Congestive Heart Failure: Question Set #3

Most important acute factor in changing the position of the force-velocity in ventricular function curves:
1. reduction in parasympathetic tone
2. circulating catecholamine levels
3. adrenergic nerve activity
Effect(s) of circulating catecholamines of cardiac function:
1. positive chronotropism
2. enhanced contractility
3. both
4. neither
Example(s) of drugs that improve ventricular performance:
1. theophylline
2. caffeine
3. dopamine
4. A & C
5. A, B & C
Physiological depressants of ventricular performance:
1. hypercapnea
2. acidosis
3. ischemia
4. hypoxia
5. all the above
For the same level of aortic pressure, afterload increases with ventricular dilatation:
1. true
2. false
Stress developed in the wall of ventricle during ejection -- dependencies:
1. ventricular dimension
2. aortic pressure
3. both
4. neither
Agents which decreased ventricular performance:
1. calcium
2. caffeine
3. cardiac glycosides
4. disopyramide (Norpace)
5. theophylline
Afterload and left ventricular stroke volume: relationship
1. inversely proportional
2. directly proportional
Ventricular performance in the failing heart (with no preload reserve) is determined by:
1. afterload
2. circulating steroid levels
3. extent of ventricular dilatation
In the failing hard, the effect on cardiac output and oxygen demand when afterload increases (increased vasoconstriction):
1. cardiac output increased; oxygen demand increased
2. cardiac output decreased; oxygen demand decreased
3. cardiac output decreased; oxygen demand increased
4. cardiac output increased; oxygen demand decreased
Effect of exercise on preload and ventricular filling:
1. decreased due to reduced venous return (peripheral pooling)
2. increased with due to enhanced venous return and ventricular filling
3. no effect in the normal heart
With exercise, what happens to arterial pressure (normal heart)?
1. notable increase
2. decrease
3. minor increase
4. no change
Adaptive mechanism(s) assisting the failing heart:
1. Frank-Starling relationship
2. myocardial hypertrophy
3. cardiac output redistribution (e.g.,from skin to brain and heart)
4. increasing intravascular volume
5. all of the above
Consequences of reninangiotensin system activation:
1. decreased angiotensin II levels
2. increased aldosterone levels
3. vasodilatation
4. increase sodium excretion
5. none of the above
Circulating norepinephrine levels in patients with heart failure:
1. typically elevated
2. typically depressed
3. no change from normal