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Cardiovascular & Respiratory Pharmacology (Karen) > Drugs influencing cardiac structure and function > Flashcards

Drugs influencing cardiac structure and function Flashcards

1
Q

Digoxin

A
  • cardiac glycoside
  • oral administration, long half-life
  • ionotropic agent
    • improves contractility by inhibiting the Na+/K+ ATPase (less Na+ pumped out means less Ca2+ pumped out), increasing intracellular Ca2+ that moves into the SR
    • tf more Ca2+ is released in subsequent APs
  • narrow margin of safetey, low therapeutic index (desired and undesired effects very close)
  • widely distributed and non-specific
    • affects all excitable tissues (gut, CNS, cardiac)
  • used to treat atrial dysrhythmia by increasing PSNS activity through the vagus nerve
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2
Q

What are the adverse effects of digoxin and other cardiac glycosides?

A
  • continuous administration shortens ventricular AP
    • leads to LADs from Ca2+ overload
      • promotes ventricular dysrhythmias
  • affects all exciteable tissues:
    • gut - anorexia, nausea, diarrhoea
    • CNS - drowsiness, confusion, psychosis
    • cardiac - ventricular dysrhythmias
  • increased toxicity with:
    • low K+ (decreased competition for binding at the Na/KATPase)
    • high Ca2+ (decreased gradient for Ca2+ efflux)
    • renal impairment
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3
Q

By what mechanism does SNS stimulation increase contractility and rate?

A
  • @ SA node
  • @ B1-aRs on myocytes
    • agonist binding activates adenyly cyclase via G protein
    • +cAMP
    • activates PKA
    • PKA phosphorylates Ca++ channel –> opens
    • cAMP is degraded to AMP by phosphodiesterase
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4
Q

Amrinone

A

phosphodiesterase inhibitor

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5
Q

What is the use of beta agonists and phosphodiesterase inhibitors in heart failure?

A
  • IV administration
  • acute, short term support for acute heart failure and cardiogenic shock
  • beta agonists:
    • noreadrenaline, adrenaline
      • activate both alpha and beta-aRs
    • dobutamine
      • selective b1-aR agonist
  • PDE inhibitors:
    • amrinone
      • inhbitis cAMP –> AMP
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6
Q

What are the adverse effects of beta agonists and PDE inhibitors in heart failure?

A
  • increased cardiac work
  • increased O2 demand
  • risk of arrhythmias
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7
Q

Dobutamine

A
  • selective b1-aR agonist
  • replaced prenalterol as it is a stronger agonist and will still work if the receptor becomes desensitized
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8
Q

What is the consequence of chronic heart failure on b1-aRs?

A
  • chronic overactivation by sympathetic compensation for reduced CO causes:
    • reduced b1-aR expression
      • tf -cAMP activation and contraction
    • impaired b1-aR coupling with adenyly cyclase and cAMP
  • leading to an overall reduced sensitivity to b1-aR agonists or sympathetic drive
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9
Q

What is the role of ionotropes in heart failure?

A
  • +contractile force of myocytes
    • this can increase work on the heart, negating symptomatic relief it overused
  • symptomatic relief of:
    • chest pain
    • fainting
    • death
  • excessive use can lead to cardiac remodelling (hypertrophy, -compliance), altering cardiac pump function
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10
Q

What are the types of drugs used to combat increased afterload and increased preload in heart failure?

A
  • beta blockers
  • ACE inhibitors
  • aldosterone antagonists
  • diuretics
  • venodilators
  • vasodilators
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11
Q

How are nitrates used in heart failure?

A
  • to reduce preload by venodilation
  • undergo first-pass metabolism tf admin under tongue or by patch
  • primarily for angina (symptomatic relief in cardiac failure)
  • can develop tolerance, tf useful in intermittent conditions
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12
Q

How is furosemide/frusemide used in heart failure?

A
  • to reduce preload as a diuretic
  • acts at loop of henle
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13
Q

What is the function of aquaretics?

A
  • vasopressin (ADH) receptor antagonists
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14
Q

What types of drugs reduce preload?

A
  • venodilators (nitrates)
  • diuretics (furosemide/frusemide)
  • aldosterone receptor antagonists
  • aquaretics (vasporessin/ADH receptor antagonists)
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15
Q

Spironolactone

A
  • aldosterone receptor antagonist
  • inhibits aldosterone action on the cortical and distal tubules
  • K+ sparing, tf can cause hyperkalaemia - must be monitored
  • can interfere with renal function
  • improves survival w/combo therapy in severe heart failure
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16
Q

What types of drugs reduce afterload?

