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Cardiology > Cardiology- Approach to heart failure > Flashcards

Cardiology- Approach to heart failure Flashcards

1
Q

What is heart failure?

A

A clinical syndrome where the heart is unable to pump sufficient blood to meet the body’s needs.

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2
Q

What are the two primary types of heart failure?

A

Heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).

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3
Q

What is HFrEF?

A

Heart failure where the left ventricular ejection fraction (LVEF) is <40%.

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4
Q

What is HFpEF?

A

Heart failure where the LVEF is ≥50%, often with diastolic dysfunction.

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5
Q

What percentage of the population is affected by heart failure?

A

Approximately 1-2% globally, with higher prevalence in those over 65 years.

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6
Q

What is the most common cause of heart failure?

A

Coronary artery disease (CAD), particularly post-myocardial infarction.

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7
Q

What are the risk factors for heart failure?

A

Hypertension, diabetes, obesity, CAD, and valvular heart disease.

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8
Q

What is the prognosis of heart failure?

A

Poor prognosis; around 50% of patients die within 5 years of diagnosis.

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9
Q

How does the prevalence of heart failure differ between men and women?

A

HFrEF is more common in men, while HFpEF is more common in women.

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10
Q

What is the impact of heart failure on hospitalization rates?

A

Heart failure is one of the leading causes of hospitalizations in patients over 65.

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11
Q

What is the primary pathophysiological problem in HFrEF?

A

Systolic dysfunction due to weakened ventricular contraction.

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12
Q

What is the primary problem in HFpEF?

A

Diastolic dysfunction due to impaired ventricular filling and relaxation.

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13
Q

How does hypertension contribute to heart failure?

A

Chronic high blood pressure causes left ventricular hypertrophy and stiffening, leading to diastolic dysfunction.

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14
Q

What role does the renin-angiotensin-aldosterone system (RAAS) play in heart failure?

A

RAAS activation leads to vasoconstriction, sodium retention, and fluid overload, worsening heart failure.

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15
Q

What is the Frank-Starling mechanism in heart failure?

A

The heart attempts to compensate by increasing preload, but this ultimately leads to inefficient pumping and congestion.

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16
Q

What is ventricular remodeling in heart failure?

A

Structural changes in the heart, including dilation and hypertrophy, in response to chronic stress.

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17
Q

What causes pulmonary congestion in heart failure?

A

Increased pressure in the left atrium leads to fluid buildup in the lungs due to backflow from the failing left ventricle.

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18
Q

What is the role of natriuretic peptides in heart failure?

A

They are released in response to myocardial stretch and act to promote vasodilation and natriuresis to counteract heart failure progression.

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19
Q

How does heart failure lead to systemic edema?

A

Reduced cardiac output leads to fluid retention, increasing hydrostatic pressure and causing fluid leakage into the tissues.

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20
Q

How does heart failure impact kidney function?

A

Decreased renal perfusion due to low cardiac output activates RAAS, causing sodium and water retention, which worsens fluid overload.

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21
Q

What are the common symptoms of heart failure?

A

Dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, and edema.

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22
Q

What is orthopnea?

A

Shortness of breath that occurs when lying flat, relieved by sitting up.

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23
Q

What is paroxysmal nocturnal dyspnea (PND)?

A

Sudden episodes of shortness of breath during the night, waking the patient from sleep.

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24
Q

What are the common signs of heart failure on physical examination?

A

Jugular venous distension, peripheral edema, crackles on lung auscultation, and an S3 gallop.

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25
Q

What causes jugular venous distension in heart failure?

A

Increased pressure in the right atrium due to right-sided heart failure or fluid overload.

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26
Q

What causes peripheral edema in heart failure?

A

Fluid retention due to poor cardiac output and increased venous pressure.

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27
Q

What is an S3 heart sound?

A

A third heart sound, also known as a ventricular gallop, heard in heart failure due to rapid filling of a stiff or dilated ventricle.

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28
Q

How does heart failure cause fatigue?

A

Reduced cardiac output leads to poor oxygen delivery to muscles, resulting in fatigue during exertion.

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29
Q

What is ascites in the context of heart failure?

A

Accumulation of fluid in the peritoneal cavity due to elevated venous pressures.

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30
Q

What causes cyanosis in heart failure?

A

Reduced oxygen delivery to tissues as a result of poor cardiac output and pulmonary congestion.

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31
Q

What is the primary imaging modality used to diagnose heart failure?

A

Echocardiography, to assess ejection fraction, wall motion, and valve function.

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32
Q

What blood test is commonly elevated in heart failure?

A

B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP).

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33
Q

What is the significance of BNP in heart failure?

A

Elevated levels indicate myocardial stretch and are used to diagnose and assess the severity of heart failure.

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34
Q

How does a chest X-ray help in heart failure diagnosis?

A

It can show pulmonary congestion, cardiomegaly, and pleural effusion.

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35
Q

What ECG findings may be present in heart failure?

A

Arrhythmias, left ventricular hypertrophy, ischemic changes, or conduction abnormalities.

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36
Q

What role does cardiac MRI play in heart failure diagnosis?

A

It provides detailed images of heart structure and function, particularly for identifying scar tissue and fibrosis.

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37
Q

How is ejection fraction measured?

A

Via echocardiogram, MRI, or nuclear imaging.

