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Pharmacology > Heart Failure Drugs > Flashcards

Heart Failure Drugs Flashcards

1
Q

Heart Failure Defined and symptoms

A

HF:
- when CO is inadequate to provide O2 needed by the body

Symptoms:
- Tachycardia, decreased exercise tolerance, peripheral/pulmonary edema, cardiomegaly

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2
Q

Risk factors for HF

A 
Hypertension
CAD
MI
Diabetes
Family History 
Use of Cardiotoxins
Obesity
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3
Q

HFrEF vs HFpEF

A

Systolic HF (contraction problem)

Diastolic HF (filling problem)
- more difficult to treat
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4
Q

Pathophysiology of HF

A

CHF:
abnormal increases in blood volume and interstitial fluid.
- LHF = dyspnea from pulmonary congestion
- RHF = peripheral edema

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5
Q

Role of Physiological Compensation in HF

A

The decrease in CO causes the SNS and RAAS to activate which increases all factors that will exacerbate heart failure
- by increasing force, preload, after load, and remodeling

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6
Q

Preload

A

force of contraction depends on how far the myocardial cells are stretched. (increasing preload will increase contractility)
** this has a limit

HF- preload is beyond stretching limits and thus increase in preload causes a decrease in contractility

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7
Q

Afterload

A

Force against which ventricles must act

- based on vascular resistance

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8
Q

Contractility

A

Force of cardiac muscle contraction is directly related to calcium levels
Sources: Voltage sensitive calcium channels, Na+/Ca2+ exchanger, and SR
Removal: Na+/Ca2+ exchanger, Reuptake into the SR

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9
Q

Therapeutic Strategies for HF

A

HF is a progressive disease - only cure is transplant

  • treatment is directed towards:
    1) reducing symptoms and slowing progression
    2) managing acute episodes
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10
Q

Chronic HF therapeutic Strategies

A 
Light aerobic exercise
Low dietary sodium 
Smoking cessation 
Decreasing weight
Fluid restriction 
Treat comorbid conditions
Use: ACEI, diuretics, beta blockers, and Inotropic agents
** DO NOT USE: NSAIDS, Ca2+ channel blockers, and alcohol
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11
Q

Drugs to Treat HFrEF (systolic)

A 
Diuretics
Spironolactone (K-sparring: aldosterone antagonist) 
ACEI/ARBs
Direct vasodilators
Beta blockers
Inotropic agents
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12
Q

Drugs to Treat HFpEF (diastolic)

A

Diuretics (be careful with reducing SV to much)
ACEI/ARBs
beta-blockers
Calcium channel Antagonist

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13
Q

AHA classification of HF

A

Stage 1: high risk for developing HF
- HTN, DM, CAD, Family history
Stage 2: Asymptomatic HF
- previous MI, LV dysfunction, Valvular heart disease
Stage 3: Symptomatic HF
- Structural heart disease. dyspnea and fatigue, impaired exercise tolerance
Stage 4: Refractory End Stage HF
- Marked symptoms at rest despite maximal medical therapy

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14
Q

NYHA classification of HF

A

Class I: No symptoms with ordinary physical activity
Class II: Ordinary physical activity somewhat limited by dyspnea (e.g climbing 2 flights of stairs)
Class III: Exercise is limited by dyspnea with moderate workload (e.g climbing 1 flight of stairs)
Class IV: Dyspnea at rest with little exertion

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15
Q

Recommended therapy for CHF

A

Diuretics. beta blocker, ACEI

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16
Q

Diuretics

A

Relieve pulmonary congestion and peripheral edema
reduces symptoms of volume overload
decrease plasma volume –> decreases VR –> decreases cardiac workload and O2 demand
Also decreases after load (reducing plasma volume and decreasing BP)

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17
Q

Clinical App. Diuretics

A

No evidence of mortality benefit alone

Thiazide infective with congestive symptoms
Loop: more effective (if edema is present)

18
Q

ACEI

A

Agents of choice for HF

  • Decrease vascular resistance and BP –> Increase CO by decreasing afterload
  • decrease in Na+ and H2O retention (dec. preload)
  • decrease in long term remodeling of the heart
19
Q

Clinical App. ACEI

A

Recommended:

  • Symptomatic HF
  • Asymptomatic patients with Decrease LFEF or history of MI

Suggested:
- patients at high risk of HF

20
Q

AE of ACEI

A 
Hypotension
Dry cough
hyperkalemia
angioedema
acute renal failure (bilateral renal artery stenosis)
Teratpgenic
21
Q

ARBS

A

Potent competitive antagonist of angiotensin II type I receptor (AT1 receptor)
do not produce dry cough
substitute for patients that can not take ACEI
AE: similar to ACEI and also teratogenic

22
Q

Direct Vasodilators

A

Hydralazine + Isosrbide dinitrate
- vasodilation –> decrease preload
- arterial dilation –> decreases PVR and afterload
(hydralazine - arterioles and nitrates- venules)

