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Medicine - Year 2 > The cardiovascular system - Heart failure and cardiomyopathy > Flashcards

The cardiovascular system - Heart failure and cardiomyopathy Flashcards

1
Q

What is heart failure?

A

Heart failure is a syndrome that results from an inability of the heart to maintain an adequate output

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2
Q

Describes the epidemiology of heart failure

A
  • Incidence increases with age
  • Median age at first presentation is 76 years
  • Men most affected
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3
Q

Describe the aetiology of heart failure

A

Vascular
- Ischaemic/coronary heart disease (50%0
- Hypertension

Muscular
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Congenital heart disease

Valvular
- Stenotic valve
- Regurgitant valves

Electrical
- Arrythmias

High output
- Anaemia
- Septicaemia
- Thyrotoxicosis
- Liver failure

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4
Q

Describe the pathophysiology of heart failure

A

As cardiac output begins to decline, compensatory mechanisms (both mechanical and neurohumeral) are activated to sustain adequate tissue perfusion

However, while these mechanisms may initially be beneficial, they eventually lead to worsening of heart failure over time as they decline their ability to compensate

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5
Q

Give 4 compensatory mechanisms that are activated to sustain an adequate cardiac output in heart failure

A
  1. Increasing preload
  2. Increasing heart rate
  3. Activation of the renin-angiotensin-aldosterone system
  4. Sympathetic nervous system activation
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6
Q

Describe how an increase in pre-load compensates for heart failure

A

Increase in pre-load causes an increase in end-diastolic volume (EDV) compensating for the reduced ejection fraction, thus maintaining cardiac output

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7
Q

Describe how the the activation of renin-angiotensin system compensates for heart failure

A

Angiotensin II increases preload and after load

This leads to increased cardiac output

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8
Q

Why does Ace inhibition cause the ace cough and angiodema

A

The ace cough develops because angiotensin converting enzyme catalyses bradykinin into inactive fragments

Ace inhibition therefore leads to an increase in bradykinin levels, which leads to side-effects of cough and angioedema

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9
Q

Give the 4 classifications of heart failure

A
  1. Acute vs chronic heart failure
  2. Systolic vs diastolic heart failure
  3. Left-sided vs right-sided heart failure
  4. High output vs low output heart failure
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10
Q

Describe acute vs chronic heart failure including the causes

A

Acute
- Characterised by rapid onset of symptoms and/or signs of heart failure that is usually life-threatening
- May present suddenly with cardiogenic shock or sub acutely with decompensation of chronic heart failure
- Requires urgent evaluation and treatment
- Most common cause include acute myocardial dysfunction, acute valvular, pericardial tamponade

Chronic
- Characterised by progressive symptoms with episodes of acute deterioration
- Due to progressive cardiac dysfunction from structural and/or functional abnormality
- Usually precipitated by conditions that affect muscle (e.g., cardiomyopathy), vessels (e.g., ischaemic heart disease), valves (e.g., aortic stenosis), or conduction (e.g., AF)

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11
Q

Describe systolic (HFrEF) vs diastolic heart failure (HFpEF) including the causes

A

Systolic
- aka heart failure with reduced ejection fraction (HFrEF)
- Poor ventricular contraction leads to reduced ejection fraction in left ventricle (< 40%)
- commonly seen because of ischaemic heart disease, dilated cardiomyopathy, myocarditis, infiltration (e.g., haemochromatosis or sarcoidosis)

Diastolic
- aka heart failure with preserved ejection fraction (HFpEF)
- Ventricles are unable to relax due to stiffness, resulting in inadequate filling of the heart during diastole (LVEF > 50%)
- Seen in restrictive cardiomyopathy, constrictive pericarditis, cardiac tamponade, hypertrophic obstructive cardiomyopathy

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12
Q

What is the LVEF in heart failure with reduced LVEF (HFrEF)?

A

LVEF < 40%

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13
Q

What is the LVEF in heart failure with reduced LVEF (HFmrEF)?

A

LVEF 40-49%

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14
Q

What is the LVEF in heart failure with preserved LVEF (HFrEF)?

A

LVEF >/= 50%

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15
Q

Describe left-sided vs right-sided heart failure

A

LHF
- Left-side is usually affected first
- Poor ventricular contraction causes blood ‘back up’ in the lungs
- This increases the pulmonary vein hydrostatic pressure, resulting in pulmonary oedema

RHF
- Most common cause of RHF is left heart failure
- An increase in the pressure of the pulmonary vasculature causes the right side of the heart to pump against increased resistance. The right side of the heat compensates with ventricular dilatation and eventual failure

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16
Q

What are the 3 broad categories that right-sided heart failure is related to?

A
  • Pulmonary hypertension
  • Pulmonary/tricsupid valve disease
  • Pericardial diseases
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17
Q

a) What is cor pulmonale?

b) What is the ECG appearance of cor pulmonale?

A

a) Right heart failure secondary to long-standing pulmonary arterial hypertension e.g., COPD

b) Shows p pulmonale, which refers to tall, peaked p wave. It reflects right atrial enlargement

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18
Q

Describe low output vs high output heart failure including the causes

A

Low output
- Compensatory mechanisms eventually fail, resulting in a reduced cardiac output
- Caused by either failure of the pump (heart), increased preload or increased after load
- Characterised by weak pulse, cool peripheries, and low blood pressure
- Low-output states are seen in ischaemic heart disease, aortic stenosis

High output
- The heart is unable to meet the increased demand of perfusion despite normal or increased cardiac output
- The problem is with reduced vascular resistance, often due to diffuse arteriole vasodilation or shunting
- LVEF > 50% and abnormal diastolic filling
- Echocardiogram is typically normal
- It is generally due to states of increased metabolic demand (e.g., hyperthyroidism aka thyrotoxicosis), reduced vascular resistance (e.g., thiamine deficiency, sepsis) or significant shunting (e.g., large arteriovenous fistula), Paget’s disease, pregnancy, anaemia
- Characterised by warm peripheries and normal pulses

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19
Q

What are is low cardiac output and high cardiac output heart failure characterised by?

A

Low output
- Weak pulse
- Cool peripheries
- Low blood pressure

High cardiac output
- Warm peripheries
- Normal pulses

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20
Q

What does the echocardiogram in high-cardiac output heart failure look like?