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38
Q

What is the clinical utility of stress testing in heart failure?

A

To assess for ischemia or viability of the myocardium in patients with suspected ischemic heart disease.

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39
Q

What laboratory tests are important in heart failure assessment?

A

Renal function, electrolytes, liver function tests, thyroid function, and complete blood count.

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40
Q

How is heart failure classified according to the New York Heart Association (NYHA)?

A

Based on symptom severity: Class I (no symptoms), Class II (mild symptoms), Class III (moderate symptoms), Class IV (severe symptoms).

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41
Q

What role does diabetes play in the development of heart failure?

A

Diabetes increases the risk of atherosclerosis, CAD, and directly damages the myocardium, promoting heart failure.

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42
Q

What valvular heart diseases can cause heart failure?

A

Conditions like aortic stenosis and mitral regurgitation can lead to heart failure by increasing the workload on the heart.

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43
Q

Can cardiomyopathy cause heart failure?

A

Yes, dilated, hypertrophic, and restrictive cardiomyopathies can impair heart function and lead to heart failure.

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44
Q

How does chronic alcohol abuse contribute to heart failure?

A

It can lead to alcoholic cardiomyopathy, where excessive alcohol consumption damages the heart muscle, reducing its ability to pump efficiently.

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45
Q

Which main components of the circulatory system can fail in heart failure?

A
  1. Endocardium: valves
  2. Myocardium
  3. Within the myocardium
    • coronary arteries
    • conduction system
  4. Pericardium: TB, malignancy
  5. Systemic blood vessels: systemic hypertension
  6. Pulmonary vessels: pulmonary hypertension & cor pulmonale
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46
Q

Textbook definition of heart failure

A

a clinical syndrome of effort intolerance due to cardiac dysfunction, with neurohormonal adaptations resulting in salt & water retention

may have features of LV, RV or biventricular failure

in end stage disease, the heart normally fails as a whole, irrespective of cause

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47
Q

Common causes of heart failure

A
  1. Hypertension
  2. Ischaemic heart disease
  3. Rheumatic heart disease (RHD)
  4. Cor pulmonale
  5. Myopathies – include ethanol and nutritional deficiencies
  6. Drugs – esp Tik & Cocaine; both can cause systemic hypertension & pulmonary hypertension
  7. Pericardial disease
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48
Q

What is pump failure in heart failure?

A

It refers to the inability of the heart to effectively pump blood, which can occur due to weakened heart muscle (systolic failure) or impaired filling (diastolic failure).

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49
Q

How can blood vessels contribute to heart failure?

A

Abnormal vasoconstriction or vasodilation can increase the workload on the heart or impair blood delivery to tissues.

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50
Q

What role does the renin-angiotensin-aldosterone system (RAAS) play in heart failure?

A

RAAS activation leads to vasoconstriction and fluid retention, increasing blood volume and worsening heart failure.

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51
Q

How can the kidneys contribute to heart failure?

A

In response to reduced cardiac output, the kidneys retain sodium and water, which increases blood volume and leads to fluid overload.

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52
Q

What is the consequence of left ventricular failure?

A

It causes pulmonary congestion and edema because of backflow and increased pressure in the pulmonary circulation.

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53
Q

What happens in right ventricular failure?

A

It causes systemic venous congestion, leading to symptoms like peripheral edema, hepatomegaly, and ascites.

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54
Q

How does the autonomic nervous system (ANS) contribute to heart failure?

A

Over-activation of the sympathetic nervous system can increase heart rate and vasoconstriction, leading to increased cardiac workload.

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55
Q

What is ventricular remodeling?

A

Structural changes to the heart, such as hypertrophy or dilation, occur in response to chronic stress and contribute to worsening heart failure.

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56
Q

What does NYHA stand for in heart failure?

A

New York Heart Association, a classification system used to describe the severity of heart failure based on symptoms.

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57
Q

What is NYHA Class I?

A

No limitation of physical activity. Ordinary physical activity does not cause symptoms of heart failure.

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58
Q

What is NYHA Class II?

A

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

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59
Q

What is NYHA Class III?

A

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms.

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60
Q

What is NYHA Class IV?

A

Unable to carry on any physical activity without discomfort. Symptoms of heart failure are present even at rest.

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61
Q

Why is the NYHA classification important in heart failure management?

A

It helps to assess the severity of the disease, guide treatment decisions, and predict outcomes and prognosis.

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62
Q

How does NYHA classification aid in treatment planning?

A

Patients with higher NYHA classes may require more aggressive therapy, including advanced interventions like device therapy or transplantation.

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63
Q

How can NYHA classification change over time?

A

With appropriate treatment and lifestyle changes, a patient’s symptoms can improve, potentially moving them to a lower NYHA class.

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64
Q

What is the significance of NYHA Class IV in terms of prognosis?

A

NYHA Class IV is associated with the worst prognosis and indicates the need for advanced therapies or palliative care.

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65
Q

Can the NYHA classification be used to track disease progression?

A

Yes, worsening NYHA class over time indicates disease progression, while improvement suggests effective management.

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66
Q

What is cardiomyopathy?

A

diseases involving the myocardium directly

not the result of:
- hypertensive heart
disease
- valvular heart disease
- coronary artery disease or
- pericardial disease

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67
Q

What are the three main types of cardiomyopathy?

