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Cardio All My Notes > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Question: What is heart failure?

A

Answer: Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation.

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2
Q

Question: What are the two main causes of chronic heart failure?

A

Answer: Chronic heart failure can be caused by either impaired left ventricular contraction (systolic heart failure) or left ventricular relaxation (diastolic heart failure).

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3
Q

Question: What are the main causes of heart failure?

A

Answer: The main causes of heart failure include ischaemic heart disease, dilated cardiomyopathy, and hypertension. Other causes include other forms of cardiomyopathy, valvular disease, arrhythmias, pericardial disease, infections, alcohol, diabetes, and congenital heart disease.

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4
Q

Question: What is ejection fraction?

A

Answer: Ejection fraction refers to the percentage of blood that is pumped out of the heart during each beat.

  • It is calculated as stroke volume divided by end-diastolic volume, multiplied by 100.
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5
Q

Question: What is heart failure with reduced ejection fraction?

A

Answer: Heart failure with reduced ejection fraction is characterized by an ejection fraction less than 40%. It is caused by reduced contractility, commonly due to ischaemic heart disease, but can also occur with valvular heart disease and hypertension.

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6
Q

Question: What happens to contractility and preload in heart failure with low stroke volume or low ejection fraction?

A

Answer:

  • contractility is reduced, and preload is increased due to conditions such as
  • anterior or lateral myocardial infarction,
  • dilated cardiomyopathy,
  • mitral regurgitation, and
  • aortic regurgitation.
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7
Q

Question: What is heart failure with preserved left ventricular ejection fraction?

A

Answer: Heart failure with preserved left ventricular ejection fraction is characterized by symptoms and signs of heart failure with an ejection fraction greater than 50%. It is caused by decreased ventricular compliance, leading to diastolic ventricular dysfunction, reduced ventricular filling, increased diastolic pressure, and decreased cardiac output.

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8
Q

Question: What happens to contractility and preload in diastolic heart failure or heart failure with preserved ejection fraction?

A

Answer:

  • contractility may be normal, but preload is decreased due to conditions such as myocardial infarction, restrictive cardiomyopathy, and constrictive pericarditis.
  • Afterload may also increase due to hypertension, aortic stenosis, coarctation of the aorta, or hypertrophic obstructive cardiomyopathy.
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9
Q

Question: What are the symptoms of left-sided heart failure?

A

Answer:

  • dyspnoea (shortness of breath), dry cough,
  • orthopnoea (needing to prop up with pillows while lying down),
  • paroxysmal nocturnal dyspnoea (PND) sudden awakening from sleep with difficulty breathing, fatigue, and
  • inspiratory rales or crackles (abnormal lung sounds).
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10
Q

Question: What are the symptoms of right-sided heart failure?

A

Answer:

  • raised jugular venous distention,
  • hepatomegaly,
  • ascites,
  • splenomegaly,
  • abdominal pain,
  • peripheral oedema (swelling in the lower extremities), and
  • cool, pale, sweaty, and clammy extremities.
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11
Q

Question: What is high-output cardiac heart failure?

A

Answer:
usually occurs due to an increased demand for cardiac output, such as in
* severe anaemia,

  • thyrotoxicosis,
  • arteriovenous fistula,
  • beriberi,
  • severe systemic arteriovenous shunting.
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12
Q

Question: What are the compensation mechanisms in heart failure?

A

Answer:
* sympathetic nervous system activation,

  • renin-angiotensin-aldosterone system activation,
  • increased heart rate,
  • myocardial hypertrophy, and
  • ventricular dilation.
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13
Q

Question: What is the New York Heart Association (NYHA) functional classification for heart failure?

A

Answer:
The New York Heart Association (NYHA) functional classification is a system used to categorize heart failure based on the severity of symptoms.

It has four classes:
Class I (no limitation of physical activity),
Class II (slight limitation of physical activity),
Class III (marked limitation of physical activity), and
Class IV (severe limitation of physical activity).

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14
Q

Question: What are some diagnostic tests used for heart failure?

A

Answer:

  • echocardiography,
  • electrocardiogram (ECG),
  • chest X-ray,
  • cardiac biomarkers (e.g., B-type natriuretic peptide),
  • stress tests,
  • cardiac catheterization, and
  • coronary angiography.
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15
Q

Question: What is the treatment approach for heart failure?

