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Pathophysiology 1 > Jan 19 - Heart Failure > Flashcards

Jan 19 - Heart Failure Flashcards

1
Q

What is vascular resistance?

A

The “squeeze” of the blood vessels outside the heart resisting blood flow

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2
Q

What is cardiac output?

A

A measure of how much blood is pumped out of the left ventricle of the heart in 1 minute (reminder: humans have about 5L of blood circulating at one time)

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3
Q

What is stroke volume?

A

The volume of blood ejected with each beat of the heart

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4
Q

What is inotropy?

A

The force at which the heart beats (squeeziness)

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5
Q

What is chronotropy?

A

The speed at which the heart beats

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6
Q

What are the 3 factors that can affect stroke volume?

A

Contractility (inotropy) - direct relationship
Afterload (squeeze/resistance) - inverse relationship
Preload (stretch/filling) - direct relationship

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7
Q

What is the LVEDV?

A

The left ventricular end diastolic volume; it’s volume of blood in the left ventricle at the end of diastole (preload)

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8
Q

How is the stroke volume affected by heart damage?

A

Even if their preload increases, their stroke volume still sucks

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9
Q

Explain what happens to the heart following an event such as an MI, stress, cardiac arrest, etc.

A

The heart becomes damaged, so that portion of the heart can’t work properly. The high blood pressure causes back up within the veins. The damage and the pressure causes a decrease in stroke volume so the heart tries to compensate

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10
Q

How does the heart compensate in heart failure?

A
  1. It increases chronotropy (heart rate) via sympathetics (norepinephrine)
  2. It increases preload via the RAAS
  3. Redirects blood flow to the heart via vasoconstriction of blood vessels, endothelin, RAAS, SNS
  4. Ventricular hypertrophy and remodeling
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11
Q

What are the pros to increasing heart rate (sympathetic activation) to compensate for heart failure?

A

It helps maintain cardiac output (CO=SVxHR)

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12
Q

What are the cons to increasing heart rate (sympathetic activation) to compensate for heart failure?

A

Short filling time, increased oxygen demand, risk of arrhythmias

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13
Q

What are the pros to increased preload using RAAS (sodium and water retention) to compensate for heart failure?

A

Increase stroke volume (more stretch, more preload)

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14
Q

What are the cons to increased preload using RAAS (sodium and water retention) to compensate for heart failure?

A

Pulmonary and/or peripheral oedema, increased oxygen demand

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15
Q

What are the pros to peripheral vasoconstriction (endothelin, RAAS, SNS) to compensate for heart failure?

A

Maintains blood pressure, recruits blood to the heart and brain

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16
Q

What are the cons to peripheral vasoconstriction (endothelin, RAAS, SNS) to compensate for heart failure?

A

Increased afterload (resistance) which decreases stroke volume

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17
Q

What are the pros to ventricular hypertrophy and remodelling to compensate for heart failure?

A

Helps to maintain cardiac output, decreases oxygen deman

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18
Q

What are the cons to ventricular hypertrophy and remodelling to compensate for heart failure?

A

Increased risk of ischemia, dysfunction, fibrosis and arrhythmias

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19
Q

Explain how the compensatory mechanisms are a vicious cycle

A

When the heart is damaged, the cardiac output sucks. So heart rate and preload are increased, blood pressure increases (good to a point), but then so does afterload (which is bad). Even though all of these things are happening, the heart still can’t push out what it wants (the cardiac output still sucks)

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20
Q

Name neurohormonal factors

A

Angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin

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21
Q

What is the mechanism of angiotensin II as a neurohormonal factor?

A

It causes vasoconstriction, activates SNS, causes sodium retention by the kidneys and aldosterone release (RAAS)

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22
Q

What is the mechanism of the norepinephrine as a neurohormonal factor?

A

It causes tachycardia, vasoconstriction, increased contractility

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23
Q

What is the mechanism of aldosterone as a neurohormonal factor?

A

It causes sodium and water retention in the kidney (RAAS), and contributes to ventricular remodelling

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24
Q

Name three natriuretic peptides

A

Atrial natriuretic peptide (ANP)
Brain natriuretic peptide (BNP) and NT-proBNP
C-type natriuretic peptide

25
Q

What is the mechanisms of natriuretic peptides as neurohormonal factor?

A

BNP is the most important, but both ANP and BNP are increased in heart failure. They have diuretic, natriuretic and hypotensive effects (trying to counteract the heart failure process)

26
Q

What is the mechanism of arginine vasopressin as neurohormonal factor?

A

It increases water retention, increases vasoconstriction, it contributes to ventricular remodelling (it’s part of RAAS; it’s aka antidiuretic hormone or ADH)

27
Q

What is special of NT-proBNP?

A

It’s specific to heart failure (can be used as biomarker)

28
Q

What is the difference between systolic and diastolic heart failure?

A

In systolic heart failure, the blood has a hard time ejecting properly from the left ventricle. In diastolic heart failure, the ventricles do not fill properly

29
Q

What causes systolic heart failure?

A 
Poor contraction (ischemic heart disease)
Volume overload (if the valves become diseased, it can cause valve stenosis)
Pressure overload (in hypertension, the blood can't be pumped out because there's too much pressure)
30
Q

What causes diastolic heart failure?

A

Small ventricle chamber (hypertrophy/fibrosis)

Diastolic filling is hindered (mitral valve stenosis, hypertrophy

31
Q

What is the difference in symptoms between left-sided and right-sided heart failure?