A

The three main types are dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM).

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68
Q

What is dilated cardiomyopathy (DCM)?

A

DCM is characterized by an enlarged and weakened heart muscle, leading to reduced systolic function and heart failure.

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69
Q

What is hypertrophic cardiomyopathy (HCM)?

A

HCM involves thickened heart muscle, often the interventricular septum, leading to impaired relaxation, diastolic dysfunction, and potential obstruction of blood flow.

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70
Q

What is restrictive cardiomyopathy (RCM)?

A

RCM is characterized by stiffened heart muscle, which impairs the heart’s ability to fill properly during diastole, leading to heart failure with preserved ejection fraction (HFpEF).

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71
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

ARVC is a rare type of cardiomyopathy where the heart muscle is replaced by fatty or fibrous tissue, particularly in the right ventricle, leading to arrhythmias and risk of sudden cardiac death.

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72
Q

How is cardiomyopathy different from other causes of heart failure?

A

Cardiomyopathy is a primary disorder of the heart muscle itself, while other causes of heart failure may stem from conditions like coronary artery disease or valvular heart disease.

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73
Q

Can cardiomyopathy lead to heart failure?

A

Yes, all forms of cardiomyopathy can lead to heart failure due to the heart’s impaired ability to pump blood effectively.

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74
Q

Is cardiomyopathy always symptomatic?

A

No, cardiomyopathy can be asymptomatic in early stages, especially hypertrophic cardiomyopathy, and may only be discovered during routine screening or due to sudden cardiac events.

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75
Q

Can cardiomyopathy be inherited?

A

Yes, many forms of cardiomyopathy, particularly hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, can be inherited in an autosomal dominant pattern.

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76
Q

What does the acronym “HEARTII PVD” stand for in the context of cardiomyopathy causes?

A

H HIV
E ethanol (thiamine deficiency: Beri Beri)
A amyloid/sarcoid/haemochromatosis/malignancy
R rhythms: includes AF, atrial flutter, ARVC
T thyroid disease: especially hyperthyroidism
I idiopathic & genetic / familial (HCM, muscular dystrophy)
I inflammatory (SLE, systemic sclerosis)

P post partum: last month of pregnancy -> 5/12 post partum
V viruses (esp. Coxsackie virus)
D drugs (Tik/cocaine); chemotherapy, radiation

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77
Q

History taking in 1st episode of heart failure

A
  • hypertension, diabetes or HIV
  • thyroid disease
  • current or recent pregnancy
  • sudden cardiac death
  • anaemia or blood loss
  • excess alcohol or substance use
  • ischaemic chest pain (angina)
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78
Q

History taking in patient with known heart failure

A
  • poor fluid & salt restriction
  • poor medication adherence
  • features of systemic infection
  • recent ischaemic chest pain, autonomic Sx
  • excessive use of NSAIDs
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79
Q

What is the primary result of left heart failure?

A

Left heart failure leads to pulmonary congestion due to impaired left ventricular function, causing a backup of blood into the lungs- pulmonary oedema

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80
Q

What is the most common symptom of left heart failure?

A

Hx of orthopnea and PND
apex displaced infero- laterally
S3 at the apex- loudest on expiration

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81
Q

What is paroxysmal nocturnal dyspnea (PND)?

A

PND is sudden shortness of breath that awakens patients from sleep, typically caused by fluid redistribution in left heart failure.

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82
Q

How does left heart failure cause a cough?

A

The buildup of fluid in the lungs can lead to a persistent cough, often productive of frothy sputum that may be blood-tinged (hemoptysis).

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83
Q

What type of lung sounds are heard in left heart failure?

A

: Bibasilar crackles (rales) are often heard on auscultation due to fluid accumulation in the lungs.

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84
Q

What cardiac findings are associated with left heart failure?

A

Findings include an S3 heart sound (due to increased filling pressures), and possibly an S4 (due to a stiffened left ventricle).

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85
Q

What is the effect of left heart failure on exercise tolerance?

A

Patients with left heart failure often have reduced exercise tolerance and fatigue due to poor oxygen delivery to tissues.

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86
Q

How can left heart failure affect blood pressure?

A

It may lead to low blood pressure (hypotension) as the heart struggles to pump blood effectively, or high blood pressure (hypertension) in early compensatory stages.

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87
Q

How does left heart failure affect the kidneys?

A

Decreased cardiac output leads to reduced renal perfusion, potentially causing fluid retention and worsening heart failure.

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88
Q

What is cardiogenic shock, and how is it related to left heart failure?

A

Cardiogenic shock occurs when the left ventricle fails to pump enough blood to meet the body’s needs, leading to hypotension, cool extremities, and organ dysfunction.

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89
Q

What is the primary result of right heart failure?

A

Right heart failure leads to systemic venous congestion due to the impaired ability of the right ventricle to pump blood to the lungs.

90
Q

What are the most common symptoms of right heart failure?

A
  • increased JVP
  • apex can displace up towards axilla
  • pleural effusions: R>L
  • ascites, pedal oedema
  • S3 at the lower sternal border- loudest on inspiration
91
Q

ow does right heart failure affect the jugular veins?

A

Elevated jugular venous pressure (JVP) or jugular vein distension (JVD) is a key sign due to venous congestion.