A

Echocardiogram is typically normal

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21
Q

Heart failure

a) Symptoms

b) Signs

A

a)
- Shortness of breath
- Wheeze
- Fatigue
- Weight loss
- Orthopnoea (breathless lying down)
- Paroxysmal nocturnal dyspnoea (waking up at night breathless)
- Palpitations

b)
- Raised JVP
- Displaced apex
- Crackles]- Ankle oedema
- Heart sounds S3/S4
- Ascites (fluid collects in spaces within your abdomen)
- Pulses alternans (an alternating strong and wake pulse) - associated with severe LHF
- Right sided heart failure: peripheral oedema (pedal, scrotal or sacral), raised JVP, hepatomegaly and bloating

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22
Q

What are the symptoms and signs of left-sided heart failure?

A

Symptoms
- Dysponea
- Fatigue
- Tachycardia - gallop rhythm
- Orthopnoea
- Paroxysmal nocturnal dysponea

Signs
- Displaced apex beat
- Pleural effusion
- Bibasall crackles
- Pulsus alternans

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23
Q

What are the signs of right sided heart failure?

A
  • Peripheral oedema (pedal, scrotal or sacral)
  • Raised JVP
  • Hepatomegaly
  • Bloating
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24
Q

What are the differential diagnosis of heart failure?

A
  • Obesity
  • Chest disease: including lung, diaphragm or chest wall
  • Venous insufficiency in lower limbs
  • Drug-induced ankle swelling (e.g., dihydropyridine calcium channel blockers)
  • edu-induced fluid retention (e.g., NSAIDs)
  • Angina
  • Hypoalbuminemia
  • Intrinsic renal or hepatic disease
    -Pulmonary embolic disease
  • Depression and/or anxiety disorder
  • Severe anaemia or thyroid disease
  • Bilateral renal artery stenosis
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25
Q

Describe the 4 class of the New York association clinical classification of heart failures based on: physical activity and symptoms

A

Class I - no limitation on physical activity and no symptoms

Class II - slight limitation on physical activity and symptoms are present with normal physical activity –> mild heart failure

Class III - marked limitation on physical activity and symptoms are present with less than normal physical activity –> moderate heart failure

Class IV - unable to do physical activity without discomfort and symptoms present at rest –> severe heart failure

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26
Q

Describe the investigations for cardiac failure, include what you are trying to exclude

A

Bedside
- Blood pressure
- ECG
- Urinalysis: for protein and glucose

Bloods
- FBC: exclude anemia, infetcive cause
U&Es: exclude renal failure as a cause of oedema
- LFT: exclude liver failure a s a cause of oedema
- TFT: exclude thyroid disease
- Cholesterol and HBA1c: cardiovascular risk stratification
- Brain natriuretic peptides (BNP and n-terminal pro BNP)

Imaging
- Echocardiogram (imaging modality): previous MI, LV strain/hypertrophy, conduction abnormalities/AF
- CXR

Other imaging
- Cardiac MRI
- Coronary angiogram
- Right heart catheterisation: reserved for the investigation of right-sided heart failure
- 24hr ECG: if arrhythmia is suspected
- Lung function tests: to exclude alternative pathology impacting on symptoms (e.g., breathlessness)

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27
Q

What are the x-ray findings in heart failure?

A

ABCDE
A: Alveolar oedema (with ‘batwing’ peripheral shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio > 0,5)
D: Upper lobe diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure

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28
Q

When would you used cardiac MRI to investigate heart failure?

A

Particularly useful when TTE images are poor/non-diagnostic due to obesity or chronic obstructive lung disease

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29
Q

What is pro brain natrieutic peptide and describe its role in heart failure (BNP)

A

pro-BNP is a protein released by cardiomyocytes in response to excessive stretching

It is used to assess the likelihood of heart failure

It has a high negative predictive value so good at excluding heart failure

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30
Q

Other than heart failure, what other conditions may raise BNP?

A
  • Diabetes
  • Sepsis
  • Old age
  • Hypoxaemia (PE and cold)
  • Kidney disease
  • Liver cirrhosis
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31
Q

a) What is a high bNP? and what must you do?

What is a raised bNP? and what must you do?

What is a normal bNP? and what must you do?

A

a) BNP>2000ng/L the patient needs an urgent 2-week referral for specialist assessment and an ECHO.

b) BNP 400-2000ng/L the patient should get a 6-week referral for specialist assessment and an ECHO.

c) BNP < 400ng/L and consider other diagnosis

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32
Q

What are the poor prognostic factors in heart failure?

A
  • Low systolic bP
  • Coronary disease
  • Raised creatinine/eGFR
  • Hyponatraemia
  • Diabetes
  • Anaemia
  • Arrythmias
  • AF
  • Low EF (<30%)
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33
Q

Give the 4 bases of heart failure management

A
  1. Lifestyle modification
  2. Pharmacological therapy
  3. Devices and surgery
  4. Continuous monitoring
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34
Q

Describe the lifestyle modification to manage heart failure

A
  • Weight control
  • Dietary measures e.g., salt avoidance, optimising nutrition
  • Reducing fluid intake including alcohol
  • Smoking cessation
  • Exercise (low intensity aerobic exercise/rehabilitation
  • Pneumococcal and annual influenza vaccination
  • Management of co-morbidities (diabetes, COPD)
  • Screen for depression
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35
Q

Describe pharmacological therapy, 1st line and 2nd line to manage heart failure

A

1st line (ACEi + beta-blcokers)
- ACEi e.g., ramipril 2.5mg OD or ARBs if intolerable to side effects (e.g., losartan, candesartan) - improves diagnosis and symptoms

AND

  • Beta-blockers e.g., bisporoplol 1.25mg OD (or carvedilol, metoprolol) - improves diagnosis and symptoms

MAYBE WITH

  • Aldosterone antagonist e.g., eplerenone 25mg, spironolactone - can be added to ACEi and beta-blocker if symptoms persist
  • Loop diuretics (e.g., furesomide), thiazides _ symptomatic relief of oedema only

2nd line
- Ivabradine
- Sacubitril/valsartan
- Hydralazine in combination with nitrates
- Digoxin

