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Abbie's Final Year Flashcards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is chronic heart failure?

A

A clinical syndrome involving reduced cardiac output because of impaired cardiac contraction

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2
Q

What are typical clinical symptoms of CHF?

A

Shortness of breath, fatigue and ankle swelling.

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3
Q

What is the prevalence of CHF?

A

1-2%, rising to 10% in over 70 year olds

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4
Q

What are three factors stroke volume requires?

A
  1. adequate preload
  2. optimal myocardial contractility (Frank-Starling mechanism)
  3. decreased afterload
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5
Q

Cardiac output =

A

stroke volume x heart rate

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6
Q

Which factors reduce cardiac output, potentially causing CHF?

A
  1. Decreased heart rate
  2. Decreased preload
  3. Decreased contractility
  4. Increased afterload
    (cardiac output = heart rate [1] x stroke volume [2,3,4])
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7
Q

How is CCF diagnosed using the Framingham criteria?

A

2 major criteria or 1 major + 1 minor

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8
Q

What is the major criteria for the Framingham criteria for CCF?

A
  1. PND
  2. +ve abdominojugular reflux
  3. Neck vein distension
  4. S3
  5. Basal creps
  6. Cardiomegaly
  7. Acute pulmonary oedema
  8. ↑ CVP (>16cmH2O)
  9. Wt. loss >4.5kg in 5d 2O to Rx
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9
Q

What is the minor criteria for the Framingham criteria for CCF?

A
  1. Bilat ankle oedema
  2. SOBOE
  3. ↑HR >120
  4. Nocturnal cough
  5. Hepatomegaly
  6. Pleural effusion
  7. 30% ↓ vital capacity
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10
Q

Most common causes of HF in the UK?

A

Coronary heart disease (MI), atrial fibrillation, valvular heart disease and hypertension

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11
Q

Other causes of HF?

A

Endocrine or medications

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12
Q

What are endocrine causes of HF?

A

Hypothyroidism, hyperthyroidism, diabetes, adrenal insufficiency, Cushing’s syndrome

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13
Q

What medications can cause HF?

A

Calcium antagonists, anti-arrhythmics, cytotoxic medication, beta-blockers

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14
Q

When does high-output cardiac failure occur?

A

In states where demand exceeds normal cardiac output such as pregnancy, anaemia and sepsis.

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15
Q

A useful acronym to remember some of the causes of CHF:

A

HIGH-VIS: hypertension, infection/immune, genetic, heart attack, volume overload, infiltration, structural

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16
Q

What are some infective/immune causes of CHF?

A

Viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis)

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17
Q

What are genetic causes of CHF?

A

Hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM)

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18
Q

What are causes of volume overload that lead to CHF?

A

Renal failure, nephrotic syndrome, hepatic failure

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19
Q

What are causes of infiltration that lead to CHF?

A

Sarcoidosis, amyloidosis, haemochromatosis

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20
Q

What are structural causes of CHF?

A

Valvular heart disease, septal defects

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21
Q

Typical symptoms of CHF?

A
  1. Dyspnoea on exertion
  2. Fatigue limiting exercise tolerance
  3. Orthopnoea: the patient may be using several pillows to reduce this symptom.
  4. Paroxysmal nocturnal dyspnoea (PND): attacks of severe shortness of breath in the night that are relieved by sitting up (pathognomonic for CHF).
  5. Nocturnal cough with or without the characteristic ‘pink frothy sputum’.
  6. Pre-syncope/syncope
  7. Reduced appetite
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22
Q

Relevant past medical history for CHF?

A

Hypertension, coronary artery disease and valvular heart disease (common causes of CHF)

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23
Q

Relevant medication history for CHF?

A

Calcium antagonists, antiarrhythmics, cytotoxic medication and beta-blockers (in the acute phase, but long term provide prognostic benefit).

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24
Q

Relevant family history for CHF?

A

Cardiomyopathy (e.g. HOCM) or coronary artery disease

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25
Q

Relevant social history for CHF?