92
Q

How does right heart failure affect the liver?

A

It can cause hepatomegaly (enlarged liver) and sometimes painful liver congestion, which can lead to liver dysfunction (congestive hepatopathy).

93
Q

What gastrointestinal symptoms are associated with right heart failure?

A

Patients may experience nausea, vomiting, and abdominal discomfort due to hepatic congestion and bowel edema.

94
Q

What type of edema is commonly seen in right heart failure?

A

Pitting peripheral edema, which typically begins in the lower extremities and progresses upward.

95
Q

How does right heart failure affect weight?

A

Patients with right heart failure often experience rapid weight gain due to fluid retention.

96
Q

What is the impact of right heart failure on urine output?

A

Nocturia (increased urination at night) is common due to fluid redistribution when lying down.

97
Q

Can right heart failure lead to ascites?

A

Yes, right heart failure can cause ascites, which is fluid accumulation in the peritoneal cavity.

98
Q

What is the relationship between right and left heart failure?

A

Right heart failure is often secondary to left heart failure, as increased pressure in the lungs from left heart failure can strain the right ventricle.

99
Q

Common precipitants of heart failure

A
  1. Anaemia, especially acute blood loss
  2. Infection – esp. pneumonia
  3. Thyrotoxicosis
  4. Pregnancy
  5. Non-adherence: medication or fluid restriction
  6. Beri-Beri (Thiamine deficiency)
  7. Tachycardia-related: AF, atrial flutter
  8. Medications: NSAIDs, corticosteroids -> fluid retention
  9. Myocardial infarction
  10. Natural progression of disease
100
Q

If there is a sudden deterioration in condition, what should you consider:

A
  1. Mitral stenosis
  2. ‘Flash pulmonary oedema’ – HPT crisis, renal artery stenosis
  3. Acute coronary syndrome
  4. Acute pulmonary embolism
    - RV failure
101
Q

What is the third heart sound (S3)?

A

The S3 heart sound is a low-frequency sound heard just after S2 during early diastole. It is caused by rapid filling of the ventricles and can indicate fluid overload or heart failure.

102
Q

In what part of the cardiac cycle does the S3 heart sound occur?

A

The S3 sound occurs in early diastole, during the rapid filling phase of the ventricles, after the mitral and tricuspid valves open.

103
Q

What is the primary cause of the S3 heart sound?

A

S3 is primarily caused by the sudden deceleration of blood flow into a dilated or noncompliant ventricle, often associated with heart failure or volume overload.

104
Q

Why does rapid ventricular filling contribute to the S3 sound?

A

When the ventricles are overloaded with volume or have impaired compliance, rapid filling creates a “sloshing” effect, leading to vibrations that produce the S3 sound.

105
Q

Is the S3 heart sound always pathological?

A

No, S3 can be physiological in young people, athletes, and pregnant women due to increased blood volume. However, in older adults, it is typically a sign of heart failure or dilated cardiomyopathy.

106
Q

How is S3 linked to systolic heart failure?

A

In systolic heart failure, reduced contractility leads to increased ventricular volumes, and rapid early diastolic filling into a dilated ventricle produces the S3 sound.

107
Q

Can S3 be heard in conditions other than heart failure?

A

Yes, S3 can also occur in conditions such as severe mitral regurgitation, dilated cardiomyopathy, and sometimes in left-to-right shunts (e.g., ventricular septal defects).

108
Q

Where is the S3 heart sound best heard?

A

The S3 sound is best heard with the bell of the stethoscope at the apex of the heart (mitral area) in the left lateral decubitus position.

109
Q

Why is S3 associated with volume overload?

A

In volume overload, the increased blood returning to the ventricles during diastole causes excessive stretching of the ventricular walls, which leads to the production of the S3 sound.

110
Q

What does the presence of S3 indicate in the context of heart disease?

A

In adults, the presence of S3 suggests heart failure, particularly with reduced ejection fraction, or severe mitral regurgitation.

111
Q

How does S3 sounds like

A

“Ken- tuc- KY’)

112
Q

What is the fourth heart sound (S4)?

A

The S4 heart sound is a low-frequency sound heard just before S1 during late diastole. It is caused by atrial contraction against a stiff or noncompliant ventricle.

113
Q

In what part of the cardiac cycle does the S4 heart sound occur?

A

The S4 sound occurs in late diastole, just before S1, during atrial contraction when blood is forced into a stiff ventricle.

114
Q

What causes the S4 heart sound?

A

S4 is caused by atrial contraction against a ventricle with reduced compliance or increased stiffness, often due to left ventricular hypertrophy or ischemic heart disease.

115
Q

Why does atrial contraction produce the S4 sound in a stiff ventricle?

A

A stiff or noncompliant ventricle does not expand easily to accommodate the incoming blood during atrial contraction, leading to turbulence and vibrations that create the S4 sound.

116
Q

Is the S4 heart sound pathological?

A

Yes, the presence of S4 is generally considered pathological and is associated with conditions that cause ventricular stiffness, such as hypertension, aortic stenosis, or myocardial ischemia, hypertrophic cardiomyopathy

117
Q

How is S4 linked to diastolic heart failure?

A

S4 is commonly heard in diastolic heart failure (heart failure with preserved ejection fraction) where ventricular compliance is reduced, leading to impaired filling.

