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Pharma Finals > Chapter 24: Treatment of CHF > Flashcards

Chapter 24: Treatment of CHF Flashcards

1
Q

Preload is proportional to the end-diastolic ventricular volume,
or the amount of blood in the ventricles immediately before systole.; the
amount of fluid the heart must pump

A

Preload

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2
Q

afterload can be related to the amount of systemic resistance
the ventricles must overcome to eject blood into the vasculature.; the
pressure that the heart must work against in the peripheral vessels

A

Afterload

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3
Q

increasing or decreasing the force of muscular contractions

A

Inotropic

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4
Q

influencing the rate especially of the heartbeat

A

Chronotropic

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5
Q

affecting the conductivity of cardiac muscle —used of the
influence of cardiac nerves

A

Dromotropic

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6
Q

Chronic condition in which the heart is unable to pump sufficient quantity
of blood to meet the needs of peripheral tissues

A

Congestive Heart Failure

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7
Q

Arises from the tendency of fluid to accumulate in the lungs and peripheral tissues

A

Congestion

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8
Q

CHF symptoms (PDD)

A

○ Peripheral edema
○ Decreased tolerance for physical activity
○ Dyspnea, SOB in pulmonary congestion

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9
Q

CHF Prognosis

A

approximately 50% of patients die within 5 years after they are
diagnosed with heart failure

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10
Q

CHF Pathophysiology

A

Mechanisms underlying chronic heart failure:
● Disturbances in the cardiac cell
● Altered genetic expression of myocardial cells
● Systemic changes in hemodynamics and
● Humoral factors
● Self-perpetuating - initiates a vicious cycle that leads to
further decrements in cardiac function

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11
Q

Primary problem: the heart is unable to push blood forward through the circulatory system -> pressure to build up in the veins returning to the heart→ blood begins to back up in the venous system → increase pressure gradient for fluid to move out of the capillaries → edema or congestion

A

Congestion in Left and Right Heart Failure

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12
Q
  • The left atrium and ventricle are unable to pump the blood coming from the lungs
  • Pressure build up in the pulmonary veins, fluid accumulates in the lungs
  • Pulmonary edema
A

Left HF

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13
Q
  • The right atrium and ventricle are unable to
    handle blood returning from the systemic
    circulation
  • Fluid accumulate in the peripheral tissues
  • Ankle edema and organ congestion
A

Right HF

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14
Q
  • Usually caused by hypertension, CAD, and valvular diesease
  • Divided into two subtypes: Systolic (reduced ED), Diastolic (preserved ventricular function)

Symptoms:
- cough
- crackles
- pink sputum
- tachycardia
- fatigue
- cyanosis
- exertional dyspnea

A

Left HF

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15
Q
  • Can be caused by left ventricular failure, right MI, or pulmonary hyptertension
  • Right ventricle cannot empty completely
  • May be secondary to pulmonary problems (COPD)

Symptoms:
- peripheral edema
- ascites
- enlarged liver and spleen
- JVD
- weight gain
- increased peripheral venous pressure

A

Right HF

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16
Q
  1. Digitalis
  2. Phosphodiesterase (PDE) inhibitors
  3. Dopamine, Dobutamine

(DPD - PIA)

A

Agents That Increase Myocardial Contraction Force (Positive Inotropic
Agents)

17
Q

○ ACE inhibitors (-pril)
○ ARBs (-sartan)
○ Direct renin inhibitor - Aliskiren
○ Beta blockers (-olol)
○ Diuretics
○ Vasodilators

A

Agents That Decrease Cardiac Workload

18
Q

● Digoxin, digitoxin
● Benefits: Improves cardiac pumping ability; increases CO at rest and during exercise; increased exercise tolerance; decrease symptoms of HF and decrease hospitalization

A

Digitalis
(Positive Inotropic Agent)

19
Q

Effects:
○ direct inhibitory effect on SNS activity; reflex stimulation of Vagus nerve
○ stabilize HR, slow impulse conduction

● Indications: systolic heart failure (heart failure with reduced ejection fraction
(HFrEF)); Ejection fraction <40% and Atrial Fibrillation, Atrial Tachycardia
● AE: GI distress, CNS disturbance (drowsiness, fatigue, confusion, visual
disturbances), arrhythmias: (PACs, PVCs, VTach, high degree AV block,
paroxysmal atrial tachycardia)