A

Smoking, excess alcohol intake and recreational drug use

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26
Q

Clinical findings of CHF in cardio exam?

A
  1. Tachycardia at rest
  2. Hypotension
  3. Narrow pulse pressure
  4. Raised jugular venous pressure
  5. Displaced apex beat (due to left ventricular dilatation)
  6. Right ventricular heave
  7. Gallop rhythm on auscultation (pathognomic for CHF)
  8. Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis)
  9. Pedal and ankle oedema
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27
Q

Clinical findings of CHF in resp exam?

A
  1. Tachypnoea
  2. Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields
  3. Reduced air entry on auscultation with stony dullness on percussion (pleural effusion)
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28
Q

Clinical findings of CHF in abdo exam?

A

Hepatomegaly, ascites

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29
Q

What bedside investigations should be done in CHF?

A

Full history, cardio/resp/cardio exams, urinalysis and ECG

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30
Q

What would an ECG show in CHF?

A
  1. Tachycardia
  2. Atrial fibrillation (due to enlarged atria)
  3. Left-axis deviation (due to left ventricular hypertrophy)
  4. P wave abnormalities (e.g. P.mitrale/P.pulmonale due to atrial enlargement)
  5. Prolonged PR interval (due to AV block)
  6. Wide QRS complexes (due to ventricular dyssynchrony)
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31
Q

Why is there AF in CHF?

A

Due to enlarged atria

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32
Q

Why is there left-axis deviation in CHF?

A

Due to left ventricular hypertrophy

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33
Q

Why are there P wave abnormalities in CHF?

A

P.mitrale or P.pulmonale due to atrial enlargement

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34
Q

Why is there a prolonged PR interval in CHF?

A

Due to AV block

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35
Q

Why are there wide QRS complexes in CHF?

A

Due to ventricular dyssynchrony

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36
Q

What bloods do you want to do in CHF?

A
  1. FBC (anaemia)
  2. U&E (renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia))
  3. LFTs (hepatic congestion)
  4. Glucose/HbA1c (ischaemic risk profile)
  5. Lipids (ischaemic risk profile)
  6. Troponin (if considering recent myocardial infarction)
  7. BNP/NT-proBNP (heart failure)
  8. TFTs
  9. cardiomyopathy screen
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37
Q

Screening for cardiomyopathy includes which blood tests?

A
  1. Serum iron and copper studies (to rule out haemochromatosis and Wilson’s disease)
  2. Rheumatoid factor, ANCA/ANA, ENA, dsDNA (to rule out autoimmune disease)
  3. Serum ACE (to rule out sarcoidosis)
  4. Serum-free light chains (to rule out amyloidosis)
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38
Q

NT-proBNP level >2000 ng/L significance:

A

refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks

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39
Q

NT-proBNP level 400-2000ng/L significance:

A

refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks

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40
Q

NT-proBNP level <400 ng/L significance:

A

heart failure unlikely

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41
Q

What are other conditions in which NT-proBNP may be raised other than CHF?

A
  1. Left ventricular hypertrophy
  2. Tachycardia
  3. Liver cirrhosis
  4. Diabetes
  5. Acute or chronic renal disease
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42
Q

What imaging can be done in CHF?

A

Transthoracic echocardiography, CXR, cardiac MRI

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43
Q

What are typical CXR findings associated with CHF?

A
  1. Alveolar oedema (perihilar/bat-wing opacification)
  2. Kerley B lines (interstitial oedema)
  3. Cardiomegaly (cardiothoracic ratio >50%)
  4. Dilated upper lobe vessels
  5. Effusions (e.g. pleural effusions – blunted costophrenic angles)
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44
Q

What is is the gold standard investigation for assessing ventricular mass, volume and wall motion?

A

Cardiac MRI

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45
Q

What is a cardiac MRI used for and why is it used?

A

To assess ventricular mass, volume and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views.

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46
Q

What can an echo show in relation to CHF?

