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1. Why we cannot give beta blocker to patient who been diagnosed with
aortic stenosis with acute heart failure?
The natural history of aortic stenosis involves a prolonged latent
period, during which progressive worsening of left ventricular (LV)
outflow obstruction leads to hypertrophic changes in the left ventricle.
As the aortic valve area becomes less than one half its normal size of 3
to 4 cm2 , a measurable pressure gradient between the left ventricle
and ascending aorta may be detected on echocardiography or by
direct measurement at cardiac catheterization. This change reflects
compensatory increases in LV pressures that contribute to the
maintenance of adequate systemic pressures. One consequence is LV
hypertrophy with subsequent diastolic dysfunction and increased
resistance to LV filling. Thus, a strong left atrial contraction is needed
to provide sufficient LV diastolic filling and support adequate stroke
volume. Increasing overall myocardial contractility and augmenting
preload with an increased atrial kick preserve LV systolic function,
typically while the patient remains asymptomatic.
As aortic stenosis worsens, with the aortic valve area decreasing to 1
cm2 or less , changes in LV function may no longer be adequate to
overcome the outflow obstruction and maintain systolic function, even
when complemented by an increase in preload. The resulting
impairment in systolic function, alone or combined with diastolic
dysfunction, may lead to clinical heart failure. Beta blockers may
depress LV systolic function and aggravate the symptoms of HF,
(decrease heart rate, decrease blood pressure, decrease contractility,
decrease cardiac output initially therefor decrease in systolic
contraction). Patients with symptoms and signs of HF are not good
candidates for this treatment option. Beta blockers may be used in AS
patients with angina pectoris or AF with rapid ventricular response.
Although the majority of these patients are also affected by heart
failure, the recommended drugs able to counteract the negative
effects of heart failure are generally precluded due to the fear that
they could worsen flow obstruction at the valve level.

Angiotensin II causes vasoconstriction increasing afterload thus increasing systemic blood pressure. severe bradycardia. Angiotensin contributes to the production of aldosterone which normally acts to retain sodium and water. ACE inhibitors can reduce the symptoms of heart failure and have been shown in multiple clinical trials to have a mortality benefit in systolic heart failure patients. It is reasonable to withhold beta-blockers in patients who were previously taking them in the outpatient setting for chronic systolic heart failure when they are admitted with a heart failure exacerbation. . Beta-blockers are contraindicated specifically in systolic heart failure when pulmonary edema is present.These drugs have been shown in multiple clinical trials to give a significant mortality benefit. This enzyme converts angiotensin I to angiotensin II. What are the indications for aortic valve replacement (AVR) in aortic stenosis and aortic regurgitation? For either aortic regurgitation or stenosis. Which medication for systolic cardiac heart failure reduce mortality? Why? Angiotensin converting enzyme inhibitors (ACE inhibitors) are a class of oral medications that act primarily through blockade of the angiotensin converting enzyme (ACE). when there are signs of cardiogenic shock.Beta-blockers should be initiated in patients hospitalized for acute systolic congestive heart failure prior to hospital discharge. 3. Doses are usually started low and titrated up to a predetermined goal dose if the patient is able to tolerate it. aortic valve replacement is indicated when symptoms occur or if the left ventricular systolic function decline. hypotension or wheezing related to asthma. Reducing the activity of the reninangiotensin-aldosterone system (RAAS) is crucial in heart failure during which it is overactive and contributes to negative remodeling. AVR is indicated even if the left ventricular ejection fraction is normal when the end systolic dimension increases to > 55 mm or end diastolic dimension to > 75 mm on echocardiography.2.

