Lecture Week 6 Flashcards

1
Q

Define Heart Failure.

A

Clinical syndrome in which the heart cannot at the same time:

1) Maintain its normal cardiac filling pressures
2) Maintain CO as needed by bodily demand

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2
Q

A failing heart can still maintain CO, but it will not maintain____.

A

cardiac filling pressure.

Failing hearts can only do one or the other.

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3
Q

Heart failure is a disease of the _______. And happens more in which sex?

A

Elderly, men (higher prevalence of coronary artery disease)

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4
Q

Why is the prevalence of Heart Failure increasing?

A

Better treatment

Aging Population

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5
Q

What are the two most common flavors of Heart Failure? Describe their pathology.

A

Heart failure secondary to:
DCM (Dilated Cardiomyopathy) –> Systolic –> Heart Failure with Reduced Ejection Fraction (HFrEF)

LVH (Left Ventricular Hypertrophy) –> Diastolic –> Heart Failure with Preserved Ejection Fraction (HFpEF)

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6
Q

What is the difference between Coronary Artery Disease (CAD) and Peripheral Artery Disease (PAD)?

A

CAD - Stenosis of coronary arteries that can lead to cardiac ischemia.

PAD - Stenosis of peripheral arteries that can lead to peripheral organ ischemia

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7
Q

In heart failure patients most symptoms are due to what? What are physical signs due to?

A

Symptoms - Retention of salt and fluid –> HTN.

Signs - Cardiac filling pressure & perfusion.

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8
Q

Difference between Right-sided HF between Left-sided HF?

A

RHF - Systemic (venous) congestion, high right atrial pressure

LHF - Pulmonary and Right heart congestion, high left atrial pressure

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9
Q

The most common cause (80% of the time) of right-sided heart failure is…? Why?

A

Left-sided heart failure.

LHF causes a pressure increase in vasculature and chambers behind it which ultimately leads to an increase in non-sustainable right atrial pressure leading to RHF.

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10
Q

What are the primary symptoms seen in Left-sided heart failure? What causes these symptoms?

A
Respiratory Symptoms (PND orthopnea, DOE, Hemoptysis)
Increased left atrial pressure leading to pulmonary HTN.
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11
Q

Left and Right-sided heart failure both lead to poor what? Why?

A

Perfusion

Both of these forms of heart failure lead to low CO and pulse pressure.

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12
Q

What are signs of left-sided heart failure? (2)

A

Rales (velcro lungs)

Wheezing

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13
Q

What are signs of right-sided heart failure? (4)

A

Elevated neck veins (JVD)
Ascites (fluid build-up in abdomen)
Hepatomegaly
Edema (pitting)

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14
Q

What are symptoms of right-sided heart failure? (4)

A

Anorexia
Abdominal bloating
Early satiety
Abdominal discomfort

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15
Q

Define “Cor Pulmonale”

A

Right-sided heart failure secondary to disease of pulmonary arteries or lungs.

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16
Q

How can right-sided heart failure lead to low CO?

A

RV & RA will compress LA & LV leading to less filling of the left heart and low CO.

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17
Q

What are symptoms of impaired perfusion? (3)

A

Low energy (Fatigue, weakness, lethargy)
Anorexia
Poor cognition

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18
Q

What are the signs of poor perfusion? (5)

A
Cool, mottled extremities
Low pulses (low pulse pressure)
Poor capillary refill
Low blood pressure
Pulsus alternans - pulse alternates b/t strong and weak
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19
Q

If the patient has edema, but no JVD can you suspect heart failure?

A

No. Patient has to have JVD (elevated JVP) to suspect HF.

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20
Q

Jugular venous pressure is measured in…?

A

centimeters of water.

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21
Q

Jugular venous pressure usually reflects the ____ which reflects the ____ assuming no occlusion or valve dysfunction.

A

Right atrial pressure, Left atrial pressure

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22
Q

How can you confirm during a physical exam if you see a jugular vein?

A

You should see respirophasic changes (changes when breathing) of the vein.

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23
Q

Patients that have Heart Failure should all have what test performed?

A

ECG - To look for further HF substrates such as (ischemia, long QRS (low EF), left ventricular hypertrophy)

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24
Q

Where would you see Kerly B lines? What are they and what do they indicate?

