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