncope is due to arrhythmia or obstructive lesions such as aortic stenosis or HOCM.
-Syncope may be associated with a prodrome of palpitations. Arrhythmias usually occur without warning, with the patient in a supine or resting position, and lasts for a few seconds. Patients will have risk factors such as left ventricular dysfunction, prior myocardial infarction or conduction system disease.
-Physical examination may show the murmur of aortic stenosis or HOCM. EKG/Holter monitoring may detect an arrhythmia.
-Neurological syncope is due to atherosclerotic disease of the cerebral circulation, and is associated with a history of focal neurological deficits.
DDX: A seizure may mimic syncope; however, patients usually have a history of tonic-clonic movements, urinary or fecal incontinence, and a postictal state. Jerky movements similar to tonic-clonic movements can occur in any patient with syncope, but the postictal confusion is very unlikely with other conditions except seizures.
Orthostatic hypotension
Orthostatic hypotension is defined as a significant drop in blood pressure upon assuming a standing position, causing symptoms of cerebral hypoperfusion. Orthostatic hypotension is diagnosed if there is a fall of at least 20 mmHg of systolic blood pressure, or a fall of at least 10 mmHg of diastolic blood pressure, within two to five minutes of standing from a supine or sitting position.
-A fall in the blood pressure with/after standing or eating (postprandial hypotension) is a commonly encountered clinical situation, especially in the elderly population. It is usually caused by autonomic dysfunction or failure, or intravascular volume depletion from various causes.
-Almost all the patients suffering from orthostatic hypotension experience a sensation of dizziness or lightheadedness, especially after rapid changes in position (i.e. from supine or sitting to standing position). In some severe cases, it can lead to a fall (presyncope), angina, acute stroke, or loss of consciousness (syncope).
-The symptoms of orthostatic hypotension are primarily caused by a rapid decrease in cerebral perfusion.
-There are multiple causes of orthostatic hypotension in elderly patients>>The two major mechanisms of orthostatic hypotension are autonomic dysfunction/failure and intravascular volume depletion. Autonomic dysfunction is caused by various neurological disorders, systemic disorders (diabetes mellitus, amyloid neuropathy) or medications. Common drugs causing orthostatic hypotension include antihypertensives, antianginal drugs, vasodilators (nitrates, calcium channel blockers), antidepressants (especially tricyclic antidepressants), and opiate analgesics.
-When a patient stands up from a supine position, there is pooling of 500 to 1000 cc of blood in the lower extremities and mesenteric circulation. This causes a decrease in the venous return to the heart, which decreases ventricular filling pressures. A drop in the cardiac output and blood pressure occurs, causing decreased cerebral perfusion. This is a normal response seen in all patients, and is counteracted by a reflex increase in sympathetic discharge, which causes vasoconstriction and an increase in cardiac output. Nitrates may cause excess vasodilation, which could reduce the venous return to and cardiac output of the heart.
-An excess drop in blood pressure and cerebral perfusion may occur, and lead to symptoms of orthostatic hypotension.
-RX->>
>>The first step in reducing the frequency and symptoms of orthostatic hypotension is to recognize and remove the potential offending medications; therefore, isosorbide nitrate should be discontinued, and the patient should be observed for any recurrence of symptoms.
>>Fludrocortisone is a synthetic mineralocorticoid. It is used as a first-line agent for most patients whose orthostatic hypotension is not controlled by nonpharmacologic measures. It causes an increase in salt and water retention, which increases the effective circulating blood volume.
Cardiac temponade
Pericardial effusion may occur in response to any cause of pericarditis or from malignancies. The pericardial effusion may develop slowly or rapidly. However, sudden filling of the pericardial space with fluid can have catastrophic consequences by limiting ventricular filling.
-Patients with pericardial tamponade often complain of shortness of breath. It is accompanied by typical physical signs and symptoms that arise from the limited filling of the ventricle. The classic Beck’s triad is hypotension, muffled or distant heart sounds, and elevated jugular venous pressure. Arterial systolic blood pressure normally drops 10 -12 mmHg with inspiration.
-Marked inspiratory drop in systolic blood pressure (> 20 mmHg) is an important physical finding in cardiac tamponade, but can also be seen in severe obstructive pulmonary disease and constrictive pericarditis. In pericardial tamponade, low limb voltage with alternating size of QRS complex due to swinging of the heart is seen.
♦CXR in cardiac tamponade will show an enlarged cardiac silhouette. When a chest
x-ray shows an enlarged heart with pulmonary edema, congestive heart failure should be suspected. In cardiac tamponade, usually, there is no pulmonary edema.
Cardiac tamponade is a surgical emergency, and an ECHO should be obtained urgently. The ECHO will reveal the large pericardial effusion, with prominent collapse of the right atrium and ventricle during diastole. Cardiac catheterization can confirm the diagnosis by showing equalization of diastolic pressures in all chambers. However, if the patient is collapsing, one should not wait for an ECHO. Rapid pericardiocentesis is life saving.
Mechanical valves
The following are the recommendations from the Sixth ACCP Consensus Conference for a mechanical valve:
A goal INR of 2.5 (range 2 to 3) is recommended for patients with AVR with bileaflet mechanical valve, provided that the patient is in sinus rhythm, left atrium is of normal size, and the left ventricular ejection fraction is normal, as in this patient.
A goal INR of 3 (range 2.5 to 3.5) is recommended for patients with MVR with bileaflet mechanical valve or for patients with a bileaflet mechanical aortic valve who have atrial fibrillation
A goal INR of 3 (range 2.5 to 3.5) in combination with low dose aspirin is recommended for patients with mechanical prosthetic valves who suffer a systemic embolism despite adequate anticoagulant therapy.
However, more data is coming in favor of a higher level of anticoagulation (target INR >3.0) for both aortic and mitral prosthetic mechanical valve
Respiratory
TB
Even though it is not common, a new pleural effusion in a patient already on anti-tuberculosis treatment may occur and must be studied, because this can progress despite the clinical improvement of the patient. There is no need to change therapy, unless there is proof of a new infection or drug resistance. Some authors advocate the use of steroids in this setting, but this is not a universally accepted practice.
Chronic Eosinophilic Pneumonia (CEP)
Chronic Eosinophilic Pneumonia (CEP) is the most common eosinophilic pneumonia in the USA. Patients with chronic eosinophilic pneumonia present with systemic symptoms such as fever, malaise, anorexia, and weight loss for several weeks to months.
Pulmonary symptoms include cough and breathlessness.
Sometimes, patients may give a history of bronchial asthma or allergic rhinitis.
-Chest auscultation shows crackles or wheezing.
-Chest x-ray reveals peripheral infiltrates that are the "photographic negative" of pulmonary edema, and this radiographic finding is pathognomonic for the disease.
♥Bronchoalveolar lavage (BAL) that reveals eosinophils greater than 40% is suggestive of the diagnosis. Glucocorticoid therapy results in rapid resolution of the symptoms and radiographic clearing.
Acute bronchopulmonary aspergillosis ABPA:
This hypersensitivity reaction to Aspergillus antigens is seen in patients with underlying asthma. When the airways of such patients become colonized with Aspergillus, the intense IgE and IgG mediated immune response leads to the characteristic recurrent episodes of fever, malaise, cough with brownish mucoid expectoration, wheezing, and symptoms of bronchial obstruction.
There is no single diagnostic test to confirm the diagnosis of ABPA.
►The diagnosis is usually made by clinical, radiographic, and immunologic criteria, which include the following:
1. A history of asthma.
2. Immediate skin test reactivity to Aspergillus antigen.
3. Precipitating serum antibodies to Aspergillus fumigatus.
4. Serum total IgE concentration of greater than 1000 ng/mL.
5. Peripheral blood eosinophilia greater than 500 per cubic millimeter.
6. Lung infiltrates, usually involving the upper lobes.
7. Central bronchiectasis.
==A skin prick test for Aspergillus should be performed initially in all asthmatic patients suspected of having ABPA.
If the skin prick test is positive, serum total IgE levels and precipitating serum antibodies to Aspergillus fumigatus should be measured. If the skin prick test is negative, the diagnosis of ABPA is extremely unlikely.
Recurrent episodes of airway inflammation and bronchial obstruction in patients with ABPA can lead to bronchiectasis and lung fibrosis; therefore, it is important to diagnose and treat such patients early to reduce the risk of progressive lung damage.
Corticosteroids are the mainstay of therapy for patients with ABPA.
Treatment with corticosteroids is effective in controlling the episodes of acute inflammation and preventing progressive lung fibrosis.
The clinical response to treatment is measured by the reduction of serum total IgE concentration, clinical improvement and resolution of radiographic findings.
Churg Strauss syndrome (CCS): is a multisystem vasculitic disorder of unknown etiology that affects the skin, kidney, nervous system, lungs, gastrointestinal tract, and heart. It is characterized by allergic rhinitis, asthma, and prominent peripheral blood eosinophilia.
A CSS-like syndrome has been noted in patients who have been successfully treated for chronic steroid-dependent asthma with leukotriene receptor antagonists.
Up to 75% of the patients have evidence of peripheral neuropathy. The disease is severe, and requires treatment with glucocorticoids and sometimes with immunosuppressants. There have been significant reports which associate the use of leukotriene inhibitors with Churg-Strauss vasculitis. To date, there are more than 28 cases of Churg Strauss vasculitis associated with its use.
ARDS:
ARDS can occur secondary to sepsis, pneumonia, severe trauma, burns, drowning, or pancreatitis. The presentation is sudden. Oxygen requirements increase very rapidly.
Criteria for ARDS diagnosis are:
1. A pulmonary capillary wedge pressure less than 18 mmHg
2. PaO2 to FiO2 ratio of 200 mmHg or less, regardless of the PEEP level
3. Diffuse bilateral infiltrates on chest x-ray
In contrast to heart failure, patients with ARDS will typically have clear lungs on exam but will show diffuse, bilateral infiltrates on the chest x-ray results.
The management of ARDS through mechanical ventilation involves the interplay of the following settings:
1. PEEP (positive pressure at the end of expiration)
2. oxygen concentration
3. tidal volume
The PEEP attempts to expand the collapsed alveoli in ARDS in order to decrease the high oxygen requirement. It also prevents the development of atelectasis.
