Heart Failure (General) Flashcards

1
Q

What is Heart Failure

A

Cardiac Output is not enough to meet metabolic demands of body

Progressive Syndrome

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2
Q

Causes of Heart Failure

A

Decreased Contractility:
- Diseases of Myocardium
- Cardiotoxic Drugs
- Pressure Overload
- Volume Overload

Restriction in Ventricular Filling:
- Diastolic Dysfunction
–> Ventricle Stiffness

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3
Q

Compensatory Mechanism during Heart Failure and their effect

A

When cardiac function significantly decreases compensatory mechanisms are triggered to maintain adequate CO
–> These mechanism make situation worse instead of better (Counter Regulatory)

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4
Q

Heart Failure
(Counter Regulatory Mechanisms)

A

Kidney interprets reduced prefusion as ineffective blood volume
- Kidney thinks body is bleeding
–> Stimulate Na+ and H2O retention (RAS)

Vasoconstriction
- Redistribute blood flow from non-essential organs to coronary and cerebral circulations

Ventricular Hypertrophy
- Remodeling of Heart and Hypertrophy

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5
Q

What are the two types of RAS Inhibitors

A

ACE Inhibitors
Angiotensin Receptor Blockers (ARBs)

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6
Q

RAS Inhibitors Mechanism of Action

A

Blocks formation of Ang II
- Inhibits release of aldosterone
- Reduced vascular resistance and afterload
- Improve tissue perfusion
- Reduces Na+ reabsorption

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7
Q

Beta-Adrenoceptor Antagonist Mechanism of Action

A

Reduces heart rate and blood pressure
- Prolongs Diastolic Filling
- Reduces Detrimental remodeling of heart
- Inhibits Renin

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8
Q

Beta-Adrenoceptor Antagonist Dosage

A

Normal Dose Beta-Adrenoceptor Antagonists reduce CO
- Need to be started at low doses and slowly increased

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9
Q

Aldosterone Receptor Antagonists Mechanism of Action

A

Competitive Antagonists of Aldosterone Receptor in Kidney
- Inhibits expression of transporters (Changes nuclear receptor’s gene expression)

Overall Effect: Inhibits Na+ reabsorption and Water Retention

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9
Q

What kind of Receptor are Aldosterone Receptors

A

Mineral Corticoid Receptor (Class 1 Nuclear)

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10
Q

Furosemide Mechanism of Action

A

Inhibits Na+/K+/2Cl- transporters in loop of Henle
- Potent Diuretic, more water eliminated
–> Decrease Na+ Reabsorption
–> Decrease Water Reabsorption
–> Decrease Blood Volume

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11
Q

Digoxin
- When to use?

A

Used in heart failure patients with:
- Chronic atrial fibrillation
- Remain symptomatic after ACEI and Diuretic treatments

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12
Q

Digoxin
- What class?

A

Cardiac Glycoside with Positive Inotropic Effect
- Changes the force of contraction of the heart

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13
Q

Digoxin
- Mechanism of Action

A

Inhibits Na+/K+ ATPase pump
- Increases Contraction Force
- Slows Heart Beat
- Increases Ventricular Filling

Less Na+ Influx and Less transport of Ca2+
- More Ca2+ in Cardiac Myocyte
–> Stronger Contractions
–> Slower Heartbeat
–> Increased Ventricular Filling

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14
Q

Isosorbide Mononitrate
- Mechanism of Action

A

Metabolized with release of NO
- Relax veins and Reduces central Venous Pressure
–> Reduces Preload

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15
Q

NO Mechanism

A

Nitric Oxide diffuses into smooth muscle
- Activates GC –> Converts GTP into cGMP
–> Causes Relaxation

16
Q

Hydralazine
- Mechanism of Action

A

Causes a fall in BP (Reduces Afterload)
- Inhibits IP-mediated intracellular Ca2+ release in SMC of arteries and arterioles
–> Imhibits Calcium release