Cardiology

·         The increased venous return of inspiration (the Müller maneuver is sucking in with the nares held closed) increases the murmurs of the right side of the heart, and expiration increases the murmurs of the left side of the heart.

·         Low-risk patients (score of 0, stroke risk 0.5%/year without warfarin) can be managed with aspirin alone. High-risk patients (score ≥3, stroke risk ≥5.2%/year without warfarin) should be managed with warfarin. Intermediate-risk patients (score 1 or 2, stroke risk 1.5% –2.5%/year without warfarin) may be managed with aspirin or warfarin, depending upon the clinician's assessment of risk, the ability to monitor the intensity of anticoagulation, the patient's risk of bleeding with anticoagulation, and patient preference. If warfarin is used, the goal INR should be 2–3.

·         The left parasternal border at the third, fourth, and fifth intercostal spaces should be palpated for a right ventricular tap, which is also called a lift or heave. It is a nondiagnostic finding and results from any etiology of right ventricular hypertrophy. A heave that is palpable at the apex is consistent with LVH.

·         An easy mnemonic to remember systematic heart auscultation is APT. M (Aortic valve, Pulmonic valve, Tricuspid valve, and Mitral valve.

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·         Prophylaxis for SABE is not recommended in isolated secundum ASD, surgical repairs of septal defects (both atrial and ventricular), and PDA.

·         Systolic ejection murmur with a THRILL ON THE UPPER LEFT STERNAL BORDER: pulmonic stenosis

·         Holosystolic murmur with a THRILL ON THE LOWER LEFT STERNAL BORDER: VSD

·         Holosystolic murmur best heard on the apex, radiating to the AXILLA: mitral regurgitation

·         Systolic murmur along with LSB THRILL RADIATING TO THE RIGHT SIDE OF THE NECK: aortic stenosis

·         Midsystolic click with late systolic murmur: mitral valve prolapsed

·         Opening snap, loud S1, diastolic rumble, atrial fibrillation: mitral stenosis

·         2^nd H.S.:

Fixed Split = ASD (the only one)

Narrow/ Paradoxical: LHAIM (LBBB, HTN, AS, IHSS, MI)

All other have wide split.

·         The uraemia leads to exudation of fibrin onto the epicardial and pericardial surfaces. Haemorrhagic pericarditis is more typical of tuberculosis or metastatic tumour. Serous pericarditis is more typical of collagen vascular diseases.

·         Antimicrobials with prolonged QTI: Erythro,Quinine,Levoflox

·         Pulmonary embolism should be considered in the differential diagnosis of patients presenting with undifferentiated chest pain or dyspnea and an elevated cardiac troponin level.

·         Patients with Hypertrophic Cardiomyopathy (HCM) are at increased risk of sudden cardiac death due to VF/VT. The five poor prognostic markers which are predictive of sudden cardiac death are:

1. Syncope
2. Family History of HCM and sudden cardiac death
3. Maximum Left Ventricular Wall Thickness >3cm
4. BP drop during peak exercise on stress testing
5. Documented runs of Non-Sustained VT on 24 hour tape.

LVOT obstruction causes symptoms and can lead to deterioration of LV function but does not predict sudden cardiac death. Asymmetric Septal Hypertrophy is a feature of HCM, in order to assess the risk for sudden cardiac death a detailed echocardiogram with measurements of the maximum left ventricular wall thickness is required. Systolic anterior movement of the mitral valve is often seen on echocardiogram and is thought to be the mechanism behind the left ventricular outflow tract obstruction.

·         IWMI pt may need temporary pacemaker if not controlled with medication.

·         systolic ejection click- signify congenital bicuspid aortic valve then acquired AS

·         Total cholesterol and HDL cholesterol can be calculated without FASTING. LDL cholesterol is calculated from the fasting triglyceride level and total and HDL cholesterol levels are calculated by the following formula:

LDL=Total-HDL+(TG/5)

·         Cigarette smoking is a greater risk factor for cardiovascular disease than obesity.

·         Cardiologists express functional status in terms of metabolic equivalent (MET) levels. One MET is equal to the oxygen consumption (3.5 mL/kg/min) of a 70-kg, 40-year-old man in a resting state. With this benchmark, functional capacity is excellent in patients who can perform at a level of > 7 METs; moderate at 4-7 METs; and poor if patients cannot meet a 4-MET demand during most daily activities. The 4-MET cut point is used in the ACC/AHA guideline.

·         Clues to the diagnosis of cholesterol emboli syndrome include a predisposing procedure in a patient with extensive vascular disease; the presence of leukocytosis, and especially eosinophilia, in the peripheral blood film; and cholesterol crystals in tissue specimens and retinal arteries.

·         The most common cause of atrial tachycardia with block is digitalis toxicity.

