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NURS 1650 - Here We Go Again > Pathophysiology of Heart Failure > Flashcards

Pathophysiology of Heart Failure Flashcards

1
Q

How does contractility shift the Frank-Starling curve?

A

Decreased contractility shifts the curve downward

HF can cause a decrease in contractility and an increase in the workload of the heart

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2
Q

Higher and higher levels of preload lead to:

A

An increase in the workload of the heart

A non-normal SV

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3
Q

What does aldosterone do to blood volume?

A

Regulates sodium (increases retention)

Leads to an increase in water retention/volume retention

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4
Q

What does vasopressin/ADH do to blood volume?

A

Regulates water

Increases retention of water –> increase in volume

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5
Q

What do ANP and BNP do to blood volume?

A

Regulate sodium

Increase excretion –> decreased water retention –> decreased volume

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6
Q

What are the two types of HF based on heart function?

A

Systolic: Heart Failure with Reduced Ejection Fraction (HFrEF)

Diastolic: Heart Failure with Preserved Ejection Fraction (HFpEF)

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7
Q

What are the two types of HF based on heart anatomy?

A

Left HF

Right HF

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8
Q

What is heart failure defined as?

A

The inability of the heart to produce enough cardiac output to meet the needs of the body

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9
Q

What is ejection fraction?

A

The % of blood volume in the LV at EDV that is actually ejected into the systemic circulation

Blood pumped out/total blood in the ventricle

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10
Q

What is systolic heart failure? What is it also called?

A

Impaired ability of the ventricle to contract, reducing stroke volume and ejection fraction to <40%

Generally occurs due to a thinned, weakened heart wall

Known as HFrEF: “Heart Failure with Reduced Ejection Fraction”

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11
Q

What has happened to the heart during HFrEF/systolic heart failure? Why has this happened?

A

The ventricle things

Chamber gets larger

Myocytes apoptose and are eventually replaced with stiff fibrotic tissue

Ventricles dilate

No longer has a good shape or structure for contracting/pumping

Occurs due to chronically increased preload and associated chronically elevated end-diastolic pressures

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12
Q

Etiology of systolic/HFrEF:

A
  • Coronary artery disease/MI
  • HTN
  • Valve disorders
  • Smoking
  • Diabetes
  • Toxic damage to the heart
  • Dilated cardiomyopathy
  • Idiopathic
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13
Q

The heart and chamber become ____ in HFrEF:

A

Bigger

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14
Q

What is diastolic heart failure? What is it also known as?

A

Impaired relaxation of the ventricle decreases the amount of filling and end-diastolic volume (SV)

Also called HFpEF: “Heart Failure with Preserved Ejection Fraction”

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15
Q

What happens to stroke volume, contractility, afterload, and ejection fraction in diastolic/HFpEF?

A

Contractility and EF are fairly normal

Afterload increases

Stroke volume is decreased due to poor filling and increased pressure (afterload)

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16
Q

How is the heart remodeled in diastolic/HFpEF? Why does this happen?

A

Ventricular wall hypertrophy, thickening (w/ accompanying stiffness)

Usually a response to chronically increased afterload, such as uncontrolled HTN

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17
Q

The chambers in diastolic/HFpEF become ___:

What does this cause?

A

Smaller

Less blood fills the chamber, decreased SV

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18
Q

Etiology of diastolic/HFpEF:

A
  • Uncontrolled HTN
  • Aging
  • Untreated obstructive sleep apnea (OSA)
  • Ischemic fibrosis (makes the ventricles stiff)
19
Q

What is hypertrophic cardiomyopathy? What are its clinical presentations?

A

Autosomal dominant disease with variable expressivity (missense mutation)

Abnormal thickening/enlargement of the septum and/or L ventricular wall; obstruction of blood flow at left ventricular outflow tract, and sarcomere disarray

Dyspnea on exertion, syncope (fainting), fatigue, chest pain, palpitations, arrhythmias

20
Q

Hypertrophic cardiomyopathy is similar to which type of heart failure?

A

HFpEF/diastolic HF

21
Q

What is the NYHA Classification Scheme of HF based on?

A

Functional capacity

22
Q

Describe the different classes in the NYHA Classification Scheme

A

Class I: No incapacity

Class II: Slight limitation

Class III: Incapacity with slight exertion

Class IV: Incapacity with rest

23
Q

What are the three main adaptive/injury response mechanisms?

A

Frank-Starling Mechanism
- increased preload via fluid retention to increase contractility and maintain SV

Neurohormonal Adaptation
- RAAS, SNS stimulation, etc.)

Dilation/hypertrophy/structural alterations
- “Remodeling”

24
Q

Why does the RAAS get activated in HF? What is it compensating for?

A

To increase perfusion

Increases blood volume

Its job is to keep normal GFR, needs enough blood to do that

25
Q

What does angiotensin II do systemically?

A

Vasoconstriction

26
Q

What happens to the Frank-Starling curve in HF? What causes this to happen?

