Congestive Heart Failure Flashcards

(46 cards)

1
Q

What is Cardiac Failure

A

Failure of cardiac function to deliver oxygenated blood to tissue and the function defined as Cardiac Output

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2
Q

What is the aim of drug therapy in CHF

A

To relieve symptoms

To improve quality of life

To improve survival

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3
Q

Determinants of Stroke Volume

A

Afterload

Preload

Contractility

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4
Q

Strategies to treat CHF

A
  1. Reduce Afterload-Artery dilators
  2. Reduce Preload-Remove water and Vein Dilators
  3. Increase contractility-Inotropes
  4. Inhibit RAAS system
  5. Inhibit Sympathetic NS activation
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5
Q

Drugs used for the treatment of CHF

A

Artery Dilators: ACEI, Hydralazine and Minoxidil

Inotropes: Digoxin, Dobutamine and Milrinone

Diuretics: Furosemide
Vein Dilator: Nitrate(NTG) and ACEI-Captopril

ACEI

B-blocker

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6
Q

Drugs proven to improve Survival

A

Aspirin

B-blockers

ACE inhibitors

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7
Q

Classes of Drugs for CHF

A
  1. Inotropics
  2. Vasodilators
  3. Neurohormonal antagonists
  4. Diuretics
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8
Q

Inotropes:

Examples

A

Digoxin

Catecholamines

Phosphodiesterase III inhibitor

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9
Q

_NEUROHORMONAL EFFECTS

A

Decreases Plasma Noradrenalin (Reduced Sympathetic tone)

Decreases Peripheral nervous system activity

Decreases RAAS activity (switches off)

Decreases Vagal tone or

Normalizes arterial baroreceptors

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10
Q

_EFFECTs (SUMMARY)

A

Positive inotropia: Na K-ATPase inhibition

Negative chronotropia

Negative dromotropia

Increased Parasympathetic tone: Decreased AV conduction & heart rate

Decreased Sympathetic tone

A dromotropic agent affects the conduction speed in the AV node, and subsequently the rate of electrical impulses in the heart.

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11
Q

Digoxin:

Long Term Effects

A

Survival similar to placebo

Fewer hospital admissions

More serious arrhythmias

More myocardial infarctions

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12
Q

Digoxin:

Clinical Uses

A

Atrial Fibrillation with rapid ventricular response.

Congestive Cardiac Failure refractory to other drugs

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13
Q

Digoxin:

Contraindications

A
  • Digoxin toxicity• RELATIVE- Advanced A-V block withoutpacemaker- Bradycardia or sick sinus without PM- Extrasystoles- Marked hypokalemia- W-P-W with atrial fibrillation
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14
Q

Digoxin Side Effects/Toxicity:

Cardiac Manifestations

A

Arrhythmias:
Ventricular
Supraventricular

Blocks:
SA and AV blocks

Exacerbates cardiac failure

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15
Q

Digoxin Side Effects/Toxicity:

Extracardiac

A

Gastrointestinal:
- Nausea, vomiting, diarrhea

Nervous System:
- Depression, disorientation, paresthesias

Visual:
- Blurred vision, scotomas and yellow-green vision

Hypoestrogenism:
- Gynecomastia, galactorrhea

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16
Q

Digoxin:

Drug Interactions

A

Antacids and Cholesteramine:
=> to reduced absorption of digoxin

Calcium Channel Blocker:
- Oppose the effect of digoxin on the heart

Drugs that cause Hypokalemia: Diuretics
- Cause digoxin arrhythmias

Drugs that block AV node: Quinidine
- worsen digoxin toxicity (bradycardia)

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17
Q

Catecholamines:

A

B-adrenergic stimulants classification:

B1 Stimulants which Increase contractility:
Dobutamine

Mixed DA, B1 & B2:
Dopamine
DOPAMINE AND DOBUTAMINE
EFFECTS
Dopamine μg/kg/ml Dobutamine
<2 2-5 >5
Receptors DA1/DA2 β1 β1+α β1
Contractility ± ++ ++ ++
Heart rate ± + ++ ±
Arterial
pressure
± + ++ ++
Renal
perfusion
\++ + ± +
Arrhythmia - ± ++ ±
POSITIVE INOTROPES:
CONCLUSIONS
• May increase mortality
• Safer in lower doses
• Use only in cardiogenic shock
• NOT for use as chronic therapy
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18
Q

Conclusion of Positive Inotropes

A

May increase mortality

Safe in lower doses

Use only in cardiogenic shock

Not for us as chronic therapy

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19
Q

Vasodilators:

Drugs

A

ACE Inhibitors & AT-1 blockers

Nitrates

20
Q

ACEI:

Advantages

A

Inhibit left ventricular remodeling post-myocardial infarction

Modify the progression of chronic congestive heart
failure
-Increases Survival
- Decreases Hospitalizations
-Improve the quality of life

In contrast to others vasodilators, do not produce neurohormonal activation or reflex tachycardia

Tolerance to its effects does not develop

21
Q

ACEI:

Side Effects

A

Inherent in their mechanism of action

  • Hypotension
  • Hyperkalemia
  • Angioneurotic edema

Due to their chemical structure:

  • Cutaneous eruptions
  • Neutropenia, thrombocytopenia
  • Digestive upset
22
Q

ACEI:

Contraindications

A

Renal artery stenosis

Renal insufficiency

Hyperkalemia

Arterial hypotension

Intolerance (due to side effects

23
Q

AT1 Receptor Blockers:

Drugs

A

Losartan

Valsartan

Ibersartan
Competitive and selective
Inhibition of AT1 receptors

24
Q

Nitrates: Hemodynamic Effects

Types

A

Venous Vasodilation

Arterial Vasodilation

Coronary Vasodilation

25
Venous Dilation:
Decrease Preload: When that happens: It also decreases the following: - Pulmonary congestion - Ventricular size - Vent. Wall stress - MVO2
26
Arterial Vasodilation
Decreases Afterload: Thus decreasing: - Cardiac Output and - Blood Pressure
27
Coronary Vasodilation
Increases myocardial perfusion:
28
Nitrates: Tolerance
" Decrease in the effect of a drug when administered in a long-acting form" Develops with all nitrates Is dose-dependent Disappears in 24 h. after stopping the drug Can be avoided or minimized - Intermittent administration - Use the lowest possible dose - Intersperse a nitrate-free interval Allow peaks and valleys in plasma levels - Vascular smooth muscle recovers its nitrate sensitivity during the nadirs - Patches: remove after 8-10 h
29
Nitrates: Contraindications
Previous hypersensitivity Hypotension (< 80 mmHg) 1st trimester of pregnancy WITH CAUTION in: - Constrictive pericarditis - Intracranial hypertension - Hypertrophic cardiomyopathy
30
Nitrates: Clinical Uses
Pulmonary congestion Orthopnea and paroxysmal nocturnal dyspnea Congestive cardiac failure with myocardial ischemia Acute congestive cardiac failure and pulmonary edema: TNT SL or IVI.
31
Neurohormonal Antagonists: B-blockers
Inhibit cardiotoxicity of catecholamines Decreases Neurohormonal activation Decreases Heart rate
32
B-Blockers: Clinical Uses
Suspected adrenergic activation Arrhythmias Hypertension Angina
33
ß-Adrenergic Blockers: Contraindications
Hypotension: BP < 100 mmHg Bradycardia: Heart rate < 50 bpm Clinical instability Chronic bronchitis, ASTHMA Severe chronic renal insufficiency
34
Diuretics: Drugs
Thiazides Loop diuretics Potassium Sparing Diuretics
35
Thiazides
Inhibit active exchange of Na-Cl in cortical diluting segment of ascending loop of Henle.
36
Loop diuretics
Inhibit exchange of Na-Cl-K in thick segment (ascending loop of Henle)
37
K- sparing
Inhibit reabsorption of Na in distal convoluted & collecting tubule
38
Thiazides: Mechanism of Action
Excrete 5 - 10% of filtered Na+ Increases Elimination of K+ Decreases Excretion of uric acid and Ca Minimal dose - effect relationship Some inhibit carbonic anhydrase: increase elimination of HCO3
39
Loop Diuretics: Mechanism of Action
Excrete 15 - 20% of filtered Na+ Increases Elimination of K+, Ca+ and Mg++ Decreases Resistance of afferent arterioles – Increases Release renal PGs – NSAIDs may antagonize diuresis
40
K-Sparing: Mechanism of Action
Eliminate < 5% of filtered Na+ Inhibit exchange of Na+ for K+ or H+ Spironolactone = competitive antagonist for the aldosterone receptor Amiloride and triamterene block Na+ channels controlled by aldosterone
41
Diuretic Effects
Volume and preload – Improve symptoms of congestion No direct effect on cardiac output, but excessive preload reduction may improve arterial distension. Neurohormonal activation: – Increased levels of renin and Angiotensin II – Exception: Reduced with spironolactone
42
Diuretics: Adverse Reactions: Thiazides and Loop Diuretics
Changes in fluid balance and electrolytes: – Reduce Volume – Reduce Na+, K+, Mg++ – Metabolic alkalosis Other changes: – Increase blood glucose and uric acid – Increase LDL cholesterol & Trigliserides Cutaneous allergic reactions Idiosyncratic effects: – Blood dyscrasia, cholestatic jaundice and acute pancreatitis Gastrointestinal effects Genitourinary effects: – Impotence and menstrual cramps Deafness, nephrotoxicity (Loop diuretics)
43
Diuretics: Adverse Reactions: K-Sparing
Changes in electrolytes: – ↑ Na+, ↑ K+, acidosis Musculoskeletal: – Cramps, weakness Cutaneous allergic reactions : – Rash, pruritis
44
Drugs used for Acute Heart Failure
In hospital: intravenous Diuretics: Furosemide Nitrates: Inotropic agents: Dopamine/ dobutamine Oxygen
45
Drugs used for Chronic Heart Failure
Systolic dysfunction: Diuretic + ACEI / ARB Beta blocker Spironolactone or eplerenone if needed Digoxin if AF Hydrallazine + nitrate Anticoagulant/ antiplatelet drugs
46
Drugs which may aggravate or induce Heart Failure
Drugs that increase fluid retention – NSAIDs – Rosiglitazone/ Pioglitazone – High salt content: Fleet enema Drugs with negative inotropic effect – Betablocker – Calcium channel blocker Direct cardiotoxicity – Cancer chemotherapy