A

Digitalis
(Positive Inotropic Agent)

20
Q

Increases myocardial
contractility by elevating
intracellular calcium levels and facilitating actin-myosin
interaction in cardiac cells; may also help normalize autonomic
effects on the heart

A

Digitalis
(Positive Inotropic Agent)

21
Q

● Inamrinone, milrinone
● Cause a cAMP-mediated increase in intracellular calcium ->
increases force of contraction
● Phosphodiesterase enzyme breaks down cAMP in cardiac cells
● cAMP is a common second messenger
○ acts on membrane calcium channels to allow more calcium
to enter the cell

A

Phosphodiesterase (PDE) inhibitors

22
Q

● Dopamine, Dobutamine
● Indications: Acute or severe HF (not used to control chronic HF)
● MOA: stimulate beta 1 receptors on the myocardium
● Effect: positive inotropic effect

A

Drugs used to stimulate the heart

23
Q

Drugs affecting RAAS
- ACE inhibitors (-pril)
- ARBs (-sartan)
- Direct renin inhibitor (Aliskiren)

A

Agents That Decrease Cardiac Workload

24
Q

○ Angiotensin II:
■ promotes abnormal growth and remodeling of the heart
■ growth and hypertrophy and thickening of peripheral blood vessels -
> reducing lumen size
■ Angiotensin III (by product): Promotes aldosterone secretion ->
increase water reabsorption
○ ACEi prevent angiotensinogen II-induced cardiac remodeling
○ Increases bradykinin(a vasodilator) levels in the bloodstream
○ AE: skin rashes, GI discomfort, dizziness, persistent dry cough

A

ACE inhibitors (-pril)

25
Q

Alternative for those unable to tolerate ACEi

A

ARBs (-sartan)

26
Q

Directly inhibit renin’s ability to convert angiotensinogen to angiotensin

A

Direct renin inhibitor - Aliskiren

27
Q

● Decrease the excessive sympathetic activity associated with HF
● MOA: Beta blockers bind to beta-1 receptors on the myocardium and block the effects of NE and Epinephrine

A

Beta Blockers

28
Q

Effects:
○ Reduce HR (negative chronotropic effect)
○ Reduce myocardial contraction force (negative inotropic effect)
● May also prevent anginas and arrhythmias

A

Beta blockers

29
Q

○ Carvedilol, nevibolol
○ MOA: block beta 1 receptors on the heart and block alpha-1(vasoconstriction)
receptors on the vasculature -> peripheral vasodilation
■ Reduce afterload and reduce myocardial stress

A

3rd generation beta blockers

30
Q

AE: excessive inhibition of the heart: slow HR and reduced contraction force
○ Adjust the dose

A

Beta blockers AR

31
Q

● Increase the excretion of sodium and water
● Ability to reduce congestion in the
lungs and peripheral tissues.
● Decrease cardiac preload
● MOA: inhibit reabsorption of
sodium from the nephron
● AE: volume depletion,
hyponatremia, hypokalemia, altered
pH balance, arrhythmia

A

Diuretics

32
Q

● Vasodilate peripheral vessels
● Reduce peripheral vascular resistance → decrease blood returning to the heart (cardiac preload)

A

Vasodilators

33
Q

MC used in HF:

A

○ Prazosin
○ Hydralazine
○ Organic nitrates (nitroglycerin, isosorbide dinitrate, sodium nitroprusside

34
Q

○ Selective inhibitor of PDE5
■ PDE6 normally inactivates cGMP
■ By inhibiting PDE 5, sildenafil prolongs the action of cGMP, enhancing vasodilation
○ Indications: erectile dysfunction, pulmonary hypertension

A

Sildenafil

35
Q

○ Alpha-1 receptor blocker
○ Blocks alpha-1 receptors on vascular smooth muscle -> vasodilation

A

Prazosin

36
Q

● All can decrease cardiac workload by decreasing peripheral vascular resistance
● AE: headaches, dizziness, hypotension, orthostatic hypotension, reflex tachycardia

A

Vasodilators

Pharma Finals (4 decks)

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