A

Chest X-ray (CXR)

Visible septa between lobes of lungs. They indicated fluid due to pulmonary edema.

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25
Q

What is B-type Natriuretic Peptide (BNP)? What is its function?

A

A hormone that is secreted by a stretched or overworked cardiac ventricle. BNP is a systemic vasodilator and diuretic.

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26
Q

Low BNP “rules out” heart failure in the differential except in cases of…? and why? (4)

A

Obesity- adipocytes “eat up” BNP

Flash Pulmonary Edema - Not enough time for BNP to be released.

Mitral stenosis - Since less blood goes into the LV BNP cannot be released much into systemic system.

Pericardial disease - BNP is only released when heart is stretched.

27
Q

What are BNP levels like during heart failure? Is this diagnostic?

A

Elevated.
Not diagnostic, there are other causes of elevated BNP. (ie heart wall stress caused by another organ disease) But we can suspect HF.

28
Q

What are the levels of BNP for each level of confidence in diagnosing heart failure?
Improbable
Probable
Very probable

A

Improbable: < 100 pg/mL
Probable: 100 pg/mL - 400 pg/mL
Very probable: > 400 pg/mL

29
Q

What key pieces of information can be gleaned about a heart failure patient with an Echocardiogram? (2)

A

If the ejection fraction is preserved or reduced.

Any cardiac structural abnormalities (ie. valves, chambers, etc.)

30
Q

In addition to estimating chamber sizes, what can an echocardiogram indirectly measure?

A

Cardiac and Pulmonary artery filling pressures.

31
Q

What are the 4 New York Heart Association (NYHA) classifications of heart failure?

A

Class 1 - HF only symptomatic in extreme conditions.

Class 2 - HF asymptomatic at rest, but symptomatic with ordinary physical activity (Hiking)

Class 3 - HF symptomatic with less than ordinary physical activity (stairs, dressing), somewhat comfortable at rest.

Class 4 - HF symptomatic at rest and any physical activity,

32
Q

Class 3 HF (NYHA) can be divided into type A & B. What is the difference?

A

Class 3A (less severe) - Walking up the stairs causes symptoms

Class 3B (more severe) - Dressing or bathing causes symptoms

33
Q

Describe the 4 stages of heart failure according to the American College of Cardiology (ACC)/American Heart Association (AHA). What class does each stage fall in?

A

Stage A - High risk for CHF, NO heart structure disorders (Class 1)

Stage B - Structural disorder of heart, no Hx of CHF symptoms (Class 1)

Stage C - Past or current symptoms of CHF associated with underlying heart disease (Class 3, ~4)

Stage D - End-stage disease (Class 4)

34
Q

Why does the rate of survival after heart transplant increase so much after 1 year?

A

Immune rejection of the transplant reduces.

35
Q

What is the normal value for PVR pressure?

A

x<3.5 Wood Units

36
Q

What are major contraindications for a heart transplant? (6)

A
Major (unmanageable) psychiatric illness
Severe pulmonary hypertension
Obesity
Advanced Age
Diabetes with end-stage organ damage
Absence of social support
37
Q

When are heart transplants indicated? (4)

A

End-stage heart disease
Severe ischemia
Recurrent symptomatic V-tach
NYHA Class 3-4 symptoms > 1 year

38
Q

What are the two ways that heartmate 3 is better than 2?

A

Increased survival

Less thrombotic events

39
Q

Where do clots typically form on heartmate? What can happen to the clot?

A

The “ruby.”

It can dislodge and cause a stroke.

40
Q

What are the less obvious risks of LVAD implantation? (2)

A

GI bleeding

LVAD dysfunction

41
Q

What are the indications for an LVAD?

A

NYHA Class 3B-4 limitations despite intervention
End-organ dysfunction due to low CO
Iontrope (agent increasing contractility) dependence
Frequent hospitalizations for HF

42
Q

What are contraindications for an LVAD?

A

Severe psychosocial limitation
Medication noncompliance
Irreversible end-organ disease

43
Q

How does an LVAD work?

A

The LVAD bypasses the aortic valve through an inflow cannula that sucks blood out of the left ventricle leading to an inflow cannula that pumps blood into the aorta.

44
Q

Why is there high infection risk in LVAD?

A

There is a cord that goes through the abdomen that has to be kept sterile, which is very hard.

45
Q

What are the main compensatory mechanisms of heart failure? (5) What is the goal of these compensatory mechanisms?