A

Answer:
involves a combination of

  • lifestyle modifications (such as sodium restriction, weight management, and regular exercise),
  • medications (such as diuretics, ACE inhibitors, beta-blockers, and aldosterone antagonists), and,
  • in some cases, interventions like cardiac resynchronization therapy or implantable cardioverter-defibrillators.
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16
Q

Question: What is the goal of pharmacological treatment in heart failure?

A

Answer:

  • to improve symptoms,
  • slow disease progression,
  • reduce hospitalizations, and
  • prolong survival.
  • It involves optimizing medication regimens based on the type and stage of heart failure.
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17
Q

Question: What is cardiac resynchronization therapy (CRT)?

A

Answer:

  • treatment option for selected heart failure patients with impaired ventricular function and electrical dyssynchrony.
  • It involves the placement of a specialized pacemaker that coordinates the contraction of the heart’s chambers to improve overall cardiac function.
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18
Q

Question: What are the complications of heart failure?

A

Answer:

  • arrhythmias,
  • pulmonary edema,
  • cardiogenic shock,
  • kidney dysfunction,
  • liver dysfunction, and
  • increased risk of thromboembolic events such as stroke or deep vein thrombosis.
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19
Q

Question: Can heart failure be prevented?

A

Answer:

  • adopting a healthy lifestyle, managing risk factors (e.g., controlling hypertension, quitting smoking), and
  • early management of underlying cardiac conditions can significantly reduce the risk of developing heart failure.
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20
Q

Question: What is the prognosis for heart failure?

A

Answer:
varies depending on the underlying cause, severity of symptoms, and response to treatment.

With appropriate management, including lifestyle modifications and medication, many individuals with heart failure can lead fulfilling lives and experience improved outcomes

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21
Q

What is the difference between systolic and diastolic heart failure?

A
  • Systolic heart failure is caused by impaired left ventricular contraction, ( siff, fibrotic and non complinace)
  • while diastolic heart failure is caused by impaired left ventricular relaxation. (Flappy, DIlated and high compliancey)
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22
Q

What is the precentage of heart failure with reduced ejection fraction?

A

The ejection fraction in heart failure with reduced ejection fraction is less than 40%.

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23
Q

What causes heart failure with reduced ejection fraction?

A

commonly caused by ischaemic heart disease,

  • but it can also occur with valvular heart disease and hypertension.
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24
Q

What are the causes of heart failure with preserved left ventricular ejection fraction? 2

A

include

  • increased stiffness of the ventricle (e.g. in long-standing hypertension with ventricular wall hypertrophy) and
  • impaired relaxation of the ventricle (e.g. constrictive pericarditis).
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25
Q

What happens to contractility and preload in heart failure with low stroke volume or low ejection fraction?

A

contractility is reduced, and preload is increased.

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26
Q

What are the causes of right-sided heart failure?

A
  • increased right ventricular afterload (e.g. pulmonary hypertension) and
  • increased right ventricular preload (e.g. tricuspid valve regurgitation).
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27
Q

What is high-output cardiac heart failure?

A

usually occurs with an underlying cardiovascular disease and is characterized by increased oxygen demand but low oxygen supply to the heart.

  • UNDERLINE DISEASE -> Diabetes, sleep apnea, smoke, hypertension, CAD, etc
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28
Q

How do compensatory mechanisms in heart failure work?

A

Compensatory mechanisms in heart failure include

  • increased SA node stimulation,
  • increased myocardial stimulation,
  • vasoconstriction in the venous and arterial system,
  • activation of the renin-angiotensin-aldosterone system (RAAS),
  • increased adrenergic activity, and
  • secretion of BNP.
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29
Q

How can compensatory mechanisms lead to exacerbation of heart failure?

A

Compensatory mechanisms can lead to exacerbation of heart failure by increasing heart rate and vasoconstriction, which can worsen afterload and preload and further strain the weakened heart.

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30
Q

What type of drugs can help reduce compensation mechanisms in heart failure?

A

Drugs such as beta blockers, ACE inhibitors, diuretics, and vasodilators can help reduce compensation mechanisms in heart failure.