A
  1. Global systolic and diastolic function (Ejection fraction normally ~60%)
  2. Focal / global hypokinesia
  3. Hypertrophy
  4. Valve lesions
  5. Intracardiac shunts
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47
Q

What is LVEF?

A

LVEF is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole.

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48
Q

How is LVEF measured?

A

LVEF is usually measured using transthoracic echocardiography, however, MRI, nuclear medicine scans and transoesophageal echocardiography can also be used.

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49
Q

New York Heart Association’s (NYHA) classification system:

A

Class I: no symptoms during ordinary physical activity
Class II: slight limitation of physical activity by symptoms
Class III: less than ordinary activity leads to symptoms
Class IV: inability to carry out any activity without symptoms

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50
Q

BNP is secreted from ventricles in response to:

A

↑ pressure → stretch, tachycardia, glucocorticoids, and
thyroid hormones

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51
Q

What are actions of BNP?

A

↑ GFR and ↓ renal Na reabsorption, ↓ preload by relaxing smooth muscle

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52
Q

What is the general management for CHF?

A

Lifestyle, vaccinations, medication review, monitoring

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53
Q

Describe lifestyle management for CHF?

A
  1. Fluid and salt restriction
  2. Regular exercise
  3. Smoking cessation
  4. Reduced alcohol intake
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54
Q

What vaccinations should you give in CHF?

A

Influenza and pneumococcal disease

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55
Q

Which medications may be harmful in the context of heart failure?

A
  1. Calcium channel blockers (e.g. verapamil, diltiazem)
  2. Tricyclic antidepressants
  3. Lithium
  4. NSAIDs and COX-2 inhibitors
  5. Corticosteroids
  6. QT-prolonging medications
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56
Q

What should be monitored in HF?

A
  1. Functional capacity
  2. Fluid status
  3. Cardiac rhythm
  4. Cognitive status
  5. Nutritional status
  6. Renal function
57
Q

How can comorbidities in CHF be managed?

A

Statins and aspirin for coronary heart disease. Oral anticoagulation for heart failure and atrial fibrillation (either paroxysmal or permanent).

58
Q

How does pharmacological treatment work in CHF?

A

Pharmacological treatment aims to increase cardiac output ­by optimising preload and contractility whilst decreasing afterload.

59
Q

What medications are used in the pharmacological treatment of CHF?

A

Diuretics, ACEi, beta-blockers, angiotensin-II receptor antagonists (ARBs), mineralocorticoid/aldosterone receptor antagonists (MRAs), sodium-glucose cotransporter-2 (SGLT2) inhibitors

60
Q

Why prescribe diuretics in CHF?

A

Diuretics should be prescribed to relieve symptoms of fluid overload (e.g. shortness of breath, peripheral oedema)

61
Q

How do diuretics work in CHF?

A

Diuretics (e.g. furosemide) work by increasing sodium excretion via diuresis, ultimately reducing cardiac afterload. (Doses should be titrated according to clinical response and renal function should be closely monitored.)

62
Q

All patients with CHF should be commenced on an ACE inhibitor if they have an ejection fraction of?

A

A reduced ejection fraction (≤40%)

63
Q

What have ACEi been shown to improve?

A

Ventricular function and reduce mortality

64
Q

When ACEi are given to heart failure patients, what should be monitored?

A

U&Es should be checked prior to starting treatment and then after 1-2 weeks of treatment.

65
Q

What are contradictions to ACEi?

A
  1. A history of angioedema
  2. Bilateral renal artery stenosis
  3. Hyperkalaemia (>5 mmol/L)
  4. Severe renal impairment (serum creatinine >220 μmol/L)
  5. Severe aortic stenosis
66
Q

When should beta blockers be given to patients with CHF?

A

Beta-blockers (e.g. bisoprolol) should be prescribed for all patients with symptomatic heart failure and reduced LVEF (≤40%) unless contraindicated.

67
Q

How do beta blockers work?

A

Decrease heart rate, myocardial oxygen demand and RAAS activation.

68
Q

What needs to be monitored when prescribing beta blockers to CHF patients?