A
Increase HR (Tachycardia)
Increase preload
Increase contractility
Fluid Retention
Selective vasoconstriction

The goal is to maintain cardiac output, vital organ perfusion, and systolic blood pressure.

46
Q

Neurohormonal activation is a key compensatory mechanism that stimulates the ____&____ systems. Why is this activation a key target for therapeutic inhibition?

A

Renin Angiotensin Aldosterone System (RAAS)
Sympathetic Nervous System

These are the primary drivers of heart failure progression (increased fluid retention & MABP/afterload)

47
Q

Where is renin made?

A

Juxtaglomerular apparatus of the kidney

48
Q

What are the long term detrimental effects of an active RAAS? (4)

A

Cardiac Fibrosis & Hypertrophy

Ischemia (2ndary to hypertrophy)

Increased afterload (from vasoconstriction) –> Ventricular remodeling (eccentric)

Salt & water retention

49
Q

Why is it better to use an ARB over and ACE inhibitor?

A

There are other enzymes (aside from ACE) that can convert ang1 to ang2 so it is better to just block the receptor.

50
Q

What is the difference between Angiotensin 1 and 2 receptors? Which angiotensin receptor do we want to block when using an ARB?

A

Angiotensin 1 Receptor - Responsible for water retention, vasoconstriction, ventricular remodeling

Angtioensin 2 Receptor - Responsible for cell differentiation, tissue repair, anti-proliferation

We want to block Ang 1 Receptor with ARB

51
Q

In heart failure, there is a neuronal imbalance between what two systems? What does this lead to?

A

There is an imbalance between the Natriuretic Peptides (ie. BNP) & RAAS.

RAAS is more active which leads to more fluid retention and vasoconstriction. NP’s promote vasodilation & diuresis.

52
Q

What is Neprilysin (NEP)? Why is it a target for therapeutic inhibition for heart failure?

A

Neprilysin breaks down Natriuretic Peptides. It is a target for inhibition by Ang receptor neprilysin inhibitor (ARNI) because we want to promote vasodilation and diuresis to reduce pressure on the heart.

53
Q

What are the major downsides to chronic sympathetic stimulation in relation to heart failure progression? (3)

A

Calcium overload –> unresponsiveness
Volume overload –> high preload
High Afterload –> hypertrophy

54
Q

What can stimulate renin release? (2)

A

Sympathetic Nervous System

Low Renal perfusion

55
Q

What is Lusitropy?

A

The rate of relaxation.

56
Q

Is ventricular relaxation passive or active? Why? What happens if afterload is increased.

A

Active.
Relaxing is an active process that uses Ca2+ ATPase to reabsorb Ca2+ back into the SR.
If afterload is increased ventricular relaxation will be blunted.

57
Q

What is the now-standard` treatment for Heart Failure? What type of heart failure is this used in?

A

Beta-Blockers.

Used to treat SYSTOLIC (HFrEF) heart failure.

58
Q

What can beta-blockers do to improve heart failure?

A

Reverse cardiac remodeling.

Improve systolic function

59
Q

Do NOT give beta-blockers to patients who are having? (2)

A

Acute decompensated heart failure (ADHF)

Cardiogenic Shock

60
Q

How do you treat HFpEF? (3)

A

Treat underlying chronic disease (ie HTN, diabetes)
Dietary sodium restriction
Diuretics

61
Q

How does increased afterload impair diastole?

A

More Ca2+ is released to generate a greater contractile force. Therefore it takes more time to reabsorb the Ca2+ leading to less relaxation.

62
Q

How does ischemia affect ventricular relaxation and why?

A

Ischemia –> Decreased blood flow –> Less ATP –> Less Calcium reuptake to SR via Ca2+ pumps –> Decreased/Prolonged atrial relaxation.

63
Q

What stressors cause symptoms in patients with HFpEF?

A
HTN - afterload impairs relaxation
Ischemia - low ventricular relaxation
Atrial Fibrillation - less blood into ventricles
Tachycardia - less filling 
Exercise - Sx with exertion
64
Q

Ischemia vs Myocardial Infarct in respect to the two types of Heart Failure?

A

Ischemia – can lead to HFpEF, contractile cells take longer to relax.

Myocardial infarct – leads to HFrEF, you lose contractile cells