118
Q

Can S4 occur in conditions other than diastolic heart failure?

A

Yes, S4 can occur in conditions such as hypertrophic cardiomyopathy, severe aortic stenosis, or after a myocardial infarction where ventricular stiffness is present.

119
Q

Where is the S4 heart sound best heard?

A

The S4 sound is best heard with the bell of the stethoscope at the apex of the heart (mitral area) in the left lateral decubitus position.

120
Q

Can S4 be heard in atrial fibrillation?

A

No, S4 cannot be heard in atrial fibrillation because there is no coordinated atrial contraction to generate the sound.

121
Q

What does the presence of S4 indicate about ventricular compliance?

A

The presence of S4 indicates that the ventricle is stiff and noncompliant, often due to conditions like left ventricular hypertrophy or myocardial fibrosis.

122
Q

Investigation modalities in heart failure

A

Urine dipstix

Blood tests
full blood count: Hb - anaemia, WCC – infection
renal function
Troponin T if suspecting myocardial infarction
+/- TSH, HIV, iron studies (selected population)

Other tests
ECG: IHD, pericardial disease, arrythmias
chest x-ray: heart size, pulmonary oedema, pleural effusion
echocardiogram: LVEF, chamber dimensions, valves
cardiac MRI: expanding role, limited access

123
Q

Why is it recommended to restrict oral fluids to 1000 ml/day in heart failure?

A

Fluid restriction helps prevent fluid overload, which can worsen heart failure symptoms like edema and dyspnea.

124
Q

When is fluid restriction most necessary in heart failure management?

A

Fluid restriction is particularly important in patients with severe heart failure, hyponatremia, or when there is evidence of volume overload.

125
Q

What is the recommended daily salt intake for heart failure patients?

A

Dietary salt should be restricted to less than 2 grams per day to minimize fluid retention and prevent worsening heart failure symptoms.

126
Q

How does salt restriction benefit heart failure patients?

A

Reducing salt intake helps control blood pressure and prevents fluid buildup, which can reduce the strain on the heart.

127
Q

What is the role of diuretics in heart failure treatment?

A

Diuretics provide symptomatic relief by reducing fluid overload, leading to less edema, shortness of breath, and improved exercise tolerance.

128
Q

Do diuretics improve mortality in heart failure patients?

A

No, diuretics are mainly for symptomatic relief and do not have a proven mortality benefit.

129
Q

What is the role of ACE inhibitors like Enalapril in heart failure with left ventricular dysfunction?

A

ACE inhibitors (e.g., Enalapril) reduce afterload and preload, improve cardiac output, slow disease progression, and reduce mortality in heart failure.

130
Q

What is the recommended dose of Enalapril for heart failure patients?

A

The usual dose is 5-10 mg twice daily.

131
Q

Why might ARBs be used instead of ACE inhibitors in some heart failure patients?

A

ARBs are used in patients intolerant to ACE inhibitors due to side effects like cough or angioedema, as they have similar benefits in reducing mortality and heart failure symptoms.

132
Q

What is the role of β-blockers like Atenolol and Carvedilol in heart failure?

A

β-blockers reduce heart rate, improve left ventricular function, reduce hospitalizations, and provide a mortality benefit in heart failure patients.

133
Q

What is the initial dose and titration schedule for Carvedilol in heart failure?

A

Start at 3.125 mg twice daily, doubling the dose every 2 weeks until reaching a maximum of 25 mg twice daily, if tolerated.

134
Q

Do β-blockers have immediate symptomatic benefits?

A

No, β-blockers may initially worsen symptoms, but they provide long-term mortality benefits and improve heart function over time.

135
Q

What is the benefit of using Spironolactone in heart failure?

A

Spironolactone reduces mortality and hospitalization rates by inhibiting the effects of aldosterone, which contributes to fluid retention and myocardial remodeling.

136
Q

What is the recommended dose of Spironolactone in heart failure?

A

Spironolactone is typically used at doses of 12.5 mg to 25 mg daily, depending on the patient’s renal function and potassium levels.

137
Q

When is Digoxin indicated in heart failure?

A

Digoxin is particularly useful in heart failure patients with atrial fibrillation to control heart rate and improve symptoms, although it does not reduce mortality.

138
Q

What is the usual dose of Digoxin in heart failure management?

A

The typical dose is 0.125 mg to 0.25 mg daily.

139
Q

Why is thiamine supplementation sometimes recommended in heart failure patients?

A

Thiamine deficiency can occur in heart failure patients, particularly in those with malnutrition or alcohol abuse, and can worsen heart function.

140
Q

How does thiamine deficiency affect heart failure?

A

Thiamine deficiency can impair myocardial energy metabolism, leading to heart failure exacerbation.

141
Q

How to differentiate between a Jugular Venous Pulse and a carotid pulse
POLICE

A

P: palpation
- non palpable

O: Occlusion
-readily occludable

L: location
- between heads of SCM, lateral to carotid

I: Inspiration
- drops with inspiration

C: Contour
- biphasic waveform

E: Erection/ Position
- drops when sitting erect

142
Q

What is the Jugular Venous Pressure (JVP)?

A

JVP is the indirectly measured pressure in the right atrium, reflected by the height of the venous column in the internal or external jugular vein.

