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Internal Medicine > Harrison - Heart Failure and Cor Pulmonale > Flashcards

Harrison - Heart Failure and Cor Pulmonale Flashcards

1
Q

HF - Number of people affected worldwide?

A

20 million.

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2
Q

Prevalence of HF in people over 65?

A

6-10%

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3
Q

What must happen in a patient to predispose to develop HF?

A

Any condition that leads to an alteration in LV structure or function.

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4
Q

Etiology of HF - 4 categories?

A
  1. Depressed ejection fraction (40-50%).
  2. Pulmonary heart disease
  3. High-output states
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5
Q

Etiology of HF - Depressed EF (<40%)?

A
  1. CAD –> MI, ischemia.
  2. Chronic pressure overload.
  3. Chronic volume overload.
  4. Non ischemic DCM
  5. Toxic/drug-induced damage.
  6. Chagas
  7. Disorders of rate and rhythm - chronic tachy/brady-arrhythmias.
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6
Q

Etiology of HF - Preserved EF (>40-50%)?

A
  1. Pathologic hypertrophy - primary (HCM), or secondary (HTN).
  2. Aging
  3. RCM
  4. Fibrosis
  5. Endomyocardial disorders
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7
Q

Etiology of HF - Pulmonary heart disease?

A
  1. Cor pulmonale

2. Pulmonary vascular disorders

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8
Q

Etiology of HF - High-output states?

A
  1. Metabolic disorders
  2. Thyrotoxicosis
  3. Nutritional disorders (beri beri)
  4. Excessive blood-flow requirements
  5. Systemic AV shunting
  6. Chronic anemia
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9
Q

MCC of HF?

A

CAD - Responsible for 60-75%.

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10
Q

HTN and HF?

A

HTN contributes to the development of HF in 75% of patients, including most patients with CAD.

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11
Q

Percentage of HF with a DEPRESSED EF in which the cause is unknown?

A

20-30%.

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12
Q

Conditions that lead to high CO - what is essential in order to result in HF?

A

The presence of underlying structural heart disease (usually).

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13
Q

Prognosis of symptomatic HF?

A

Poor:
30-40% die within 1yr.
60-70% die within 5yrs.
mainly from worsening of HF or as a sudden event (probably v-arrhythmia).

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14
Q

NYHA class IV - annual mortality rate?

A

30-70%.

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15
Q

NYHA class II - annual mortality rate?

A

5-10%.

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16
Q

NYHA class I - Objective assessment?

A

Patients with cardiac disease but without resulting limitation of physical activity.
Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea, or anginal pain.

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17
Q

NYHA class II - Objective assessment?

A
  1. Patients with cardiac disease resulting in slight limitation of physical activity.
  2. They are comfortable at rest.
  3. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
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18
Q

NYHA class III - Objective assessment?

A
  1. Patients with cardiac disease resulting in marked limitation of physical activity.
  2. They are comfortable at rest.
  3. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
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19
Q

NYHA class IV - Objective assessment?

A
  1. Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort.
  2. Symptoms of HF or the anginal syndrome may be present even at rest.
  3. If any physical activity is undertaken, discomfort is increased.
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20
Q

Index event in the pathogenesis of HF with a depressed EF?

A

Regardless of he nature of the inciting event, the feature that is common to each of these index events is that they ALL in some manner produce a decline in the pumping capacity of the heart.

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21
Q

After the initial decline in pumping activity, are the patients symptomatic?

A

In most instances, patients remain asymptomatic or minimally symptomatic after the initial decline in pumping activity of the heart or develop symptoms only after dysfunction has been present for some time.

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22
Q

At some point, asymptomatic patients become overtly symptomatic with a resultant striking increase in morbidity and mortality rates. What causes this transition?

A

Exact cause not known:
–> The transition to symptomatic HF is accompanied by increasing activation of neurohormonal adrenergic, and cytokine systems that lead to a series of adaptive changes within the myocardium collectively referred to as LV REMODELING.

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23
Q

Overview of LV remodeling - 3 categories of alterations?

A
  1. Alterations in myocyte biology
  2. Myocardial changes
  3. Alterations in LV chamber geometry
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24
Q

LV remodeling - Alternations in myocyte biology?

A
  1. Excitation-contraction coupling
  2. Myosin heavy chain (fetal) gene expression
  3. Beta adrenergic desensitization
  4. Hypertrophy
  5. Myocytolysis
  6. Cytoskeletal proteins
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25
Q

LV remodeling - Myocardial changes?

A
  1. Myocyte loss –> Necrosis/Apoptosis/Autophagy

2. Alterations in ECM –> Matrix degradation/Myocardial fibrosis

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26
Q

LV remodeling - Alterations in LV chamber geometry?

