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Pharmacology > Drugs and Heart Failure > Flashcards

Drugs and Heart Failure Flashcards

1
Q

What is heart failure?

A

The heart is failing to pump sufficient blood to meet the needs of the body
Most failure is low output failure

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2
Q

Describe low output failure

A

The pump is slowly failing, the body compensates. Initially the failure is not perceived by the patient due to compensation.
As failure increases, compensatory mechanisms keep increasing but as some point they are no longer able to improve the condition, creating decompensated heart failure
The compensatory mechanisms become part of the problem

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3
Q

How does the body try to correct heart failure?

A

Increased sodium retention (slow benefit)
Activation of RAAS
Sympathetic nerve activation (fast benefit)

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4
Q

How does activation of RAAS help to correct heart failure?

A

Angiotensin constricts arteries and veins (fast benefit)

Aldosterone causes sodium retention (slow benefit) and potassium loss

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5
Q

How does sympathetic nerve activation help to correct heart failure?

A 
Increased heart rate (beta 1)
Increased contractility (beta 1)
Vasoconstriction (alpha 1)
Renin release (beta 2)
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6
Q

How do the compensatory mechanisms initially benefit the patient?

A

They all work to correct the drop in blood pressure
Increased plasma volume and constriction of the veins causes an increase venous return, which stretches the ventricles and increases contraction
Increased constriction of the arteries causes increased peripheral resistance but the heart is still strong enough to pump against increased resistance
Cardiac stimulation allows the heart to respond to increased sympathetic nerve activity and increased heart rate and contraction

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7
Q

What happens when the heart starts to fail? How does the heart compensate?

A

When the heart starts to fail, for the same LVEDV, you now have a lower SV or CO and your blood pressure drops
The heart tries to compensate by increasing the LVEDV. But if the heart becomes decompensated, increasing the LVEDV causes pulmonary congestion but not increasing it causes hypotension

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8
Q

How do the compensatory mechanisms affect late heart failure?

A

They worsen the condition
Overly increased plasma volume and constriction of veins
Overly increased constriction of arteries
Cardiac overstimulation
The patient is no longer able to compensate and overt signs of heart failure appear
But now the heart must deal with large increases in RAAS, SNS and blood volume

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9
Q

What happens with overly increased plasma volume and construction of veins?

A

Increased venous return stretches already overstretched ventricles
Heart is no longer able to increase force of contraction
Heart size enlarges (dilates) and muscle thickens (hypertrophy)
Venous pressure increases (peripheral and pulmonary oedema)

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10
Q

What happens with overly increased constriction of the arteries?

A

Greatly increased peripheral resistance makes it hard for the heart to empty against
Increased resistance to outflow is more than the heart can now overcome

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11
Q

What happens with cardiac overstimulation?

A

Overstimulation of the beta-adrenergic receptors causes down regulation of these receptors, increased fibrosis, increased apoptosis (cell death)

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12
Q

What are the symptoms of left-sided heart failure?

A

Shortness of breath
Need to sit or stand to breath easily
Shortness of breath at night
Fatigue

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13
Q

What are the physical findings of left-sided heart failure?

A 
Sweating
Increased heart rate
Rapid breathing
Pulmonary oedema
Maybe peripheral oedema
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14
Q

What are the symptoms of right-sided heart failure?

A

Peripheral oedema

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15
Q

What are the physical findings of right-sided heart failure?

A

Jugular venous distention

Peripheral oedema

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16
Q

What are the different drug classes for heart failure?

A 
Inhibitors of RAS
Aldosterone antagonists
Beta adrenergic receptor blockers
Diruetics
Inotropes
Vasodilators
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17
Q

What are the different stages/classes of heart failure?

A 
AHA stage A/NYHA prefailure
AHA stage B/NYHA class I
AHA stage C/NYHA class II/III
AHA stage D/NYHA class IV
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18
Q

Describe stage A/prefailure

A

No symptoms but there are risk factors

Treat obesity, hypertension, diabetes, hyperlipidemia, etc.

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19
Q

Describe stage B/class I

A

Symptoms with severe exercise

Treat with ACEi/ARB, beta blockers and diuretics

20
Q

Describe stage C/class II/III

A

Symptoms with marked (II) or mild (III) exercise

Add aldosterone antagonist, digoxin, hydralazine with a nitrate

21
Q

Describe stage D/class IV

A

Severe symptoms at rest

Treatment: transplant

22
Q

Why do we decrease the formation/action of angiotensin II?

A

Compensation to heart failure involves the RAAS

In the long term, this vasoconstriction and volume retention become a problem

23
Q

How do ACEi and ARBs treat heart failure?

A 
Decreased constriction in arteries and veins (decreased preload and afterload, so the heart works less)
Decreased aldosterone by decreased angiotensin II (decreased blood volume, meaning decreased venous return)
Decreased remodelling (decreased thickening of the heart tissue)
24
Q

What are the many benefits of ACEi/ARBs?

A 
Increased survival
Decreased symptoms
Increase quality of life
Increase exercise tolerance
Decreased hospitalization and ER visits
Increased ejection fraction and hemodynamics
25
Q

What is normal ejection fraction? What is considered low? What is symptomatic?