143
Q

Why is JVP clinically important?

A

JVP provides valuable information about the right heart’s hemodynamics, particularly in conditions like heart failure, pericardial disease, and volume overload.

144
Q

How is JVP measured clinically?

A

JVP is measured with the patient reclined at a 45-degree angle. The height of the pulsation in the internal jugular vein is measured in centimeters above the sternal angle, with more than 3 cm considered elevated.

145
Q

What vein is typically used to assess JVP?

A

The internal jugular vein is typically used because its pressure is directly transmitted from the right atrium.

146
Q

What are common causes of elevated JVP?

A

Elevated JVP is most commonly caused by heart failure, particularly right heart failure. It can also be due to conditions like constrictive pericarditis, tricuspid regurgitation, and fluid overload.

147
Q

What does a prominent JVP indicate?

A

A prominent JVP suggests increased right atrial pressure, which may indicate right heart dysfunction, pulmonary hypertension, or volume overload.

148
Q

What is considered a normal JVP?

A

A normal JVP is 6-8 cm H2O when adding the height of the venous column above the sternal angle (usually measured as 3 cm + 5 cm from the right atrium to the sternal angle).

149
Q

What does a JVP higher than 8 cm above the right atrium suggest?

A

A JVP higher than 8 cm suggests elevated central venous pressure and can be a sign of conditions like heart failure, fluid overload, or pulmonary hypertension.

150
Q

What are the components of the normal JVP waveform?

A

he normal JVP waveform consists of the a wave, c wave, x descent, v wave, and y descent.

151
Q

What does the “a wave” in the JVP represent?

A

The “a wave” represents atrial contraction. It occurs just before the first heart sound (S1), and its absence may indicate atrial fibrillation or atrial flutter.

152
Q

What does the “c wave” in the JVP represent?

A

The “c wave” represents the bulging of the tricuspid valve into the right atrium during early ventricular contraction (isovolumetric contraction).

153
Q

What does the “x descent” in the JVP represent?

A

The “x descent” represents atrial relaxation and the downward pull of the atrioventricular (AV) septum during ventricular systole.

154
Q

What does the “v wave” in the JVP represent?

A

The “v wave” represents passive filling of the right atrium when the tricuspid valve is closed during ventricular systole.

155
Q

What does the “y descent” in the JVP represent?

A

The “y descent” represents the opening of the tricuspid valve and the rapid emptying of blood from the right atrium into the right ventricle.

156
Q

What does a large “a wave” in the JVP indicate?

A

A large “a wave” indicates increased resistance to right atrial contraction, such as in tricuspid stenosis or pulmonary hypertension.

157
Q

What does a “cannon a wave” in the JVP indicate?

A

A “cannon a wave” occurs when the atrium contracts against a closed tricuspid valve, often seen in complete heart block or atrioventricular dissociation, PVCs.

158
Q

What does an absent “a wave” in the JVP indicate?

A

An absent “a wave” is seen in atrial fibrillation, atrial fluuter as the atria do not contract effectively.

159
Q

What does a prominent “v wave” in the JVP indicate?

A

A prominent “v wave” can indicate tricuspid regurgitation, where blood flows back into the right atrium during ventricular systole.

160
Q

What is Kussmaul’s sign, and what does it indicate?

A

Kussmaul’s sign is the paradoxical rise in JVP during inspiration, which is abnormal and suggests impaired right ventricular filling, commonly seen in constrictive pericarditis or right heart failure.

161
Q

Causes of heart failure in HIV

A

pericardial disease
valvular heart disease
HIV cardiomyopathy
pulmonary hypertension

162
Q

What is the role of the RAAS in heart failure?

A

It helps regulate blood pressure and fluid balance but is overactivated in heart failure, worsening the condition.

163
Q

What triggers the activation of the RAAS in heart failure?

A

Reduced renal perfusion due to decreased cardiac output.

164
Q

What is the function of renin in the RAAS?

A

Renin converts angiotensinogen to angiotensin I.

165
Q

How is angiotensin II formed?

A

Angiotensin I is converted to angiotensin II by the enzyme angiotensin-converting enzyme (ACE).

166
Q

What are the effects of angiotensin II in heart failure?

A

It causes vasoconstriction, sodium and water retention, and stimulates aldosterone release.

167
Q

How does aldosterone contribute to heart failure progression?

A

Aldosterone promotes sodium and water retention, leading to increased blood volume and worsened congestion.

168
Q

What are the long-term effects of RAAS activation in heart failure?

A

It leads to cardiac remodeling, fibrosis, and worsening of heart function.

169
Q

What medications target the RAAS in heart failure?

A

ACE inhibitors, ARBs (angiotensin receptor blockers), and aldosterone antagonists.

170
Q

What is the role of the sympathetic nervous system in heart failure?

A

It increases heart rate and contractility to compensate for reduced cardiac output.

171
Q

What triggers the activation of the SNS in heart failure?

A

Reduced cardiac output and low blood pressure stimulate the baroreceptors to activate the SNS.

172
Q

What neurotransmitters are involved in SNS activation?

A

Norepinephrine and epinephrine.

173
Q

How does chronic SNS activation affect the heart in heart failure?

A

It leads to tachycardia, increased myocardial oxygen demand, and eventually worsens heart function.