·         Three ECG findings are virtually pathognomonic of VT: AV dissociation, capture beats, and fusion beats

·         The normal range for the PR interval is 0.12-0.20 sec. It is not significantly related to age, sex, or heart rate.

The normal range for the QT interval also is unrelated to age, but it does vary with heart rate. As the heart rate increases, the QT interval shortens. To help evaluate a QT interval independent of heart rate, the corrected QT interval (QTc) can be calculated:

QTc (in msec) = measured QT (in msec)/square root of the R-R interval (in sec)

The normal range for the QTc is 0.36-0.44 sec. A prolonged QTc is defined as QTc > 0.44 sec.

·         Diagnostic criteria for left anterior fascicular block: QRS axis -60° to -90°, Small q-wave in lead I, Small r-wave in lead III

·         Prolongation of the QT interval is associated in certain patients with a definite increase in risk of VF and death.

·         Some patients exhibit ECG changes similar to those of MI but do not have any other definitive evidence of an MI. Such patients are said to have ECG evidence of "pseudoinfarction." Causes include:

o   LV or RV hypertrophy

o   LBBB

o   Wolff-Parkinson-White syndrome

o   Hypertrophic cardiomyopathy

o   Hyperkalemia

o   Early repolarization

o   Cardiac sarcoid or amyloid

o   Intracranial hemorrhage

·         The primary angioplasty in myocardial infarction (PAMI) trial is the first published clinical trial designed specifically to compare balloon angioplasty with t-PA as the primary reperfusion therapy in patients with acute ST-elevation MI. Survival rates (at 30 days and at 2 years) after primary angioplasty were similar to those with t-PA in acute MI, but angioplasty conferred greater freedom from recurrent ischemia, reinfarction, and need for readmission to the hospital. Another important advantage of balloon angioplasty over thrombolytic drug therapy is freedom from intracranial hemorrhage, a dreadful complication of thrombolysis, particularly in elderly patients.

·         Acute coronary syndrome is a clinical syndrome characterized by ischemic cardiac chest pains associated with ST or T-wave changes, but, unlike classic acute MI, there is no acute ST segment elevation. Thus, it is called the non-ST elevation acute coronary syndrome. This includes two diseases: unstable angina and non-Q-wave MI, which are differentiated based on the presence or absence of an elevation of the creatinine kinase MB fraction (MB CK) or troponin I or T levels.

·         Digoxin  is successful in decreasing hospitalization for heart failure—an important clinical end point—but did not decrease mortality. It has no role in preventing maladaptive ventricular remodeling.

·         A presystolic, or S4, gallop indicates reduced compliance of the left ventricle but not a failing left ventricle per se. Pulsus alternans, characterized by alternating weaker and stronger pulsations in the peripheral arteries, indicates a diseased left ventricle with poor systolic function. Pulsus alternans will usually be accompanied by an S3 gallop.

·         In patients with severe and chronic systemic venous congestion, the prothrombin time can be prolonged. Thus, an abnormal international normalized ratio does not automatically indicate liver disease. Similarly, chronic congestion may produce mild elevations in bilirubin and alkaline phosphatase levels. An elevation of transaminase levels is more likely to be associated with acute liver congestion with hypoxia and hepatocellular damage. Splanchnic congestion in right heart failure can lead to nausea, diarrhea, and malabsorption.

·         The oral bioavailability of furosemide varies widely (10% to 100%), but absorption of torsemide and bumetanide is nearly complete, ranging from 80% to 100%.

·         ABPM is the best method to establish the presence of isolated clinic hypertension (socalled white-coat hypertension), which is defined as an elevation in BP that occurs only in the clinic setting, with normal BP in all other settings, in the absence of evidence of target-organ injury.

·         The JNC VII report suggests initiation of therapy with two drugs rather than a single agent if the systolic blood pressure is higher than 20 mm Hg above the treatment goal or if the diastolic blood pressure is higher than 10 mm Hg above the goal. Generally, a two-drug regimen should include a diuretic appropriate for the level of renal function.

·         Establishment and maintenance of sinus rhythm is not superior to ventricular rate control in patients with AF.

·         Although success rates are high with DC cardioversion in AF, a number of risk factors for cardioversion failure have been identified. These include longer duration of AF (notably, longer than 1 year), older age, left atrial enlargement, cardiomegaly, rheumatic heart disease, and transthoracic impedance. Pretreatment with amiodarone, ibutilide, sotalol, flecainide, propafenone, disopyramide, and quinidine have been shown to increase DC cardioversion success rates.

·         The most feared arrhythmia in the WPW syndrome involves atrial fibrillation with dominant conduction over an accessory pathway that has rapid conduction properties. These patients may experience extraordinarily rapid ventricular rates and are at risk for sudden cardiac death from ventricular fibrillation.

·         It is not uncommon for trained athletes to have type I second-degree AV block and be asymptomatic. Pacemaker therapy is not indicated.