Although the physiologic PEEP is around 5 cmH2O, the mechanical ventilator settings of ARDS patients are usually around 9 cmH2O. Oxygen is set at high concentrations, while the tidal volume is set to the lowest possible value.
ARDS is associated with a mortality rate of 35-40%. Among the different strategies, mechanical ventilation that delivers lower tidal volumes (< 6 ml/kg) and limits plateau pressure (< 30 CmH2O) has been shown to be relatively more effective.
Studies comparing the effects of low tidal volume and limited plateau pressure to that of high tidal volume and plateau pressure have shown a significant reduction in mortality in the first group (32% vs. 40%).
Mechanical ventilation in the management of ARDS is a dynamic process.
When the patient improves, FiO2 and PEEP should be decreased stepwise, as tolerated.
The objective is to maintain the patient on the following settings: a PaO2 more than 60mmHg, an oxygen saturation more than 90%, and a normal or slightly acidic pH (permissive hypercapnia).
Once this is achieved, the patient should be weaned as soon as possible, in order to avoid complications such as barotrauma, ventilator-associated pneumonia, prolonged sedation, and hypotension.
PE:
Pulmonary thromboembolism is difficult to diagnose, and usually requires the combination of several diagnostic modalities. It is therefore important to know the order in which to order these diagnostic tests.
=The first test that is usually employed is ventilation/perfusion scanning.
►If the results reveal the classic pattern of mismatched perfusion; it is advisable to proceed directly with treatment.
►If the scan is normal, significant pulmonary thromboembolism should be ruled out; however, ventilation/perfusion scanning results are inconclusive in a substantial number of patients. Since the usual source of emboli causing this condition is deep venous thrombosis (DVT) of the lower extremities, ►the next best step in this case is Venous ultrasonography to reveal DVT or CT angiogram of the chest. A diagnosis of DVT makes the probability of pulmonary thromboembolism very high, and warrants immediate treatment.
►Pulmonary angiogram is the gold standard test for the diagnosis of pulmonary embolism (PE); however, this procedure is rarely being performed since it is invasive and CT angiogram is readily available.
♥ Mild fever and leukocytosis can be seen in the setting of PE.
-Pulmonary embolism (PE) is generally treated by starting the patient on heparin first, and then adding warfarin (Coumadin) after 24-48 hours.
The recommended duration of pharmacotherapy depends on the setting in which the PE occurred, as indicated below:
1. Occurrence of PE in the setting of reversible risk factors (e.g., use of oral contraceptive pills, immobilization, or surgery) should be treated with 3-6 months of warfarin therapy.
2. If the first episode of thromboembolism occurs in a setting that involves an underlying malignancy, anticardiolipin antibody, and antithrombin deficiency, the patient should be treated with at least 12 months of warfarin therapy.
3. Patients with a first episode of idiopathic thromboembolism should be treated for at least six months with warfarin; three months of therapy is inadequate in this patient group.
4. Patients with recurrent thromboembolism or a continuing risk factor should be treated indefinitely.
The indications for an inferior vena caval (IVC) or Greenfield filter insertion include patients with:
1. a documented recurrent venous thromboembolism while on therapeutic anticoagulation
2. a recurrent venous thromboembolism and absolute contraindications to anticoagulation
3. a history of massive pulmonary embolism in whom a recurrent episode may be life-threatening
4. Chronic recurrent pulmonary embolism and a history of pulmonary hypertension
►It is also considered prophylactically in patients with severe chronic obstructive pulmonary disease, cor pulmonale, or a previous history of venous thromboembolism who develop a predisposing risk factor for pulmonary embolism, such as an acute fracture or cancer.
►A chest x-ray should be obtained in all post-operative patients who complain of shortness of breath before performing more specific tests that will determine or exclude the diagnosis of PE. Chest x-ray findings may suggest the presence of PE and may help exclude other chest pathology.
►Septic pulmonary emboli may result from septic thrombophlebitis and/or tricuspid endocarditis.
Asthma:
♫ the allergen most frequently associated with asthma is house dust mites.
♥Cough induced by forced expiration is characteristic of airway hyperreactivity, and is usually suggestive of asthma; however, this presentation has also been described in some patients with COPD who can occasionally have an overlapping condition with asthma.
♥It is important to recognize and initiate early interventions in a patient with acute exacerbation of asthma. Early recognition, rapid assessment and treatment are crucial in preventing significant morbidity and mortality.
♥Measurement of the peak expiratory flow rate with a peak flow meter is an excellent method to assess the degree of severity of airflow limitation, and subsequent serial measurements of the peak flow rate are useful in assessing the response to therapy.
►The goal of treatment is to rapidly correct the airflow obstruction. This is most rapidly achieved by the administration of inhaled beta-2 adrenergic agonists, either by continuous nebulization or with the use of metered dose inhalers with a spacer.
►Systemic corticosteroids should also be administered early in the treatment of acute asthmatic exacerbation; however, their effect is usually not apparent in the first few hours. Their use should be preceded or accompanied by inhaled beta-2 agonist therapy.
♥In a patient with an acute, severe, asthma exacerbation, it is important to periodically assess the response to initial therapy during the first few hours. Failure to recognize early signs of clinical deterioration and impending respiratory failure is responsible for majority of the morbidity and mortality seen in patients with status asthmaticus.
♥Some of the clues to a patients clinical deterioration and poor outcome include a history of prior intubation, exhaustion or extreme fatigue, diaphoresis, change in consciousness (confusion and drowsiness), use of accessory muscles, presence of suprasternal retractions, depressed respiratory drive, marked tachycardia, pulsus paradoxus, PaCO2 greater than 40 mmHg, and a peak expiratory flow rate less than 25% of the normal predicted.
►Any patient with the above signs and symptoms of impending respiratory failure should be immediately intubated to secure and protect the airways.
Patients with hypoxemia due to an acute asthma exacerbation should be immediately managed with oxygen inhalation, followed by administration of an inhaled beta-2 agonist, which is the mainstay of therapy.
►Hospital admission for asthma exacerbation is recommended if the peak flow reading is 40-50% lower than the patient’s baseline, if there are signs of respiratory distress, if oral steroid therapy fails, or if the patient’s clinical condition worsens. Ipratropium nebulization may be given in the emergency department, but this is not the mainstay of therapy. For any acute exacerbation, oral or parenteral steroid therapy with prednisone, prednisolone, methylprednisolone, or hydrocortisone is essential for therapeutic success.
Solitary pulmonary nodule
Solitary pulmonary nodules represent a common clinical problem in the primary care setting. They are usually detected in an asymptomatic patient and present a clinical dilemma for the primary care physician.
The clinical and diagnostic workup of a solitary pulmonary nodule is aimed towards differentiating between a benign lesion from a malignant lesion (lung cancer).
►Some of the factors that suggest a malignant cause of a solitary pulmonary nodule include:
Age greater than 50 years,
History of smoking or asbestos exposure, presence of another primary cancer elsewhere in the body (malignant melanoma, colon, breast, kidney, testis),
Size greater than 3 cm, irregular or speculated borders of the nodule, and certain patterns of calcification within the lesion (eccentric calcification).
Another important clue is the growth of the pulmonary lesion over time.
Malignant lesions usually have a doubling time of 20-400 days, whereas the doubling time of benign lesions is either less than 20 days (infectious cause) or greater than 450 days.
►As a general guideline, any solitary pulmonary nodule with the absence of any changes in size over the last two years is strongly suggestive of a benign lesion; therefore, a comparison of the pulmonary nodule on chest x-ray with the previous chest radiographs to document any changes in the size of the lesion is a critical initial part of the diagnostic workup of this patient.
►A chest CT scan should be obtained to characterize the pulmonary nodule before performing any invasive procedures. It demonstrates the pattern of calcification within the nodule, and identifies any mediastinal lymph node involvement and small pleural effusions. Particular CT scan findings that suggest malignant lesions include an irregular or speculated border and the presence of eccentric, reticular or punctate calcifications within the lesion. Such findings can help distinguish between a benign from a malignant cause of the solitary nodule.
►BENIGN: Certain patterns of calcification within the pulmonary nodule, as seen on chest x-ray or CT scan, are strongly suggestive of a benign cause of the lesion or nodule. These include popcorn calcifications, concentric or laminated calcifications, central calcifications and diffuse homogenous calcifications. Popcorn calcifications are characteristically seen on radiographic imaging in patients with pulmonary hamartoma.
►Any patient with a solitary peripheral lung nodule suspicious for malignancy should undergo video-assisted thoracoscopic surgery (VATS) and excisional biopsy of the lesion. This is the procedure of choice in most patients for the removal and definite diagnosis of a peripherally located pulmonary nodule. It is a relatively safe procedure and has a low risk of complications if performed by a skilled surgeon.
Sarcoidosis
Sarcoidosis is a chronic granulomatous disease seen more frequently in young African-American patients. It is characterized by the formation of non-caseating granulomas in various involved tissues and organs. It usually involves the lungs, but can also involve other organ systems including the skin, lymph nodes, liver, spleen, eyes, exocrine glands (salivary and lacrimal glands), heart, kidneys, and central nervous system. It is usually asymptomatic and is frequently detected as an incidental finding on a routine chest x-ray.
Patients with pulmonary sarcoidosis usually present with cough, chest pain, or dyspnea. Some other nonspecific features include generalized weakness, lethargy, fever, and weight loss.
-Sarcoidosis- Initial test/screening:
-The chest radiograph in patients with pulmonary sarcoidosis classically reveals
Bilateral hilar adenopathy with or without right paratracheal lymph node enlargement
Serum ACE levels are elevated [screening test] in more than half of the patients with sarcoidosis, but this is a nonspecific finding. Although serum ACE levels have little role in diagnosing the disease, these may prove to be useful in monitoring disease activity
CONFIRMATORY TESTS:
-The biopsy of accessible tissues [not erythema nudosum] for confirmation of the diagnosis is not required in an asymptomatic patient with the typical history and chest x-ray findings.
-Hypercalciuria occurs in 50% of cases of sarcoidosis. Macrophages in the sarcoid granulomas produce calcitriol, which is the active form of vitamin D, and as a result, calcium absorption from the gut increases.