A
  1. LV dilation
  2. Incr. LV sphericity
  3. LV wall thining
  4. MV incompetence
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27
Q

Biologic stimuli for LV remodeling?

A
  1. Mechanical stretch of the myocyte
  2. Circulating neurohormones (NE, ANG II)
  3. Inflammatory cytokines
  4. Other peptides and GFs (endothelin)
  5. ROS
    - -> Now you understand the benefit from ACEIs + beta blockers in HF.
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28
Q

Mechanism of DIASTOLIC dysfunction seen in HF?

A
  1. Slowed myocardial relaxation (ATP dependent process –> SERCA2A –> Take up of Ca/ REDUCTION OF ATP in ischemia).
  2. LV compliance is reduced (hypertrophy or fibrosis).
  3. Can occur alone or in combination with systolic dysfunction in patients with HF.
29
Q

Ventricular remodeling refers to what basically?

A

To the changes in LV mass + volume + shape + composition of the heart that occur after cardiac injury and/or abnormal hemodynamic loading conditions.

30
Q

Cardinal symptoms of HF?

A
  1. Fatigue

2. Shortness of breath

31
Q

Mechanism of fatigue in HF?

A

Although fatigue traditionally has been ascribed to the low cardiac output in HF, it is likely that skeletal-muscle abnormalities and other noncardiac comorbidities (eg anemia) also contribute to this symptom.

32
Q

Origin of dyspnea in HF?

A

Probably multifactorial:

  1. Most important –> Pulmonary congestion –> interstitial or intra-alveolar fluid –> activates J receptors –> Stimulate rapid, shallow breathing characteristic of cardiac dyspnea.
  2. Reduction in pulmonary compliance.
  3. Incr. airway resistance.
  4. Respiratory muscle and/or diaphragm fatigue
  5. Anemia
33
Q

Can dyspnea become less frequent in HF?

A

With the onset of RV failure and TV regurgitation.

34
Q

Orthopnea occurs after or before exertional dyspnea in HF?

A

Usually after.

35
Q

What is the main symptom in orthopnea?

A

Nocturnal cough.

36
Q

Can orthopnea be seen in conditions other than HF?

A
  1. Abdominal obesity
  2. Ascites
  3. Patients with pulmonary disease whose lung mechanics favor an upright posture.
37
Q

Cardiac asthma is?

A

Closely related to PND –> Characterized by wheezing secondary to bronchospasm, and must be differentiated from primary asthma and pulmonary causes of wheezing.

38
Q

Cheyne-Stokes in HF?

A

It is present in 40% of patients with advanced HF and usually is associated with LOW CO.

39
Q

Cause of Cheyne-Stokes respiration?

A

Diminished sensitivity of the respiratory center to arterial Pco2.

40
Q

How is the Cheyne-Stokes respiration perceived by the patient or the patient’s family?

A

As severe dyspnea or as a transient cessation of breathing.

41
Q

GI symptoms in HF?

A
  1. Anorexia
  2. Nausea
  3. Early satiety
  4. Abdominal pain and fullness (edema of the bowel wall and/or congested liver).
  5. Congestion of liver and its capsule –> RUQ pain.
42
Q

Cerebral symptoms in HF?

A
  1. Confusion
  2. Disorientation
  3. Sleep and mood disturbances
    –> In severe HF.
    Also nocturia is common and may contribute to insomnia.
43
Q

Purpose of physical exam in HF?

A
  1. Help determine the cause of HF.

2. Assess the severity of the syndrome.

44
Q

SBP in HF?

A

Early –> May be normal or high.

Advanced –> Generally reduced due to LV dysfunction.

45
Q

Can rales be absent in patients with chronic HF, even when filling pressures are elevated?

A

Yes - Because of increased lymphatic drainage of alveolar fluid.

46
Q

Where do the pleural veins drain?

A

Into both systemic and the pulmonary veins –> Pleural effusions occur most commonly with biventricular failure.

47
Q

Are pleural effusions in HF always bilateral?

A

Although pleural effusions are often bilateral in HF, when they are unilateral –> More frequently in the right pleural space.

48
Q

Mechanism of cardiac cachexia in severe chronic HF?

A

Multifactorial:
1. Elevation of resting metabolic rate
2. Anorexia
3. Nausea
4. Vomiting
–> Due to congestive hepatomegaly + abdominal fullness.
5. Elevation of cytokines
6. Impairment of intestinal absorption due to congestion of the intestinal veins.
When present, cardiac cachexia –> poor prognosis.

49
Q

Routine laboratory testing in suspected HF?

A
  1. Complete blood count
  2. Panel of electrolytes
  3. BUN
  4. Creatinine
  5. Hepatic enzymes
  6. Urinalysis
    Selected patients should have:
    a. Fasting serum glucose (DM)
    b. Fasting lipid panel (dyslipidemia)
    c. Thyroid abnormalities (TSH-level)
50
Q

ECG role in HF diagnosis?

