Heart Failure Treatment 1 Flashcards

1
Q

Define Heart Failure

A

Pathological state when the heart is unable to pump blood (reduce stroke volume & cardiac output) at a rate that meets the requirements of tissue

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2
Q

Normal conditions = dynamic relationship between

A

venous capacitance, ventricular preload, CO, afterload, peripheral resistance

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3
Q

Define Acute Hemodynamic Stress

A

Sharp decrease in blood volume –> decreased cardiac output –> activation of compensatory mechanisms to support the circulation

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4
Q

RAS –> BP and CO

A

Increased AngII which leads to peripheral resistance and increased sodium and water which allows recovery of BP and CO

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5
Q

SNS –> BP and CO

A

Increased myocardial contractility and increased heart rate via beta 1
Increased peripheral resistance via alpha 1 and 2

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6
Q

Therapy for HF involves:

A

Reduction of preload and/or afterload

Enhancement of inotropic state (contraction force)

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7
Q

Vasodilators

A

ACEi

Direct vasodilators

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8
Q

Positive inotropic drugs

A

Cardiac glycosides
Adrenergic/dopaminergic receptor agonists
Phosphodiesterase inhibitors

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9
Q

Diuretics in HF work on

A

Vasoconstriction and sodium/water retention

- Long term effects via: decrease peripheral resistance

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10
Q

Loop Diuretics are

A

Furosemide
Dumetanide
Torsemide

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11
Q

Loop Diuretics MOA

A

Inhibit NKCC symporter

Act in the thick ascending limb of loop of Henle

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12
Q

Loop Diuretics Main effects

A
Profound diuresis (25%) which increases urine flow
Increased excretion of Na, Cl, K, Ca and Mg
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13
Q

Loop diuretics Main Adverse Effects

A

Ototoxicity
Hypokalemia
Hyperglycemia

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14
Q

Thiazide diuretics main representatives

A

HCTZ (microzide)
Chlorthalidone (Hygroton)
Indapamide (Lozol)
Metolazone (zaroxolyn)

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15
Q

Thiazide diuretics MOA

A

Act in the distal convoluted tubule (5% of Na reabsorption)

Inhibit Na Cl symporter

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16
Q

Thiazide diuretics effects on urine flow and ion excretion

A

Moderate increase in urine flow

Increased excretion of Na, Cl and increased excretion of K

17
Q

Chronic use of thiazide diuretics

A

Decreased excretion of Ca and uric acid

18
Q

Thiazide Main Adverse Effects

A

Hypokalemia
Increased risk of gout
Hyperuricemia

19
Q

Aldosterone antagonists drugs

A

Spironolactone and eplerenone

20
Q

Aldosterone antagonists MOA

A

Aldosterone (steroid hormone) binds to receptors then are translocated to the nucleus where it binds DNA and stimulates expression of aldosterone induced proteins

21
Q

ACEi drugs

A

End in -pril

22
Q

ACEi MOA

A

Reduction of Ang II which is involved in vasoconstriction, increased peripheral resistance, decreased sodium and water, slight decrease in aldosterone secretion and decreased sympathetic tone

23
Q

Alternative MOA of ACEi

A

Increased bradykin which decreased peripheral resistance via vasodilation and Ang 1-7 which is an antagonists of Ang II and natriuresis

24
Q

ACEi side effects

A

Dry cough, angioedema

25
Direct vasodilators
Nitroglycerin Nitroprusside (Nipride) Nesiritide (Natrecor)
26
Direct vasodilators MOA
Nitropresside and nitroglycerin either breakdown into NO or are NO and stimulate the process
27
Nitroglycerin
Prodrug metabolized into NO Infused IV Selective for venous capacitance vessels (reduction of left ventricular filling pressure)
28
Limitations of Nitroglycerin
Severe headache Have to taper off Development of resistance with chronic use Long infusion + increased EtOH
29
Na nitroprusside
Metabolized into cyanide and NO IV administered Dilates both arteries and veins so it can reduce ventricular filling pressure and peripheral restance
30
Na nitroprusside Limitations
Hypotension Cyanide toxicity Can cause tissue hypoxia, decreased oxidative metabolism, and liver or renal toxicity
31
Cyanide toxicity causes
Altered mental status CV instability Anion gap metabolic acidosis
32
Nesiritide
Recombinant brain natiuretic peptide Causes vasodilation of arteries and veins, nauresis and diuresis IV administration
33
Nesiritide Limitations
Hypotension Expensive Debatable effectiveness