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36
Q

Describe pharmacological therapy, 1st line and 2nd line to manage heart failure

A

1st line (ACEi + beta-blcokers)
- ACEi e.g., ramipril 2.5mg OD or ARBs if intolerable to side effects (e.g., losartan, candesartan) - improves diagnosis and symptoms

AND

  • Beta-blockers e.g., bisporoplol 1.25mg OD (or carvedilol, metoprolol) - improves diagnosis and symptoms

MAYBE WITH

  • Aldosterone antagonist e.g., eplerenone 25mg, spironolactone - can be added to ACEi and beta-blocker if symptoms persist
  • Loop diuretics (e.g., furesomide), thiazides _ symptomatic relief of oedema only

2nd line
- Ivabradine
- Sacubitril/valsartan
- Hydralazine in combination with nitrates
- Digoxin

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37
Q

What are the devices and surgery options to manage heart failure

A
  • Cardiac resynchronisation (CRT)
  • Implantable cardiac defibrillator (ICD)
  • Revascularisation (PCI/CABG)
  • Cardiac transplant
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38
Q

What are the 3 indications of an ICD in patients with cardiac failure

A
  • QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
  • QRS interval 120-149ms without LBBB, NYHA class I-III
  • QRS interval 120-149ms with LBBB, NYHA class I
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39
Q

Describe the initial management of acute heart failure (pulmonary oedema)

A
  • Sit the patient up
  • Oxygen therapy (aiming saturations > 94%)
  • IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
  • SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
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40
Q

Describe the advanced manage of acute heart failure (pulmonary oedema) - occurring usually in ITU settings

A
  • Continuous positive airway pressure (CPAP) : reduces hypoxia and may help push fluid out of alveoli
  • Intubation and ventilation
  • Furosemide infusion: continuous IV furosemide given over 24 hours to maximise diuresis
  • Dopamine infusion: Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility.
  • Intra-aortic balloon pump: if the patient is in cardiogenic shock
  • Ultrafiltration: If resistant to or contraindicated diuretics
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41
Q

What are the common adverse effects of the following heart failure medications:

a) Beta-blockers

b) ACEi

c) Spironolactone

d) Furosemide

e) Hydralazine

f) Digoxin

A

a) Bradycardia, hypotension, fatigue, dizziness

b) Hyperkalaemia, renal impairment, dry cough, light- headedness, fatigue, GI disturbances, angioedema

c) Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes libido

d) Hypotension, hyponatraemia/kalaemia

e) Headache, palpitations, flushing

f) Dizziness, blurred vision, GI disturbances

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42
Q

What are the monitoring requirements ACEi when managing heart failure

A

Check renal function prior to initiation ; repeat tests within 1-2 weeks

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43
Q

What are the common adverse effects of the following heart failure medications:

a) Beta-blockers

b) ACEi

c) Spironolactone

d) Furosemide

e) Hydralazine

f) Digoxin

A

a) Bradycardia, hypotension, fatigue, dizziness

b) Hyperkalaemia, renal impairment, dry cough, light- headedness, fatigue, GI disturbances, angioedema

c) Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes libido

d) Hypotension, hyponatraemia/kalaemia

e) Headache, palpitations, flushing

f) Dizziness, blurred vision, GI disturbances

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44
Q

What is the genetic basis of Marfan syndrome?

A

inherited in an autosomal dominant pattern

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45
Q

What is the genetic basis of long QT syndrome?

A

Inherited in an autosomal dominant pattern

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46
Q

What is the genetic basis of Fabry disease?

A

Inherited as an X-linked disorder

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47
Q

Define cardiomyopathy

A

A disorder in which heart muscle is structurally and functionally abnormal (in the absence of other heart conditions severe enough to cause the heart abnormality)

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48
Q

a) Name the 2 most common cardiomyopathies

b) Name 3 uncommon cardiomyopathies

A

a)
- Hypertrophic cardiomyopathy
- Dilated cardiomyopathy

b)
- Arhythmogenic right ventricular cardiomyopathy
- Restrictive cardiomyopathy
- Unclassified cardiomyopathies: left ventricular non-compaction, takotsubo’s cardiopathy

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49
Q

What investigation is the diagnosis of cardiomyopathy deterred by?

A

Echocardiogram

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50
Q

What is hypertrophic cardiomyopathy?

A

An autosomal dominant genetic disorder that causes increased ventricular wall thickness or mass not caused by pathological loading

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51
Q

What is the genetic inheritance of hypertrophic cardiomyopathy

A

Autosomal dominnat

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52
Q

Describe the epidemiology of hypertrophic cardiomyopathy

A
  • Commonest genetic cardiovascular condition
  • Increase prevalence in males and the afro-caribbean and asian populations
  • Most common cause of sudden death in under 35 years old
  • Obstructive form i.e., hypertrophic obstructive cardiomyopathy (HOCM) seen in 2/3 of cases
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53
Q

Describe the aetiology of hypertrophic cardiomyopathy

A

HCM is commonly due to an abnormal gene that encodes one of the sarcomere proteins needed for myocardial contraction, which include:
- Cardiac troponin T and I
- Myosin regulatory light chains

The most common mutation is in the gene that encodes the beta myosin heavy chain and the inheritance is usually autosomal dominant

The myosin binding protein C is next commonly affected

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54
Q

What gene, is the most common mutation in hypertrophic cardiomyopathy found?

A

The gene that encodes the beta myosin heavy chain

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55
Q

Describe the pathophysiology of hypertrophic cardiomyopathy

A

In HCM there are mutations in genes encoding proteins that make up the sarcomere complex

Incorporation of these mutated peptides into the sarcomere –> impaired contractile function –> increased myocyte stress –> compensatory hypertrophy and increased fibroblasts –> chaotic and disorganised myocardial fibres

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56
Q

a) Describe the pathological consequences of HCM

b) Explain what these pathological changes lead to?

A

a) 1. Obstructive - left ventricular outflow obstruction

  1. Non-obstructive
    - Mitral regurgitation
    - Diastolic dysfunction
    - Systolic dysfunction
    - Arrhythmia

b) Heart failure with features of breathlessness, fatigue and overload. This is because of abnormal relaxation and filling, abnormal contraction and/or outflow obstruction.