A

55-70%
Low is less than 40%
Constant symptoms are seen at 25%

26
Q

What are precautions/adverse reactions of ACEi/ARBs?

A

Should not be used in pregnant women (can cause birth defects)
May cause hyperkalemia
Commonly causes a dry cough (switch to ARB)
May cause angioedema (breathing problems)
Metabolically neutral (no effects on lipids or blood glucose)

27
Q

Should beta blockers be used in heart failure?

A

You give them a small dose, then monitor them over the next few weeks then increase their dose slightly and you continue to do this.
Beta blockers reduce heart rate and oxygen consumption
Cardiac output it increased after several months

28
Q

What does carvedilol do in heart failure?

A

Blocks beta and alpha adrenergic receptors
Alpha adrenergic receptor blockade helps to relax (dilate) arteries (the heart does not have to work as hard to eject blood and it decreases afterload)
Beta adrenergic receptor blockade slows the heart and decreases force of contraction
It’s a first line treatment in heart failure

29
Q

What does metoprolol do in heart failure?

A

Similar benefits to carvediol

Selectively blocks only beta1-adrenergic receptors

30
Q

When should beta blockers be avoided?

A

When the heart rate is less than 60 bp, or when the patient has second or third degree heart block, asthma, COPD, peripheral vascular disease, insulin dependant diabetes, or is physically active

31
Q

What co-morbidities benefit from beta blockers?

A 
May increase plasma potassium levels
Hypertension
Glaucoma
Certain arrhythmias
Myocardial infarction
Angina
32
Q

Why are diuretics used in heart failure?

A

If the patient is wet (you can hear congestion), it relieves pulmonary congestion and peripheral oedema

33
Q

What diuretics are used in heart failure? Why?

A

Furosemide is the most often diuretic used in heart failure. It is effective even if renal function is poor. In pulmonary oedema/congestion, it may improve congestion even before urine production. Aspirin may decrease the effectiveness of diuretics
Metolazone (thiazide) is added if response to furosemide is poor

34
Q

When are the benefits of diuretics in heart failure seen?

A

The benefits can be seen within hours to days (while other medications may take weeks to months)

35
Q

What is the goal with loop diuretics in heart failure?

A

To reduce weight by 1 kg/day

If the patient doesn’t respond, increase the dose of the loop diuretic (may need to add a thiazide if refractory)

36
Q

What are the problems with diuretics in heart failure?

A

Caution of excessive decreasing of blood volume (decreased venous pressure, which causes decreased filling pressure, also need to remove fluid from the plasma space at the same rate fluid from the interstitial space can replace it)
Monitor blood glucose and lipid levels

37
Q

How do hydralazine and nitrates affect heart failure?

A

Combination provides symptomatic and mortality benefits
Decrease preload (nitrate) and afterload (hydralazine)
Beneficial when added to patients with continued symptoms despite optimal treatment (ACEi, beta blocker, aldosterone antagonist)
White and black patients both benefit but more so with black patients
Hydralazine vasodialtes partially by releasing nitric oxide (presence of sildenafil may drastically increase the vasodilation with this combination)

38
Q

What are inotropes?

A

Agents which alter the force of contraction of the heart (“positive” interpose are of interest here)
Digoxin, dobutamine

39
Q

What do digoxine and dobutamine do?

A

They increase contractility of the heart
They provide symptomatic relief (long term benefit is unclear)
Chronic use may be associated with increased mortality (the patient doesn’t live longer but they feel better)

40
Q

Describe dobutamine use in heart failure

A

Must be given by intravenous infusion
Stimulates beta1-adrenergic receptors in the heart to increase heart rate and more importantly, contractility
May also stimulate beta2-adrenergic receptors in arterial vessels (vasodilation would decrease TPR)
Must carefully monitor as it may increase the heart rate, myocardial oxygen consumption and blood pressure
May aggravate schema (increased oxygen demand) and provoke arrhythmias

41
Q

Describe digoxin use in heart failure

A

Increases heart contractility (increases calcium in myocardial cells)
Blocks sodium/potassium ATPase
Must carefully monitor as increased contractility causes increased myocardial oxygen consumption which causes an increase in blood pressure
May aggravate ischemia (increased oxygen demand) and provoke arrhythmias
Provides symptomatic relief (improved exercise capacity, decreases hospitalization for heart failure)
Does not improve mortality but improves quality of life
Patients first stabilized on appropriate medications (ACEi, beta blockers, diuretics) when these are no longer sufficient, digoxin is used (long term plan)

42
Q

How does digoxin work?

A

It inhibits Na/K exchange by Na/K ATPase
The concentration of intracellular Na increases, and the concentration gradient across the membrane decreases
Increased Na decreases the driving force for the Na/Ca exchanger, so there is decreased extrusion of Ca into the extracellular space

43
Q

What needs to be monitored when on digoxin?

A

Potassium levels; hypokalemia increases digoxin toxicity

High aldosterone levels in heart failure decreases plasma potassium

44
Q

How does response to treatment vary among sex?

A

Women may not respond as well to ACEi/ARBs as men

Women and men benefit from beta blockers to the same degree

45
Q

How does response to treatment vary among race?

A

Blacks do not respond as well to ACEi as white

Hydralazine and nitrates appeared to be more effective in blacks than in whites

Pharmacology (15 decks)

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