HF Flashcards

1
Q

What COMPENSATORY RESPONSES BECOME MALADAPTIVE LONG TERM

A

• Myocyte dysfunction • Ventricular remodeling • Hypertrophy, fibrosis • Myocyte death

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2
Q

HF treatment
Preload, afterload, contractility> SV>CO

A

^ preload + ^ afterload = decreased SV } decreased
Decreased contractility= decreased SV }. CO

Therefore we want to reduce preload+ afterload
AND INCREASE Contractility

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3
Q

HF + tx aims to

A

Causes breathlessness and distress
Treatment aims to:
 Prolong life
 Relieve symptoms
 Improve quality of life

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4
Q

ACEIs/ARBs
(Afterload, preload)

A

 Reduce cardiac afterload
 Reduce cardiac preload
 Delay progression of the disease
 Prolong life
 ACEIs may be used
as first-line treatment
 ARBs are a reasonable alternative
in case of ACEI intolerance

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5
Q

Angiotensin Receptor-Neprilysin Inhibitor (ARNI)
Examples

A

Some patients may be candidates for initial
therapy with an ARNI
—> (sacubitril-valsartan)

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6
Q

ARNI MoA

A

•Neprilysin degrades natriuretic peptides and ATII •Natriuretic peptides (B-type natriuretic peptide-
BNP): hormones released in HF to counteract the
effects of compensation:
-Natriuresis (counteracts NA retention)
-Vasodilation (counteracts Vasoconstriction)
-Inhibition of renin, ATII, aldosterone, ADH release
and action RAAS pathway

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7
Q

Eligibility criteria for initial therapy with an ARNI

A

 Current or prior elevated B-type natriuretic
peptide (BNP) level or N-terminal proBNP
 Hemodynamic stability (BP ≥100 mmHg)
 No history of angioedema
 Access to medication

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8
Q

Adverse effects of ARNI

A

-Hypotension
-hyperkalemia (RAAS pathway)
-cough
-dizziness (from hypotension)

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9
Q

β-BLOCKERS IN HF

A

 Considered first line treatment in combination with ACEIs, ARBs or ARNI
 But NOT in acute, decompensated HF

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10
Q

β-BLOCKERS IN HF
Examples

A

Metoprolol, carvedilol, bisoprolol

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11
Q

EFFECTS OF β-BLOCKERS IN HF

A

 SA node: Decrease heart rate
 Myocardium: Decrease contractility
 Renal: Decrease renin release, decrease RAAS
activation, reverse vasoconstriction, prevent fluid
retention —> Decrease blood pressure
 Save energy and oxygen demand
 Reduce Ca cycling and propensity for arrhythmias  Halt progression of the disease
 Improved survival

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12
Q

DIURETICS
Chronic tx and combination + monitor

A

 Chronic treatment with ACEIs leads to ‘aldosterone escape’’
—Circulating aldosterone concentrations return towards pre-treatment values
 Combining ACEIs/β-blockers with aldosterone antagonists (spironolactone, eplerenone) further reduces mortality in more advanced HF
 Monitor K+ levels with ACEIs/ARBs/ARNI in combination with aldosterone antagonist
 Other diuretics e.g. loop/thiazide diuretics used to treat congestion but do not prolong life

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13
Q

ALDOSTERONE ANTAGONISTS MoA

A

Aldosterone
 ↑Na+ & H2O retention —->↑ Preload & BP
 Myocardial fibrosis
 Endothelial dysfunction
 Promotes arrhythmias

Aldosterone antagonists in HF
Decrease preload
Improve prognosis

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14
Q

OTHER DRUGS FOR SECONDARY TREATMENT OF HF

1.Hydralazine plus nitrate (isosorbide nitrate)

A

• Hydralazine reduces afterload, while nitrates
reduce preload
• Addition to HF regimen, especially in black patients, improves survival

Reduces TPR

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15
Q

OTHER DRUGS FOR SECONDARY TREATMENT OF HF

  1. Digoxin
  2. Ivabradine
A

2.
• Does not reverse/retard progression of HF
• Reduces hospitalization (in combination with
other HF drugs)

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16
Q

OTHER DRUGS FOR SECONDARY TREATMENT OF HF
4. Sodium-Glucose Co-Transporter Inhibitor 2

A

• Recent guidelines recommend use of a
SGLT2i to reduce hospitalization for HF and
CV mortality, irrespective of presence of T2D

17
Q

DIGOXIN

A

 Inhibition of Na+/K+ ATPase

 Increases intracellular Ca2+

 Positive inotropic agent

18
Q

DIGOXIN Effects on the heart

A

 Cardiac slowing and reduced rate of conduction
through the AV node
-Due to increased vagal activity
 Increased force of contraction
 Disturbances of rhythm
-Block of AV conduction, increased ectopic
pacemaker activity

19
Q

Digoxin indications

A

 Treatment of HF in patients who remain
symptomatic despite optimal use of ACEIs
and diuretics
 Atrial fibrillation: due to AV conduction
slowing

20
Q

Digoxin Adverse effects

A

Common and severe
 Narrow therapeutic index
-Care in elderly and renal impairment
-Monitoring may be useful
 Disturbs sinus rhythm
-Can progress to AV block
 Anorexia, nausea
 Ectopic beats
 Visual effects (yellow, blurry vision)

21
Q

Digoxin
The effect of extracellular potassium

A

 Effect of digoxin increased if less K+, thus more
toxicity i.e. arrhythmias
 If more K+, then less effective
 Important: Diuretics-digoxin interaction
 Treatment of digoxin toxicity: normalize K+ levels,
anti-digoxin Fab fragments, anti-arrhythmics,
pacing

22
Q

Acute HF TX

A

 Loop diuretic-drugs of choice

 IV glyceryl trinitrate (GTN): Predominantly mediates venorelaxation
-Central venous pressure reduction (reduced preload)
 Mild effects on arteries
-Reduced afterload
 Can be combined with diuretics, if symptoms persist, especially with elevated BP

23
Q

ACUTE HF WITH SYSTOLIC DYSFUNCTION: INOTROPES

A
  1. Dobutamine
  2. Dopamine
  3. PDE3 inhibitors : amrinone, milrinone
24
Q

ACUTE HF WITH SYSTOLIC DYSFUNCTION: INOTROPES
1. Dobutamine

A

 Selective β1-adrenergic receptor agonist
 Drug of choice in !systolic dysfunction !

25
Q

ACUTE HF WITH SYSTOLIC DYSFUNCTION: INOTROPES
2.Dopamine

A

 Positive inotrope
 May increase renal blood flow

26
Q

ACUTE HF WITH SYSTOLIC DYSFUNCTION: INOTROPES

  1. PDE3 inhibitors: amrinone, milrinone
A

 Increase cAMP in heart muscle & smooth muscle: positive
inotropy, decreased TPR
 Improve hemodynamic indices
 Worsen survival: arrhythmias