A
  • arterial vasodilators
  • ACE inhibitors
  • AT1 antagonists (alternative to ACE inhibitors)
  • b-aR antagonists
17
Q

What is the risk of using arterial vasodilators to reduce afterload in heart failure?

A
  • the vasodilation causes a drop in BP triggering a baroreflex tachycardia
  • this causes the heart to work harder
  • tf not used as front-line therapy
18
Q

What are the first line therapy drugs in heart failure?

A
  • ACE inhibitors
  • decrease angiotensin II production
    • this decreases vasoconstriction (-afterload)
    • and decreases fluid retention (-preload)
  • tf limiting progression of hypertrophy
    • RAS involved in remodelling
19
Q

How do ACE inhibitors function in heart failure?

A
  • first-line therapy
  • decrease angiotensin II
    • decreases vasoconstriction (-afterload)
    • decreases fluid retention (-preload)
    • slows cardiac hypertrophy
20
Q

How are angiotensin I antagonists used in heart failure?

A
  • afterload reduction
  • used when ACE inhibitors do not work
21
Q

How do beta blockers function in heart failure?

A
  • adjuncts to ACE inhibitors and diuretics
  • reduce HR
  • decrease renin secretion
    • lowers O2 demand at heart by lowering the extracellular volume and increasing the O2 carrying capacity of blood
22
Q

What are the benefits of using ACE inhibitors and agiotensin receptor blockers (ARBs) in heart failure?

A
  • nb: also used in hypertension
  • effective at all grades of HF
  • improve symptoms, delay progression of remodelling
  • reduce mortality up to 30-40%, reduce morbidity
23
Q

What are the adverse effects of ACE inhibitors and ARBs in treating heart failure?

A
  • first-dose hypotension - titrate dosage
  • dry cough
  • loss of taste
  • hyperkalaemia (rx: thiazide diuretic)
  • acute renal failure
  • itching, rash, angioedema
  • foetal malformations (contratx in pregnancy)
24
Q

In what patients with heart failure are ACE inhibitors and ARBs contraindicated?

A
  • bilateral renal stenosis
  • angioneurotic oedema
  • pregnancy
25
Q

When treating heart failure, ACE inhibitors and ARBs should be used in adjunct with

A
  • diuretics
    • thiazide for hyperkalaemia
  • glycosides
  • b-aR antagonists
26
Q

What are the side effects of beta blockers?

A
  • hypotension, fatigue (cadiac & b2 mediated)
  • bronchoconstriction (b2 block)
  • cold extremities (a1 mediated)
  • cause or mask signs of hypoglycemia

therefore, contraindicated in:

  • asthma
  • PVD (peripheral vascular disease)
  • diabetes
27
Q

How do beta blockers cause increased stroke volume if they block b1 receptors?

A
  • b1 blockade removes NA influence, decreasing cardiac output
  • stroke volume increases because working at a high CO is inefficient (frank-starling)
  • tf reducing CO with beta blockers increases efficiency which increases SV
28
Q

Why is the use of beta blockers in heart failure considered counter-intuitive?

A
  • some side effects actually worsen the symptoms
  • often used to inhibit the early stages of the disease process
29
Q

Metoprolol

A
  • cardiac b1 blockade in heart failure:
    • reduces tachycardia and cardiac work (inhibits compensation)
    • inhibits renin release and subsewuent AII effects
    • protects against receptor downregulation
  • used in early and mild to moderate CHF
30
Q

Carvedilol

A
  • b1 and a1 vascular blockade in heart failure
    • vasodilation reduces afterload, cardiac work
  • can improve ejection fraction (SV)
  • can reduce mortality
  • can reduce chance of fatal stroke or MI
  • used in early and mild to moderate CHF
31
Q

What are the aims of heart failure treatment?

A
  • decrease cardiac work and improve cardiac function
    • preload, afterload, contractility
  • reduce signs and symptoms
    • oedema, fatigue, arrhythmias, ventricular remodelling
  • increase survival
    • one-year mortality rate is ~10% for mild and moderate CHF
32
Q

Symptomatic relief in heart failure is achieved by

A
  • ionotropes to improve contractility
  • diuretics and venodilators to decrease preload
33
Q

Mortality in heart failure is reduced by

A
  • angtiotensin inhibitors, beta blockers, and aldosterone antagonists decreasing afterload and preload
34
Q

What are the alternatives to pharmacological treatment of heart failure?

A
  • surgical:
    • pacemaker, defib, valve replacement, transplant
  • complements to pharm and surgical approaches:
    • reduce salt, dluid, alcohol intake
    • stop smoking
    • exercise
    • consider risk factors and attenuate them with lifestyle changes

Cardiovascular & Respiratory Pharmacology (Karen) (15 decks)

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