-Nephrocalcinosis may result in chronic renal failure (CRF) and end stage renal disease.
-Hypercalcemia occurs in 10-20% of cases of sarcoidosis [high vitamin D].
-Thrombocytopenia may occur in patients with sarcoidosis.
►Definitive diagnosis of sarcoidosis can be made from the biopsy of the easily accessible lesions, including:
1. Any palpable lymph node
2. Skin lesion [except erythema nodosum]
3. Enlarged parotid
4. Lacrimal glands
NEXT STEP IF NOT ACCESSIBLE LESION ►LUNG BIOPSY with fiberoptic bronchoscopy and transbronchial lung biopsy is the procedure of choice.
•Nerve and liver biopsies are not recommended unless all other approaches fail.
♥Hypercalcemia, non-caseating granulomas, depressed-cell mediated immunity, and activated humoral immunity are characteristic features of sarcoidosis.
♥Asymptomatic pulmonary sarcoidosis generally does not need treatment.
-Hilar adenopathy associated with erythema nodosum represents a very favorable variant of sarcoidosis that is associated with a high rate of spontaneous remission and good prognosis.
♥Symptomatic pulmonary disease is usually an indication for corticosteroid therapy in patients with sarcoidosis, especially if it is accompanied by systemic symptoms such as severe fatigue, fever and hypercalcemia. Severe extrapulmonary manifestations of sarcoidosis such as cardiac, ocular and neurologic involvement may require high-dose corticosteroid therapy.
-Alternative agents (e.g. methotrexate) may be indicated if corticosteroids are not effective or if intolerable side effects of corticosteroid therapy occur.
OSA:
Although there are no specific physical findings consistent with obstructive sleep apnea (OSA), some general observations can contribute to the diagnosis. Truncal obesity and a large neck circumference (collar size > 17.5 inches) are common, and the oropharynx may be visibly "crowded." In some patients, the uvula is enlarged.
-Systemic hypertension is seen in approximately half of the patients with OSA.
-Hypothyroidism should be screened for, especially in older patients or those with symptoms suggestive of hypothyroidism (e.g., constipation and hair loss, as seen in this patient). Therefore, physical examination and thyroid function testing should be performed next.
-Sleep studies are typically performed to confirm the diagnosis of OSA.
-Polysomnography in particular is considered the gold standard for diagnosis.
-After completing the physical and laboratory evaluation of the patient, polysomnography is indicated.
PPH:
►The diagnosis of primary pulmonary hypertension is made when there is evidence of increased pulmonary arterial pressure in the absence of other identifiable causes.
-Pulmonary hypertension may be primary or secondary to interstitial lung disease, chronic venous thromboembolism, valvular or myocardial disease, connective tissue disease, or congenital heart disease.
-All patients with primary pulmonary hypertension should receive anticoagulation therapy because of an increased risk of pulmonary thromboembolism. This increased risk is due to slow pulmonary blood flow, a dilated right heart, and venous stasis.
-The anticoagulant of choice for this purpose is warfarin, and a target INR of 2 should be achieved.
-Oral vasodilators prolong survival and provide hemodynamic and clinical benefit in those patients of primary pulmonary hypertension who show vasoreactivity to nitric oxide and other vasodilators.
Patients who do not show vasoreactivity may experience an acute cardiopulmonary decompensation if oral vasodilators are used. It is therefore recommended that all patients with primary pulmonary hypertension be tested for vasoreactivity before starting therapy with oral vasodilators.
==Untreated primary pulmonary hypertension ►can lead to cor pulmonale.
COPD:
It is important to recognize that some patients with COPD will be oxygen dependent at some point of their disease. Oxygen therapy in this setting will decrease mortality and delay the development of pulmonary hypertension or cor pulmonale as a consequence of chronic hypoxia.
►The current recommendations to use home oxygen therapy are:
1. PaO2 less than or equal to 55 mmHg or an arterial oxygen saturation (SaO2) less than or equal to 88 percent.
2. PaO2 between 56 to 59 mmHg (or) a SaO2 of 89 percent, if there is evidence of cor pulmonale, right heart failure, or erythrocytosis (hematocrit above 55 percent).
HY:
♥Recurrent pneumonia in an elderly smoker may be the first manifestation of bronchogenic carcinoma.
►Flexible bronchoscopy is a primary diagnostic tool to evaluate patients with persistent or nonresolving pneumonia or pulmonary infiltrates (HRCT scan is an alternative, but it does not provide confirmatory information).
►The best diagnostic test for endobronchial obstructive lesions is flexible bronchoscopy. If the question had asked for the next best step in management, then the answer would have been CT scan.
►Syndrome of inappropriate antidiuretic hormone (SIADH) is associated with normovolemic hyponatremia and can be caused by small cell carcinoma of the lung.
Water restriction (with the possible inclusion of salt administration) is the preferred means of correcting mild to moderate hyponatremia associated with SIADH.
♥Postoperative complications:
-Are a common cause of perioperative morbidity and mortality. Some of the factors that increase the risk of developing postoperative complications are upper abdominal and thoracic surgeries, underlying chronic lung disease, a history of smoking within the last eight weeks, baseline PaCO2 > 45 mmHg, duration of surgery of more than 3-4 hours, and the use of general anesthesia.
♥The most common complications include atelectasis, bronchospasm, worsening of the underlying lung disease, postoperative pneumonia, and prolonged need for mechanical ventilation.
♥All patients undergoing upper abdominal or thoracic surgery with one or more additional risk factors are at a high risk for postoperative complications. These patients should be the target of risk reduction strategies. Antibiotics should be given prior to surgery only in patients with clinically apparent respiratory infection. These include patients with purulent sputum or a recent change in the color of the sputum.
They should not be used routinely in stable COPD patients.
Silicosis:
Is pneumoconiosis caused by exposure to silica crystals.
-There are three patterns of disease: acute, accelerated, and chronic silicosis. High-risk professions include glass maki
Cardiology
CAD
Multiple risk factors increase the risk of acute CAD.
The risk can be significantly reduced by decreasing LDL cholesterol and, to a lesser degree, by adequately controlling the blood pressure (in diabetic patients, as well as in patients with previous CAD, a blood pressure lower than 130/80 mmHg is recommended). The contribution of other interventions such as smoking cessation, diabetes control, exercise, and HDL increase is also beneficial, but not as critical as the first two measures.
♥In patients with hypercholesterolemia and hypertriglyceridemia ► a statin is the best initial drug of choice. The primary target of therapy is normalizing LDL-cholesterol; the secondary target is normalizing non-HDL cholesterol(total cholesterol – HDL cholesterol).
♥If the statin fails to control hypertriglyceridemia► gemfibrozil or niacin can be added.
In prospective studies of healthy patients, those with higher plasma fibrinogen concentrations developed coronary heart disease more frequently. Fibrinogen levels decrease only 20 years after smoking cessation; while certain drugs such as atorvastatin and lovastatin can produce hyperfibrinogenemia. Even though it is uncertain how dangerous hyperfibrinogenemia can be, it is currently recommended to maintain fibrinogen levels as low as possible and to discontinue any medication that can increase them, unless the benefits outweigh the risks.
Exercise electrocardiography should be the initial test of choice for evaluation of suspected CAD in patients with a normal resting EKG and the ability to exercise.
Exercise stress testing is useful for the diagnosis and risk stratification of patients with stable angina. Exercise testing is useful to identify a high-risk group that will benefit from coronary angiography.
♥Patients at high risk have one of the following findings on exercise testing:
1. failure to increase their blood pressure with exercise
2. Inability to complete stage I of Bruce protocols
3. Appearance of horizontal or down sloping ST segment during exercise
♥Pharmacological stress testing is an alternative to exercise stress testing, and is indicated in the setting of CAD, when the patient is unable to exercise due to some underlying medical disorder (amputation), when an exercise stress test is relatively contraindicated (MI, unstable angina), or in patients in whom interpretation of an EKG is difficult because of preexisting changes, such as left bundle branch block, baseline ST/T changes from left ventricular hypertrophy, etc.
♠Both adenosine and dipyridamole scans are contraindicated in patients with COPD because they can induce bronchospasm.
♥The American College of Cardiology/American Heart Association (ACC/AHA) defines a positive exercise stress test as ►1 mm or more of down sloping or flat ST segment depression during exercise or during the recovery period.
♥Exercise echocardiography is more sensitive than the resting echocardiogram or stress EKG, and is also commonly done in patients with stable angina.
♥Resting echocardiography or EKG is useless in stable angina when the patient has no active chest pain.
-Principles and practice of stress testing are based on the relative development of manifestations of myocardial ischemia as the stress to the myocardium is increased. Regional wall motion defects are the first to appear (detected by stress echocardiography). This is followed by significant perfusion defects (detected by perfusion scans), pulmonary capillary wedge elevation, ST segment changes on electrocardiogram, and finally, anginal pain.
-Stress imaging should therefore be pursued if there are no EKG changes during or after the stress test. It is also the modality of choice in patients with bundle branch block, WPW syndrome, paced ventricular rhythm, and baseline ST changes before exercise (ventricular hypertrophy, digitalis therapy, etc.). A positive stress test result in a patient with symptoms warrants further intervention, preferably with a coronary angiogram.
-Nuclear scans should be performed in subsets of patients with baseline ST segment changes.
-It is important to recognize the advantages and limitations of different available testing modalities for the evaluation of myocardial ischemia.
--Adenosine, along with dipyridamole and dobutamine, is one of the most frequently used pharmacologic agents to induce ischemia in patients with poor functional status.
--Sestamibi test is one of the three available technetium-99m labeled tracers used frequently for radionuclide imaging.
-In patients with angina and a prior history of revascularization (PTCA or CABG), technetium-99m (sestamibi) and thallium perfusion imaging are the two types of radionuclide perfusion imaging modalities used for characterizing the ischemia, establishing the functional effects of lesions, and determining the viability of myocardium.
-The two modalities are also used in patients with complete left bundle branch block (LBBB), electronically-paced ventricular rhythm, preexcitation (WPW) syndromes, > 1 mm ST segment depression at rest, LVH with repolarization changes, and in patients who are unable to exercise.