174
Q

What effect does the SNS have on blood vessels in heart failure?

A

It causes vasoconstriction, which increases afterload and worsens heart failure.

175
Q

What are the consequences of excessive norepinephrine release in heart failure?

A

It can lead to arrhythmias, further cardiac dysfunction, and increased mortality.

176
Q

How do beta-blockers work in heart failure?

A

They inhibit the effects of the SNS, reducing heart rate, myocardial oxygen demand, and improving survival.

177
Q

What are examples of beta-blockers used in heart failure?

A

Carvedilol, metoprolol succinate, and bisoprolol.

178
Q

What are natriuretic peptides, and how are they involved in heart failure?

A

They are hormones (e.g., BNP and ANP) released in response to increased heart wall stretch, promoting diuresis and vasodilation.

179
Q

What is the role of B-type natriuretic peptide (BNP) in heart failure?

A

BNP counteracts the effects of the RAAS and SNS by promoting sodium excretion and vasodilation.

180
Q

How does the body respond to increased BNP levels in heart failure?

A

BNP acts to reduce fluid overload, decrease blood pressure, and alleviate heart failure symptoms.

181
Q

Why is BNP often measured in patients with suspected heart failure?

A

Elevated BNP levels are a marker of heart failure and indicate increased cardiac stress.

182
Q

What are the effects of natriuretic peptides on the kidneys?

A

They promote sodium and water excretion, reducing blood volume and relieving symptoms of heart failure.

183
Q

How does neprilysin affect natriuretic peptides?

A

Neprilysin degrades natriuretic peptides, reducing their beneficial effects in heart failure.

184
Q

What medication inhibits neprilysin to enhance the effects of natriuretic peptides?

A

Sacubitril (found in the combination drug sacubitril/valsartan).

185
Q

What is endothelin, and how is it involved in heart failure?

A

Endothelin is a potent vasoconstrictor that is overproduced in heart failure, leading to increased vascular resistance.

186
Q

How does endothelin affect the heart and vasculature in heart failure?

A

It increases afterload, promotes cardiac hypertrophy, and contributes to worsening heart failure.

187
Q

What triggers the release of endothelin in heart failure?

A

Stress on the heart, inflammation, and activation of the RAAS and SNS stimulate endothelin production.

188
Q

What is the role of vasopressin in heart failure?

A

Vasopressin, also known as antidiuretic hormone (ADH), promotes water retention and vasoconstriction.

189
Q

How does vasopressin worsen heart failure?

A

By increasing blood volume and vasoconstriction, it contributes to fluid overload and increases the heart’s workload.

190
Q

What stimulates the release of vasopressin in heart failure?

A

Low cardiac output and reduced arterial pressure.

191
Q

How can vasopressin antagonists be used in heart failure?

A

They block the effects of vasopressin, reducing fluid overload and relieving symptoms.

192
Q

What role does inflammation play in heart failure?

A

Chronic inflammation contributes to cardiac remodeling, fibrosis, and progression of heart failure.

193
Q

What are pro-inflammatory cytokines, and how do they contribute to heart failure?

A

Cytokines like TNF-α and IL-6 are elevated in heart failure and promote tissue damage and fibrosis.

194
Q

How does oxidative stress influence heart failure progression?

A

Oxidative stress leads to damage of cardiac cells, promoting apoptosis and worsening heart function.

195
Q

Why is neurohormonal activation initially beneficial in heart failure?

A

It compensates for reduced cardiac output by increasing heart rate, blood pressure, and fluid retention.

196
Q

What is the long-term impact of neurohormonal activation in heart failure?

A

Chronic activation leads to worsening heart function, cardiac remodeling, and progression of the disease.

197
Q

Why is it important to inhibit neurohormonal activation in heart failure?

A

To prevent further damage to the heart, improve symptoms, and reduce mortality.

198
Q

What are the key neurohormonal systems targeted by heart failure treatments?

A

RAAS, SNS, and the natriuretic peptide system.

199
Q

How do ACE inhibitors improve outcomes in heart failure?

A

By blocking the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and fluid retention.

200
Q

What role do aldosterone antagonists play in heart failure treatment?

A

They block the effects of aldosterone, reducing sodium retention and cardiac fibrosis.

201
Q

What is the benefit of using beta-blockers in heart failure?

A

They reduce the harmful effects of chronic SNS activation, improving heart function and survival.

202
Q

How do sacubitril/valsartan improve outcomes in heart failure?

A

By inhibiting neprilysin and blocking angiotensin receptors, they enhance natriuretic peptide effects and reduce RAAS activation.

203
Q

How does the inhibition of vasopressin help in heart failure?

A

It reduces water retention and vasoconstriction, relieving symptoms of congestion.

204
Q

What is the importance of diuretics in heart failure treatment?

A

They reduce fluid overload, improving symptoms like edema and shortness of breath.

205
Q

What is cardiac remodeling, and how is it related to neurohormonal activation?

A

Cardiac remodeling is the structural changes in the heart due to chronic stress from neurohormonal activation.

206
Q

How can cardiac remodeling be prevented or reversed in heart failure?

A

Through the use of RAAS inhibitors, beta-blockers, and controlling other contributing factors.

