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Cardio Pharm > Congestive Heart Failure > Flashcards

Congestive Heart Failure Flashcards

1
Q

TREATMENT OF CONGESTIVE HEART FAILURE goals

A
  1. Improve contractility (inotropes) 2. ↓ AL w/ ace inhib. & some vasodil 3. ↓ PL w/ diuretics & vasodil
    Acute HF: recent onset SOB. (Pulmonary Edema). Cardiogenic shock due to vasoconstriction & low systolic BP (<90).
    Chronic HF: when untx: symptoms of salt & H2O retention
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2
Q

Digitalis compounds

A

DIGOXIN ( more widely used), DIGITOXIN
= cardiac glycosides
-increase calcium at rest

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3
Q

DIGOXIN

A
  • Digitalis compound
  • Mechanism: Major: inhibit Na/K ATPase, and increase calcium at rest
  • Admin/Use: only orally active positive inotropes
  • Start low dose, titrate up and be careful with increasing doses
  • Digoxin: renal metab. (quinidine, verapamil decreases renal clearance → ↑[2x] which ↑ toxicity)
  • t½ 40 hrs
  • Doesn’t ↓ mortality and has many side effects so is not a primary drug!
  • CHF w/ AF (↓AV nodal conduction)
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4
Q

DIGITOXIN

A
  • Digitalis compound
  • Mechanism: Major: inhibit Na/K ATPase, and increase calcium at rest
  • Admin/Use: only orally active positive inotropes
  • Start low dose, titrate up and be careful with increasing doses
  • Digitoxin: hepatic metab
  • long t½ 170 hrs
  • Doesn’t ↓ mortality and has many side effects so is not a primary drug!
  • CHF w/ AF (↓AV nodal conduction)
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5
Q

Digitalis Compounds Mechanism

A

-Mechanism: Major: inhibit Na/K ATPase
→ ↑intracellular Na
→ ↓Na/Ca exchange
→ ↑intracellular “resting/trigger” Ca
→ ↑total Ca which means there is more Ca present during an action potenional → ↑force of contraction
Minor: direct/autonomic effect on cardiac electrical activity: brady and slowing of AV nodal conduction
- @ [low] → vagomimetic: ↓AV nodal conduction, ↓HR (↑filling → ↑CO and also ↓ 02 demand), sympatholytic: ↓renin, vasodilation
- @ [high]: sympathomimetic: ↑HR, ↓AP duration (→ ectopic beats, arrhythmias)

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6
Q

Risks of Digitalis Compounds

A

BOTH ↑ risk of toxicity w/ non-K+-sparing (thiazide & loop) diuretics⇒ diuretics cause hypokalemia and K+ is a competitive antagonist for digoxin
Reversal: - withdrawal (but long t½)
- K+ supplements (digoxin binds K+ site @Na/K ATPase)

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7
Q

AE of Digitalis Compounds

A 
-Therapeutic index: 1.6-2.5  
 Cardiac:
- AV junctional rhythm because the SA node is slowed significant
- premature vent. depol 
- AV blockade → leads to premature ventricular contractions
Extra-cardiac:
- anorexia
- nausea
- diarrhea
- color vision abnormality
- disorientation
- gynecomastia (in males; rare)
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8
Q

Sympathetomimetic Inotropes

A
  • Dobutamine, Dopamine, Amrinone, Milrinone, Norepinephrine

- Increase calcium at AP

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9
Q

Dobutamine

A
  • Sympathetomimetic Inotrope
  • Increase calcium at AP
  • Mechanism: β1-selective agonist w/ high inotropic & low chronotropic activity b/c ↑cAMP
  • ↑ contractility, ↓ afterload
  • pure agonist → receptor desensitization
  • Admin: short acting, not orally active IV
  • Use: ** Acute Heart Failure used in cardiogenic shock
  • AE: arrhythmias
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10
Q

Dopamine

A
  • Sympathetomimetic Inotrope
  • Increase calcium at AP
  • Mechanism: low doses: ↑NE release at heart → β1 stimulation→ ↑ inotropy
  • @ periphery (DA receptor): ↓NE release → vasodil, ↑ renal and cerebral blood flow
  • at high doses, also has alpha1 activity, leading to vasoconstriction
  • Admin: IV
  • Use: Acute Heart Failure (esp. w/ renal failure, it’s a better option than dobutamine)
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11
Q

AMRINONE

A

-Sympathetomimetic Inotrope, via PDE inhibition
-Increase calcium at AP
-Mechanism: PDE: cAMP → AMP
- PDE inhibition → ↑cAMP → ↑ β adrenergic effect (because of increased calcium from increased cAMP!!)
- “inodilators”
↑ contractility, ↓ preload, ↓ afterload
-Admin: orally-active (only used IV, short-term treatment)
- somewhat selective cardiac isoform (type III)
- bypass the receptor & problem of desensitization
Use: * acute heart failure
-AE: hepatotoxicity, nausea

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12
Q

Milrinone

A

-Sympathetomimetic Inotrope, via PDE inhibition
-Increase calcium at AP
-Mechanism: PDE: cAMP → AMP
- PDE inhibition → ↑cAMP → ↑ β adrenergic effect (because of increased calcium from increased cAMP!!)
- “inodilators”
↑ contractility, ↓ preload, ↓ afterload
-Admin: orally-active (only used IV, short-term treatment)
- somewhat selective cardiac isoform (type III)
- bypass the receptor & problem of desensitization
Use: * acute heart failure
-AE: not hepatotoxic, but ↑ mortality in chronic use

