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Module 9 - Cardiovascular disorders > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is heart failure?

A

A clinical syndrome resulting from any structural or functional impairment of ventricular filling or ejection of blood.

It is a common final pathway for a variety of heart conditions including:
- CAD
- HTN
- Arrhythmia’s
- Cardiomyopathy
- Congenital heart defects
- Valvular heart disease

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2
Q

What is the pathophysiological outcome of HF (low output) (3)?

A

1) decreased CO = decreased tissue perfusion

2) compensation for the decline in CO

3) back up of blood into vessels supplying the heart (congestive heart failure = old terminology)

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3
Q

What is the cause of high output HF?

A

Occurs when cardiac demands (and CO) increase, but the heart can’t keep up (e.g. severe anemia or thyrotoxicosis)

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4
Q

What is the mortality rate for HF?

A

50% mortality within 5 years of diagnosis.

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5
Q

Treatment for HF is aimed at (3)?

A
  • relieving symptoms
  • reducing frequency of exacerbations
  • slowing progression
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6
Q

Describe acute vs chronic HF.

A

Acute:
- rapid onset
- caused by an acute MI (cardiogenic shock), a massive PE, cardiac tamponade, or a sever infection (myocarditis)

Chronic:
- slowly developing (progressive decline in cardiac function)
- most often caused by coronary artery disease (CAD), chronic HTN or valvular heart disease

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7
Q

What is left-sided HF?

A
  • ineffective left ventricular function
  • blood backs up into the left atrium and pulmonary circulation
  • CO decreases (decreased forward flow)
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8
Q

What is right-sided HF?

A
  • ineffective right ventricular function
  • blood backs up into the right atrium and systemic venous system
  • decreased blood flow into the pulmonary circulation
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9
Q

What is systolic dysfunction (HFrEF)?

A

= Heart failure with reduced ejection fraction

  • impaired pumping causes a decrease in SV and CO
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10
Q

Describe how myocardial damage occurs and can lead to systolic dysfunction.

A

Myocardial damage impairs contractility.
Causes of damage:
- acute MI
- viral infection of the myocardium
- cardiotoxins
- chronically under-perfused myocardium/ repeated ischemic episodes d/t CAD)

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11
Q

Describe how ventricular dilation contributes to systolic dysfunction.

A

Ventricle wall becomes excessively dilated which impairs contractility. A volume overload causes excessive preload.

  • dilated cardiomyopathy
  • aortic or mitral valve regurgitation
  • congenital heart disease (septal defects)
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12
Q

Describe how excessive afterload contributes to systolic dysfunction.

A

Contractility is insufficient to overcome afterload.
- chronic (long-standing) HTN
- aortic stenosis
At some point the heart decompensates.

Note: if the pressure overload causes hypertrophy - coronary blood flow might be insufficient to meet metabolic demands of hypertrophied muscle causing ischemic damage.

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13
Q

What is Takotsubo (stress) cardiomyopathy?

A

An acute, reversible heart failure syndrome (< 21 days) caused by impaired ventricular contractility typically in response to a stressful trigger.

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14
Q

Who does Takotsubo cardiomyopathy typically effect?

A

Postmenopausal women presenting with acute or subacute onset of chest pain (>75%) and/or shortness of breath (approx 50%), often with dizziness (>25%) and occassional syncope (5-10%)

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15
Q

What is diastolic dysfunction (HFpEF)?

A

= Heart failure of preserved ejection fraction. EF is preserved as both EDV and SV are reduced in diastolic dysfunction (EF = SV/EDV)

Impaired filling decreases EDV (preload) = less blood is available to be pumped out causing a decrease in SV and CO.

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16
Q

How does decreased compliance contribute to diastolic dysfunction?

A

increased wall stiffness that impairs filling.
- ventricular hypertrophy d/t HTN
- scar tissue d/t MI or radiation
- infiltrative disorders (amyloidosis, hemochromatosis)

17
Q

How does obstructed ventricular filling contribute to diastolic dysfunction?

A
  • mitral valve stenosis
  • compression of the ventricle (cardiac tamponade, chronic pericarditis)
18
Q

How does impaired heart relaxation contribute to diastolic dysfunction?

A

Shortened diastole impairs filling.
- ventricular tachyarrhythmias
- atrial fibrillation (increase in HR and loss of atrial kick)

19
Q

What is ejection fraction?

A

EF = SV (amount of blood pumped out of the ventricle)/ EDV (amount of blood in ventricle)

  • the percentage of blood ejected during systole
  • reflects myocardial contractility
  • hallmark of systolic dysfunction = EF < or equal to 40% (indicates impaired contractility)
20
Q

What are the Canadian Cardiovascular Society CPGs on EF?

A

> or equal to 50% is normal/ preserved (HFpEF)

41-49% is borderline/ mildly reduced (HFmrEF)

< or equal to 40% is low/ reduced (HFrEF)

Normal range is 50-70% (we don’t eject 100% of EDV)

21
Q

What are S3 and S4 heart sounds?

