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Pharm block 4 hemostasis and cardiac > CHF treatment > Flashcards

CHF treatment Flashcards

1
Q

COMMON CAUSES OF ACUTE CONGESTIVE HEART FAILURE

A

Acute Myocardial Infarction

Global Myocardial Ischemia (‘Stunned Myocardium’)

Acute Viral Myocarditis

Acute Valvular Regurgitation (AR, MR)

Arrhythmias - VT, VF, SVT with rapid ventricular response (WPW)

Acute Pericardial Tamponade

Massive Pulmonary Embolism

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2
Q

COMMON CAUSES OF CHRONIC

CONGESTIVE HEART FAILURE

A

Ischemic Cardiomyopathy (most common cause of CHF in US)

Hypertrophic Cardiomyopathy

Dilated Cardiomyopathy

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3
Q

TREATMENT OBJECTIVES IN ACUTE CHF

A

Early recognition and treatment
Decrease symptoms (primarily pulmonary congestion)
Increase cardiac output (Increase cardiac contractility, Reduce afterload)

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4
Q

why are diuretics used in CHF and how do they work

A

used to decrease pulmonary congestion by:

Reduce intravascular volume to reduce filling pressure (preload)

Reduce pulmonary venous pressure and interstitial pulmonary edema

Improve oxygenation

*Preload reduction may have little effect on cardiac output in patients with CHF (flat portion of Starling Curve)

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5
Q

diuretics commonly used in CHF

A

Loop and Thiazide diuretics

*** Furosemide (Lasix®) others (Bumetanide, Torsemide)

Thiazide diuretics (chlorothiazide, and chlorthalidone)

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6
Q

how does furosemide work

A
  • Loop diuretic – inhibits Na+/K+/2Cl- Cotransporter in Loop of Henle
  • Intravenous and oral preparations
  • Rapid onset of action; relatively short duration
  • Very potent!!!
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7
Q

How do thiazide diuretics work

A
  • Inhibit Na+ and Cl- reabsorption in distal tubules

- Can be used in combination with loop diuretics in patients resistant to furosemide

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8
Q

ADVERSE EFFECTS OF DIURETICS

A

Overdiuresis

Hypokalemia
- Precipitate arrhythmias, especially digitalis-induced arrhythmias

Hypomagnesemia

Hyperuricemia
- Precipitate acute gout

Ototoxicity and Hearing Loss

Allergies (Loop and Thiazide diuretics are sulfa drugs)

Diuretic Resistance

  • Reduce GFR because of volume reduction
  • Overcome by using drugs in combination
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9
Q

what is the function of nitroglycerine and other organic nitrates in CHF

A

Venodilate (reduces venous return, reduced preload, reduced afterload)

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10
Q

NISERITIDE (Natricor ®) MOA

A

Human Recombinant Brain Natriuretic Peptide (hBNP)

“Normally” produced by ventricular myocardium in response to “chronic” stretch

Activates vascular smooth muscle NPR1 and NPR2 receptors

Raises cGMP levels in VSMC-vasodilation

Decreases Na reabsorption in the Distal tubule

Therefore NISERITIDE induces both vasodilatation and natriuresis

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11
Q

overall effect of NISERITIDE (Natricor ®)

A

NISERITIDE induces both vasodilatation and natriuresis

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12
Q

what is the affect of CHF on contractility

A

contractility is decreased in many forms of acute CHF

Acute reduction in LV contractility (for example, global ischemia, acute MI)

Chronic reduction in LV contractility (for example, chronic valvular regurgitation, ishcemic cardiomyopathy)

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13
Q

what types of drugs are used to increase contractility in CHF (inotropic agents)

A

Beta Adrenergic Agonists

- Isoproterenol
- Dopamine
- Dobutamine
- Norepinephrine

Phosphodiesterase Inhibitors

- Inamrinone
- Milrinone
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14
Q

what do activation of B1 receptors in the heart cause

A

increased cAMP (through Gs) which results in

  • Increased Opening of L-type Ca channels
  • Increased Reuptake of Ca into SR stores
  • Increased Pacemaker Current
  • Increased Rate of Conduction
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15
Q

what drugs increase cAMP levels

A 
Beta Adrenergic Agonists:
Isoproterenol (nonselective β1, β2-ARs)
Dopamine (low-dose β1-selective; high dose α1-AR)
Dobutamine (β1-selective)
Norepinephrine (nonselective)

Phosphodiesterase Inhibitors:
Inamrinone (aka Amrinone)
Milrinone

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16
Q

Nitroprusside’s effect

A

increases CO by reducing afterload (raises the contractility curve)

The magnitude of reduction in vascular resistance is GREATER than the decrease in mean arterial blood pressure - increased output maintains the arterial pressure.

Particularly useful in patients with hypertension and acute CHF.

17
Q

would you use CCB in CHF

A

NO - Ca Channel blockers - although they are potent arteriolar vasodilators, they are CONTRAINDICATED IN ACUTE CHF BECAUSE OF NEGATIVE INOTROPIC EFFECTS

18
Q

how are Arteriolar Vasodilators Like Nitroprusside useful in mitral regurgitation

A

by reducing afterload you reduce regurgitant fraction and increases forward C.O.

