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
What is B-type Natriuretic Peptide (BNP)? What is its function?
A hormone that is secreted by a stretched or overworked cardiac ventricle. BNP is a systemic vasodilator and diuretic.
26
Low BNP "rules out" heart failure in the differential except in cases of...? and why? (4)
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
What are BNP levels like during heart failure? Is this diagnostic?
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
What are the levels of BNP for each level of confidence in diagnosing heart failure? Improbable Probable Very probable
Improbable: < 100 pg/mL Probable: 100 pg/mL - 400 pg/mL Very probable: > 400 pg/mL
29
What key pieces of information can be gleaned about a heart failure patient with an Echocardiogram? (2)
If the ejection fraction is preserved or reduced. Any cardiac structural abnormalities (ie. valves, chambers, etc.)
30
In addition to estimating chamber sizes, what can an echocardiogram indirectly measure?
Cardiac and Pulmonary artery filling pressures.
31
What are the 4 New York Heart Association (NYHA) classifications of heart failure?
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
Class 3 HF (NYHA) can be divided into type A & B. What is the difference?
Class 3A (less severe) - Walking up the stairs causes symptoms Class 3B (more severe) - Dressing or bathing causes symptoms
33
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?
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
Why does the rate of survival after heart transplant increase so much after 1 year?
Immune rejection of the transplant reduces.
35
What is the normal value for PVR pressure?
x<3.5 Wood Units
36
What are major contraindications for a heart transplant? (6)
``` Major (unmanageable) psychiatric illness Severe pulmonary hypertension Obesity Advanced Age Diabetes with end-stage organ damage Absence of social support ```
37
When are heart transplants indicated? (4)
End-stage heart disease Severe ischemia Recurrent symptomatic V-tach NYHA Class 3-4 symptoms > 1 year
38
What are the two ways that heartmate 3 is better than 2?
Increased survival | Less thrombotic events
39
Where do clots typically form on heartmate? What can happen to the clot?
The "ruby." | It can dislodge and cause a stroke.
40
What are the less obvious risks of LVAD implantation? (2)
GI bleeding | LVAD dysfunction
41
What are the indications for an LVAD?
NYHA Class 3B-4 limitations despite intervention End-organ dysfunction due to low CO Iontrope (agent increasing contractility) dependence Frequent hospitalizations for HF
42
What are contraindications for an LVAD?
Severe psychosocial limitation Medication noncompliance Irreversible end-organ disease
43
How does an LVAD work?
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
Why is there high infection risk in LVAD?
There is a cord that goes through the abdomen that has to be kept sterile, which is very hard.
45
What are the main compensatory mechanisms of heart failure? (5) What is the goal of these compensatory mechanisms?
``` 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
Neurohormonal activation is a key compensatory mechanism that stimulates the ____&____ systems. Why is this activation a key target for therapeutic inhibition?
Renin Angiotensin Aldosterone System (RAAS) Sympathetic Nervous System These are the primary drivers of heart failure progression (increased fluid retention & MABP/afterload)
47
Where is renin made?
Juxtaglomerular apparatus of the kidney
48
What are the long term detrimental effects of an active RAAS? (4)
Cardiac Fibrosis & Hypertrophy Ischemia (2ndary to hypertrophy) Increased afterload (from vasoconstriction) --> Ventricular remodeling (eccentric) Salt & water retention
49
Why is it better to use an ARB over and ACE inhibitor?
There are other enzymes (aside from ACE) that can convert ang1 to ang2 so it is better to just block the receptor.
50
What is the difference between Angiotensin 1 and 2 receptors? Which angiotensin receptor do we want to block when using an ARB?
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
In heart failure, there is a neuronal imbalance between what two systems? What does this lead to?
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
What is Neprilysin (NEP)? Why is it a target for therapeutic inhibition for heart failure?
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
What are the major downsides to chronic sympathetic stimulation in relation to heart failure progression? (3)
Calcium overload --> unresponsiveness Volume overload --> high preload High Afterload --> hypertrophy
54
What can stimulate renin release? (2)
Sympathetic Nervous System | Low Renal perfusion
55
What is Lusitropy?
The rate of relaxation.
56
Is ventricular relaxation passive or active? Why? What happens if afterload is increased.
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
What is the now-standard` treatment for Heart Failure? What type of heart failure is this used in?
Beta-Blockers. Used to treat SYSTOLIC (HFrEF) heart failure.
58
What can beta-blockers do to improve heart failure?
Reverse cardiac remodeling. | Improve systolic function
59
Do NOT give beta-blockers to patients who are having? (2)
Acute decompensated heart failure (ADHF) | Cardiogenic Shock
60
How do you treat HFpEF? (3)
Treat underlying chronic disease (ie HTN, diabetes) Dietary sodium restriction Diuretics
61
How does increased afterload impair diastole?
More Ca2+ is released to generate a greater contractile force. Therefore it takes more time to reabsorb the Ca2+ leading to less relaxation.
62
How does ischemia affect ventricular relaxation and why?
Ischemia --> Decreased blood flow --> Less ATP --> Less Calcium reuptake to SR via Ca2+ pumps --> Decreased/Prolonged atrial relaxation.
63
What stressors cause symptoms in patients with HFpEF?
``` HTN - afterload impairs relaxation Ischemia - low ventricular relaxation Atrial Fibrillation - less blood into ventricles Tachycardia - less filling Exercise - Sx with exertion ```
64
Ischemia vs Myocardial Infarct in respect to the two types of Heart Failure?
Ischemia -- can lead to HFpEF, contractile cells take longer to relax. Myocardial infarct -- leads to HFrEF, you lose contractile cells