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31
Q

What are the consequences of decompensated heart failure? 2

A

The consequences of decompensated heart failure include

  • forward failure, which can lead to multisystem organ failure, and
  • backward failure, which can cause pulmonary edema and systemic venous congestion.
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32
Q

What is paroxysmal nocturnal dyspnea (PND)?

A

Paroxysmal nocturnal dyspnea is a symptom of heart failure characterized by sudden shortness of breath that wakes the person up from sleep, often accompanied by a feeling of suffocation.

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33
Q

What signs can be observed in heart failure?

A

the new ones include
* Elevated jugular venous pressure (JVP)
* Hepatojugular reflux (an increase in JVP when pressure is applied to the liver)
* Peripheral edema (swelling in the legs, ankles, or feet)
* S3 gallop (an extra heart sound indicative of impaired ventricular filling)
* Pulmonary rales (abnormal lung sounds caused by fluid accumulation)
* Cyanosis (bluish discoloration of the lips or extremities due to poor oxygenation)
* Pleural effusion (fluid accumulation in the pleural cavity)
* Cardiomegaly (enlarged heart) on chest X-ray
* Ascites (fluid accumulation in the abdominal cavity)
* Weight gain due to fluid retention

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34
Q
  • what causes S3
A

caused by dialtoed ventricles stretch during diastole and you hear S3 sound

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35
Q
  • what causes S4
A

thick non compliance ventricles fill to short point where filling Stops producing S4

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36
Q

Q: What is the role of phosphodiesterase (PDE) enzymes ?

A

A: PDE enzymes are responsible for the degradation of cAMP, which leads to a decrease in cardiac contractility.

37
Q

Q: Why are PDE inhibitors not used in clinical practice for heart failure?

A

A: Despite improving haemodynamic parameters, PDE inhibitors are not used in clinical practice because they have the potential to cause arrhythmias THUS increase mortality.

38
Q

what is Pulsus alternans

A

Pulsus alternans (an alternating strong and weak pulse) is associated with severe left heart failure due to it reflects an abnormality in the contraction of the left ventricle.

39
Q

Signs on CXR of HF: mnemonic- DABCE

A
  • Dilated prominent upper lobe vessels
  • Alveolar oedema (bat wing opacities)
  • Kerley B lines
  • Cardiomyopathy
  • Plural Effusion
40
Q

what is the treatment of### Heart failure with preserved ejection fraction EF more or equall to 50%)

A
  • Loop diuretic e.g. furosemide to relieve symptoms of fluid overload
  • Manage cause/precipitating factors
41
Q

treatment of heart failure with reduced ejection fraction< 40%) - ABAL

A
  • ACE inhibitor (e.g.ramipril)
  • β blocker (e.g.bisoprolol)
  • Aldosterone antagonist when symptoms not controlled with A and B (spironolactoneoreplerenone)
  • Loop diuretics improvessymptoms(e.g.furosemide) meaning pain relief
42
Q

Q: What are the radiographic findings associated with pulmonary edema? 3

A

A:

  • Hazy opacities in the perihilar region,
  • Kerley B lines, and
  • bat-wing shadowing (also known as alveolar edema).
43
Q

Q: What is another term used to describe the radiographic appearance of alveolar edema?

A

A: Bat-wing opacities.

44
Q

Q: What is the purpose of the BNP blood test in the context of pulmonary edema?

A

A:

The BNP blood test, specifically measuring N-terminal pro-B-type natriuretic peptide (NT-proBNP), is used as a marker to assess the severity of heart failure.

  • An NT-proBNP level greater than 2000 is indicative of significant cardiac compensation.
45
Q

Q: What is the recommended management when initiating sacubitril/valsartan in a patient?

A

A: Stop ACE inhibitors/ARBs but continue beta-blockers and spironolactone.

46
Q

Q: What is the mechanism of action of ivabradine?

A

A:

  • Ivabradine slows ionic depolarization through the pacemaker cells, resulting in a decreased heart rate.
  • This allows for more filling time during diastole
47
Q

Q: In which group of patients is the combination of hydralazine and nitrates indicated for the treatment of heart failure?

A

A: Hydralazine plus nitrates is recommended for Afro-Caribbean patients with moderate-severe heart failure.

48
Q

Q: Which three medications can potentially cause electrolyte disturbances?