A

Blood pressure and heart rate need to be monitored carefully when adjusting doses.

69
Q

What are contraindications to beta-blockers?

A

Contraindications include asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.

70
Q

If a patient is unable to tolerate an ACE inhibitor (usually due to persistent cough), what can be given instead?

A

An ARB (e.g. candesartan) should be prescribed as an alternative

71
Q

What must be ensured before starting an ARB?

A

Patients must have normal serum potassium and adequate renal function to commence an ARB.

72
Q

When should a low-dose aldosterone antagonist (e.g. spironolactone or eplerenone) be prescribed?

A

If a patient continues to have symptoms of heart failure despite diuretics, ACE inhibitors and beta-blockers

73
Q

How do MRAs work?

A

MRAs antagonise aldosterone, increasing sodium excretion via diuresis, ultimately decreasing cardiac afterload.

74
Q

When is SGLT2 inhibitor used in CHF?

A

SGLT2 inhibitors (e.g. dapagliflozin) can be used as add-on therapy in patients with a reduced LVEF (<40%).

75
Q

Dapagliflozin (SGLT2 inhibitor) has been shown to reduce the risk of?

A

Cardiovascular events and hospital admission. This benefit occurs regardless of the patient’s glycaemic control.

76
Q

What are some specialist pharmacological treatments in CHF?

A

Ivabradine and ARNI (angiotensin receptor and neprilysin inhibitor)

77
Q

How does ivabradine work in CHF?

A

Ivabradine inhibits the sinoatrial node, slowing the heart rate of patients in sinus rhythm, increasing stroke volume whilst preserving myocardial contractility.

It has been shown to reduce cardiovascular death or hospitalisation for heart failure by 18%.

78
Q

How do ARNIs work in CHF?

A

ARNI’s increase BNP levels by inhibiting the neprilysin enzyme which breaks down BNP.

Higher BNP causes natriuresis/diuresis, therefore decreasing cardiac afterload.

79
Q

What are other management options for heart failure?

A

If heart failure is caused or worsened by other conditions, these should be managed appropriately:

  1. Revascularisation (e.g. coronary artery bypass grafting)
  2. Valve surgery (e.g. aortic valve replacement)
  3. Implantable cardiac defibrillator (ICD): inserted if EF <30% for prevention of fatal arrhythmias
  4. Cardiac resynchronisation therapy + defibrillator (CRT-D)
  5. Cardiac transplantation (rare and strict criteria must be met for consideration).
80
Q

What is CRT-D?

A

Cardiac resynchronisation therapy + defibrillator (CRT-D): a biventricular pacemaker for EF <30% + QRS >130 m/sec to re-synchronise left and right ventricular contraction to improve EF

81
Q

Complications of CHF?

A

Arrhythmias: atrial fibrillation and ventricular arrhythmias
Depression and impaired quality of life
Loss of muscle mass
Sudden cardiac death

82
Q

What is the prognosis of CHF?

A

Prognosis is poor overall, with approximately 50% of people with heart failure dying within five years of diagnosis.

83
Q

What does the cardiac cycle involve?

A

Contraction (systole) and relaxation (diastole) of the atria and ventricles to effectively pump blood

84
Q

The cardiac cycle starts with the atria and ventricles in…

A

Diastole

85
Q

When blood enters the right atrium (from the vena cava) and the left atrium (from the pulmonary vein), which valves are open?

A

Mitral and tricuspid valves are open, allows blood to flow freely into the right and left ventricles from the atria. Aortic and pulmonary valves are shut.

86
Q

What comes after the initial diastole in the cardiac cycle?

A

Atrial systole

87
Q

What happens in atrial systole?

A

Contraction of the atria to finish “filling” the ventricles with blood

88
Q

What happens in ventricular systole?

A

Ventricles contract -> increasing the pressure within the ventricles -> closure of the mitral and tricuspid valves -> this prevents regurgitation of blood from the ventricles into the atria

89
Q

What is isovolumetric contraction?