19
Q

what are types of “NONPHARMACOLOGICAL”

THERAPY FOR ACUTE CHF

A

PCI/SURGICAL THERAPY

- Acute Revascularization
- Urgent Valve Repair/Replacement

ULTRAFILTRATION

INTRA-AORTIC BALLOON PUMP (IAPB)

VENTRICULAR ASSIST DEVICES (VADs)
Impella Percutaneous LVAD
Implantable LVAD (HeartMate II)

20
Q

TREATMENT OBJECTIVES IN CHRONIC CHF

A

• Early Recognition of Ventricular Dysfunction even in the ABSENCE of symptoms
• Prevent Ventricular Remodeling
• Decrease Symptoms (Reduce pulmonary congestion and
Increase cardiac output)
• Prolong Survival

21
Q

which drug classes can prevent ventricular remodeling in chronic CHF

A

ACE Inhibitors/ARB’s/LCZ696
Beta Blockers
Aldosterone Antagonists

22
Q

which drug classes can prolong survival in chronic CHF

A

ACE Inhibitors
Nitrates+Hydralazine
Beta Blockers (carvedilol, metoprolol)
Aldosterone antagonists (spironolactone, eplerenone)

23
Q

which drug classes can reduce pulmonary congestion in chronic CHF

A
  • Thiazides, Loop Diuretics, Aldosterone Antagonists

- Venodilators (ACE inhibitors, ARBs, nitrates)

24
Q

which drug classes can increase CO in chronic CHF

A 
Increase Contractility (Digitalis)
 Reduce Afterload (ACE inhibitors, ARBs, hydralazine)
25
Q

DIGITALIS GLYCOSIDES cellular MOA

A
  • Partial inhibition of Na/K ATPase (Sarcolemmal Na Pump)
  • Increased [Na+]i leads to enhanced extrusion of Na+ out of cell and Ca2+ into the cell via the Na/Ca Exchanger (so called “reverse-mode Na/Ca exchange”)
  • Increased [Ca2+]i stored in Sarcoplasmic Reticulum
  • More Ca2+ released from SR stores during each contraction
26
Q

what are the Mechanical Effects of Digitalis Glycosides on Cardiac Performance

A
  • Increased velocity of fiber shortening and force of contraction
  • Increased ventricular emptying (SV increases)
  • Decreased end-systolic and end-diastolic volume
27
Q

Systemic (overall) Effects of Digitalis Glycosides in CHF

A

Increased cardiac output

  • Increased renal perfusion
  • Decreased sympathetic tone (reduced heart rate, vasoconstriction)
28
Q

DIGITALIS GLYCOSIDES – Side Effects

A

Very Narrow Therapeutic Window!!!

- Therapeutic range of Digoxin = 1-2 ng/ml
- Toxic range >2.5 ng/ml

Renal Clearance – Digoxin is often given to patients with decreased GFR, complicating its administration

Cardiac Toxicity

- Delayed afterdepolarizations (DAD’s) and abnormal automaticity
- Digitalis Intoxication - VPBs, V tach, junctional tachycardia, etc.
29
Q

how do you prevent and treat digitalis toxicity

A

prevent by frequent measurement of serum levels

Digibind antibodies used to treat life-threatening Digitalis Toxicity

30
Q

what is digitalis used for

A

Because of potential for side-effects, digoxin is now primarily used in patients with CHF and Atrial Fibrillation with rapid ventricular response (slows ventricular rate)

31
Q

ARTERIOLAR VASODILATORS IN CLINICAL USE FOR Acute vs chronic CHF

A

ACUTE CHF (intravenous; rapid onset of action)

- Nitroprusside
- Nitroglycerin

CHRONIC CHF (oral agents; slower onset of action)

- ACE Inhibitors
- Angiotensin II Receptor Blockers
- Hydralazine
- Minoxidil
- Prazocin
- LCZ696 (Valsartan+sacubritil)
32
Q

How do ACEI improve survival in chronic CHF

A
  • Angiotensin II is a potent cardiomyocyte growth factor (hypertrophy) and fibroblast mitogen (hyperplasia)
  • Inhibition of local RAAS System (autocrine/paracrine effects)
  • ACE Inhibitors also reduce systolic and diastolic wall stress, decreasing stretch-induced hypertrophy and remodeling
  • ACE Inhibitors improve survival regardless of etiology of CHF
33
Q

LCZ696 MOA

A

Combination of Valsartan and sacubitril

Valsartan blocks AT1a receptor on cardiac and vascular smooth muscle.

Sacubitril is converted into a neutral endopeptidase inhibitor. Neutral endopeptidases degrade natriuretic peptides,bradykinin, andadrenomedullin. Thus, sacubitril increases the levels of these peptides, causing vasodilation and reduction of ECF volume via sodium excretion.

34
Q

how are BB used in the treatment of CHF

A

Must be used with caution! - precipitate worsening of CHF symptoms- use low doses (reduced cardiac performance initially)

35
Q

what are the beneficial affects of using BB in CHF

A

increase survival and prevent deterioration of LV performance over time in patients with mild-moderate CHF.

Thought to involve reduction in heart rate and prevention of deleterious effects of chronic sympathetic stimulation

  • Prevents activation of the “fetal gene program” (ie., prevents downregulation of αMHC, SERCA2a)-makes more adult like
  • Prevents SR Ca Leak
  • Prevents β-adrenergic receptor down-regulation
  • Prevents myocardial apoptosis
  • Decreases LV remodeling
36
Q

“NONPHARMACOLOGICAL”

THERAPY FOR CHRONIC CHF

A

SURGICAL THERAPY

- Revascularization for Ischemic Heart Disease
- Valve Repair/Replacement for Valvular Heart Disease
- Aneurysmectomy

LEFT VENTRICULAR ASSIST DEVICES (LVADs)
“Bridge to Transplant”
“Destination Therapy”

BIVENTRICULAR PACING (“Cardiac Resynchronization Therapy” or “CRT”) ± Implantable Cardioverter Defibrillators (ICDs)

CARDIAC TRANSPLANTATION

Pharm block 4 hemostasis and cardiac (12 decks)

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