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HF Flashcards

1
Q

In heart failure, the heart is unable to pump sufficient blood to meet the needs of the body

A

True
It’s also progressive

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2
Q

HF is due to..

A

Impaired ability of the heart to full with blood or/and eject blood

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3
Q

HF is accompanied with an increase in..

A

Abnormal increade in blood volume + interstitial fluid

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4
Q

Underlying causes of HF?

A
  1. Arteriosclerosis heart diseases (atherosclerosis)
  2. Myocardial infraction (heart attack)
  3. Dilated cardiomyopathy (enlarged heart)
  4. HTN
  5. Vulvular heart diseases (invloves one of the 4 heart valves)
  6. Cingential heart disease (heart defects)
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5
Q

What are the 11 classes of drugs for HF?

A

ACEi, ARBs, B-blockers
Diuretics, ARNI (sacubitril/valsartan)
SGC stimulators, SGLT2 inhibitors
Inontropic agents
Aldosterone antagonists
Mineralcocorticoid receptor antagonist
And dilators

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6
Q

What is the pharmacological (the medication) intervention in HF?

A
  1. Lower workload on myocardium
  2. Lower extracellular fluid volume
  3. Lower cardiac remodeling rate
  4. ENHANCE CONTRACTILITY
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7
Q

What is the inontropic effect?

A

Force of contraction is related to calcium concentration (in free cystolic form)
So, agents that increase calcium levels intracellularly (or increase contractility to calcium sensitivity) ———> increase force of contraction
This is the inontropic effect

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8
Q

Stimulation of cardiac tissues if it was sustained & inappropriate leads to?

A

Impaired calcium homeostasis
Heart failure
Arrhythmia

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9
Q

T/F increased calcium concentration initiates the contractile process

A

True

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10
Q

What are the compensatory mechanisms of HF?

A
  1. Increased sympathetic activity (it increases the work of the heart)
  2. Activation of RAAS (increases the work of the heart)
  3. Activation of natriuretic peptides (due to increase in preload, a beneficial response)
  4. Myocardial hypertrophy (stretching of the heart, which leads to more contraction)
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11
Q

Talk about the first compensatory mechanism, increased sympathetic activity

A
  1. It is due to a decrease in blood pressure that the baroceptors (B-adrenoceptors) have sensed
  2. When the decrease in blood pressure is sensed, the sympathetic nervous system is activated, stimulation B1 and a1 receptors
  3. What happens next? Increaded heart rate & increased contraction force
  4. In addition, vasoconstriction (a1 mediated) enhances venous return and increases preload
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12
Q

Increased sympathetic activity in a nutshell:

A

Decreased blood pressure — increase in heart rate — increased force of contraction (B1 & a1 stimulated)

Vasocontriction — enhanced venous return — increased cardiac preload (from a1)

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13
Q

Compensatory mechanism: activation of RAAS

A
  1. Due to a decrease in cardiac output
  2. Decreased blood flow to kidneys
  3. Renin is relased — angiotensin II is relased — aldosterone is released
  4. Blood volume is increased
  5. More blood is returned to the heart
  6. Can cause peripheral edema, pulmonary edema, and venous pressure if the heart cant pump the extra volume
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14
Q

What increases the release of natriuretic peptides

A

An increase in preload

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15
Q

What do natriuretic peptides include (only 2 are important in cardiac function)

A
  1. Atrial natriuretic peptides (ANP)
  2. B-type natriuretic peptides
  3. C-type
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16
Q

Compensatory mechanism 3: activation of natriuretic peptides

A

Results in:

1) vasodilation

2) natriuresis (exceretion)

3) inhibition of the release of renin + aldosterone

4) reduced myocardial fibrosis

Beneficial and can improve cardiac function

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17
Q

Myocardial hypertrophy/ types of heatt failure?

A

Systolic heart failure or HFrEF
Happens due to excessive elongation/stretching of the heart which leads to weaker contraction and diminished ability to eject blood
It is the result of the ventricle inability to pump/eject effectively
*symptoms can be reduced

Diastolic heart failure/HFpEF
the inability of the ventricles to RELAX and ACCEPT blood due to structural changes such as hypertrophy
Due to thickening of ventricular walls and decrease in ventricular volume
*the ventricles do not fill adequately
**medication cannot improve survival

Both types coexist in HF

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18
Q

Inadequacy of cardiac output is termed:

A

Diastolic dysfunction or HFpEF

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19
Q

Resistance to natriuretic peptides

A

Happens due to poor cardiac output
High levels of these peptides lead to vasodilation and natruresis
Resistance lead to: hypertrophy, fibrosis, Vasocontriction, and reduced renal blood flow

Because without Resistance, they increase blood flow, cause vasodilation, decreased RAAS and sympathetic activity, decrease hypertrophy

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20
Q

When is heart failure compensated?

