SITI NUR WARDAH BINTI MUSTAPA

KAMIL
C1112848

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.

2. What are the indications for aortic valve replacement (AVR) in aortic
stenosis and aortic regurgitation?
For either aortic regurgitation or stenosis, aortic valve replacement is
indicated when symptoms occur or if the left ventricular systolic
function decline. 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.
3. 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). This enzyme converts angiotensin I to
angiotensin II. Angiotensin II causes vasoconstriction increasing
afterload thus increasing systemic blood pressure. Angiotensin
contributes to the production of aldosterone which normally acts to
retain sodium and water. Reducing the activity of the reninangiotensin-aldosterone system (RAAS) is crucial in heart failure during
which it is overactive and contributes to negative remodeling. 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. Doses are usually started low and titrated up to
a predetermined goal dose if the patient is able to tolerate it.
Beta-blockers are contraindicated specifically in systolic heart failure
when pulmonary edema is present, when there are signs of cardiogenic
shock, severe bradycardia, hypotension or wheezing related to
asthma.Beta-blockers should be initiated in patients hospitalized for
acute systolic congestive heart failure prior to hospital discharge. 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.These drugs
have been shown in multiple clinical trials to give a significant
mortality benefit.

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

occur in late diastole, during active left ventricle filling, requires anoncompliant left ventricle and can be a sign of diastolic cardiac heart
failure.
7. What is cardiomyopathy?
In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid.
In rare cases, the muscle tissue in the heart is replaced with scar
tissue. As cardiomyopathy worsens, the heart becomes weaker. It's
less able to pump blood through the body and maintain a normal
electrical rhythm. There are three types of cardiomyopathy:
Dilated cardiomyopathy: This results in left ventricular systolic
dysfunction and clinical manifestations of congestive heart failure.
Etiologies include viral, alcoholic, idiopathic, familial and other rare
causes.
Hypertrophic cardiomyopathy: Also known as hypertrophic obstructive
cardiomyopathy (HOCM), this results in abnormal hypertrophic changes
most commonly in the interventricular septum with pathologic
myocardial disarray. HOCM is familial in about 50% of cases and
transmitted in an autosomal dominant fashion. HOCM can result in
clinic heart failure, life-threatening arrhythmias, mitral regurgitation
and sudden cardiac death.
Restrictive cardiomyopathy: This results in heart failure related to
severe diastolic dysfunction. Causes include amyloid heart disease,
infiltrative disorders, and familial.
8. What is the treatment for coronary vasospasm?
Coronary vasospasm is a sudden, intense vasoconstriction of an
epicardial coronary artery that causes vessel occlusion or near
occlusion. It can cause Prinzmetal's angina. It can occur in multiple
vessels. Coronary artery vasospasm, or smooth muscle constriction of
the coronary artery, is an important cause of chest pain syndromes
that can lead to myocardial infarction (MI), ventricular arrhythmias,
and sudden death.Dont give beta-blocker so they say this causes
unopposed agonism at alpha receptors since the circulating
catecholamines cant act on the beta-receptors if a beta-blocker is
given. The catecholamines decide to go to the alpha receptors and
stimulate them which can worsen vasospasm. Use a nondihydropyridine calcium channel blocker.

9. What are the signs/symptoms and issues with digoxin toxicity?

The sign and symptoms are nausea/Vomiting/Abdominal pain,
weakness/dizziness , symptoms of arrhythmia, Altered mental status,
Vision changes (yellow vision or Xanthopsia).
Digoxin causes EVERY arrhythmia EXCEPT rapidly conducted atrial
rhythms (atrial fibrillation or flutter with a rapid ventricular rate). The
classic ECG has the "reverse check" sign. The two pathognomonic
rhythms in digoxin toxicity are atrial tachycardia with 2:1 block and
bidirectional ventricular tachycardia. Digoxin toxicity can cause
hyperkalemia. In the setting of digoxin toxicity and hyperkalemia,
giving IV calcium may be potentially fatal. 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" .

10.
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. This then
strains the right heart and eventually causes right heart failure.