A

A: Diuretics, ACE inhibitors, and aldosterone antagonists can all lead to electrolyte imbalances.

49
Q

Q: When should cardiac resynchronization therapy (CRT) devices be offered to patients?

A

A: Patients with a wide QRS and an ejection fraction of less than 35% should be considered for CRT devices if they are not stabilized with current medications.

50
Q

Q: When is cardiac resynchronization therapy plus defibrillator (CRT-D) indicated?

A

A:

  • patients in sinus rhythm with a prolonged QRS duration (>130 milliseconds).
  • OR patients without pacing capabilities.
51
Q

Q: What is the compensatory mechanism that causes an increase in heart rate in heart failure?

A

A: The increase in heart rate as a compensatory mechanism in heart failure is due to sympathetic nervous system activity.

52
Q

Q: In heart failure with preserved ejection fraction, which derangement is commonly found?

A

A: Myocyte hypertrophy is commonly found in heart failure with preserved ejection fraction.

53
Q

Q: Which symptomatology is correctly paired with its respective type of heart failure?

A

A: Heart failure with reduced ejection fraction is associated with the S3 heart sound.

54
Q

Q: The symptoms of cough, shortness of breath, and positive crackles on both lungs are hemodynamically due to what?

A

A: due to volume overload of the left ventricle.

55
Q

Q: In a patient with pedal edema and ascites, which diagnosis may suggest the presence of signs of volume overload?

A

A: Aortic regurgitation may suggest the presence of signs of volume overload in this patient.

56
Q

Q1: What is the definition of systolic heart failure?

A

A1: characterized by either structural or functional impairment of ventricular filling or ejection of blood.

57
Q

Q2: What are the clinical manifestations of systolic heart failure?

A

A2: include dyspnea, fatigue, and signs of heart failure such as edema and rales.

58
Q

Q3: What is the formula for cardiac output (CO)?

A

A3: Cardiac output (CO) is calculated as heart rate (HR) multiplied by stroke volume (SV): CO = HR x SV.

59
Q

Q4: How does increased blood pressure affect stroke volume (SV)?

A

A4: Increased blood pressure leads to a decreased volume of blood (mL) pushed out, resulting in a decrease in stroke volume (SV).

60
Q

Q5: What factors affect or increase stroke volume (SV)?

A

A5: Factors that affect or increase stroke volume (SV) include

  • preload (increased myocardial stretch),
  • contractility (increased force generated), and
  • afterload (decreased pressure or load the heart pumps against).
61
Q

Q6: What is dilated cardiomyopathy, and what can cause it?

A

A6:
* Dilated cardiomyopathy is a condition characterized by thin and weak ventricles, leading to decreased strength in pumping blood.
* It can be caused by factors such as bacterial and viral infections, idiopathic reasons, autoimmune disorders, infiltrative disorders (cancer, sarcoidosis, hemochromatosis), and alcohol (holiday heart syndrome).

62
Q

Q7: How does decreased contractility affect stroke volume (SV)?

A

A7:
* leads to a decrease in stroke volume (SV) and
* subsequently a decrease in cardiac output (CO) over time.

63
Q

Q8: What happens in mitral regurgitation?

A

A8:
* In mitral regurgitation, the left ventricular contraction pumps blood into the aorta,
* but due to a damaged valve, some blood leaks back into the left atrium (LA), resulting in bidirectional flow.

64
Q

Q1: What is the definition of diastolic heart failure?

A

A1: Diastolic heart failure is characterized by a stiff left ventricle, fibrosis, noncompliance, impaired relaxation, and increased end-diastolic pressure.

65
Q

Q2: What are the clinical manifestations of diastolic heart failure?

A

A2: dyspnea, fatigue, and signs of heart failure such as edema and rales.

66
Q

Q3: What can lead to a decrease in preload in diastolic heart failure?

A

A3:
Conditions such as
* myocardial infarction, restrictive cardiomyopathy (caused by amyloidosis, cancer, hemochromatosis, sarcoidosis),

  • constrictive pericarditis, and
  • cardiac tamponade can lead to a decrease in preload.
67
Q

Q4: What factors can increase afterload in diastolic heart failure? 4

A

A4:

  • Hypertension,
  • aortic stenosis (caused by rheumatic heart disease or bicuspid aortic valve),
  • coarctation of the aorta, and
  • hypertrophic obstructive cardiomyopathy can increase afterload.
68
Q

Q5: How does tachyarrhythmia (increased heart rate) affect diastolic heart failure?