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13
Q

Norepinephrine

A
  • Sympathetomimetic Inotrope
  • Increase calcium at AP
  • Mechanism: alpha1, alpha2, beta1 agonist
  • Use: Acute heart failure where systolic pressure needs to be increased due to cardiogenic shock
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14
Q

Diuretics

A

Thiazide (“low-ceiling”): hydrochlorthazide; Loop (“high-ceiling”): FUROSEMIDE; K+ sparing: SPIRONOLACTONE, ELPERENONE

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15
Q

hydrochlorthazide

A
  • Thiazide (“low-ceiling”) diuretic
  • Mechanism: ↓Na/H20 retention → ↓PL → ↓edema & ↓cardiac size → ↑pumping efficiency
  • Provides symptom relief
  • Use: * Mild to moderate CHF (w/ Na diet restriction)
  • 1st drug put pt on: diet ↓ Na + HCTZ
  • AE: Hypokalemia (use w/ K+ supplements, bananas)
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16
Q

FUROSEMIDE

A
  • Loop (“high-ceiling”) diuretic
  • Mechanism: ↓Na/H20 retention → ↓PL → ↓edema & ↓cardiac size → ↑pumping efficiency
  • Provides symptom relief
  • Use: * Mild to moderate CHF (w/ Na diet restriction)
  • 1st drug put pt on: diet ↓ Na + HCTZ
  • Use: * Severe CHF → used as drug of choice when the “ceiling” for HCTZ has been reached
  • ACUTE setting
  • AE: Hypokalemia (use w/ K+ supplements, bananas)
17
Q

SPIRONOLACTONE

A

-K+ sparing diuretic
-Mechanism: Aldosterone Antagonist: blocks effects of aldosterone: blocks myocyte fibrosis, blocks ↑ vascular sensitivity to Angtensin, blocks inhib NO release
- ↓Na/H20 retention → ↓PL
-Use: * ↓ Mortality because of effects on aldosterone!
-CHRONIC setting
D.O.C. 1st line- diuretic to ↓ edema symptoms
-AE: hyperkalemia

18
Q

ELPERENONE

A

-K+ sparing diuretic
-Mechanism: Aldosterone Antagonist: blocks effects of aldosterone: blocks myocyte fibrosis, blocks ↑ vascular sensitivity to Angtensin, blocks inhib NO release
- ↓Na/H20 retention → ↓PL
-Use: * ↓ Mortality because of effects on aldosterone!
-CHRONIC setting
D.O.C. 1st line- diuretic to ↓ edema symptoms
-AE: hyperkalemia

19
Q

HYDRALAZINE

A

-Vasodilator
-Mechanism: K+ channel opener → ↓voltage-dependent Ca entry
- Arteriole dilator → ↓AL (↓work, ↓ O2 demand) * Use: CHF for patients w/ low ventricular output
Only when other drug classes don’t respond

20
Q

Vasodilators

A

HYDRALAZINE
NITRATES
BiDil
Nesiritide

21
Q

NITRATES

A

-Venodilator
-Mechanism: Venodilator → ↓PL (↓ edema, ↓ O2 consump)
-Use: * CHF w/ high filling pressures, pulmonary congestion
Only when other drug classes don’t respond - -AE: reflex tachycardia (not used alone)

22
Q

BiDil

A
  • Vasodilator
  • Combination of isosorbide dinitrate and hydrazaline
  • mechanism unclear
  • Use: African Americans
  • not effective and does not reduce mortality
23
Q

Nesiritide

A
  • Vasodilator
  • Mechanism: ANP release→ activates guanylate cyclase (like nitrates) → ↑ NO→ vasodilation
  • usefulness of drug not proven
24
Q

ACE inhibitors

A

CAPTOPRIL

ENALALPRIL

25
Q

CAPTOPRIL

A
  • ACE inhibitors
  • Mechanism: ↓TPR → ↓AL
  • ↓aldosterone → ↓PL by ↓ in water and salt retention
  • ↓Ang II → ↓sympathetic activity, ↓remodeling *
  • Use: ↓ Mortality
  • ACE inhibitors when given with angiotensin receptor blockers provide a significant improvement in cardiac function
  • AE: ACE inhibitors may causer hyperkalemia
26
Q

ENALALPRIL

A
  • ACE inhibitors
  • Mechanism: ↓TPR → ↓AL
  • ↓aldosterone → ↓PL by ↓ in water and salt retention
  • ↓Ang II → ↓sympathetic activity, ↓remodeling *
  • Use: ↓ Mortality
  • ACE inhibitors when given with angiotensin receptor blockers provide a significant improvement in cardiac function
  • AE: ACE inhibitors may causer hyperkalemia
27
Q

Beta Blockers

A

CARVEDILOL NS (some alpha antag)
BISPROLOL S B1
METAPROLOL S B1

28
Q

CARVEDILOL
BISPROLOL
METAPROLOL

A

-Beta blockers used in CHF
-Counter-intuitive
-Mechanism: Counteracts SNS overload catecholamine overload:
-↓ RAS, ↓ HR (improves filling), protects myocytes: anti-apoptotic
- ↓ PL & ↓ AL
-Use: start at low dose, titrate up
* mild CHF
↓ Mortality
-Carvediol seems to be most effective
-Contraindication: severely Decompensated Heart Failure

Cardio Pharm (5 decks)

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