23
Q

Clinical app. Direct Vasoldilators

A

Patients who can not take ACEI or ARB
or
In African Americans with advanced stage HF (as adjunct)

24
Q

Direct vasodilators AE

A

Headache, dizziness. tachycardia. peripheral neuritis, and lupus like syndrome

Contraindicated: Sildenafil (severe hypotension)

25
Q

Beta Blockers

A

studies shown some reverse of Cardiac remodeling

  • Decrease HR and contractility and inhibit renin release
  • prevent deleterious effects of NE on cardiac muscle fibers (decrease remodeling)
    • can get initial exacerbation of symptoms (titrate the dose up)
26
Q

Clinical App. Beta blockers

A

recommended in addition with ACEI/ARB in patients with:

  • symptomatic HF
  • asymptomatic HF with decrease LVEF
    • use cautiously in decompensated HF or cardiogenic shock (can not take the initial exacerbated symptoms)
27
Q

Spironolactone

A

Patients with advanced Heart Disease have elevated aldosterone levels

MOA: aldosterone antagonism - prevents Na+ retention, myocardial hypertrophy, and hypokalemia

28
Q

Clinical App. and AE of spironolactone

A

CA:
- Plus ACEI are shown to decrease morbidity and mortality

AE:

  • Hyperkalemia
  • GI disturbances
  • CNS effects
  • Endocrine abnormalities
29
Q

Inotropic Agents

A

digoxin

  • cardiac glycoside
  • derivative from foxglove plant
  • widely used treatment in HF
  • Digoxin can decrease the symptoms of heart failure, increase exercise tolerance and decrease rate of hospitalization, but DOES NOT increase survival
30
Q

Digoxin disadvantages

A

Narrow therapeutic margin
unfavorable and complicated PK
Drug sensitivity varies between patients and with in therapy
sever and lethal side effects

31
Q

Digoxin MOA

A

Positive Iontropic:
increases cytosolic calcium by blocking Na+/K+ ATPase
** if extensively inhibited –> dysrhythmias

Negative Chronotropic: (dec HR)
- enhances vagal tone

32
Q

Digoxin PK

A 
Very potent (narrow TW)
Widely distributed (including CNS)
half life: 36-40 hours
Large Vd (loading dose required)
33
Q

digoxin AE

A

cardiac: arrhythmias, (slowing of AV conduction)
GI: anorexia and N/V
CNS: headache, fatigue, confusion, blurred vision, yellow-green color perception, and halos on dark objects

34
Q

Precipitating factors of digoxin toxicity

A
  • Hypokalemia
  • Overdose
  • hypomagnesemia or hypercalemia
  • hyperthyreosis
  • abnormal renal function
  • respiratory disease
  • acid-base imbalance
    • drugs causing digoxin displacement from tissue:
  • Quinidine, verapamil, and amiodarone
35
Q

Treatment of digoxin toxicity

A

withdraw drug
monitor plasma levels of digoxin and K+
adjust electrolytes
if Ventricular tachyarrhythmia: lidocaine or magnesium

Sever digoxin toxicity:

  • bradyarrthythmias, suppressed automaticity –> temp cardiac pacemaker
  • treat with digitalis antibodies (digoxine immune fab, digibind)
36
Q

Digoxin Contraindications

A

patients Right side HF
presence of uncontrolled HTN
presence of bradyarrhythmias
non-responders or intolerant patients

37
Q

Treatment of HFpEF (diastolic)

A

Diuretics: treat pulmonary edema, but caution because of reduction in SV (not wanted in diastolic HF)

ACEI/ARB: same benefits with systolic HF

Calcium Channel blockers: Decrease inotropic which increase relaxation time and increase filling

Beta-blockers: Similar to Calcium channel blockers

38
Q

Inotropic Agents used in treatment if Acute HF

A

PDE III inhibitors
Dopamine
Dobutamine
Glucagon

39
Q

PDE III inhibitors

A

Inamrinone
Milrinone

inhibits myocardial cAMP PDE activity thus increases cAMP levels (positive inotropic effect and increase CO)
possess systemic and pulmonary vasodilator effects (reduces preload and after load)
shown slightly to increase AV conduction
Short term therapy

40
Q

Dopamine

A

Stimulates both adrenergic and dopaminergic receptors
(dose dependent)
- Higher doses: affects both dopaminergic and b1 (produces cardiac stimulation- b1 as well as renal vasodilation- d1)

41
Q

Dobutamine

A

administered as a racemic mixture

  • (-) isomer is a1 receptor agonist and weak b1 agonist
  • (+) isomer is an a2 antagonist and a potent b1 agonist and a mild b2 agonist
  • therapeutic levels stimulates b1 receptors most
  • used to increase CO in acute management
42
Q

Glucagon

A

Stimulates Adenylyl cyclase to produce cAMP (binds to GPCR) leading to potent inotropic and chronotropic effects

  • produces similar effects of beta agonist but without using beta receptors
  • Used for cardiac stimulation in beta blocker overdose

Pharmacology (20 decks)

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