rivaroxiban. but an echo will show a pericardial effusion and if the right ventricle is collapsing in diastole. Pericardiocentesis is therapeutic. requires a very compliant left ventricle and can be a sign of systoliv cardiac heart failure. muffled heart sounds. aneurysm aortic atheroma) NOTE: Female gender is also included in this scoring system = 1 point! 5. The S4 heart sound is almost always pathologic and can occur in the setting of diastolic heart failure and/or myocardial ischemia. Which atrial fibrillation patient can we use only aspirin for and who needs full anticoagulation to prevent stroke? Use the CHA2DS2 Vasc Score: If 0-1 points then aspirin 81 mg . Beck’s triad: Hypotension. so collapses first. It usually occur in early diastole. not an echocardiographic one. dabigatran.heart shaped like a canteen Treat with IV fluids to increase preload and prevent right ventricular collapse. a.a. then tamponade is thought to be present (right ventricle is lowest pressure chamber. but can also be there in normal healthy hearts.325 mg If > 2 points then full anticoagulation (warfarin. Pressure is lower in diastole than systole). the ventricular gallop can be present in systolic heart failure. previous MI. It usually .k. How to diagnose and treat cardiac tamponade? Cardiac tamponade is a CLINICAL diagnosis. elevated neck veins Pulsus paradoxus: Abnormal if > 12 mmHg. > 75 = 2 points) Diabetes Stroke/TIA (2 points) Vascular disease (peripheral arterial disease. during passive Left ventricle filling.4. 6. What are the causes of S3 and S4 heart sound? An S3 heart sound. apixiban) Congestive heart failure Hypertension Age ( > 65 = 1 point. Water Bottle Heart: Chest x-ray finding .

What is the treatment for coronary vasospasm? Coronary vasospasm is a sudden. and sudden death. the heart becomes weaker. requires anoncompliant left ventricle and can be a sign of diastolic cardiac heart failure. It can occur in multiple vessels. HOCM can result in clinic heart failure. intense vasoconstriction of an epicardial coronary artery that causes vessel occlusion or near occlusion. What is cardiomyopathy? In cardiomyopathy.occur in late diastole. There are three types of cardiomyopathy: Dilated cardiomyopathy: This results in left ventricular systolic dysfunction and clinical manifestations of congestive heart failure. the heart muscle becomes enlarged. As cardiomyopathy worsens. familial and other rare causes. life-threatening arrhythmias. during active left ventricle filling. infiltrative disorders. Hypertrophic cardiomyopathy: Also known as hypertrophic obstructive cardiomyopathy (HOCM). 8. The catecholamines decide to go to the alpha receptors and stimulate them which can worsen vasospasm.Dont give beta-blocker so they say this causes “unopposed” agonism at alpha receptors since the circulating catecholamines can’t act on the beta-receptors if a beta-blocker is given. is an important cause of chest pain syndromes that can lead to myocardial infarction (MI). In rare cases. and familial. It can cause Prinzmetal's angina. It's less able to pump blood through the body and maintain a normal electrical rhythm. Etiologies include viral. thick. this results in abnormal hypertrophic changes most commonly in the interventricular septum with pathologic “myocardial disarray”. ventricular arrhythmias. or rigid. Coronary artery vasospasm. alcoholic. . idiopathic. 7. the muscle tissue in the heart is replaced with scar tissue. HOCM is familial in about 50% of cases and transmitted in an autosomal dominant fashion. Causes include amyloid heart disease. or smooth muscle constriction of the coronary artery. Restrictive cardiomyopathy: This results in heart failure related to severe diastolic dysfunction. mitral regurgitation and sudden cardiac death. Use a nondihydropyridine calcium channel blocker.

What are the signs/symptoms and issues with digoxin toxicity? The sign and symptoms are nausea/Vomiting/Abdominal pain. Why left heart failure is the common cause of right heart failure? When anything causes left heart failure the LV pressure increases and transmits back to the lungs causing pulmonary hypertension. . 10. symptoms of arrhythmia. The classic ECG has the "reverse check" sign. Digoxin causes EVERY arrhythmia EXCEPT rapidly conducted atrial rhythms (atrial fibrillation or flutter with a rapid ventricular rate). In the setting of digoxin toxicity and hyperkalemia.9. Digoxin toxicity can cause hyperkalemia. The massive influx of calcium into myocytes after the IV calcium is given has been theorized to induce a non-contractile state and has been termed "Stone Heart" . weakness/dizziness . giving IV calcium may be potentially fatal. Altered mental status. Vision changes (yellow vision or “Xanthopsia”). This then strains the right heart and eventually causes right heart failure. The two pathognomonic rhythms in digoxin toxicity are atrial tachycardia with 2:1 block and bidirectional ventricular tachycardia.