A

If compensatory mechanisms restore cardiac output

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21
Q

When is heart failure acute/decompensated?

A

If compensatory mechanisms fail to restore cardiac failure

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22
Q

What drugs may perciptate or exacerbate HF?

A
  1. Non dihydropyridine ccb
  2. NSAIDs
  3. Alcohol
  4. Some antiarrhythmics
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23
Q

T/F inontropic agents are reserved for ACUTE signs and symptoms of HF and mostly used in INPATIENT setting

A

True

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24
Q

Part of the standard pharmacotherapy in HFrEF?

A

ACEi
- For symptomatic + asymptomatic HFrEF
- for all stages of LEFT ventricular failure
- for long term use in recent MI

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25
How do ACEi work?
Decrease circulating levels of angiotensin II — inhibit degradation of bradykinin Decreased angiotensin lead to: 1. Decreased output of sympathetic system 2. Increased vasodilation of smooth muscles 3. Decreased retention of sodim and water All lead to DECREASED preload + afterload INCREASED cardiac output
26
Renal elimination is important for most ACEi except ..... which undergoes excertion in feces
Fosinopril
27
T/F ARBs are highly plasma protein-bound
True
28
Why do we need aldosterone antagonists in HF?
Because patients with HF have high levels of aldosterone due to angiotensin II stimulation + reduced hepatic clearance of the hormone
29
Talk about spironolactone & epleronone?
- both are aldosterone antagonists - they prevent retention, hypertrophy, and hypokalemia - for SYMPTOMATIC HFrEF - for HFrEF with recent MI **spironolactone had affinity for androgen + progesterone so it has endocrine related side effects: dysmonorrhea and gynecomastia
30
What is Neprilysin in ARNI?
It is an enzyme responsible for breaking down vaso-active peptides (ang I and II, Bradykinen, and natriuretic peptides) So ARNI inhibits it, what happens if neprilyin is inhibited? 1.Augments the activity of vasoactive peptides 2. Increases their concentration 3. Natriuresis 4. Diuresis 5. Vasodilation 6. Inhibition of fibrosis
31
What does ARNI therapy decrease:
Afterload Preload Myocardial FIBROSIS **BETTER THAN ACEI
32
Randoms about ARNI
- hypotension is more common because of the added reduction of afterload - contraindicated in angioedema due to increase in bradykinin due to sacubitril inhibition of neprilysin - to minimize risk of angioedema with ARNI: acei must be stipped at least 36 hours before startiing ARNI
33
Why are B blockers used in HF?
- They prevent changes that occur because of the chronic activation of SNS - they prevent direct deleterious effects of norepinephrine decreasing remodeling, hypertrophy, cell death
34
B blockers are recommended for patients with...
Chronic & stable HFrEF
35
What do diuretics decrease in hf?
1. Diuretics decrease signs of volume overload (symptoms of hf such as orthopnea, dyspnea) 2. Diuretics decrease plasma volume ——》 decrease venous return to the heart (decrease preload) ——》 decrease workload & oxygen demand 3. Diuretics decrease afterload by reducing plasma volume, decreasing blood pressure
36
Randoms about diuretics:
- loop diuretics are most commomly used in HF - they do not show to improve survival in HF, only for signs and symptoms
37
HCN blockers?
- inhibition of HCN channel results in slowed depolarization & low heart rate - HR reduction is dose dependent - it's related to SA node
38
Ivabradine?
An HCN channel blocker Which inhibits If current (selective) to slow HR and depolarization WITHOUT a reduction in contractility, AV conduction, blood pressure, or repolarization
39
Therapeutic uses of Ivabradine
-In patients with HFrEF because a slower HR increases stroke volume -It improves symptoms in HFrEF especially for patients who are in SINUS rhythm with heart rate above 70 And their therapy is OPTIMIZED - So to take ivabradine you should also take b blocker or you should have contraindication to b blocker to have it optimized
40
Ivabradine kinetics
- bradycardia (solved by dose reduction) - luminous phenomena (by dose reduction) - half life is 6 hours, twice a day administration - inhibited by CYP3A4
41
Arterial vasodilators?