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57
Q

How does left ventricular outflow obstruction in hypertrophic cardiomyopathy occur?

A

There is narrowing of the ventricular outflow tract due to thickened interventricular septum

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58
Q

Explain how the symptoms: syncope, sudden death, shortness of breath and chest pain come about in myocyte hypertrophy

A

Myofibres in disarray –> ventricular arrhythmia and sudden death

Left ventricular hypertrophy –> impaired relxation –> increased Left ventricular end-diastolic pressure (LVEDP) –> SOB

Left ventricular hypertrophy –> increased myocardial O2 demand –> chest pain

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59
Q

Hypertrophic cardiomyopathy

a) Symptoms

b) Signs

A

a)
- Most people are asymptomatic
- Fatigue
- Shortness of breath
- Orthopnoea
- Ankle swelling
- angina
- Presyncope or syncope
- Palpitations (AF)
- Sudden death

b)
- May be normal
- Ejection systolic murmur (left ventricular outflow obstruction)
- Mid-late systolic murmur (mitral regurgitation): occurs at the apex/may be pansystolic
- Heave (visible or palpation pulsation)
- Thrill
- Signs of LV outflow obstructions are exaggerated by standing up (reduce venous return), inotropes and vasodilators (e.g., GTN spray)
- Features of heart failure: raised JVP, crackles on lung auscultation, peripheral oedema

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60
Q

What exaggerates the signs of LV outflow obstruction?

A
  • Standing up (reduced venous return)
  • Inotropes
  • Vasodilators (e.g., GTN spray)
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61
Q

Describe the 1st line and 2nd line investigations for hypertrophic cardiomyopathy?

A

1st line
- Echocardiography (gold standard)
- ECG
- Bloods: including LFTs, electrolytes, BNP, TNTs
- Genetic testing

2nd line
- Cardiac MRI

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62
Q

Describe the ECG appearance of hypertrophic cardiomyopathy

A
  • Amplitude of QRS increased (shows LV hypertrophy with a strain pattern)
  • T wave inversion
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63
Q

What re the 4 principles of management in hypertrophic cardiomyopathy?

A
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64
Q

What are the 4 principle of management in hypertrophic cardiomyopathy?

A
  1. Education and reassurance
  2. Management of symptoms and complications
  3. Risk stratification/prevent complication in HCM
  4. Family screening
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65
Q

Describe education and reassurance needed to be provided to patients with hypertrophic cardiomyopathy

A
  • Most patients have no symptoms and a normal life expectancy
  • Encourage ALL patients to undertake low-moderate intensity exercise
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Not at all
2
3
4
5
Perfectly
66
Q

Describe the management of symptoms and complications in hypertrophic cardiomyopathy

A
  1. Beta-blocker or rate limiting calcium channel blocker
  2. Myomectomy/alcohol septal ablation (for those who do respond best to medical therapy)
67
Q

Describe the role of beta-blockers and rate limiting calcium channel blockers in hypertrophic cardiomyopathy

A

They decrease heart rate and force of contraction –> increased diastolic filling time and decrease myocardial oxygen demand

68
Q

When is myomectomy/alcohol septal ablation given as a method of treatment in hypertrophic cardiomyopathy?

A

For those with obstruction form that do not respond best to medical therapy

69
Q

Describe the risk stratification/management required in hypertrophic cardiomyopathy to prevent complications

A
  • Anti-arrhythmic drugs for any arrhythmia
  • Patients with AF should receive treatment with DOAC/Warfarin
  • Patients at risk of sudden death may benefit from an implantable cardioverter defibrillator (ICD)
70
Q

a) What features make a patient with hypertrophic cardiomyopathy at highest risk?

b) What treatment is recommended?

A

a)
- Risk of sudden cardiac death
- Sustained VT

b) ICD

71
Q

a) What features make a patient with hypertrophic cardiomyopathy at intermediate risk?

b) What treatment should be considered?

A

a)
- FH of sudden cardiac death
- Massive LVH
- Syncope
- LV aneurysm
- Impaired LV function
- NSVT
- Extensive scar on cardiovascular magnetic resonance (CMR)

b) ICD

72
Q

Describe the family screening management in hypertrophic cardiomyopathy

A
  • Genetic counselling should be offered to all patients (as 50% chance of passing gene to children)
  • If detected, then cascade family screening can be offered to first degree relatives
  • If no clear mutation detected, then first degree relatives should undergo regular follow up with ECG and ECHO
73
Q

a) What is the role of mavacamten in hypertrophic cardiomyopathy

b) Describe how it works

A

a) It is a targeted inhibitor of cardiac myosin that improve symptoms in the obstructive form of HCM

b) Reduces the number of crossbridges in HCM sarcomere –> decrease contractility –> increased relaxation

74
Q

What is dilated cardiomyopathy (DCM)

A

DCM is enlargement of one or both ventricles leading to impaired contractile function i.e., systolic dysfunction

75
Q

Describe the aetiology of dilated cardiomyopathy

A

Idiopathic

Genetic - familial and neuromuscular

Inflammatory
- Infections: post viral (e.g., influenza, adenovirus, Coxsackie A and B)
- Non-infectious: connective tissue disease, permpartum cardiomyopathy, sarcoidosis

Toxic - alcohol, chemotherapy

Metabolic - hypothyroidism, hereditary hemochromatosis

Tachycardia induced

76
Q

Describe the pathophysiology of dilated cardiomyopathy

A

Myocyte injury –> systolic dysfunction (decrease contractility) –> decrease stroke volume –> increased ventricular filling pressure (leads to pulmonary and systemic congestion) + LV dilatation (leads to mitral regurgitation) + decrease CO

77
Q

Dilated cardiomyopathy

a) Symptoms

b) Signs

A

a)
- Asymptomatic
- Heart failure symptoms: breathlessness, peripheral oedema, fatigue, syncope, sporadic chest pain
- Arrhythmia e.g., AF or sudden cardiac death due to ventricular arrhythmia
- Thromboembolism

c)
- Displaced heartbeat secondary to LV dilatation
- Signs of heart failure
- S2 and S4 gallop

78
Q

Describe the 1st and 2nd line investigations for dilated cardiomyopathy

A

1st line
- Echocardiography (gold standard)
- ECG: changes are non-specific
- CXR: features of heart failure, cardiomegaly
- Bloods

2nd line
- Cardiac biopsy (an establish definitive diagnosis but its use is controversial)
- Cardiac MRI

79
Q

Describe the management of dilated cardiomyopathy

A

Management of DCM = management of systolic heart failure
- Beta-blockers and ACEi/ARBs
- Loop and thiazide diuretics
- Spironolactone

Prevent complications - anticoagulation if AF/LV thrombus

Cardiac transplantation

80
Q

What is restrictive cardiomyopathy?