♥Coronary angiography is indicated in the setting of stable angina pectoris when the angina is refractory to medical treatment, or when exercise testing identifies the patient as high-risk.
►Studies have shown that compared to angioplasty, Coronary artery bypass graft (CABG) improves long-term survival in diabetic patients with multivessel disease and recent Q-wave infarction.
-Good, perioperative control of the blood glucose levels is advocated during CABG. An insulin drip achieves better blood glucose control during CABG, and decreases the incidence of sternotomy wound infections.
-According to the ACC/AHA guidelines, patients who are unable or unfit to exercise should undergo adenosine or dipyridamole myocardial perfusion imaging for the diagnosis and risk stratification of CAD. Adenosine, along with dipyridamole and dobutamine, is one of the most frequently used pharmacologic agents to induce ischemia in patients with poor functional status.
►All patients with chronic stable angina should undergo an exercise stress test for prognostic and risk stratification.
►All patients with coronary artery disease and stable angina should be referred for an exercise stress test for further risk stratification.
♥Patients with a low risk treadmill score (able to exercise more with a normal EKG) have less than 1% annual mortality rate.
♥On the other hand, patients who have a high-risk treadmill score (presence of chest pain or EKG changes with minimal exercise) have greater than 3% annual mortality rate and require more aggressive management.
►Metformin use is contraindicated in patients with renal failure, sepsis, hepatic dysfunction, and severe heart failure. It should also be stopped in patients who are at risk to develop renal failure, such as those who will undergo angiography, a procedure that involves infusion of a high load of contrast agent
►In patients whose chest pain may be ischemic in origin, supplemental oxygen and ASA aspirin should be administered immediately, followed by Nitroglycerin, Morphine, and Beta-blockers (presuming no contraindications exist).
►Calcium channel blockers can be harmful in patients with acute MI.
►Beta blockers, ACE inhibitors, and statins have significant effects on the secondary prevention of coronary artery disease, and should be continued indefinitely unless absolutely contraindicated.
►The only indications of calcium channel blockers in the setting of acute myocardial infarction include:
♥Intolerance to beta blockers, post-infarction angina refractory to beta blockers and nitrates, and rapid atrial fibrillation with contraindications to beta-blocker use (COPD, pulm. disease)
♠Peripheral edema is a well-known side effect of calcium antagonist therapy. It is more common with dihydropyridine agents (e.g. nifedipine, amlodipine), but also occurs in 2 to 15% of patients taking diltiazem [cardizem]. The exact mechanism of calcium antagonist-associated edema is not known; arteriolar dilatation seems to be responsible for increased interstitial fluid accumulation in these patients
Acute pericarditis
Acute pericarditis (infarct associated or infarction pericarditis) can occur within one to four days as a direct complication of a transmural myocardial infarction. The recurrence of chest pain three days after a myocardial infarction, which gets worse with position changes and deep inspiration, is suggestive of infarction pericarditis. It is usually a clinical diagnosis, and is supported by the presence of pericardial friction rub and EKG changes of pericarditis (sinus tachycardia, diffuse ST segment elevations with PR segment depression).
-A pericardial rub is usually heard over the left sternal border and can be present during any of the phases of the cardiac cycle. It is heard as a superficial scratchy or grating sound, which gets more pronounced when the patient leans forward.
-The EKG changes of pericarditis are not always seen, but usually resemble that of an acute myocardial infarction.
Infarction pericarditis
-Is seen less frequently in patients with early and complete reperfusion. It is usually a transient episode and does not affect the management of acute myocardial infarction, unless it is complicated by a large pericardial effusion or tamponade.
>>It should be managed with close clinical observation and adequate pain control.
>>Nonsteroidal anti-inflammatory medications (NSAIDs) are effective in alleviating the pain associated with acute pericardial inflammation, although there are some concerns that they may increase the risk of myocardial rupture after a transmural MI.
D/DX:
1. Chordae tendineae or papillary muscle rupture is a life threatening mechanical complication of an acute myocardial infarction. It usually occurs two to seven days after the infarction and causes acute hemodynamic instability. Patients also develop acute pulmonary edema.
2. Dressler’s syndrome, or post-cardiac injury syndrome, occurs in patients with myocardial infarction and after cardiac surgery. It is an autoimmune mediated syndrome, which usually develops weeks to months after an acute MI. It usually presents with fever, leukocytosis, pleuritic chest pain, and a pericardial rub.
3. A left ventricular aneurysm usually occurs as a late complication of a transmural myocardial infarction (usually a large anterior wall MI). It may result in heart failure, ventricular arrhythmias, or peripheral arterial embolization due to the formation of a left ventricular thrombus. It develops over a longer period of time, and is usually not associated with chest pain. Persistent ST elevation can be present in these patients.
►Sinus bradycardia is commonly seen as a complication of an inferior wall myocardial infarction.
-It is usually present transiently, immediately after or within the first six hours, and resolves within 24 to 48 hours of acute myocardial infarction. Most of the episodes are asymptomatic, and resolve without any therapy or intervention.
>>BUT: Active intervention is required in patients with sinus bradycardia after myocardial infarction, if the patient exhibits signs and symptoms of hemodynamic compromise.
>>The definite treatment is by reperfusion of the infarcted myocardium, either with thrombolysis or percutaneous transluminal coronary angioplasty (PTCA).
>>If bradycardia persists after reperfusion, the patients can still respond to the administration of intravenous Atropine.
>>VERY HD UNSTABLE: Temporary transvenous cardiac pacing is usually required in patients with persistent bradycardia and hemodynamic instability after myocardial infarction, despite the above measures.
►Recent myocardial infarction and atrial fibrillation are two most common causes of arterial thromboembolism.
►The single most important step in the early management of the patients with acute arterial occlusion diagnosed by history and physical examination is immediate IV heparin therapy followed by continuous heparin infusion.
►Heparin therapy will prevent further propagation of thrombus, and inhibit thrombosis distally in the arterial and venous systems due to low flow and stasis.
♥An important issue for many patients after a myocardial infarction is when sexual activity can be safely resumed
-Therefore, this should be addressed in all sexually active patients before hospital discharge.
-A consensus panel concluded that patients resuming sexual activity 6 weeks after an uncomplicated myocardial infarction are at low risk for future myocardial events.
On the other hand, those resuming sexual activity within six weeks are at intermediate risk, and those resuming activity within two weeks are at high risk.
•Patients with complications such as post-infarction chest pain, evidence of arrhythmias, or heart failure are also at intermediate or high risk
•Patients at intermediate risk should receive further evaluation and subsequent reclassification into the low-risk or high-risk category, while patients at high risk should be stabilized with appropriate therapy before resuming sexual activity.
•Consultation with a cardiologist prior to resuming sexual activity is recommended in all high-risk patients
Radionuclide ventriculography [RVG]
-The anthracyclines (doxorubicin, daunorubicin, idarubicin, epirubicin, and mitoxantrone) are the most common cause of cardiovascular complications in cancer patients.
-Patients who are about to receive such cardiotoxic chemotherapy are therefore recommended to undergo baseline testing and serial reevaluation of systolic function to identify early signs of cardiotoxicity.
-Noninvasive serial monitoring of cardiac function with radionuclide ventriculography (RVG) has been the most effective way to detect early toxicity and reduce the risk of anthracycline toxicity.
-Radionuclide ventriculography [also known as radionuclide angiography (RNA) or multiple-gated cardiac blood pool imaging (MUGA scan)] is performed by labeling a patient’s red cells with a radioactive tracer and measuring radioactivity over the anterior chest with a gamma camera.
-It is the ideal and most reproducible test for providing longitudinal quantitative assessment of LV systolic function in patients receiving doxorubicin or other anthracyclines. It should be used when detection of slight changes in the ejection fraction are of importance, such as during chemotherapy, before and after cardiac transplantation, and severe CHF
HTN
-According to the new JNC VII guidelines, thiazide diuretics are the initial drugs of choice for the treatment of essential hypertension.
-Approximately 90% of patients with secondary HTN will have an unidentified cause. Of the remaining, around 3% will be due to renovascular HTN. Other less common causes account for less than 1% each, and are comprised of the following: primary hyperaldosteronism, drug-induced HTN, acute stress, and renal parenchymal disease.
-Abdominal or flank bruits are present in 50% of the patients with renovascular HTN. This makes this clinical finding the most common and expected clinical finding in a patient with suspected secondary HTN.
-Almost all guidelines recommend non-pharmacologic measures that can be preventive, adjunctive or sometimes definitive in the treatment of hypertension.
-Weight loss enhances the effect of anti-hypertensive drugs. It is the single most effective non-pharmacologic measure to decrease blood pressure in overweight individuals, and it is believed to reduce the overall cardiovascular risk in such patients.
♥ Note: Smoking cessation is an important component of lifestyle modification that reduces the risk of future cardiovascular events.
CHF
►Ischemic heart disease is the most common cause of congestive heart failure (CHF), especially dilated cardiomyopathy, in the United States. Approximately 50 to 75% of the patients with heart failure (HF) have coronary disease as the etiology.
-Other known etiologies are: hypertension (13%), valvular disease (10-to12%), renovascular disease, and very rare causes, such as obstructive sleep apnea, myocarditis, alcohol or cocaine abuse, etc.
-In a new case of CHF with unknown etiology, efforts must first be made to rule out the presence of coronary lesions which may be corrected by an angioplasty.
-Congestive heart failure is a clinical syndrome that results from impaired or inadequate ventricular emptying (systolic dysfunction) or impaired ventricular relaxation (diastolic dysfunction).
-It is characterized by specific symptoms that are either due to reduced cardiac output (fatigue, weakness) or excessive fluid retention (peripheral or pedal edema, dyspnea).
-All symptoms are exacerbated by exertion, and the degree of these symptoms helps in assessing the severity of heart failure.
♥Heart failure is primarily a clinical diagnosis and is based on a detailed history and physical examination. A detailed history and physical examination can also provide clues to the specific cause of heart failure.
♥CHF: The major criteria include the presence of paroxysmal nocturnal dyspnea, orthopnea, raised jugular venous pressure, pulmonary rales, presence of third heart sound, increased cardiac silhouette, and pulmonary vascular congestion on chest x-ray.
