Cardiovascular IV - CHF Flashcards Preview

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Flashcards in Cardiovascular IV - CHF Deck (32):

When do symptoms of CHF become noticeable?

What are the adaptive responses to cardiac myocyte loss/dysfunction and/or persistant overload?

Only when the LV remodeling process is nearly completed


Myocardial hypertrophy and LV chamber dilation


In CHF what does chamber dilation augment? What does this result in?

Chamber dilation augments diastolic wall stress --> this leads to deformation of the LV wall, functional mitral regurgitation, as well as myocyte apoptosis


In response to CHF local neurohumoral systems become activated with increased? What occurs to the parasympathetic tone?


The structural and functional alterations constitue what is termed ____ ____.

Increased NE and angiotensin II; Parasympathetic tone is reduced


Ventricular remodeling


What is ventricular remodeling characterized by?


An increase in ventricular volume helps to maintain cardiac output but at the cost of? What produces further damage?

Myocyte hypertrophy and elongation


Maintain CO at the cost of increasing ventricular filling pressures; increase in diastolic stretch and pressure produces futher damage


Neurohumeral activation occurs with a decreased __ tone and increased ___ tone. Can result in?


What causes arterial vasoconstriction with resultant maldistribution of flow?

vagal; sympathetic; tachycardia


Activation of the renin-angiotensin system and increased sympathetic tone


Treatment of chronic CHF is directed initially at?

Goals for the treatment of CHF?

Improving organ perfusion and relieving excess fluid accumulation


a. Improve peripheral organ perfusion

b. Reduce ventricular size (decrease stress on myo.)

c. Reduce pulmonary congesion (decrease stress)

d. Reduce ventricular remodeling and cell death


5 Major classes of drugs used to treat CHF?

a. ACE Inhibitors

b. Beta-blockers

c. Diuretics (thiazides or loop)

d. Vasodilators (hydralizine or nitroprusside)

e. Digitalis


Thiazide or loop diuretics can relieve ____ with what two detriments?

Congestion; they dont improve long term surival and may exacerbate malignant remodeling


What is the only positive ionotrope CHF medication?



What can beta-blockers do?

Improve ejection fraction and mortality outcome with chronic treatment as well as decrease risk of sudden death


Vasodilator therapy:

1. The failing heart could benefit by reducing what?

2. How would this reduction help the patient?

1. Reducing afterload (via arterial dilation) and pre-load (through venodilation)


2. This would increase organ perfusion, relieve pulmonary congestion, and reduce ventricular chamber size.


Vasodilator therapy:

1. Decrease in afterload causes a greater augmentation of ____ ____ in the failing heart than in the normal heart.

2. Reduction of preload allows alleviation of? This is especially beneficial in what?

1. stroke volume


2. pulmonary congestion without severe reductions in stroke volume; this ies especially beneficial in reducing the phenomena of decompensation and acute severe congestion


Vasodilator therapy:

1. In the presence of ventricular failure, the ___ length in ___ is increased.

2. For the same relative change in afterload, the increase in shortening is greater where? Why?

1. fiber; diastole


2. Fiber shortening is greater in the failing ventricle due to the relative flattening of the end systolic force:length relationship


Vasodilator therapy:

1. Normally, the ventricle operates on a steep starlinc curve with LVEDP < ____mmHg, where small changes in filling pressure yield? 


2. Also, normally, stroke volume is largely independent of the ____. 

1. 12; a large change in stroke volume


2. afterload


Vasodilator therapy:

1. In failure, what occurs to the Starling curve? 


2. The failing ventricle is highly afterload ____.

1. It moves down and to the right


2. dependent


Vasodilator therapy:

1. What is the net result in normal circulation of reducing afterload and incurring venodilation?

2. When afterload is reduced in the presence of failure, what occurs to stroke volume? Since the starling curve is relatively flattened, what does a simultaneous decrease in venous tone lead to?

1. decrease in stroke volume

2. Increased stroke volume; Bc the curve is flattened there is a decrease in LVEDP with only a small decrease in stroke volume. The net result of these opposing consequences may be an increase in stroke volume


Vasodilator therapy:

Only two types of vasodilator therapy have proven to improve patient mortality outcomes: what are they?

a. Combined hydralazine with isosobide (Hyd-iso)

b. ACE inhibitors


Beta-adrenergic antagonist:

1. Beta adrenergic receptor blockade improves?

2. Mechanisms for doing this?

3. Drug examples?

1. Beta blockers improve overall prognosis and ventricular function

2. They do this (above) by reducing potential for sudden death due to arrhythmias, reducing Na/H2O retention (RAAS inhibition), reducing myocyte apoptosis, and reducing/reversing remodeling