A

The ventricles becomes stiff, non-dilated which leads to abnormal ventricular filling with preserved systolic function

81
Q

Describe the aetiology of of restrictive myocarditis

A

Commonly the result of infiltrative diseases where there is a deposition of substance in the myocardium such as amyloid, iron or granulomas:
- Amyloidosis
- Hemochromatosis (iron overload)

82
Q

Describe the pathophysiology of restrictive myocarditis

A

Stiff ventricular myocardium –> increased diastolic ventricular pressure –> venous congestion –> signs of right sided heart failure (raised JVP, hepatomegaly and ascites, peripheral oedema)

Stiff ventricular myocardium –> decreased ventricular filling –> decreased CO –> weakness and fatigue

83
Q

Describe the 1st line and 2nd line investigations for restrictive cardiomyopathy

A

1st line
- Echocardiography
- ECG: changes are non-specific
- CXR: reveals features of heart failure
- Bloods

2nd line
- Endomyocardial biopsy
- Complex imaging modalities (e.g., CT, MRI) and diagnostic angiography are particularly used to distinguish restrictive cardiomyopathy from constrictive pericarditis because of latter is correctable with surgery

84
Q

Describe the CXR appearance in restrictive cardiomyopathy

A

Reveals feature of heart failure - alveolar effusion, kerley b lines, cardiomegaly, upper blood diversion

“sparkling” on ECG

85
Q

Why are complex imaging modalities (e.g., CT, MRI) and diagnostic angiography used when investigating for restrictive cardiomyopathy

A

They are used to distinguish restrictive cardiomyopathy from constrictive pericarditis because constructive pericarditis is correctable with surgery

86
Q

What are the symptoms and signs of restrictive cardiomyopathy?

A

Symptoms
- Weakness
- Fatigue

Signs
- Jugular vein distention
- Hepatomegaly and ascite
- Peripheral oedema

87
Q

Describe the management of restrictive cardiomyopathy

A
  • Aim to treat the underlying cause, other symptomatic treatment
  • May require heart transplantation in later stages
  • Prevent complications
  • Individuals with AF must be offered anticoagulation unless contraindicated as they are at an increased risk of thromboembolism
88
Q

What is arrhythmogenic cardiomyopathy?

A

It is an inherited heart muscle disease characterised by progressive replacement of the myocardium by fibrofatty tissue

89
Q

Describe the epidemiology of arrhythmogenic cardiomyopathy

A

Presents in young-middle age

90
Q

Describe the aetiology of arrhythmogenic cardiomyopathy

A

Genetics - due to mutation in a desmosomal gene in 40-60% of cases

Acquired - e.g., Chagas disease

91
Q

Describe the pathophysiology of arrhthmogenic cardiomyopathy

A

It is a disease of the desmosome

92
Q

Arrhthmogenic cardiopathy is a progressive disease with 3 clinical phases. Describe the 3 phases

A

Concealed phase - patient is asymptomatic but still at risk sudden cardiac death

Electrical phase - symptomatic ventricular arrythmias

Advanced phase - characterised by RV or biventricular failure

93
Q

Arrythmogenic cardiomyopathy is a progressive disease 3 clinical phase: concealed phase, electrical phase and advanced phase.

Describe the features of each phase

A

Concealed phase - patient is asymptomatic but still at risk sudden cardiac death

Electrical phase - symptomatic ventricular arrythmias

Advanced phase - characterised by RV or biventricular failure

94
Q

Describe the symptoms of arrythmogenic cardiomyopathy

A
  • Asymptomatic
  • Palpitations
  • Syncope
  • Chest pain
  • Breathlessness
  • Features of heart failure
  • Sudden death
95
Q

Describe the investigations for arrythmogenic cardiomyopathy

A
  • Echocardiography with/without cardiac MRI
  • ECG
  • CXR
96
Q

Describe the ECG appearance in arrhythmogenic cardiomyopathy

A
  • T wave inversion
  • Localised prolongation of QRS interval in right precordial leads (V1-V3)
  • LBBB VT if arrhythmogenic cardiomyopathy of RV and RBBB if arrhythmogenic cardiomyopathy of LV
97
Q

Describe the 4 principles of management of arrhythmogenic cardiomyopathy

A
  1. Risk stratification for sudden death
    - defibrillators are indicated in the highest risk patients
  2. Improve symptoms and quality of life
    - Ventricular arrhythmias: beta lockers, antiarrhtymic drugs, catheter abaltion
    - Heart failure: diuretics, beta blockers and ACEi, aldosterone antagonists
  3. Prevent disease progression (exercise restriction)
    - Vigorous exercise associated with accelerated progressive of disease and greater risk of ventricular arrhythmias
    - Participation in high intensity recreational exercise or competitive sports is NOT recommended in patients with arrhythmogenic cardiomyopathy
  4. Screening of family members
98
Q

Takatosubo’s cardiomyopathy?

a) What is is also known as?

b) Aetiology

b) Epidemiology

c) Pathophysiology

d) Pathognomonic features of echocardiogram

e) Symptoms and signs

f) Management

A

a) ‘broken-heart syndrome’ or stress-induce cardiomyopathy

b) Cause is unknown but often brought on by stressful situations which are usually acute and severe

c) Preferentially affects postmenopausal women

d) Apical ballooning of the LV

e) Symptoms and signs may mimic MI (e.g., central crushing chest pain with ST elevation – which is often anterior) but patients have non-obstructive coronary arteries on angiography

f) The condition is self-limiting, but there is a risk of sudden death due to arrhythmia or ventricular free-wall rupture so monitoring in early stages and treatment with beta blockers and ACEi recommended

99
Q

What is myocarditis?