♥CHF: The minor criteria include the presence of bilateral lower extremity edema, nocturnal cough, dyspnea on exertion, tachycardia, presence of pleural effusion, and hepatomegaly.
►The diagnosis of heart failure is based on the presence of two major criteria or one major and two minor criteria, provided the minor criteria cannot be explained by the presence of any concurrent medical illness.
♥Chest radiograph findings suggestive of congestive heart failure include cardiomegaly, pulmonary vascular congestion (especially in the upper lobes), Kerley B lines and bilateral pleural effusions.
-The presence or absence of such findings will help to differentiate heart failure from dyspnea secondary to a primary pulmonary pathology.
-Plasma B type natriuretic peptide levels are useful at times to differentiate between cardiogenic versus non-cardiogenic causes of dyspnea.
♥Rupture of chordae tendineae should be suspected in healthy individuals who develop flash pulmonary edema (heart failure) associated with an acute mitral regurgitation.
-The differential diagnosis of this condition includes infective endocarditis, papillary muscle rupture secondary to ischemia, and mitral valve rupture secondary to trauma.
♥ACE inhibitors are the main therapy for CHF. ]They are indicated even in the asymptomatic phase. Although there is currently insufficient data to show its benefits to the mortality rate of African-Americans and women, their use in CHF is always recommended.
♥The only reasons for not giving ACE inhibitors are=
(1) Poor tolerance to the drugs (presence of severe adverse effects) and
(2) The presence of contraindications, such as renal failure
(Creatinine greater than or equal to 3 mg/dL) or hyperkalemia)
♥ Hydralazine and isosorbide combination is frequently used in the management of congestive heart failure in patients intolerant of ACE inhibitors.
-Patients should be informed regarding the possible adverse reactions that may result from the use of these drugs, and instructed to stop the medication if they develop any of these reactions.
♣The development of drug-induced lupus-like syndrome
-has been associated with the use of hydralazine.
-Other drugs that have been associated with lupus include procainamide, penicillamine, isoniazid, minocycline, diltiazem, methyldopa, chlorpromazine, and interferon-alfa.
-Patients with drug-induced lupus can develop a variety of flu-like symptoms such as fever, malaise, arthralgias, myalgias, and maculopapular facial rash. They can also develop lymphadenopathy, splenomegaly, pleurisy, and pericarditis. An important immunological marker of drug-induced lupus is the presence of antihistone antibodies.
Remember:
All patients with flash pulmonary edema of unknown etiology should be evaluated with an Echocardiogram.
Patients with acute pulmonary edema are initially managed with oxygen, morphine and loop diuretics (IV furosemide).
The two most commonly used antihypertensive agents in the management of hypertensive crisis complicated by acute pulmonary edema are => IV nitroglycerine and IV nitroprusside.
Marfans
Marfan or Ehlers-Danlos syndrome must be suspected in patients with connective tissue abnormalities and an acute mitral regurgitation secondary to chordae tendineae rupture, although a primary, pre-existing mitral valve prolapse (MVP) is the most common cause.
Some cases may be idiopathic (individuals who experience rupture of the chordae tendineae without previous MVP or connective tissue disease), but an etiology can be found in most occasions.
Cardiac risk factors
-Diabetes mellitus is the single most important predictor of adverse cardiovascular outcomes, especially in women. It is considered to be an equivalent of coronary heart disease (CHD).
-The role of glycemic control in the development of macrovascular disease in patients with type-2 diabetes is not firmly established.
=Hypertension is a well-established risk factor.
=The blood pressure should be kept below 130/85 mmHg in diabetics, unlike non-diabetic individuals whose target blood pressure is below 140/90 mmHg.
=Smoking is an important modifiable risk factor. The risk of cardiovascular events declines rapidly after smoking cessation, and approaches that of non-smokers in several years
MAT
Multifocal or multiform atrial tachycardia (MAT) is characterized by the presence of:
3 or more P waves of different morphologies
The QRS complexes are narrow
While the PR segments and the R-R intervals are variable
The heart rate can reach up to 200 beats per minute.
MAT is usually secondary to the following conditions:
1) hypoxia
2) chronic obstructive pulmonary disease (COPD)
3) hypokalemia
4) hypomagnesemia
5) coronary/ hypertensive/ valvular disease
6) medications (i.e., theophylline, aminophylline, isoproterenol)
Treatment M A T:
#1= Correct cause: Do ABGs because Hypoxia and COPD are the most common etiologies that affect mainly elderly patients. -Therapy is aimed at correcting the underlying cause.
#2-If the patient fails to improve >>electrolyte abnormalities (e.g., hypokalemia or hypomagnesemia) should be wanted.
If therapy is not effective and there are no contraindications, beta-blockers can be used successfully. In patients with asthma or COPD, verapamil is the drug of choice.
-SVT and sinus tachycardia are the most frequent types of tachyarrhythmias.
--Narrow and regular QRS complexes, and absent P waves >> suggest supraventricular tachycardia.
--Narrow and regular QRS complexes, and presence of P waves >> Sinus tachycardia
WPW Syndrome can be identified in around 0.2% of the population.
=It is characterized by a short PR interval (less than 0.12sec), a delta wave at the beginning of the QRS complex, QRS duration of 0.12sec or wider, and non-specific ST segments or T wave abnormalities.
=Although WPW Syndrome is not common, its diagnosis is important because it can present as SVT.
=If verapamil or beta-blockers are given, AV nodal conduction will be slow, and the accessory pathway conduction will increase.
=These can lead to ventricular fibrillation (especially if the patients already have atrial fibrillation) and death.
♦ Blocks:
-In comparison to Mobitz I, second-degree AV Block (Wenckebach’s), the PR does not prolong progressively, {PR is fixed] but QRS complexes are suddenly lost periodically
-Mobitz II AV Block can cause dizziness, episodes of syncope, or transient altered mental status, thus explaining the symptoms of the patient. Because Mobitz II can progress to third-degree AV Block, it needs to be managed with a permanent pacemaker. Even if the patient is asymptomatic, the AHA/ACC (American Heart Association/American College of Cardiology) consensus advises the use of a permanent pacemaker inserted through a venous access.
Nonsustained ventricular tachycardia
-Is defined as the presence of three or more consecutive ventricular beats with a heart rate greater than 120 beats/min, and with the episode lasting for less than 30 seconds. It is seen most commonly in patients with some form of structural heart disease, possibly because structural abnormalities lead to ventricular arrhythmia.
-Some structural abnormalities that can lead to nonsustained ventricular tachycardia include scarred myocardium from prior myocardial infarctions (coronary artery disease), ventricular hypertrophy (LVH or hypertrophic obstructive cardiomyopathy), dilated left ventricle (dilated cardiomyopathy), and valvular abnormalities such as mitral valve prolapse.
Although nonsustained ventricular tachycardia can also be seen in patients without any evidence of structural heart disease, it is important to recognize that structural heart disease is the most common cause, and a 2D-echocardiogram and stress test should be obtained to rule out ischemia.
-Patients with multiple risk factors for developing cardiac arrhythmias need proper evaluation for possible implantable cardiac defibrillator placement to prevent sudden cardiac death.
Atrial fibrillation
◘ Treatment of atrial fibrillation in a hemodynamically stable patient is different from one who is unstable.
1-If the patient is hemodynamically unstable (low BP, patient not responding to commands), the treatment of choice is electrical cardioversion.
2-If the patient is hemodynamically stable, the atrial fibrillation has to be categorized first as either an acute or a chronic process.
►If it is an acute process, the patient may undergo either Cardioversion [electrical or pharmacological with anti arrhythmic drugs class III agents (amiodarone, sotalol, ibutilide, etc.).
] or Rate control [B-blocker or CCB] to convert his arrhythmia to sinus rhythm. [If > 48 hrs, cardioversion need 1 month of anticoagulation in high risk pt]
►If it is a chronic process, then the patient should be managed with Rate control and Anticoagulation –heparin/Warfarin
Cardioversion -can be either electrical or chemical.
►Electrical cardioversion is indicated in hemodynamically unstable patients.
►Synchronized cardioversion (electrical shock administered in synchrony with the ‘R’ wave) is the procedure of choice.
-Electrical cardioversion should not be performed without 3-4 weeks of anticoagulation first in chronic atrial fibrillation (> 48 hours), as the risk of embolization is high. -The required joules are about 100-200 joules.
-Atrial fibrillation is generally more resistant to convert to normal sinus rhythm than atrial flutter, and the energy required is much higher.
-If you choose to do chemical cardioversion, the drugs of choice are class III agents (amiodarone, sotalol, ibutilide, etc.).
Lone atrial fibrillation in a patient younger than 60 years of age and without structural or functional cardiac abnormalities [CHF, valvular disease…] does not increase the risk of stroke. However, small studies suggest that there can be some risk, especially if the patient has other risk factors, such as advanced age, diabetes, or hypertension.
For this reason, ASA Aspirin is recommended as prophylactic therapy. The risk of anticoagulation with Coumadin outweighs the benefits in this setting.
♥Amiodarone interacts with Warfarin, prolonging its effect and increasing the risk of bleeding. Its clinical response is predictable; it is known that the Warfarin dose needs to be decreased about 25% in order to avoid over coagulation.
♥ Strokes and Warfarin use:
-The use of FFP or intravenous vitamin K is only necessary if the patient is bleeding or has an INR greater than 20.
-If the INR is supratherapeutic, but not higher than 5, it is enough to hold the Coumadin or decrease its dose.
-All other cases of excessive anticoagulation with Coumadin can be successfully managed with oral vitamin K
TCA toxicity
-TCA overdose is the leading cause of hospitalization and death. The signs of TCA overdose include hypotension, anticholinergic effects, CNS manifestations, and cardiac arrhythmias.
-Cardiotoxic effects are responsible for most of the mortality in patients with TCA overdose.
-TCAs inhibit fast sodium channels, which result to slowing of the phase 0 depolarization in His-Purkinje tissue and the myocardium.
-This may lead to QRS prolongation and reentrant arrhythmias, like ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
►Sodium bicarbonate is the most effective agent for the management of TCA-induced cardiotoxic effects.
►Lidocaine is the antiarrhythmic drug of choice for TCA-induced ventricular dysrhythmias.