A

S3 = ventricular gallop. Occurs early in diastole during passive LV filling. Can be normal at times. Requires a very compliant (dilated) LV. Can be a sign of systolic dysfunction. The sound is actually caused by the large amount of blood striking a very compliant LV.

S4 = atrial gallop. Occurs at the end of diastole during active LV filling. Almost always abnormal. Requires a non-compliant (hypertrophied) LV. Can be a sign of diastolic dysfunction. Sound is forceful and rapid contraction of atria forcing blood into a non-compliant SV.

22
Q

Describe how pulmonary edema occurs in Left-sided HF.

A
  1. Back up of blood into left atrium and pulmonary circulation
  2. Decreased forward flow of blood and CO
  3. Increased pulmonary capillary hydrostatic pressure (d/t congestion)
  4. Fluid enters the interstitium and alveoli = pulmonary edema
23
Q

Describe the worsening levels of dyspnea in pulmonary congestion/ edema.

A
  1. Exertional dyspnea
  2. Orthopnea (lying supine)
  3. Paroxysmal nocturnal dyspena (redistribution of daytime edema fluid at night)
  4. resting dyspnea
24
Q

What is hemoptysis?

A

Rupture of congested pulmonary vessels.

25
Q

What is a pleural effusion?

A
  • possible complication of Left-sided HF
  • edema fluid leaks into pleural cavity
  • causes worsening dyspnea and chest pain
26
Q

What are signs and symptoms of decreased CO?

A
  • decreased BP (orthostatic hypotension is common)
    reduced tissue perfusion:
  • fatigue
  • muscle weakness
  • skin pallor, cool extremities
  • confusion (more common in older adults)
  • oliguria
    + signs of compensation (increased HR)
27
Q

What is cor pulmonale?

A

right-sided HF caused by a pathological pulmonary process (e.g. COPD).

RV hypertrophies in response to increased workload, but eventually decompensates.

28
Q

What are common causes of right-sided HF?

A
  • secondary to Left-sided HF (backward flow of blood)

Isolated right-sided HF:
- large PE
- pulmonary or tricuspid valvular disease
- right ventricular MI
- pulmonary HTN d/t sleep apnea

29
Q

What are S&S of systemic venous congestion in right-sided HF?

A
  • edema (feet/ankles, sacrum)
  • RUQ pain (hepatomegaly)
  • firm, distended abdomen (ascites)
  • nausea, anorexia (GI tract congestion)
  • weight gain
  • jugular vein distension, flushed face, headache (venous congestion of the superior vena cava)
  • positive abdominal jugular reflex (increased jugular venous pressure when pressure is applied to the liver)
30
Q

What is acute decompensated HF?

A

Decompensation occurs when compensatory mechanisms fail to maintain adequate CO.

31
Q

Describe the sympathetic compensatory response to HF (baroreceptor reflex)?

A
  • increased HR & contractility = increased CO
  • venoconstriction = increased VR and preload (SV)
  • peripheral arterial vasoconstriction = increase BP
32
Q

Describe RAAS activation as a compensatory response to HF.

A
  • angiotensin II is a potent vasoconstrictor = increases BP
  • aldosterone stimulates Na+ and H2O reabsorption = increased BV and preload (SV)
  • ADH stimulates renal water reabsorption
33
Q

What is ventricular remodeling?

A

A compensatory response to HF.

Ventricle walls thicken (muscle fibres increase in width) in response to conditions that increase afterload (improves pumping).

OR

Ventricles enlarge (muscle fibres increase in length) in response to conditions that increase preload (improves filling).

34
Q

What are the negative consequences of increased preload and afterload as compensatory mechanisms?

A

Chronic increase in preload:
- excessive dilation of the ventricle decreases contractility
- fluid retention worsens symptoms (edema, etc.)

Chronic increase in afterload:
- increased workload of the heart
- increased O2 demand

35
Q

What are some key clinical signs that indicate volume overload?

A
  • weight gain of 2 kg over two days or 2.5 kg in one week
  • elevated jugular venous pressure
  • edema
  • crackles
  • elevated BNP
36
Q

Describe management of chronic HF.

A

Goals = symptom reduction, improve functional capacity, slow disease progression, prevent hospitalization, reduce the risk of death.

  1. Manage underlying cause (e.g. HTN, smoking, a-fib etc.)
  2. Self-management (e.g. fluid and Na+ restriction, physical activity, daily weights)
  3. Medications
  4. Devices (e.g. LVAD = left ventricular assist device)
37
Q

What defines the transition to advanced HF?

A
  • HF therapies are not working as well as they did
  • symptoms return more frequently
  • symptoms are more challenging to treat
  • more frequent primary care or hospital visits
  • more time spent in the yellow HF zone

Module 9 - Cardiovascular disorders (6 decks)

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