A
  1. Important to assess cardiac rhythm + determine the presence of LV hypertrophy or a prion MI (presence/absence of Q waves).
  2. To determine the QRS width, to ascertain whether the patient will benefit from resynchronization therapy.
  3. A normal ECG virtually excludes LV systolic dysfunction.
51
Q

Will patients with chronic HF have findings in a chest X-ray?

A

Although patients with acute HF have evidence of pulmonary HTN + Interstitial edema +/- pulmonary edema, the majority of patients with chronic HF do NOT!
–> Increased capacity of the lymphatics to remove interstitial +/- pulmonary fluid.

52
Q

What is today the gold standard for assessing LV mass and volumes?

A

MRI

53
Q

BNP and ANP are elevated in which type of HF?

A

Relatively sensitive for the presence of HF with DEPRESSED EF.
–> Also elevated in HF patients with a preserved EF, albeit to a lesser degree.

54
Q

Important to keep in mind about ANP?

A
  1. Natriuretic peptide levels increase with AGE + RENAL IMPAIRMENT.
  2. Also –> MORE ELEVATED IN WOMEN.
  3. Can be elevated in right HF from any cause.
  4. Can be falsely LOW in obese patients.
55
Q

Is BNP recommended as a guide to HF therapy?

A

No, for now.

56
Q

Mention other biomarkers that provide prognostic info in HF?

A
  1. Troponin T/I
  2. CRP
  3. TNF receptors
  4. Uric acid
57
Q

DDx in HF patients?

A
  1. Conditions in which there is circulatory congestion secondary to abnormal salt and water retention but in which there is no disturbance of cardiac structure or function (eg renal failure).
  2. Non cardiac causes of pulmonary edema (eg ARDS).
58
Q

Factors that may precipitate acute decompensation in patients with chronic HF?

A
  1. Dietary indiscretion
  2. Myocardial ischemia/infarction
  3. Arrhythmias (tachycardia/bradycardia)
  4. Discontinuation of HF therapy
  5. Infection
  6. Anemia
  7. Initiation of medications that worsen HF
  8. Alcohol consumption
  9. Pregnancy
  10. Worsening HTN
  11. Acute valvular insufficiency
59
Q

Medications that worsen HF?

A
  1. CCBs - Verapamil, diltiazem
  2. Beta blockers
  3. NSAIDs
  4. All class I antiarrhythmics, sotalol (III)
  5. Anti-TNF antibodies
60
Q

Cor Pulmonale - Definition?

A

Cor pulmonale often referred to as pulmonary heart disease, is defined as dilation + hypertrophy of the RV in response to diseases of pulmonary vasculature and/or lung parenchyma.
–> Historically, this definition has excluded congenital heart disease and those diseases in which the right heart fails secondary to dysfunction of the left side of the heart.

61
Q

Etiology of chronic cor pulmonale - 3 categories?

A
  1. Diseases leading to hypoxemic vasoconstriction
  2. Diseases that cause occlusion of the pulmonary vascular bed
  3. Diseases that lead to parenchymal disease
62
Q

Etiology of chronic cor pulmonale - Diseases leading to hypoxemic vasoconstriction?

A
  1. Chronic bronchitis
  2. COPD
  3. CF
  4. Chronic hypoventilation - Obesity, Neuromuscular disease, Chest wall dysfunction.
  5. Living at high altitudes.
63
Q

Etiology of chronic cor pulmonale - Diseases that cause occlusion of the pulmonary vascular bed?

A
  1. Thromboembolic disease, acute or chronic.
  2. Pulmonary HTN
  3. Pulmonary veno-occlusive disease
64
Q

Etiology of chronic cor pulmonale - Diseases that lead to parenchymal disease?

A
  1. Chronic bronchitis
  2. COPD
  3. Bronchiectasis
  4. CF
  5. Pneumoconiosis
  6. Sarcoidosis
  7. Interstitial lung disease
65
Q

What is the common pathophysiologic mechanism for cor pulmonale?

A

Pulmonary HTN that is sufficient to lead to RV dilation, with or without the development of concomitant RV hypertrophy.

66
Q

What may aggravate decompensation of chronic cor pulmonale?

A

Intermittent events that induce pulmonary vasoconstriction and RV afterload:

  1. Hypoxemia - Especially hypercarbia-induced resp. acidosis.
  2. COPD exacerbations
  3. Acute pulm. emboli
  4. Positive pressure (mechanical) ventilation
67
Q

ECG in severe pulmonary HTN shows?

A
  1. P pulmonale
  2. Right axis deviation
  3. RV hypertrophy
68
Q

Definition of heart failure?

A

A clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy.

Internal Medicine (107 decks)

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