Valvular disorders
-Mitral stenosis is a narrowing of the outflow tract from the left atrium to the left ventricle, resulting in increased pressure in the left atrium, pulmonary vasculature, and right side of the heart.
-It is more common in women, and is most commonly linked to a remote episode of rheumatic fever, though congenital mitral stenosis may be found as well.
-On physical examination, mitral stenosis produces a diastolic thrill palpable over the apex and a low-pitched, rumbling diastolic murmur best heard over the apex when the patient is lying in a left lateral decubitus position.
Mitral regurgitation causes an apical holosystolic murmur, and is most often secondary to myocardial infarction, mitral valve prolapse, rheumatic heart disease, or coronary artery disease.
Aortic stenosis causes a crescendo-decrescendo systolic murmur with a normal S1, a diminished A2, and a paradoxical splitting of S2. It is most often secondary to senile degenerative calcification, or congenital malformation.
An aortic valve area of less than 1.0 cm2 is considered severe stenosis. The onset of symptoms markedly affects the prognosis in patients with aortic stenosis; therefore, prompt intervention is recommended in patients who have cardinal symptoms of aortic stenosis (dyspnea of heart failure, anginal pain, and syncope). Aortic valve replacement is associated with marked reduction in symptoms and mortality in patients with symptomatic aortic stenosis, and is considered the treatment of choice.
Critical aortic stenosis and angina at rest >> Highest risk factors for peri-operative cardiac risk
Aortic insufficiency causes a diastolic murmur best heard adjacent to the sternum in the second to fourth intercostal space. It is most often secondary to infective endocarditis, congenital malformation, connective tissue disorders, or rheumatic heart disease.
Pulmonic stenosis causes a systolic crescendo-decrescendo ejection murmur in the left upper sternal border. It is most often secondary to congenital malformation, rheumatic heart disease, or carcinoid.
COA: This is usually associated with a congenital bicuspid aortic wall.
-In a previously undiagnosed patient, the classic presenting sign is hypertension. Most patients are asymptomatic unless severe hypertension is present, which can lead to headaches, epistaxis, heart failure, or dissecting aneurysm. The major clinical manifestation in children and adults with COA is a difference in the systolic blood pressure between the upper and lower extremities. In most cases, the diastolic blood pressures are similar.
-The classic findings are hypertension in the upper extremities, diminished or delayed femoral pulses, and lower unobtainable arterial blood pressures in the lower extremities.
♦ Magnetic resonance imaging (MRI) is the best noninvasive modality to diagnose COA because it can usually clearly define the location of severe coarctation of the aorta. MRI can also detect associated cardiac abnormalities and can be used for serial follow-up after surgical repair or balloon angioplasty.
Delirium
-Acute infections are a common cause of delirium, especially in elderly patients being admitted to the hospital. An important goal of treatment in such patients is to avoid the use of medications that can potentially worsen the acute delirious state.
-Diuretics, ACE inhibitors, spironolactone, beta-blockers, and digoxin are all a part of standard therapy for patients with heart failure or cardiomyopathy due to any cause. ACE inhibitors (lisinopril) have consistently been shown in multiple, large, randomized trials to have a significant beneficial effect on patients with heart failure. They have a very low incidence of central nervous system (CNS) side effects, and do not cause worsening of confusional states or delirium. Lisinopril can be safely started in this patient without the risk of exacerbating his confusion and agitation.
-Digoxin is a cardiac glycoside frequently used in patients with congestive heart failure due to systolic dysfunction and atrial dysrhythmias; however, its use has been associated with significant CNS side effects.
-These include blurred vision, dizziness, confusion, mental disturbances, anxiety, delirium, and hallucinations. Its use should be avoided in patients with ongoing acute mental confusion or delirium.
-Spironolactone is a useful adjunct in the management of patients with congestive heart failure, especially in patients with a low ejection fraction; however, its use can also cause CNS disturbances such as drowsiness, lethargy, and mental confusion.
♥Digoxin toxicity is characterized by nausea, vomiting, anorexia, fatigue, confusion, visual disturbances, and cardiac abnormalities. Verapamil, quinidine, and amiodarone can potentially cause digoxin toxicity.
Syncope
Vasovagal syncope is associated with prodromal symptoms of nausea, lightheadedness, pallor and diaphoresis. It usually occurs when the patient is erect, and recovery occurs in the supine position. Patients are usually young and otherwise healthy. Precipitating events include prolonged standing, exertion, venipuncture, or a painful stimulus.
-Cardiovascular syncope is due to arrhythmia or obstructive lesions such as aortic stenosis or HOCM.
-Syncope may be associated with a prodrome of palpitations. Arrhythmias usually occur without warning, with the patient in a supine or resting position, and lasts for a few seconds. Patients will have risk factors such as left ventricular dysfunction, prior myocardial infarction or conduction system disease.
-Physical examination may show the murmur of aortic stenosis or HOCM. EKG/Holter monitoring may detect an arrhythmia.
-Neurological syncope is due to atherosclerotic disease of the cerebral circulation, and is associated with a history of focal neurological deficits.
DDX: A seizure may mimic syncope; however, patients usually have a history of tonic-clonic movements, urinary or fecal incontinence, and a postictal state. Jerky movements similar to tonic-clonic movements can occur in any patient with syncope, but the postictal confusion is very unlikely with other conditions except seizures.
Orthostatic hypotension
Orthostatic hypotension is defined as a significant drop in blood pressure upon assuming a standing position, causing symptoms of cerebral hypoperfusion. Orthostatic hypotension is diagnosed if there is a fall of at least 20 mmHg of systolic blood pressure, or a fall of at least 10 mmHg of diastolic blood pressure, within two to five minutes of standing from a supine or sitting position.
-A fall in the blood pressure with/after standing or eating (postprandial hypotension) is a commonly encountered clinical situation, especially in the elderly population. It is usually caused by autonomic dysfunction or failure, or intravascular volume depletion from various causes.
-Almost all the patients suffering from orthostatic hypotension experience a sensation of dizziness or lightheadedness, especially after rapid changes in position (i.e. from supine or sitting to standing position). In some severe cases, it can lead to a fall (presyncope), angina, acute stroke, or loss of consciousness (syncope).
-The symptoms of orthostatic hypotension are primarily caused by a rapid decrease in cerebral perfusion.
-There are multiple causes of orthostatic hypotension in elderly patients>>The two major mechanisms of orthostatic hypotension are autonomic dysfunction/failure and intravascular volume depletion. Autonomic dysfunction is caused by various neurological disorders, systemic disorders (diabetes mellitus, amyloid neuropathy) or medications. Common drugs causing orthostatic hypotension include antihypertensives, antianginal drugs, vasodilators (nitrates, calcium channel blockers), antidepressants (especially tricyclic antidepressants), and opiate analgesics.
-When a patient stands up from a supine position, there is pooling of 500 to 1000 cc of blood in the lower extremities and mesenteric circulation. This causes a decrease in the venous return to the heart, which decreases ventricular filling pressures. A drop in the cardiac output and blood pressure occurs, causing decreased cerebral perfusion. This is a normal response seen in all patients, and is counteracted by a reflex increase in sympathetic discharge, which causes vasoconstriction and an increase in cardiac output. Nitrates may cause excess vasodilation, which could reduce the venous return to and cardiac output of the heart.
-An excess drop in blood pressure and cerebral perfusion may occur, and lead to symptoms of orthostatic hypotension.
-RX->>
>>The first step in reducing the frequency and symptoms of orthostatic hypotension is to recognize and remove the potential offending medications; therefore, isosorbide nitrate should be discontinued, and the patient should be observed for any recurrence of symptoms.
>>Fludrocortisone is a synthetic mineralocorticoid. It is used as a first-line agent for most patients whose orthostatic hypotension is not controlled by nonpharmacologic measures. It causes an increase in salt and water retention, which increases the effective circulating blood volume.
Cardiac temponade
Pericardial effusion may occur in response to any cause of pericarditis or from malignancies. The pericardial effusion may develop slowly or rapidly. However, sudden filling of the pericardial space with fluid can have catastrophic consequences by limiting ventricular filling.
-Patients with pericardial tamponade often complain of shortness of breath. It is accompanied by typical physical signs and symptoms that arise from the limited filling of the ventricle. The classic Beck’s triad is hypotension, muffled or distant heart sounds, and elevated jugular venous pressure. Arterial systolic blood pressure normally drops 10 -12 mmHg with inspiration.
-Marked inspiratory drop in systolic blood pressure (> 20 mmHg) is an important physical finding in cardiac tamponade, but can also be seen in severe obstructive pulmonary disease and constrictive pericarditis. In pericardial tamponade, low limb voltage with alternating size of QRS complex due to swinging of the heart is seen.
♦CXR in cardiac tamponade will show an enlarged cardiac silhouette. When a chest
x-ray shows an enlarged heart with pulmonary edema, congestive heart failure should be suspected. In cardiac tamponade, usually, there is no pulmonary edema.
Cardiac tamponade is a surgical emergency, and an ECHO should be obtained urgently. The ECHO will reveal the large pericardial effusion, with prominent collapse of the right atrium and ventricle during diastole. Cardiac catheterization can confirm the diagnosis by showing equalization of diastolic pressures in all chambers. However, if the patient is collapsing, one should not wait for an ECHO. Rapid pericardiocentesis is life saving.
Mechanical valves
The following are the recommendations from the Sixth ACCP Consensus Conference for a mechanical valve:
A goal INR of 2.5 (range 2 to 3) is recommended for patients with AVR with bileaflet mechanical valve, provided that the patient is in sinus rhythm, left atrium is of normal size, and the left ventricular ejection fraction is normal, as in this patient.
A goal INR of 3 (range 2.5 to 3.5) is recommended for patients with MVR with bileaflet mechanical valve or for patients with a bileaflet mechanical aortic valve who have atrial fibrillation
A goal INR of 3 (range 2.5 to 3.5) in combination with low dose aspirin is recommended for patients with mechanical prosthetic valves who suffer a systemic embolism despite adequate anticoagulant therapy.
However, more data is coming in favor of a higher level of anticoagulation (target INR >3.0) for both aortic and mitral prosthetic mechanical valve
Respiratory
TB
Even though it is not common, a new pleural effusion in a patient already on anti-tuberculosis treatment may occur and must be studied, because this can progress despite the clinical improvement of the patient. There is no need to change therapy, unless there is proof of a new infection or drug resistance. Some authors advocate the use of steroids in this setting, but this is not a universally accepted practice.