- Hydralazine - decreases afterload - in combination for chronic HF - may decrease calcium in arterial muscles —— 》 vasodilation & reduced afterload, preload - in case of ACEi, ARBs intolerance - in case of vasodilation effect required (in combination of hydralazine and isosorbide) - increases survival in black patients on standard treatment (b blocker + acei/arb) - acute hf
42
Arterial and venous dilators?
1) Nitrates (nitroglycerin and isosbride dintrate) — veno-dilation 2) Nitrourisside — for both dilation For acute hfref
43
Difference between veno dilation and arterial dilation?
Venous dilation: decrease in preload by increasing venous capacity Artieral dilation: reduces resistance, afterload, and increase output
44
Why are hydralzaine and isosbride in combo?
Isosbride is rapidly absorbed with high first pass metabolism With quick onset and DOA of 4-6hours
45
SGLT2 INHIBITORS?
- inhibit the myocardial SODIUM HYDROGEN exchanger preventing calcium overload - cardioprptective effects Actions of SGLT2I: - reduce reabsorption of glucose + sodium - reulsts in: glucosuria, naturesis - reduced volume, afterload, preload
46
Therapeutic uses and adverse effects of SGLT2I?
it's for patients with optimized symptomatic HFrEF It causes: 1. Volume depletion 2. Renal impairment 3. Urogenital infections
47
Oxidative stress and inflammation happens in heart failure. It results in:
1. Inactivation of nitric oxide 2. Reduced activation of sGC 3. Reduced production of cGMP which contribute to Vasocontriction, fibrosis, inflammation
48
Vericiguat?
- long acting oral sGC stimulator - increases sensitivity of the enzyme to endogenous nitric oxide because in HF theres a deficit in it - nitric oxide stimulated sGC to synthesize cGMP ——》 actibates protein kinase G
49
When to use vericiguat?
In recently hospitalized patients on guidline medications **it has minimal side effects related to hypotension
50
What do positive inontropic agents do?
They enhance cardiac contractility increasing cardiac output It happens due to an increased calcium concentration in cytoplasm this is why contraction is enhanced
51
Why are inontropic agents used for a short period of time mainly in inpatient setting?
(Except Digoxin) Because they uncrease intracellular calcium concentration and they've been associated with reduced survival
52
A group that can increase contractility of heart muscles?
Digitalis gkycosides
53
T/F Digoxin reduces the ability of myocytes to actively pump sodium ions from the cell
True
54
Who should take digoxin?
HFrEF patients who are SYMPTOMATIC on optimal hf therapy. A low serum conc (0.5-0.9) is beneficial
55
Digoxin causes neurohormonal inhibition, how?
Low dose of digoxin inhibits sympathetic activation with minimal effects on contractility, this is why a low conc is needed
56
Does digoxin slows down conduction velocity through AV node?
Yes it does. Which is why its used in ATRIAL FIBRILLATION
57
Adverse effects of digoxin?
1. Increased risk of arrhymia (na/kATPase inhibition) 2. Hypokalemia (digoxin competes with potassium)
58
What is contraindicated in digoxin?
P-gp inhibiotrs Not grapefruit Should be used in caution with meds that SLOW the AV conduction such as b blockers
59
Dobutamine and dopamine?
- both are given IV - for short term treatment of acute HF in hospital - B adrenergic agonists - they increase entry of calcium into myocardial cells ——》 enhanced contraction
60
Milrinone
- increases cAMP concentration - phosphodiesterase inhibitor - IV for short treatment of acute HF - can be considered for intermediate term treatment with dovutamine for PALLIATIVE care
61
Polytherapy is initiated as the HF progresses
True
62
When are loop diuretics introduced first?
If HF is overt for relief of symptoms
63
When are ACEi/ARBS are introduced?
After optimization of loop diuretic therapy, gradullay titratef
64
Most patients newly diagnosed with HFrEF are initiatives on both low dose ACEi and Bblocker
True, for initial stabilization
65
What medications are initiated in patients who continue to have HF symptoms despite optimal therapy?
• Aldosterone Antagonists • hydralzaine/isosorbide dinitrate • SGLT2I
66
Lastly added medications for HF for asymptomatic benefiy only:
Digoxin Ivabradine Verciciguat
67
When to replace ACEi/ARBs with sacubitril/valsartan?
Once at an optimal dose of either of them and the patient remains asymptomatic Without them using b blocker only monotherapy

Pharma 1 (2 decks)

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