A

Inflammation of the myocardium

100
Q

Describe the aetiology of myocarditis

A

External triggers
- Infection (most commonly viral e.g., Coxsackie and influenza A and B)
- Drugs/Toxins

Internal triggers (immune mediated)
- Hypersensitivity reaction to vaccines
- Autoimmune disease

101
Q

What are the 4 main clinical presentation of myocarditis

A
  1. Asymptomatic
  2. Symptomatic
    - Chest pain
    - Arrhythmias (AV block, ventricular arrhythmias)
    - Heart failure (acute/chronic)
102
Q

Describe the investigations for myocarditis

A
  • ECG
  • Troponin
  • Echocardiogram
  • Cardiac MRI
  • Endomyocardial biopsy via cardiac catheterisation is the gold standard diagnostic
103
Q

a) What is the gold standard diagnostic tool for for myocarditis?

b) What are the risks?

A

a) Endomyocardial biopsy via catheter catheterisation

b) Invasive test so bleeding can occur

104
Q

Describe the ECG appearance in myocarditis

A

Non-specific ST segment and T wave changes (which may be regional, depending on degree and location of myocardial involvement), along with ectopic beats and arrhythmias if present

105
Q

Describe the troponin levels in myocarditis

A

Markedly elevated

106
Q

Describe the echocardiogram changes in myocarditis

A

Can reveal ventricular dysfunction if present (in the form of diastolic dysfunction or regional wall motion abnormalities)

107
Q

Describe the structure of the pericardium

A

A two-layered sac that encircles the heart
1. Parietal pericardium –> bought outer fibrous layer
2. Visceral pericardium –> inner serial layer

Pericardial space: contains a small amount of serous fluid <50ml

108
Q

What are the 3 main role of the pericardium?

A
  1. Anchors the heart to the thorax
  2. Acts as barrier to the infection
  3. Limits sudden dilatation of the heart
109
Q

Is the pericardium essential for life?

A

No

110
Q

Describe the aetiology of pericardial disease

A

Idiopathic

Infectious
- Bacteria
- TB
- Viral

Non-infectious
- Auto immune
- Cancer
- Metabolic
- Trauma
- Radiation
- Drugs

111
Q

What 3 things can go wrong in the pericardium?

A
  1. Effusion
  2. Pericarditis (inflammation)
  3. Constriction (fibrosis)
112
Q

What is acute pericarditis?

A

The inflammation of the pericardium

113
Q

Describe the epidemiology of acute pericarditis

A

Majority of patients are males aged 20-50

114
Q

Describe the pathophysiology of acute pericarditis

A

The pericardial sac is acutely inflamed with infiltration of immune cells secondary to an acute infection or as a manifestation of systemic disease

115
Q

Describe the aetiology of acute pericarditis

A

Usually idiopathic/viral (often due to coxsackievirus B but also influenza, adenovirus etc)

Can also be
- Uraemia
- Surrounding organ involvement
- Malignant disease
- Autoimmune hypersensitivity
- Inflammatory disorders e.g., Behcets syndrome

116
Q

Clinical features of acute pericarditis

a) Symptoms

b) Signs

A

a)
- Chest pain: pleuritic (worse on inspiration), worse lying down and better on leaning forward and sitting up
- Fever: usually low grade
- Breathlessness
- Fatigue
- Cough

b)
- Pericardial friction rub (high pitched scratchy sound best heard at left sternal border with patient leaning forward with held inspiration)
- Features of cardiac tamponade: muffled hear sounds, distended KBP, pulses paradoxus (fall n BP > 10mmHg during inspiration), hypotension

117
Q

Describe the 1st line and 2nd investigations for acute pericarditis

A

1st line
- 12 lead ECG
- Blood tests: FBC (for infection), troponin
- CXR
- Echocardiography (for structural heart abnormality)

2nd line - to detect other possible aetiologies and in diagnostic uncertainty
- ANA testing
- HIV serology
- Tuberculin skin test (tuberculosis)

118
Q

Describe the findings for pericarditis for the following investigations

a) Bloods

b) CXR

A

a) Elevated WCC, ESR and CRP and elevated troponin (may suggest myocardial involvement - myopericarditis)

b) Often normal, but may show pericardial effusion - globular appearance of heart

119
Q

Describe the ECG appearance of acute pericarditis

A

Widespread saddle-shaped ST elevating with PR depression and a downward sloping T-P line (Spodick’s sign)

120
Q

Describe the management of acute pericarditis

A

1st line - Ibuprofen

2nd line - Colchicine (can be given as an adjunct to NSAID treatment or a primary therapy in patients with contraindications)

3rd line - Corticosteroids

121
Q

What are the complications of acute pericarditis

A
  • Haemodynamic compromise
  • Pericarditis affection +/- tamponade
122
Q

Describe how rapid effusion and slow effusion affects the haemodynamic impact in cardiac tamponade

A

Rapid effusion - if accumulation occurs acutely it can lead to rapid development of haemodynamic compromise (i.e., hypotension)

Slow effusion - if accumulation occurs slowly, it may take several weeks before clinical symptoms and features of haemodynamic compromise occur

123
Q

What is cardiac tamponade

A

A life-threatening condition that causes compression of heart from pericardial content

124
Q

Describe the aetiology of cardiac tamponade

A

Common causes
- Pericarditis
- Tuberculosis
- Iatrogenic
- Trauma
- Post pacemaker implantation or post cardiac surgery
- Malignancy

Uncommon causes
- Connective tissue disease
- Radiation-induced
- Uraemia
- Post-myocardial infraction
- Aortic dissection
- Bacterial infection

125
Q

Describe the investigations for cardiac tamponade

A
  • Echocardiography (urgent)
  • ECG
  • CXR
  • CT/MRI
  • Pericardiocentesis
126
Q

What are the findings on ECG for cardiac tamponade

A
  • Sinus tachycardia
  • Electrical alternans
  • Low voltage of the QRS complex
  • PR segment depression
127
Q

Describe the ECG appearance for cardiac tamponade

A

In large pericardial effusion the QRS complexes may be small and vary in height from heart to beat (electrical alternates)