Chronic Eosinophilic Pneumonia (CEP)
Chronic Eosinophilic Pneumonia (CEP) is the most common eosinophilic pneumonia in the USA. Patients with chronic eosinophilic pneumonia present with systemic symptoms such as fever, malaise, anorexia, and weight loss for several weeks to months.
Pulmonary symptoms include cough and breathlessness.
Sometimes, patients may give a history of bronchial asthma or allergic rhinitis.
-Chest auscultation shows crackles or wheezing.
-Chest x-ray reveals peripheral infiltrates that are the "photographic negative" of pulmonary edema, and this radiographic finding is pathognomonic for the disease.
♥Bronchoalveolar lavage (BAL) that reveals eosinophils greater than 40% is suggestive of the diagnosis. Glucocorticoid therapy results in rapid resolution of the symptoms and radiographic clearing.
Acute bronchopulmonary aspergillosis ABPA:
This hypersensitivity reaction to Aspergillus antigens is seen in patients with underlying asthma. When the airways of such patients become colonized with Aspergillus, the intense IgE and IgG mediated immune response leads to the characteristic recurrent episodes of fever, malaise, cough with brownish mucoid expectoration, wheezing, and symptoms of bronchial obstruction.
There is no single diagnostic test to confirm the diagnosis of ABPA.
►The diagnosis is usually made by clinical, radiographic, and immunologic criteria, which include the following:
1. A history of asthma.
2. Immediate skin test reactivity to Aspergillus antigen.
3. Precipitating serum antibodies to Aspergillus fumigatus.
4. Serum total IgE concentration of greater than 1000 ng/mL.
5. Peripheral blood eosinophilia greater than 500 per cubic millimeter.
6. Lung infiltrates, usually involving the upper lobes.
7. Central bronchiectasis.
==A skin prick test for Aspergillus should be performed initially in all asthmatic patients suspected of having ABPA.
If the skin prick test is positive, serum total IgE levels and precipitating serum antibodies to Aspergillus fumigatus should be measured. If the skin prick test is negative, the diagnosis of ABPA is extremely unlikely.
Recurrent episodes of airway inflammation and bronchial obstruction in patients with ABPA can lead to bronchiectasis and lung fibrosis; therefore, it is important to diagnose and treat such patients early to reduce the risk of progressive lung damage.
Corticosteroids are the mainstay of therapy for patients with ABPA.
Treatment with corticosteroids is effective in controlling the episodes of acute inflammation and preventing progressive lung fibrosis.
The clinical response to treatment is measured by the reduction of serum total IgE concentration, clinical improvement and resolution of radiographic findings.
Churg Strauss syndrome (CCS): is a multisystem vasculitic disorder of unknown etiology that affects the skin, kidney, nervous system, lungs, gastrointestinal tract, and heart. It is characterized by allergic rhinitis, asthma, and prominent peripheral blood eosinophilia.
A CSS-like syndrome has been noted in patients who have been successfully treated for chronic steroid-dependent asthma with leukotriene receptor antagonists.
Up to 75% of the patients have evidence of peripheral neuropathy. The disease is severe, and requires treatment with glucocorticoids and sometimes with immunosuppressants. There have been significant reports which associate the use of leukotriene inhibitors with Churg-Strauss vasculitis. To date, there are more than 28 cases of Churg Strauss vasculitis associated with its use.
ARDS:
ARDS can occur secondary to sepsis, pneumonia, severe trauma, burns, drowning, or pancreatitis. The presentation is sudden. Oxygen requirements increase very rapidly.
Criteria for ARDS diagnosis are:
1. A pulmonary capillary wedge pressure less than 18 mmHg
2. PaO2 to FiO2 ratio of 200 mmHg or less, regardless of the PEEP level
3. Diffuse bilateral infiltrates on chest x-ray
In contrast to heart failure, patients with ARDS will typically have clear lungs on exam but will show diffuse, bilateral infiltrates on the chest x-ray results.
The management of ARDS through mechanical ventilation involves the interplay of the following settings:
1. PEEP (positive pressure at the end of expiration)
2. oxygen concentration
3. tidal volume
The PEEP attempts to expand the collapsed alveoli in ARDS in order to decrease the high oxygen requirement. It also prevents the development of atelectasis.
Although the physiologic PEEP is around 5 cmH2O, the mechanical ventilator settings of ARDS patients are usually around 9 cmH2O. Oxygen is set at high concentrations, while the tidal volume is set to the lowest possible value.
ARDS is associated with a mortality rate of 35-40%. Among the different strategies, mechanical ventilation that delivers lower tidal volumes (< 6 ml/kg) and limits plateau pressure (< 30 CmH2O) has been shown to be relatively more effective.
Studies comparing the effects of low tidal volume and limited plateau pressure to that of high tidal volume and plateau pressure have shown a significant reduction in mortality in the first group (32% vs. 40%).
Mechanical ventilation in the management of ARDS is a dynamic process.
When the patient improves, FiO2 and PEEP should be decreased stepwise, as tolerated.
The objective is to maintain the patient on the following settings: a PaO2 more than 60mmHg, an oxygen saturation more than 90%, and a normal or slightly acidic pH (permissive hypercapnia).
Once this is achieved, the patient should be weaned as soon as possible, in order to avoid complications such as barotrauma, ventilator-associated pneumonia, prolonged sedation, and hypotension.
PE:
Pulmonary thromboembolism is difficult to diagnose, and usually requires the combination of several diagnostic modalities. It is therefore important to know the order in which to order these diagnostic tests.
=The first test that is usually employed is ventilation/perfusion scanning.
►If the results reveal the classic pattern of mismatched perfusion; it is advisable to proceed directly with treatment.
►If the scan is normal, significant pulmonary thromboembolism should be ruled out; however, ventilation/perfusion scanning results are inconclusive in a substantial number of patients. Since the usual source of emboli causing this condition is deep venous thrombosis (DVT) of the lower extremities, ►the next best step in this case is Venous ultrasonography to reveal DVT or CT angiogram of the chest. A diagnosis of DVT makes the probability of pulmonary thromboembolism very high, and warrants immediate treatment.
►Pulmonary angiogram is the gold standard test for the diagnosis of pulmonary embolism (PE); however, this procedure is rarely being performed since it is invasive and CT angiogram is readily available.
♥ Mild fever and leukocytosis can be seen in the setting of PE.
-Pulmonary embolism (PE) is generally treated by starting the patient on heparin first, and then adding warfarin (Coumadin) after 24-48 hours.
The recommended duration of pharmacotherapy depends on the setting in which the PE occurred, as indicated below:
1. Occurrence of PE in the setting of reversible risk factors (e.g., use of oral contraceptive pills, immobilization, or surgery) should be treated with 3-6 months of warfarin therapy.
2. If the first episode of thromboembolism occurs in a setting that involves an underlying malignancy, anticardiolipin antibody, and antithrombin deficiency, the patient should be treated with at least 12 months of warfarin therapy.
3. Patients with a first episode of idiopathic thromboembolism should be treated for at least six months with warfarin; three months of therapy is inadequate in this patient group.
4. Patients with recurrent thromboembolism or a continuing risk factor should be treated indefinitely.
The indications for an inferior vena caval (IVC) or Greenfield filter insertion include patients with:
1. a documented recurrent venous thromboembolism while on therapeutic anticoagulation
2. a recurrent venous thromboembolism and absolute contraindications to anticoagulation
3. a history of massive pulmonary embolism in whom a recurrent episode may be life-threatening
4. Chronic recurrent pulmonary embolism and a history of pulmonary hypertension
►It is also considered prophylactically in patients with severe chronic obstructive pulmonary disease, cor pulmonale, or a previous history of venous thromboembolism who develop a predisposing risk factor for pulmonary embolism, such as an acute fracture or cancer.
►A chest x-ray should be obtained in all post-operative patients who complain of shortness of breath before performing more specific tests that will determine or exclude the diagnosis of PE. Chest x-ray findings may suggest the presence of PE and may help exclude other chest pathology.
►Septic pulmonary emboli may result from septic thrombophlebitis and/or tricuspid endocarditis.
Asthma:
♫ the allergen most frequently associated with asthma is house dust mites.
♥Cough induced by forced expiration is characteristic of airway hyperreactivity, and is usually suggestive of asthma; however, this presentation has also been described in some patients with COPD who can occasionally have an overlapping condition with asthma.
♥It is important to recognize and initiate early interventions in a patient with acute exacerbation of asthma. Early recognition, rapid assessment and treatment are crucial in preventing significant morbidity and mortality.
♥Measurement of the peak expiratory flow rate with a peak flow meter is an excellent method to assess the degree of severity of airflow limitation, and subsequent serial measurements of the peak flow rate are useful in assessing the response to therapy.
►The goal of treatment is to rapidly correct the airflow obstruction. This is most rapidly achieved by the administration of inhaled beta-2 adrenergic agonists, either by continuous nebulization or with the use of metered dose inhalers with a spacer.
►Systemic corticosteroids should also be administered early in the treatment of acute asthmatic exacerbation; however, their effect is usually not apparent in the first few hours. Their use should be preceded or accompanied by inhaled beta-2 agonist therapy.
♥In a patient with an acute, severe, asthma exacerbation, it is important to periodically assess the response to initial therapy during the first few hours. Failure to recognize early signs of clinical deterioration and impending respiratory failure is responsible for majority of the morbidity and mortality seen in patients with status asthmaticus.
♥Some of the clues to a patients clinical deterioration and poor outcome include a history of prior intubation, exhaustion or extreme fatigue, diaphoresis, change in consciousness (confusion and drowsiness), use of accessory muscles, presence of suprasternal retractions, depressed respiratory drive, marked tachycardia, pulsus paradoxus, PaCO2 greater than 40 mmHg, and a peak expiratory flow rate less than 25% of the normal predicted.
►Any patient with the above signs and symptoms of impending respiratory failure should be immediately intubated to secure and protect the airways.