3. Metoprolol (longer acting) and carvedilol



1. The positive inotriopic effect of digitalis is due to its ability to?

2. What does digitalis do for phase 2?

1. Increase Ca__ within myocytes

2. Enhances influx of Ca++



1. What pump does digitalis block? How?

2. By increasing intracellular calcium what is it increasing?

3. What pump is being depressed by digitalis?


1. Na/K+ pump by competitive inhibition of K+

2. Increasing contractile strength (making it a true +inotrope)

3. The exchange site of Calcium out for sodium in. Thus there is an increase of intracellular calcium and a decrease of sodium



Digitalis improves ______ performance in the failing heart by ____ ___ and reduces _____ ____.

Ventricular; decreasing EDP (end diastolic pressure); congestive symptoms


Primary elecrophysiological effects of digitalis:

Purkinje fibers:

1. What does it do to Vmax?

2. What does it do to action potential duration?

3. Increases _____ spontaneously in phase 4. 

1. Decrease

2. Decrease

3. automaticity


Primary elecrophysiological effects of digitalis:

1. Effect on phase three?

2. Effect on phase four?

3. Because it causes the signal to pass from cell to cell more slowly it is the perfect way to allow ____ ___.

1. At phase 3, digitalis causes a more rapid repolarization due to increased intracellular Ca++

2. Phase four can be stimulated by itself (not good)

3. re-entry arrhythmias


Primary elecrophysiological effects of digitalis:

1. What does digitalis do to the SA node?

2. What does it do the atria and ventricles: Vm? Action potentials? dV/dt?

1. High doses partially depolarize the node and lock it in the inactivated state

2. Digitalis decreases resting Vm; Decreases AP amplitude (thus decreases refractory period); decreases dV/dt in phase 0


Primary elecrophysiological effects of digitalis:

Indirect myocardial electrical effects of digitals?

a. Increase vagal and decrease sympathetic impulses to the heart (can be used to suppress SV tachycardia bc it slows nodal conduction but it can also block the SA node)

b. Increase sympathetic impulses to the heart at toxic doses 


Untoward effects of digitalis:

1. Therapeutic ratio?

2. Common effects?

3. CNS effects?

4. Contraindication? Why?

1. Low therapeutic ratio

2. Arrhythmias and heart block

3. HA, fatigue, malaise, disorientation, mental confusion, aphasia, delirium, hallucinations, blurred vision, anoxia

4. NEVER use quinidine, it increases the concentration of digitalis in the plasma.



1. Treat what part of CHF?

2. When can they be used?

1. "congestion"

2. Diuretics can be used in both acute decompensation CHF emergencies or in classic CHF associated with excessive water/salt retention



1. When are thiazides ineffective?

2. What is furosimide effective for?

3. Potential adverse effect?

1. Thiazides are innefective if GFR <30%

2. Furosimide is effective in decompensation emergencies and in patients with excessive Na/H20 retention

3. Hypokalemia from the diuretic may predispose patients to digitalis toxicity



1. What type of remodeling occurs when asymptomatic? Symptomatic?

2. When does the LVEF% significantly drop?

3. When does peak VO2 significantly drop?

4. What are the best early/long term drugs?

1. ventricular; peripheral

2. LVEF drops when symptomatic

3. Peak VO2 also drops when symptomatic

4. ACE Inhibitors or Beta blockers


1. What drug(s) should be used when the systolic BP is greater than or equal to 90mmHg?

2. What drug(s) should be used when systolic BP is less than 90mmHg?

3. Function of nitroprusside?

1. Nitroprusside and furosemide

2. Dopamine

3. Nitrodilator to arteries over veins causing a relief in afterload --> increase perfusion. Increase Co>>decrease in TPR


1. Function of furosemide?

2. Function of Amrinone?

3. Function of dobutamine?

4. Function of A+Dob (amrinone + dobutamine)?

1. Treats congestion only

2. Increases cAMP and thus also is a poisitive inotrop and can stimulate the heart

3. Beta agonist: stimulates the heart, can be used short term

4. Amrinone potentiates dobutamine --> additional stimulation effect


1. Function of Levosimenden?

2. Function of dopamine?

3. Function of N+Dop (Nitroprusside plus dopamine)

1. Ca++ sensitizer - makes the heart more sensitive to calcium to increase contraction

2. Dopamine is a peripheral constrictor and renal vasodilator

3. If BP is high, add nitroprusside to Dopamine and it wont bottom out because the increase in CO is much much greater than the decrease in TPR