A

A5:
1. leads to an increased heart rate,
2. resulting in a decreased diastolic time period for filling,
3. decreased preload to the ventricles,
4. decreased stroke volume (SV), and
5. decreased cardiac output (CO).

69
Q

Q6: How does bradyarrhythmia (decreased heart rate) affect diastolic heart failure?

A

A6: Bradyarrhythmia
1. leads to a decreased heart rate,
2. resulting in decreased cardiac output (CO) over time,
3. decreased blood pressure, and
4. decreased perfusion to tissues,
5. eventually leading to congestive heart failure.

70
Q

Q7: What is the impact of hypertrophy in chronic hypertension?

A

A7: In chronic hypertension, the myocardium
1. initially adapts by increasing in size (hypertrophy) to handle increased blood pressure and workload. ,
2. However, over time, the myocardium becomes weak and flabby,
3. leading to diastolic heart failure and potentially progressing to systolic heart failure.

71
Q

Q8: How does aortic regurgitation affect the heart?

A

A8: In aortic regurgitation,
during left ventricular contraction,
blood leaks back into the left ventricle (LV) due to a damaged valve,
leading to bidirectional flow. thus pulmonarry edema.

72
Q

Q1: What is the relationship between right-sided heart failure and left-sided heart failure?

A

A1:

  • Right-sided heart failure is more commonly caused by left-sided heart failure.
  • The increased backflow of blood into the pulmonary circulation in left-sided heart failure leads to pulmonary hypertension
  • , which can eventually result in right-sided heart failure.
73
Q

Q2: What are some diseases that can lead to an increase in afterload in right-sided heart failure?

A

A2:
1. Pulmonary hypertension (caused by conditions such as idiopathic pulmonary hypertension, pulmonary embolism, underlying lung disease), pulmonic stenosis (caused by rheumatic heart disease), and
2. cor pulmonale (caused by conditions such as COPD, severe bronchiectasis, chronic bronchitis, emphysema)

  • can all increase afterload in right-sided heart failure.
74
Q

Q3: How does pulmonary regurgitation and tricuspid regurgitation affect the right ventricle?

A

A3:
* In pulmonary regurgitation, during right ventricular contraction, blood flows back into the right ventricle, leading to increased right ventricular expansion.
* In tricuspid regurgitation, blood backflows into the right atrium during right ventricular contraction, causing increased right ventricular expansion.

75
Q

Q4: What can cause a decrease in contractility in right-sided heart failure?

A

A4:
1. Inferior myocardial infarction,

  1. infiltrative diseases,
  2. autoimmune diseases, and
  3. myocarditis
  • can all contribute to a decrease in contractility in right-sided heart failure.
76
Q

Q5: What are some causes of high-output cardiac heart failure?

A

A5:

  • High-output cardiac heart failure typically occurs in the presence of underlying cardiovascular diseases such as
    1. diabetes,
    2. sleep apnea,
    3. s moking,
    4. hypertension, and
    5. coronary artery disease (CAD).
77
Q

Q6: How does very severe anemia contribute to high-output cardiac heart failure?

A

A6: Very severe anemia leads to
1. increased hypoxia, which triggers compensatory mechanisms to increase cardiac output.
2. The body tries to compensate for the decreased oxygen supply by increasing heart rate and pumping harder.

78
Q

Q7: What is the impact of thiamine deficiency (Wet Beri Beri) in chronic alcoholics on the heart?

A

A7:
1. It lead to altered mental status, ataxia (loss of balance), and ophthalmoplegia.
2. Without adequate thiamine, the synthesis of pyruvate dehydrogenase (PDH) is impaired,
3. resulting in lactic acid buildup, vasodilation, and increased heart workload due to AV shunting No arterioles to regulate the blood pressure stright to vinus

79
Q

Q8: What is the effect of thyrotoxicosis (elevated thyroid levels) on the heart?

A

A8:
1. Thyrotoxicosis increases the metabolic rate, oxygen usage, and demand.
2. This causes the heart to pump harder and increases oxygenation for processes such as caloric breakdown, muscle contraction, and heat generation.