Patients with hypoxemia due to an acute asthma exacerbation should be immediately managed with oxygen inhalation, followed by administration of an inhaled beta-2 agonist, which is the mainstay of therapy.
►Hospital admission for asthma exacerbation is recommended if the peak flow reading is 40-50% lower than the patient’s baseline, if there are signs of respiratory distress, if oral steroid therapy fails, or if the patient’s clinical condition worsens. Ipratropium nebulization may be given in the emergency department, but this is not the mainstay of therapy. For any acute exacerbation, oral or parenteral steroid therapy with prednisone, prednisolone, methylprednisolone, or hydrocortisone is essential for therapeutic success.
Solitary pulmonary nodule
Solitary pulmonary nodules represent a common clinical problem in the primary care setting. They are usually detected in an asymptomatic patient and present a clinical dilemma for the primary care physician.
The clinical and diagnostic workup of a solitary pulmonary nodule is aimed towards differentiating between a benign lesion from a malignant lesion (lung cancer).
►Some of the factors that suggest a malignant cause of a solitary pulmonary nodule include:
Age greater than 50 years,
History of smoking or asbestos exposure, presence of another primary cancer elsewhere in the body (malignant melanoma, colon, breast, kidney, testis),
Size greater than 3 cm, irregular or speculated borders of the nodule, and certain patterns of calcification within the lesion (eccentric calcification).
Another important clue is the growth of the pulmonary lesion over time.
Malignant lesions usually have a doubling time of 20-400 days, whereas the doubling time of benign lesions is either less than 20 days (infectious cause) or greater than 450 days.
►As a general guideline, any solitary pulmonary nodule with the absence of any changes in size over the last two years is strongly suggestive of a benign lesion; therefore, a comparison of the pulmonary nodule on chest x-ray with the previous chest radiographs to document any changes in the size of the lesion is a critical initial part of the diagnostic workup of this patient.
►A chest CT scan should be obtained to characterize the pulmonary nodule before performing any invasive procedures. It demonstrates the pattern of calcification within the nodule, and identifies any mediastinal lymph node involvement and small pleural effusions. Particular CT scan findings that suggest malignant lesions include an irregular or speculated border and the presence of eccentric, reticular or punctate calcifications within the lesion. Such findings can help distinguish between a benign from a malignant cause of the solitary nodule.
►BENIGN: Certain patterns of calcification within the pulmonary nodule, as seen on chest x-ray or CT scan, are strongly suggestive of a benign cause of the lesion or nodule. These include popcorn calcifications, concentric or laminated calcifications, central calcifications and diffuse homogenous calcifications. Popcorn calcifications are characteristically seen on radiographic imaging in patients with pulmonary hamartoma.
►Any patient with a solitary peripheral lung nodule suspicious for malignancy should undergo video-assisted thoracoscopic surgery (VATS) and excisional biopsy of the lesion. This is the procedure of choice in most patients for the removal and definite diagnosis of a peripherally located pulmonary nodule. It is a relatively safe procedure and has a low risk of complications if performed by a skilled surgeon.
Sarcoidosis
Sarcoidosis is a chronic granulomatous disease seen more frequently in young African-American patients. It is characterized by the formation of non-caseating granulomas in various involved tissues and organs. It usually involves the lungs, but can also involve other organ systems including the skin, lymph nodes, liver, spleen, eyes, exocrine glands (salivary and lacrimal glands), heart, kidneys, and central nervous system. It is usually asymptomatic and is frequently detected as an incidental finding on a routine chest x-ray.
Patients with pulmonary sarcoidosis usually present with cough, chest pain, or dyspnea. Some other nonspecific features include generalized weakness, lethargy, fever, and weight loss.
-Sarcoidosis- Initial test/screening:
-The chest radiograph in patients with pulmonary sarcoidosis classically reveals
Bilateral hilar adenopathy with or without right paratracheal lymph node enlargement
Serum ACE levels are elevated [screening test] in more than half of the patients with sarcoidosis, but this is a nonspecific finding. Although serum ACE levels have little role in diagnosing the disease, these may prove to be useful in monitoring disease activity
CONFIRMATORY TESTS:
-The biopsy of accessible tissues [not erythema nudosum] for confirmation of the diagnosis is not required in an asymptomatic patient with the typical history and chest x-ray findings.
-Hypercalciuria occurs in 50% of cases of sarcoidosis. Macrophages in the sarcoid granulomas produce calcitriol, which is the active form of vitamin D, and as a result, calcium absorption from the gut increases.
-Nephrocalcinosis may result in chronic renal failure (CRF) and end stage renal disease.
-Hypercalcemia occurs in 10-20% of cases of sarcoidosis [high vitamin D].
-Thrombocytopenia may occur in patients with sarcoidosis.
►Definitive diagnosis of sarcoidosis can be made from the biopsy of the easily accessible lesions, including:
1. Any palpable lymph node
2. Skin lesion [except erythema nodosum]
3. Enlarged parotid
4. Lacrimal glands
NEXT STEP IF NOT ACCESSIBLE LESION ►LUNG BIOPSY with fiberoptic bronchoscopy and transbronchial lung biopsy is the procedure of choice.
•Nerve and liver biopsies are not recommended unless all other approaches fail.
♥Hypercalcemia, non-caseating granulomas, depressed-cell mediated immunity, and activated humoral immunity are characteristic features of sarcoidosis.
♥Asymptomatic pulmonary sarcoidosis generally does not need treatment.
-Hilar adenopathy associated with erythema nodosum represents a very favorable variant of sarcoidosis that is associated with a high rate of spontaneous remission and good prognosis.
♥Symptomatic pulmonary disease is usually an indication for corticosteroid therapy in patients with sarcoidosis, especially if it is accompanied by systemic symptoms such as severe fatigue, fever and hypercalcemia. Severe extrapulmonary manifestations of sarcoidosis such as cardiac, ocular and neurologic involvement may require high-dose corticosteroid therapy.
-Alternative agents (e.g. methotrexate) may be indicated if corticosteroids are not effective or if intolerable side effects of corticosteroid therapy occur.
OSA:
Although there are no specific physical findings consistent with obstructive sleep apnea (OSA), some general observations can contribute to the diagnosis. Truncal obesity and a large neck circumference (collar size > 17.5 inches) are common, and the oropharynx may be visibly "crowded." In some patients, the uvula is enlarged.
-Systemic hypertension is seen in approximately half of the patients with OSA.
-Hypothyroidism should be screened for, especially in older patients or those with symptoms suggestive of hypothyroidism (e.g., constipation and hair loss, as seen in this patient). Therefore, physical examination and thyroid function testing should be performed next.
-Sleep studies are typically performed to confirm the diagnosis of OSA.
-Polysomnography in particular is considered the gold standard for diagnosis.
-After completing the physical and laboratory evaluation of the patient, polysomnography is indicated.
PPH:
►The diagnosis of primary pulmonary hypertension is made when there is evidence of increased pulmonary arterial pressure in the absence of other identifiable causes.
-Pulmonary hypertension may be primary or secondary to interstitial lung disease, chronic venous thromboembolism, valvular or myocardial disease, connective tissue disease, or congenital heart disease.
-All patients with primary pulmonary hypertension should receive anticoagulation therapy because of an increased risk of pulmonary thromboembolism. This increased risk is due to slow pulmonary blood flow, a dilated right heart, and venous stasis.
-The anticoagulant of choice for this purpose is warfarin, and a target INR of 2 should be achieved.
-Oral vasodilators prolong survival and provide hemodynamic and clinical benefit in those patients of primary pulmonary hypertension who show vasoreactivity to nitric oxide and other vasodilators.
Patients who do not show vasoreactivity may experience an acute cardiopulmonary decompensation if oral vasodilators are used. It is therefore recommended that all patients with primary pulmonary hypertension be tested for vasoreactivity before starting therapy with oral vasodilators.
==Untreated primary pulmonary hypertension ►can lead to cor pulmonale.
COPD:
It is important to recognize that some patients with COPD will be oxygen dependent at some point of their disease. Oxygen therapy in this setting will decrease mortality and delay the development of pulmonary hypertension or cor pulmonale as a consequence of chronic hypoxia.
►The current recommendations to use home oxygen therapy are:
1. PaO2 less than or equal to 55 mmHg or an arterial oxygen saturation (SaO2) less than or equal to 88 percent.
2. PaO2 between 56 to 59 mmHg (or) a SaO2 of 89 percent, if there is evidence of cor pulmonale, right heart failure, or erythrocytosis (hematocrit above 55 percent).
HY:
♥Recurrent pneumonia in an elderly smoker may be the first manifestation of bronchogenic carcinoma.
►Flexible bronchoscopy is a primary diagnostic tool to evaluate patients with persistent or nonresolving pneumonia or pulmonary infiltrates (HRCT scan is an alternative, but it does not provide confirmatory information).
►The best diagnostic test for endobronchial obstructive lesions is flexible bronchoscopy. If the question had asked for the next best step in management, then the answer would have been CT scan.
►Syndrome of inappropriate antidiuretic hormone (SIADH) is associated with normovolemic hyponatremia and can be caused by small cell carcinoma of the lung.
Water restriction (with the possible inclusion of salt administration) is the preferred means of correcting mild to moderate hyponatremia associated with SIADH.
♥Postoperative complications:
-Are a common cause of perioperative morbidity and mortality. Some of the factors that increase the risk of developing postoperative complications are upper abdominal and thoracic surgeries, underlying chronic lung disease, a history of smoking within the last eight weeks, baseline PaCO2 > 45 mmHg, duration of surgery of more than 3-4 hours, and the use of general anesthesia.
♥The most common complications include atelectasis, bronchospasm, worsening of the underlying lung disease, postoperative pneumonia, and prolonged need for mechanical ventilation.
♥All patients undergoing upper abdominal or thoracic surgery with one or more additional risk factors are at a high risk for postoperative complications. These patients should be the target of risk reduction strategies. Antibiotics should be given prior to surgery only in patients with clinically apparent respiratory infection. These include patients with purulent sputum or a recent change in the color of the sputum.
They should not be used routinely in stable COPD patients.
Silicosis:
Is pneumoconiosis caused by exposure to silica crystals.
-There are three patterns of disease: acute, accelerated, and chronic silicosis. High-risk professions include glass maki