A

After the mitral and tricuspid valves close, the ventricles continue to contract while the volume of blood stays constant, increasing the pressure. The aortic and pulmonary valves are closed (until the pressure in the ventricles exceeds the pressure in the pulmonary artery and aorta).

90
Q

What is the ventricular ejection phase?

A

The pressure within the ventricles exceeds the pressure in the pulmonary artery and aorta -> the pulmonary and aortic valves open -> blood is ejected from the ventricles during ventricular ejection phase

91
Q

What is ventricular diastole?

A

The ventricles then begin to relax following contraction. The drop in pressure within the ventricle causes the aortic and pulmonary valves to close, to prevent backflow (regurgitation) of blood into the ventricles.

92
Q

What is S1?

A

The first heart sound (S1) is caused by the closure of the mitral and tricuspid valves. It marks the start of ventricular systole, and a peripheral pulse is felt at the same time (or shortly after) S1.

93
Q

What is S2?

A

The second heart sound (S2) is caused by the closure of aortic and pulmonary valves. It marks the end of ventricular systole and the start of diastole.

94
Q

How do the valves close in a split S2?

A

(um check) The pulmonary valve may close just after the aortic valve. Closure of the pulmonary valve just after the aortic valve is prolonged during inspiration, or in defects which cause more blood to be pumped out of the right ventricle.

95
Q

What is the Levine scale for?

A

Grading cardiac murmurs according to intensity

96
Q

Levine scale grade 1:

A

Very faint. Heard by an expert in optimum conditions

97
Q

Levine scale grade 2:

A

Heard by a non-expert in optimum conditions

98
Q

Levine scale grade 3:

A

Easily audible, no thrill

99
Q

Levine scale grade 4:

A

A loud murmur, with a thrill

100
Q

Levine scale grade 5:

A

Very loud, often heard over a wide area, with thrill

101
Q

Levine scale grade 6:

A

Extremely loud, heard without a stethoscope

102
Q

What kind of murmur does aortic stenosis have?

A

Ejection systolic

103
Q

Where is aortic stenosis heard the loudest?

A

Aortic valve

104
Q

How does the aortic stenosis murmur sound?

A

Ejection systolic with ‘crescendo-decrescendo’ quality (it appears as diamond-shaped on a phonogram)

105
Q

Where does the aortic stenosis murmur radiate to?

A

Carotid arteries

106
Q

What are causes of aortic stenosis?

A

Calcification (elderly, most common cause in the developed world), congenital (bicuspid valve), rheumatic heart disease

107
Q

When is the aortic stenosis murmur loudest?

A

Loudest on expiration and when the patient is sitting forwards

108
Q

Apart from a murmur, what are other clinical features of aortic stenosis?

A
  1. Slow rising pulse with narrow pulse pressure
  2. Non-displaced, heaving apex beat (if present indicates left ventricular hypertrophy)
  3. Reduced or absent S2 (a sign of moderate-severe aortic stenosis)
  4. Reverse splitting of S2: aortic valve closes after pulmonary valve (due to the longer time required for blood to exit the left ventricle)
109
Q

When does mitral regurgitation occur?

A

Mitral regurgitation (MR) occurs when there is backflow (regurgitation) of blood from the left ventricle into the left atria (through the mitral valve) during ventricular systole.

110
Q

What murmur is heard in mitral regurgitation?

A

Pansystolic

111
Q

Where is mitral regurgitation loudest?

A

Over the mitral area, radiating to the axilla

112
Q

What are causes of mitral regurgitation?

A
  1. Infective endocarditis
  2. Acute myocardial infarction with rupture of papillary muscles
  3. Rheumatic heart disease
  4. Congenital defects of the mitral valve
  5. Cardiomyopathy
113
Q

When is mitral regurgitation murmur loudest?

A

Loudest over the mitral area and loudest on expiration in the left lateral decubitus position

114
Q

Other clinical features of mitral regurgitation, apart from a murmur?