128
Q

Clinical features of cardiac tamponade

a) Symptoms

b) Signs

A

a)
- Chest pain
- Dysponea
- Collapse
- Fatigue
- Confusion
- Peripheral oedema (subacute)

b)
“Tamponade quadrad’
1. Hypotension
2. Tachycardia
3. Raised JVP
4. Pulsus paradoxus (fall in blood pressure > 10mmHg during inspiration)

+ Pericardial friction rub
+ other features of shock: cool extremities, peripheral cyanosis, reduced urine output
+ Beck’s triad (hypotension, muffled heart sound, raised JVP

129
Q

Describe the management off cardiac tamponade

A

Urgent needed pericardiocentsis (drainage of the pericardial fluid via a needle)

130
Q

Give 4 complications of pericardiocentesis

A
  • Pneumothorax
  • Damage to the myocardium
  • Coronary vessels
  • Thrombus
  • Arrhythmias/cardiac arrest
  • Damage to the peritoneum
131
Q

What is restrictive pericarditis

A

Progressive thickening, fibrosis and calcification of the pericardium, which limits the filling of the chambers

132
Q

Describe the aetiology of restrictive pericarditis

A
  • Most commonly idiopathic (but can be due to any cause of pericarditis)
  • Post-cardiac surgery
  • Radiotherapy
  • Connective tissue disorders
  • Tuberculosis
  • Others: malignancy, trauma, uraemia pericarditis
133
Q

Describe the pathophysiology of restrictive pericarditis

A

Chronic damage to the pericardium causes thickening, fibrosis and calcification of the sac. This makes it relatively inelastic and unable to expand optimally during diastole

As the disease progresses, venous return is impeded as the right atrium fails to expand leading to a fluid overload state

Eventually there is reduced ventricular and stroke volume, leading to a low cardiac output

134
Q

Clinical features of constrictive pericarditis

a) Symptoms

b) Signs

A

a)
- Fatigue
- Breathlessness
- Peripheral oedema

b)
- Kussmaul’s sign (raised JVP on inspiration)
- Pericardial knock
- Raised JVP
- Pulsus paarodxus
- Signs of heart failure (peripheral oedema, ascites, hepatomegaly)
- Pleural effusion
- Cachexia (in severe disease)

135
Q

Describe the 1st line and 2nd line investigations for constrictive pericarditis

A

1st line
- Echocardiogram (diagnostic)
- ECG
- CXR

2nd line
- CT chest (to evaluate pericardial calcification associated with constrictive pathology and can identify extent of pericardial effusion)
- Coronary angiogram (if echocardiography is non-diagnostic and before pericardiectomy to visualise the coronary vessel anatomy)

136
Q

Describe the management of constrictive pericarditis

A

Pericardiectomy - indicated in both acute and chronic pericardial constriction

Medical therapy - NSAIDs, colchicine and/or steroids can be used to control symptoms if unsuitable or as a bridge to surgery

137
Q

Describe the prognosis of restrictive pericarditis

A
  • Curable if diagnosed early
  • Long-term prognosis after medical therapy alone is poor
  • Life expectancy is also poor in untreated children and patients with acute onset of symptoms
138
Q

What is syncope?

A

A transient loss of consciousness due to global cerebral hypoperfusion

139
Q

Describe the causes of transient loss of conscious

A
  1. Non-traumatic
    - Global cerebral hypoperfusion
    - NOT due to global cerebral hyoperfusion –> epilepsy, psychogenic
  2. Traumatic (head injury)
140
Q

Describe the characteristics of syncope due to global cerebral hypoperfuion causes vs not due to global cerebral hypoperfuon

A

Global cerebral hypoperfusion characterised by:
- Rapid onset
- Short duration
- Spontaneous complete recovery

NOT due to global cerebral hypoperfusion is NOT characterised by:
- rapid onset
- Short duration
- Spontaneous complete recovery

141
Q

Give the 4 causes of syncope and how common they are

A

Reflex - 60%

Orthostatic - 15%

Cardiac - 15%

Unknown - 10%

142
Q

Describe the characteristics of reflex syncope

A
  • Can occurs at any age (but more common in younger patients and less common in elderly)
  • Occurs in response to a trigger (emotional stress or real/threatened/imagine injury due to e.g., pain, sight of blood or having blood taken)
  • Mainly occurs when standing up
  • There is usually a prodrome lasting between 30 seconds to several minutes where the patient feels fatigue, yawns, feels hot, sweat, nauseous and has dimming of their vision followed by a loss of consciousness)
  • During the episode the patient appears pale and diaphoretic
  • Sometime the prodrome is vert short or not present at all
  • Loss of consciousness is brief (30 to a few minutes)
  • Occasionally there is a seizure-like activity (happens because of lack of blood flow to brain)
  • Recovery is rapid although patient can feel fatigued afterwards
143
Q

What are the 3 types of reflex syncope?

A
  1. Vasovagal
  2. Situational
  3. Carotid sinus syndrome
144
Q

Give 4 common triggers of vasovagal syncope

A
  1. Prolong standing
  2. Pain
  3. Fear
  4. Having blood taken
145
Q

Describe the pathophysiology of vasovagal syncope

A

In vasovagal syncope messages from higher brain centres (triggered by pain or emotion or from the heart triggered by prolonged standing) go to the brainstem and trigger an abnormal reflex consisting of withdrawal of sympathetic activity.

This leads to peripheral vasodilatation and hypotension - this is call the vasopressor effect. Also leads to increase vagal parasympathetic activity which results in slowing of the heart, called the cardioinhibitory effect

These cause cerebral hypoperfusion and syncope

146
Q

What are the symptoms of vasovagal syncope?