80
Q

Q1: What are the compensatory mechanisms within the sympathetic nervous system in left-sided heart failure?

A

A1:
Within the sympathetic nervous system, the compensatory mechanisms include
1. increased stimulation of the SA node (increased heart rate)
2. , myocardial stimulation (increased contractility),
3. vasoconstriction in the venous and arterial systems (increased total peripheral resistance), and
4. activation of the renin-angiotensin-aldosterone system (RAAS) to increase fluid retention and blood volume.

81
Q

Q2: How does increased stimulation of the SA node compensate for decreased cardiac output in left-sided heart failure?

A

A2:
1. Increased stimulation of the SA node leads to an increased heart rate (HR),
2. which helps to compensate for the decreased cardiac output by increasing the number of times the heart contracts per minute,
3. thereby increasing the overall cardiac output.

82
Q

Q3: What is the role of vasoconstriction in the arterial and venous systems in left-sided heart failure?

A

A3:
1. Vasoconstriction in the arterial system increases total peripheral resistance (TPR) and blood pressure (BP), helping to maintain adequate perfusion to the tissues.
2. Vasoconstriction in the venous system increases venous return (VR) and preload, leading to an increased stroke volume (SV) and cardiac output.

83
Q

Q4: How does the renin-angiotensin-aldosterone system (RAAS) compensate for decreased cardiac output in left-sided heart failure?

A

A4:
1. The activation of the RAAS in left-sided heart failure leads to the secretion of renin, which converts angiotensinogen into angiotensin I.
2. Angiotensin I is then converted to angiotensin II, which has several effects including
3. vasoconstriction, increased release of antidiuretic hormone (ADH), and
4. increased aldosterone secretion.
5. These actions result in increased blood volume, venous return, preload, and stroke volume.

84
Q

Q5: What are some drugs used to manage left-sided heart failure?

A

A5:
Beta blockers,
ACE inhibitors, diuretics (for fluid and volume overload), and
vasodilators (arteriodilators and venodilators) are commonly used to manage left-sided heart failure.

85
Q

Q1: What are the symptoms and physical examination findings of left-sided heart failure?

A

A1:
Symptoms of left-sided heart failure include
1. dyspnea (shortness of breath),
2. dry cough,
3. orthopnea (difficulty breathing when lying flat),
4. paroxysmal nocturnal dyspnea (awakening from sleep with shortness of breath), and
5. inspiratory rales or crackles on lung auscultation.
Physical examination findings may include
1. thickened respiratory membrane,
2. pulmonary edema, and
3. signs of pulmonary hypertension.

86
Q

Q2: What are the symptoms and physical examination findings of right-sided heart failure?

A

A2:
Symptoms of right-sided heart failure include
1. jugular venous distention (JVD), hepatomegaly (enlarged liver),
2. ascites (fluid accumulation in the abdomen),
3. splenomegaly (enlarged spleen),

  1. abdominal distention,
  2. edema in the lower extremities (bilateral pitting edema), and
  3. cool, pale, sweaty, and clammy extremities.
  4. Physical examination findings may also include a **positive hepatojugular reflux test **and a positive fluid wave test.
87
Q

Q3: How do the symptoms and physical examination findings differ between left-sided and right-sided heart failure?

A

A3:
primarily involve the respiratory system, such as dyspnea, cough, and pulmonary congestion.
Physical examination findings are related to pulmonary edema and impaired gas exchange.

In right-sided heart failure, symptoms and findings are primarily related to venous congestion and fluid accumulation in various systems, including JVD, hepatomegaly, ascites, splenomegaly, abdominal distention, and peripheral edema.

88
Q

Q4: What are the symptoms and physical examination findings specific to systolic heart failure?

A

A4:
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and the presence of an** S3 heart sound**.
Physical examination findings may include a displaced point of maximal impulse (PMI) and the presence of an S3 heart sound heard with the bell of the stethoscope in the left lateral decubitus position.

89
Q

Q5: What are the symptoms and physical examination findings specific to diastolic heart failure?

A

A5:
dyspnea and the presence of an S4 heart sound.

  • Physical examination findings may include a thickened, fibrotic, and noncompliant heart leading to the cessation of filling and the presence of an S4 heart sound.

Cardio All My Notes (13 decks)

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