207
Q

A 40-year-old woman with recently diagnosed human immunodeficiency virus . presents with grade four dyspnoea for the last month. She has pedal oedema, with a raised jugular venous pressure, ascites and a diffuse, hypodynamic apical impulse.

What is the most likely cause of her presentation?

A. Restrictive cardiomyopathy
B. Pericardial effusion
C. Viral myocarditis
D. Dilated cardiomyopathy

A

D. Dilated cardiomyopathy

208
Q

A 54-year-old man known with an ischaemic cardiomyopathy presents in decompensated cardiac failure.

Which one of the following clinical signs may be found on examination?

A. Soft aortic component of the second heart sound
B. Loud first heart sound
C. Mid-diastolic murmur at the apex
D. S3 gallop

A

D. S3 gallop

209
Q

Which of the following is NOT a risk factor for heart failure with preserved systolic heart failure (HFpEF)?

A. Diabetes
B. Obesity
C. Hypertension
D. Peripheral vascular disease

A

D. Peripheral vascular disease

210
Q

A 58-year-old man presents with a month history of progressive dyspnoea and pedal oedema. He has a heart rate of 118 beats per minute with a blood pressure of 126/84mmHg, a raised jugular venous pressure, bilateral coarse crackles and ascites.

What is the most appropriate initial drug to start?

A. Furosemide
B. Spironolactone
C. Carvedilol
D. Enalapril

A

A. Furosemide

211
Q

A 32-year-old man presents complaining of a three week history of fever and bilateral leg swelling. On examination he is found to have pallor and pyrexia. In addition he has a raised jugular venous pressure with a pansystolic murmur at the apex radiating to the axilla and bi-basal crackles. He has an absent right foot pulse. Urine dipstick shows 1 + blood.

What is the most likely aetiology of congestive cardiac failure?

A. Infective endocarditis
B. Sepsis
C. Hypertrophic obstructive cardiomyopathy
D. Rheumatic heart disease

A

A. Infective endocarditis

212
Q

Which of the following is an appropriate therapy for your patient with heart failure?

A. Salt and water restriction in your patient with dilated cardiomyopathy
B. Amlodipine in a patient with HFpEF (heart failure with preserved ejection fraction)
C. ACE-Inhibitor in a patient with calcific constrictive pericarditis
D. Beta blocker therapy in a patient with Aortic Regurgitation

A

A. Salt and water restriction in your patient with dilated cardiomyopathy

213
Q

Which of the following hormones causes vasodilation, diuresis and inhibits cardiac fibrosis in patients with heart failure?

A. Aldosterone
B. Norepinephrine (noradrenaline)
C. Brain natriuretic peptide
D. Angiotensin II

A

C. Brain natriuretic peptide

214
Q

A 35-year-old man with prior history of heavy alcohol consumption presents with congestive cardiac failure.

Which of the following pathophysiological changes is occurring?

A. Increased secretion of atrial natriuretic peptide
B. Activation of the parasympathetic nervous system
C. Decreased secretion of atrial natriuretic peptide
D. Decreased collagen synthesis

A

A. Increased secretion of atrial natriuretic peptide

215
Q

A 79-year-old man presents with acute onset of grade 4 dyspnoea and palpitations. His pulse rate is 195 beats per minute and irregular with a blood pressure of 64/46 mmHg. He has bilateral pedal oedema, a raised jugular venous pressure with bilateral crackles audible on auscultation.

What is the most like aetiology of the congestive cardiac failure?

A. First degree heart block
B. Myocardial infarction
C. Atrial Fibrillation
D. Cor pulmonale

A

C. Atrial Fibrillation

216
Q

Which of the following findings on the ECG does NOT suggest chronic underlying structural heart disease?

A. Left atrial hypertrophy
B. Left ventricular hypertrophy
C. Left bundle branch block
D. Right bundle branch block

A

D. Right bundle branch block

217
Q

Which of the following is NOT a common cause of heart failure in South Africa?

A. Rheumatic Heart Disease
B. Atrial Septal Defect
C. Dilated Cardiomyopathy
D. Hypertensive heart disease

A

B. Atrial Septal Defect

218
Q

Which of the following is NOT a common precipitant of heart failure in the appropriate context?

A. Poor glucose control
B. Urinary tract infection
C. Infective endocarditis
D. New onset atrial fibrillation

A

A. Poor glucose control

219
Q

A 45-year-old man known with an HIV induced cardiomyopathy presents with congestive cardiac failure.

Which of the following pathophysiological changes is occurring?

A. Decreased secretion of atrial natriuretic peptide
B. Activation of the sympathetic nervous system
C. Activation of the parasympathetic nervous system
D. Decreased collagen synthesis

A

B. Activation of the sympathetic nervous system

220
Q

In patients with heart failure, which of the following statements is TRUE?

A. Right ventricular function is always abnormal
B. The effective stroke volume is inadequate to meet the body’s physiologic needs
C. Patients cannot sleep using fewer that 2 pillows
D. Left ventricular systolic function is always reduced

A

B. The effective stroke volume is inadequate to meet the body’s physiologic needs

221
Q

Which of the following is NOT a typical symptom of heart failure?

A. Bilateral swelling of the legs
B. Exertional fatigue
C. Orthopnea
D. Haemoptysis

A

D. Haemoptysis

Cardiology (4 decks)

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