A

In right-sided heart failure, the blood gets backed up in the superior and inferior vena cava and fluid builds up in the arms, legs and organs. In left-sided heart failure, the blood pools in the lungs and patients experience a drowning sensation

32
Q

What are five symptoms of heart failure?

A

Fluid retention and oedema (peripheral/pulmonary)
Shortness of breath (dyspnea, orthopnea)
Fatigue (especially with activity)
Confusion
Cyanosis (oxygen depletion - blue colouring of fingers, toes lips)

33
Q

Explain the different symptoms the arise from fluid retention and oedema

A

Rales (crackling sounds on auscultation with stethoscope)
Weight gain (rapid, e.g., 10 lbs in a week)
Pitting oedema (fluid buildup in the feet
Elevated jugular venous pressure (JVP)

34
Q

What is dyspnea?

A

Irregular breathing

35
Q

What is orthopnea?

A

The patient feels like they’re drowning when they lie down. It’s good to ask the patient how many pillows they are using

36
Q

What diagnostics are used for the diagnosing of heart failure?

A

Imaging (chest X-ray, echocardiogram)
Lab work
Physical assessment (JVP, pulmonary oedema, peripheral oedema, ascites)

37
Q

How does a chest X-ray diagnose heart failure?

A

It enlarges cardiac sihouettes. They measure the largest diameter of the chest then measure the largest part of the heart. If the ratio is more than 50%, the patient has an enlarged heart

38
Q

How does an echocardiogram diagnose heart failure?

A

It uses ultrasound waves to image the beating heart. It detects abnormalities in both the structure and the function of the heart. ECHO’s also detect hypertrophy; the ventricle will be smaller and the myocardium will be fatter

39
Q

What type of lab work is done to diagnose heart failure?

A

Test the levels of brain natriuretic peptide (BNP) and plasma N-terminal pro-BNP; both peptides have elevated levels in heart failure. They have diuretic, natriuretic and hypotensive effects that try to counteract the compensatory mechanisms occurring in heart failure

40
Q

How is jugular venous pressure used to diagnose heart failure?

A

The physican is measuring where they see the heart beat in the jugular vein. Wherever they can see the pulse in the jugular vein above the sternal angle and is measured in centimetres. Normal = 1 cm. Elevation (5-6 cm) of the JVP indicates volume overload

41
Q

How is pulmonary oedema used to diagnose heart failure?

A

Rales/orthorpnea

Crackles heard with the stethoscope are due to fluid build up

42
Q

How is peripheral oedema used to diagnose heart failure?

A

Aka pitting oedema

Greater the “pit” = greater volume overload. It’s graded (0=normal, 3=the worst)

43
Q

How is ascites used to diagnose heart failure?

A

Fluid accumulation in the peritoneal space (right-sided back-up)

44
Q

What are non-pharmacological treatments for heart failure? What is the most important one?

A 
Salt restriction! (t eat soup)
Stop smoking
Monitor weight daily (consult physician if they gain 2-3 kg over three days)
Exercise (once symptoms are controlled)
Control blood pressure
Control high cholesterol
Control diabetes
Control arrhythmias
45
Q

What are pharmacologic treatments available for heart failure?

A 
ACEI/ARBs
Beta-blockers
Diuretics
Aldosterone antagonists
Digoxin
Nitrates
Hydralazine
46
Q

How do ACEI/ARBs work to treat heart failure?

A

They inhibit the RAAS, which reduces preload, cause vasodilation and reduce remodelling

47
Q

How do beta-blockers work to treat heart failure?

A

They block B1 receptors on the heart and block SNS activity to reduce heart rate and act as anti-arrhythmics

48
Q

How do diuretics work to treat heart failure?

A

They increase sodium and water excretion and decrease oedema to reduce preload

49
Q

How do aldosterone antagonists work to treat heart failure?

A

They block sodium and water retaining activities of aldosterone to reduce preload and reduce remodelling. These drugs are very important in heart failure as they reduce the risk of death

50
Q

How does digoxin work to treat heart failure?

A

It acts as Na/K-ATPase inhibitor to increase contractility (inotropy)

51
Q

How do nitrates work to treat heart failure?

A

They dilate the veins to reduce preload and afterload. Nitrates are often given with hydralazine

52
Q

How does hydralazine work to treat heart failure?

A

It dilates arterioles to reduce afterload. Hydralazine is often given with nitrates

53
Q

Why is reducing the heart rate actually a good thing to treat heart failure?

A

Although reducing heart rate isn’t good for cardiac output, it allows for better contractility (organizes the heart a bit better)

54
Q

What drugs need to be watched for/avoided in heart failure?

A 
NSAIDS
Steroids/hormones
Anti-arrhythmics
Alcohol
Illicit drugs
55
Q

Why is it important to avoid NSAIDS in heart failure?

A

NSAIDS, such as naproxen and aspirin, contribute to fluid accumulation. They constrict the afferent arteriole in the kidney and the pressure in the kidney drops (and filtration drops) so the patient can’t pee out as much fluid

56
Q

Why is it important to avoid illicit drugs in heart failure?

A

Illicit drugs, cocaine in particular, kills heart tissue

57
Q

Why is it important to avoid steroids/hormones in heart failure?

A

They can cause fluid accumulation

58
Q

Why is it important to watch for anti-arrhythmics in heart failure?

A

Because in doses that exceed the require dose, they can actually cause arrhythmias, making cardiac output worse

59
Q

Why is it important to avoid alcohol in heart failure?

A

Alcohol can be very stressful on the heart and can contribute to fluid accumulation. It can also cause arrhythmias

Pathophysiology 1 (11 decks)

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