A

Shifts downward

Overworking of the heart (SNS increasing oxygen demand, RAAS activation, increased contractility) in an attempt to attain normal SV ends up damaging the heart, resulting heart failure and a shift downward (decrease SV –> perfusion)

27
Q

In a healthy heart, why is increasing preload a good idea?

A

It increases stroke volume and cardiac output

28
Q

What do ANP and BNP do?

A

Cause vasodilation

Increased excretion of sodium by the kidneys

Decreases blood volume and blood pressure

29
Q

What happens to ANP and BNP as HF progresses?

A

The release of ANP and BNP becomes less and less effective at decreasing blood volume

30
Q

ANP/BNP and the RAAS cascade have _____ effects. Name them

A

Opposite effects

ANP/BNP:
- decrease BP
- decrease SNS activation

RAAS cascade:
- vasoconstriction
- increase BP
- increased SNS activity

31
Q

Describe how short-term compensation can bring negative long-term consequences in HF (fluid retention, increased cardiac sympathetic stimulation, increased vascular sympathetic stimulation, RAAS)

A

Fluid retention
- increased preload/ventricular filling leads to increased ventricular wall tension + ventricular dilation

Increased cardiac (B1) sympathetic activation
- increased HR, increased oxygen demand, and remodeling
- downregulation of B1 receptors in the heart
- not responds normally to SNS stimulation

Increased vascular sympathetic (alpha-1) stimulation
- increased afterload leading & remodeling

RAAS activation
- vasoconstriction
- fluid retention
- increased afterload and preload
- remodeling

32
Q

If the LEFT ventricle requires extra filling and pressure to eject an adequate SV, which structure will have to be even at higher pressure? What will the signs and symptoms be?

A

The atrium, lungs, and pulmonary circuit

The systemic circuit will not have adequate perfusion

WIll result in forward effects

33
Q

What are the forward effects of left HF? Why do these effects occur?

A
  • Fatigue (tissues not being perfused)
  • Peripheral coolness
  • Oliguria (kidneys not being perfused –> decr GFR –> decr urine output)
  • Increased HR (trying to compensate & get more blood pumped out)
  • Faint pulses

Brain not getting enough blood:
- Restlessness
- Confusion
- Anxiety

34
Q

If the LEFT ventricle cannot contract forcefully, which circuit will have inadequate perfusion? What will the s/sx be?

A

Pulmonary circuit will not be perfused

Causes backwards effects (lungs)

35
Q

What are the backward effects in left HF?

A
  • Orthopnea
  • Sudden nocturnal dyspnea
  • SOB
  • DOE
  • Cough
  • Cyanosis
  • Basilar crackles
36
Q

If the RIGHT ventricle requires extra filling and pressure to eject and adequate SV, which structures will have to be at a higher pressure? What will the s/sx be?

A

The right atrium. There will then be backup in the superior and inferior vena cava

This leads to peripheral edema, venous congestion (enlarged liver, spleen), and jugular venous distention

37
Q

What is the most common cause of RV failure?

A

LV failure

May also occur alone, secondary to chronic lung disease

38
Q

What are the backward effects of Right HF?

A
  • Hepatomegaly
  • Ascites
  • Splenomegaly
  • Anorexia
  • Subcutaneous edema
  • Jugular vein distention
39
Q

What are the clinical manifestations of HF?

A

Fatigue, exercise intolerance due to inadequate SV/CO

SOB in LHF due to pulmonary congestion

Fatigue + SOB –> impact ADLs

RHF congestion affects systemic circulation –> dependent edema, jugular venous distention, liver distention, GI discomfort/nausea

40
Q

How do you diagnose HF? What do these diagnostic tools tell us?

A
  • History and physical
  • Labs (including BNP or NT-pro-BNP)
  • ECG
  • Chest x-ray (cardiomegaly)
  • Echocardiogram (chamber size, structure, and function; estimate EF)
  • Exercise testing
41
Q

What is decompensated HF? What can cause it?

A

An exacerbation of HF symptoms (increased edema, dyspnea, signs of volume overload)

A common cause of hospitalization of people with HF

May be due to infections, not taking meds as prescribed, not maintaining fluid and sodium restrictions

42
Q

How does pulmonary edema occur in HF? Which type of HF do you see this in?

A

Alveolar capillaries, which are normally at low pressure, have higher and higher pressures inside them leading to fluid leaking into the interstitium

Eventually leaks into the alveolar lumen –> sensation of drowning & edema

Pt. will not be able to tolerate laying flat at all (orthopnea)

LHF Backward effect

43
Q

How does dependent edema occur in HF? Which type of HF do you see this in?

A

Caused by increased venous hydrostatic pressure causing fluid to leak out of the veins

Retention of sodium and water by the kidneys also contributes

RHF backward effect

44
Q

What are some sequelae of HF?

A

Atrial fibrillation/arrhythmias due to dilation of atria and ventricles impeding impulse conduction

Inflammation and fibrosis due to injury to the myocardium

Liver disease (RHF)

Kidney disease

Lung disease and pulmonary hypertension

Depression

NURS 1650 - Here We Go Again (20 decks)

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