A
  • Fainting
  • Feeling warm
  • Nausea
  • Skin feels cold and clammy
  • Ringing in ears
  • Dizziness or light-headedness
  • Blurred or tunnel vision
  • Turning pale
147
Q

Situation syncope is a form of reflex syncope caused by specific triggers. Describe the specific triggers

A

GI tract
- micro nutrition syncope: fainting occurring shorter after or during urination

GI
- Defaecation

Respiratory
- Coughing
- Laughing

148
Q

Describe the carotid sinus reflex

A

Increase in BP –> carotid baroreceptors stimulated by arterial stretch –> send messages to brain stem

This leads to:

  • Decrease sympathetic activity to ventricular muscle –> decreased contractility and decreased SV -> decreased CO (BP = TPR X CO)
  • Decreased sympathetic activity to venous system causing increased compliance
  • Decreased peripheral arterial vascular resistance –> decreased BP (BP = TPR X CO)
  • Increase parasympathetic activity (decrease HR and contractility) –> decrease CO –> decrease BP ( BP = TPR x CO)
149
Q

What is the carotid sinus massage and what is a normal response to it?

A

A simple bedside test to test the carotid sinus reflex

A normal response is a slight drop in HR and/or BP

150
Q

Carotid sinus syndrome

a) What is it?

b) Who does it occurs in the most?

c) Name 3 triggers

d) What can help it?

A

a) Syncope without warning and exaggerated carotid sinus massage response with reproduction of syncope

b) Occurs in older patients (particularly men)

c) Head turning, shaving, tight collar

d) Pacing can help if carotid massage causes a decrease in HR

151
Q

What is orthostatic hypotension?

A

Drop in systolic blood pressure ≥ 20mmHg (or ≥ 10mmHg DPB) ≤ 3 mins of standing

OR

Drop in systolic blood < 90mmHg on standing

152
Q

Describe the pathophysiology of orthostatic hypotension

A

Standing from a Supine position causes 10-15% of our blood volume to be redistributed to the abdomen and lower limbs thereby reducing venous return –> undefilled LV –> reduced stroke volume –> reduced cardiac output –> and without compensatory mechanisms there would be a drop in BP

Underfilled LV –> vigorous LV contraction –> Inappropriately activates stretch receptors in LV (this overrides baroreceptor reflex) –> decrease sympathetic activity and increase parasympathetic activity –> vasodilatation and decrease HR –> BP decreased

153
Q

What causes orthostatic hypotension?

A

Drugs
- anti-hypertensives
- anti-anginals
- anti-BPH
- anti-depressants
- anti-psychotics
- anti-parkisonian
- alcohol

Hypovolaemia - dehydration, Addison’s disease

Autonomic failure - Primary (Parkinson’s) and secondary (ageing, diabetes)

154
Q

Why are elderly patients more susceptive to hypotensive effects of drugs?

A

Because of reduced baroreceptor sensitivity, decreased cerebral blood flow, renal sodium wasting and impaired thirst mechanism that develops with ageing

155
Q

When is orthostatic symptoms worse and when are they better?

A

Symptoms are worse
- On standing
- In the morning
- After meals
- After exercise
- In hot environments

Symptoms are better
- When lying down or sitting

156
Q

Describe the management of reflex syncope and orthostatic hypotension

A
  1. Reassurance, education, and lifestyle changes
    - Let patient know it’s benign and not life threatening
    - Patient should be educated about triggers and prodromal symptoms of feeling hot, sweaty, light-headedness and to sit down if possible and about counter-pressure manoeuvres
    - Advise patients to drink 6 pints of water daily and increase salt intake (to 120 mol/day)
  2. Counter-pressure manoeuvres
    - Crossing the leg and squeezing them together
    - Squatting
    - Linking the fingers together without letting them go
157
Q

Describe the management of reflex syncope and orthostatic hypotension

A
  1. Reassurance, education, and lifestyle changes
    - Let patient know it’s benign and not life threatening
    - Patient should be educated about triggers and prodromal symptoms of feeling hot, sweaty, light-headedness and to sit down if possible and about counter-pressure manoeuvres
    - Advise patients to drink 6 pints of water daily and increase salt intake (to 120 mol/day)
  2. Counter-pressure manoeuvres
    - Crossing the leg and squeezing them together
    - Squatting
    - Linking the fingers together without letting them go
  3. If symptoms due to low BP –> give drugs that increase BP
    - Fludrocortisones
    - Midodrine
  4. Stop/reduce BP lowering drugs
  5. If symptoms due to slow HR then consider pacing (selected patients with reflex syncope)
158
Q

When should you consider pacing in patients with reflex syncope?

A

In recurrent syncope despite medical therapy (particularly if little warning and associated injury + bradycardia or systole pauses)

159
Q

What causes cardiac syncope

A

Arrhythmia (2/3)
- Bradycardia –> sinus node disease, AV block
- Tachycardia –> VT, SVT

Strutural (1/3)
- Cardiac –> Aortic stenosis, ACS, cardiomyopathy
- Vascular –> PE, aortic dissection

160
Q

What are the 6 key point in the history taking of syncope

A

Before
- Provoking factors
- Posture
- Prodrome (symptoms beforehand)
- PMH, DH, FH

During
- Passer-by account

After
- Post event

161
Q

Describe the investigations for syncope

A
  • ECG
  • ECHO (if structural heart disease is suspected)
  • Cardiac rhythm monitoring
    1. Holter
    2. Loop recorder
  • Tilt test
162
Q

What are high risk features on ECG of syncope

A
  • Signs of acute MI
  • Arrhythmias e.g., sinus node disease, complete heart block, VT
  • Conduction disease e.g., LBBB, Left ventricular hypertrophy, Q wave
  • Structural heart disease e.g., channelopathy, long QT interval
163
Q

Describe the role of an implantable loop recorder in syncope

A
  • Useful in diagnosis of recurrent syncope of unknown origin
  • Suggests arrhythmic syncope when high risk arrhythmias are detected in an asymptomatic patient
  • Can still be useful in patient without an arrhythmic cause for syncope by excluding arrhythmia at the time of the patient’s symptoms
164
Q

a) Describe the tilt table test

b) Describe the role of the tilt table test in syncope

c) What is a positive test?

A

a) Patient starts off supine, gradually tilt to upright position

b)
- Used to provoke reflex syncope in laboratory setting
- Used to confirm a diagnosis of reflex syncope in a patient with syncope of unknown cause (where reflex syncope is suspected but not proven)
- Not used much

c)
Decrease systolic BP (vasopressor response) or decrease heart rate (cardioinhibitory response) or decrease BP and decrease HR (mixed response)

Medicine - Year 2 (27 decks)

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