·         The three basic functions of a pacemaker—pacing, sensing, and action—are determined by basic pacemaker programming. Five-position code currently in use. The first position denotes the chamber or chambers paced; the second denotes the chamber or chambers sensed; the third denotes the action or actions performed; the fourth denotes rate response; and the fifth denotes multiple site pacing. The simplest mode of pacing is VVI, otherwise known as ventricular demand pacing or ventricular inhibited pacing. The most commonly used mode in dual-chamber pacing is DDD. The most basic timing cycle is the lower rate, which reflects how long the pacemaker will wait after a paced or sensed beat before initiating pacing.

·         Exercise ECG is the diagnostic test of choice for the average patient with an intermediate pretest probability of IHD and a normal resting ECG. Exercise-induced falls in blood pressure or the development of an exercise-induced S3 heart sound are strongly suggestive of ischemic left ventricular dysfunction. Specific exercise-induced ECG changes include changes ≥ 1 mm horizontal or downward-sloping ST segment depression or elevation during or after exercise. Exercise-induced changes in lead V5 are most reliable for the diagnosis of IHD.

·         Calcium channel blockers are contraindicated in the presence of decompensated congestive heart failure, although the vasoselective dihydropyridine agents amlodipine and felodipine are tolerated in patients with clinically stable left ventricular dysfunction.

·         Exercise testing is most useful for diagnosing coronary artery disease in patients with an intermediate pretest probability (e.g., 20% to 80%).

·         Approximately 35% to 50% of patients with unstable angina will not have chest pain as their presenting symptom. 51.7% of patients with unstable angina had the following atypical symptoms: dyspnea (69.4%), nausea (37.7%), diaphoresis (25.2%), syncope (10.6%), arm pain (11.5%), epigastric pain (8.1%), shoulder pain (7.4%), and neck pain (5.9%).

·         Type B dissection is frequently accompanied by hypertension, whereas type A dissection more often occurs in the presence of normal or low blood pressure.

Emergency surgery is crucial for patients with type A aortic dissections. Type B dissection cases are managed medically by means of aggressive blood pressure control with beta blockers.

·         Depression of the PR segment, which reflects superficial injury of the atrial myocardium, is as frequent and specific as ST segment elevation and is often the earliest electrocardiographic manifestation of Acute Pericarditis. The diffuse distribution and the absence of reciprocal ST segment depression distinguish the characteristic pattern of acute pericarditis from acute myocardial infarction.

A finding of diffuse ST segment elevations without reciprocal changes or PR depressions would confirm the diagnosis of viral pericarditis.

·         The constitutional symptoms may be caused by production of interleukin-6 by the myxoma.

·         The most important complication of myocardial contusion is cardiac arrhythmia. Hypotension, intracardiac thrombus, congestive heart failure, and cardiac tamponade occur occasionally.

·         Left axis deviation is present in the majority of patients with AVSD; in contrast, right axis deviation is found in patients with ostium secundum ASD.

·          All patients with bicuspid aortic valves—even those with no significant stenosis or regurgitation—should be given instructions regarding endocarditis prophylaxis.

·         Patients with Down syndrome have roughly a 40% chance of congenital cardiac anomalies. The most common are the endocardial cushion defects (especially ostium primum defects). They are also at risk for AR, tetralogy of Fallot, and pulmonary hypertension. Tetralogy of Fallot is much less common than the endocardial cushion defects. Interestingly, these patients are also at increased risk for mitral valve prolapse.

·         The exceptions, in which IE prophylaxis is not recommended, include isolated secundum ASD, surgical repairs of septal defects (both atrial and ventricular), and PDA.

·         LMWH is more effective than standard low-dose heparin in general surgical patients, patients undergoing elective hip surgery, and patients with stroke or spinal injury. For those undergoing genitourinary, neurologic, or ocular surgery, intermittent pneumatic compression, with or without graduated compression stockings, is effective prophylaxis against venous thrombosis and does not increase the risk of bleeding.

·         The ALLHAT trial is the largest multicenter, double-blind, controlled clinical trial designed to evaluate the effects of four different classes of antihypertensive drugs (e.g., thiazide diuretics, ACE inhibitors, alpha blockers, and calcium blockers) on CHD and stroke risk. It showed no superiority of ACE inhibitors, calcium blockers, or alpha blockers over diuretics in preventing CHD events.

·         Mitral valve prolapse (MVP) in the absence of other systemic manifestations of Marfan's syndrome has been called Marfan syndrome-forme fruste, in view of the similar pathologic appearance of the myxomatous mitral valve in both disorders. Isolated mitral valve prolapse is more common than Marfan syndrome.

·         The most common site of origin of atrial myxomas is the fossa ovalis. To prevent recurrence of myxoma, a wide resection of the fossa ovalis area of the interatrial septum is performed during surgical excision.