A

Displaced, hyperdynamic apex beat

115
Q

What is aortic regurgitation?

A

Aortic regurgitation (AR) occurs when there is a backflow of blood from the aorta into the left ventricle during ventricular diastole.

116
Q

What murmur is heard in aortic regurgitation?

A

Early diastolic murmur

117
Q

Where is aortic regurgitation heard loudest?

A

At the left sternal edge

118
Q

Which aortic regurgitation is asymptomatic?

A

Chronic

119
Q

What are two reasons aortic regurgitation can occur?

A

Disease process affecting the valve itself, or due to dilatation of the aortic root

120
Q

What are diseases affecting the valve?

A
  1. Congenital bicuspid aortic valve
  2. Rheumatic heart disease
  3. Infective endocarditis
121
Q

What are causes of aortic root dilatation?

A
  1. Aortic dissection: can result in acute aortic regurgitation
  2. Connective tissue diseases (e.g. Marfan’s syndrome)
  3. Aortitis
122
Q

Typical features of an aortic regurgitation murmur?

A
  1. Decrescendo early diastolic murmur
  2. Heard loudest at the left sternal edge (the direction that the turbulent blood flows) sometimes heard loudest over the aortic area
  3. Austin Flint murmur
123
Q

What is an Austin Flint murmur?

A

A low pitched rumbling mid-diastolic murmur heard best at the apex.

124
Q

What causes an Austin Flint murmur?

A

This is caused by the regurgitated blood through the aortic valve mixing with blood from the left atrium, during atrial contraction.

125
Q

What is Austin Flint murmur a sign of?

A

An Austin Flint murmur is a sign of severe aortic regurgitation.

126
Q

What are other clinical features of aortic regurgitation?

A

Collapsing pulse (a ‘water hammer pulse’ with wide pulse pressure); a displaced, hyperdynamic apex beat

127
Q

What are eponymous clinical signs associated with aortic regurgitation?

A

Corrigan’s sign, De Musset’s sign, Quincke’s sign,
Traube’s sign, Muller’s sign

128
Q

What is Corrigan’s sign?

A

Visible distention and collapse of carotid arteries in the neck

129
Q

What is De Musset’s sign?

A

Head bobbing with each heartbeat

130
Q

What is Quincke’s sign?

A

Pulsations are seen in the nail bed with each heartbeat when the nail bed is lightly compressed

131
Q

What is Traube’s sign?

A

‘Pistol shot’ sound heard when stethoscope placed over the femoral artery during systole and diastole

132
Q

What is Muller’s sign?

A

Uvula pulsations are seen with each heartbeat

133
Q

What is mitral stenosis?

A

Mitral stenosis (MS) involves narrowing of the mitral valve, which results in decreased filling of the left ventricle during systole and increased left atrial pressure (due to incomplete left atrial emptying).

134
Q

What murmur is seen in mitral stenosis?

A

A low-pitched, rumbling, mid-diastolic murmur heard loudest over the apex

135
Q

Where is the mitral stenosis murmur heard loudest?

A

Over the apex, and in left lateral decubitus position on expiration

136
Q

What is the commonest cause of mitral stenosis?

A

Rheumatic heart disease

137
Q

What are rarer causes of mitral stenosis?

A
  1. Congenital
  2. Left atrial myxoma
  3. Connective tissue disorders
  4. Mucopolysaccharidosis
138
Q

What are features of a mitral stenosis murmur?

A
  1. Low-pitched, rumbling mid-diastolic murmur with an opening click (click heard in mid-diastole when the mitral valve opens)
  2. Murmur is heard loudest over the apex
  3. Loudest in left lateral decubitus position on expiration
139
Q

What are other clinical features of mitral stenosis?

A
  1. A low-volume pulse which may be irregularly, irregular (atrial fibrillation is common in mitral stenosis)
  2. Loud first heart sound with tapping apex beat (due to a palpable closing of the mitral valve)
  3. A malar flush (plum-red discolouration of the cheeks)

Abbie's Final Year Flashcards (1 decks)

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