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Y3 MedEd > Cardiac causes of SOB > Flashcards

Cardiac causes of SOB Flashcards

1
Q

Which valvular disease is most common through HF

A

Mitral regurgitation

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2
Q

Which is the biggest sign of CHF

A

Breathlessness with pulmonary oedema due to abnormal salt and water retention

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3
Q

Three ways chronic low CO LHF manifests

A

Valvular pathology
Heart muscle pathology
Systemic pathology

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4
Q

What are the valvular causes of low CO LHF (3)

A

Aortic stenosis,
Aortic Regurgitation
Mitral Regurgitation

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5
Q

What are the heart muscle causes of low CO LHF (4)

A

Ischaemic Heart Disease
Cardiomyopathy
Myocarditis
Arrhythmias (AF)

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6
Q

What are the systemic causes of low CO LHF (3)

A 
Hypertension, 
 Amyloidosis
 Drugs (e.g. cocaine, alcohol, chemotherapeutics - eg doxorubicin)
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7
Q

Which drugs can cause low CO LHF (4)

A

cocaine, alcohol, BBs*, chemotherapeutics - eg doxorubicin

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8
Q

How does aortic stenosis cause low CO LHF

A

causes excessive afterload. Basically the ventricle has to push harder to eject blood from a stenosed aortic valve. (NB: afterload = the pressure the heart must work against to eject blood during systole)

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9
Q

How does aortic regurg cause low CO LHF

A

There is increased pressure in the LV due to the regurgitant blood form the aorta to the LV (the LV in addition to having to pump the normal volume of blood, has to pump the regurgitant blood as well). These changes lead to cardiac remodeling (dilatation, hypertrophy) leading to heart failure.

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10
Q

How does mitral regurg cause low CO LHF

A

If significant (moderate to severe) MR is present, the Left Ventricle must work harder to keep up with the body’s demands for oxygenated blood. Over time, the heart muscle and circulatory system undergo a series of changes to maintain this increased demand – due to mechanical overload the LV overtime can become, hypertrophied, fibrotic, dilated and scarred, ending up with an impaired myocardial function. This can lead to LHF (mitral regurgitation increases preload)

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11
Q

How does hypertension cause LHF

A

increases afterload. LV has to push harder in order to push blood against high systemic pressures. This over time puts strain in the LV leading to LHF.

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12
Q

How does amyloidosis cause LHF

A

In amyloidosis, an abnormal protein called amyloid builds-up in tissues and organs. If amyloid gets deposited in the heart, the heart becomes increasingly stiff and eventually the pumping function deteriorates

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13
Q

Three ways chronic low CO RHF manifests

A

LHF
Lungs
Heart valves

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14
Q

What are the lung causes of low CO RHF (3+3 examples)

A 
Pulmonary HTN (can lead to cor pulmonale)
 PE
Chronic Lung Disease (interstitial lung disease, pulmonary fibrosis, cystic fibrosis)
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15
Q

What is cor pulmonale

A

Enlargement and failure of RV due to increased pressure in the lungs/vascular resistance

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16
Q

Which interstitial lung diseases can cause low CO RHF (3)

A

interstitial lung disease, pulmonary fibrosis, cystic fibrosis

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17
Q

Which valvular diseases can cause low CO RHF (2)

A

TR

Pulmonary valve Disease

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18
Q

How do chronic lung diseases cause heart failure

A

Chronic lung disease can result in chronic hypoxia: The pulmonary vasculature results to chronic hypoxia by vasoconstriction. This increases vascular resistance and and results in increased pulmonary arterial pressure. The right heart reacts to this by remodeling (hypertrophy and dilatation). Over time it can lead to RHF.

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19
Q

What can cause high output HF (8)

A

NAP MEALS

Nutritional (B1: thiamine)
Anaemia
Pregnancy
Malignancy (multiple myeloma)
Endocrine (hyperthyroidism)
AV malformations
Liver cirrhosis
Sepsis
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20
Q

How does high CO HF present

A

High output HF presents initially with features of RHF and then LHF becomes more apparent

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21
Q

What are the main symptoms of RHF due to

A

RHF: symptoms due to fluid accumulation in the periphery

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22
Q

What are the main symptoms of LHF due to

A

LHF: respiratory symptoms due to fluid accumulation in the lungs

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23
Q

Which HF gives pulmonary symptoms

A

LHF

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24
Q

Which HF gives systemic symptoms

A

RHF

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25
Q

LHF symptims (6)

A 
Exertional dyspnea
Orthopnoea (SOB when lying flat)
Paroxysmal nocturnal dyspnea –
      PND (attacks of SOB at night)
Fatigue
Nocturnal Cough (+/- pink frothy 
      sputum)
Wheeze
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26
Q

Which murmurs are seen in LHF

A

Murmur (AS, MR, AR)

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27
Q

Which heart sounds are added in LHG

A

S3 Gallop rhythm

S4 in severe HF

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28
Q

What signs are seen in the lung in LHF (2)

A

Fine end-inspiratory crackles at lung bases (pulmonary oedema)
Wheeze (cardiac asthma)

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29
Q

What are the signs of LHF (10 heart 2 lung)

A 
↑HR, ↑RR
Irregularly Irregular heart beat 
Pulsus alternans
Displaced apex beat
S3 Gallop rhythm
S4 in severe HF
Murmur (AS, MR, AR)
Fine end-inspiratory crackles at lung bases (pulmonary oedema)
Wheeze (cardiac asthma
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30
Q

RHF symptoms (7)

A 
Swelling (ankles, facial engorgement, ascites)
Weight gain (due to oedema)
Fatigue
Reduced exercise tolerance
Anorexia
Nausea
Nocturia
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31
Q

Main 3 causes of raised JVP

A

RHF
Tricuspid regurg
Constrictive pericarditis

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32
Q

Signs of RHF (8)

A 
Face: face swelling
Neck: ↑JVP
Heart/Chest: TR murmur, ↑HR, ↑RR
Abdomen: Ascites, hepatomegaly
Other: pitting oedema in ankles & sacrum
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33
Q

HF Ix

A

ECG
FBC, U&Es, LFTs, TFTs BNP
CXR TTE - DIAGNOSTIC

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34
Q

What is HFrEF also known as and what does it suggest

A

systolic HF

Indicates inability of the ventricle to contract normally

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35
Q

What is HFpEF also known as and what does it suggest

A

diastolic HF

Indicates inability of the ventricle to relax and fill normally

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36
Q

What is a normal EF

A

50-70%

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37
Q

What % is HFrEF

A

<40%

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38
Q

What % is HFpEF

A

> 50%

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39
Q

CXR features of HF (5)

A 
Alveolar oedema
B-lines (kerley)
Cardiomegaly
Dilated upper lobe vessels
Effusion (pleural, transudative)
40
Q

Conservative Mx of HF (3)

A

smoking cessation, weight management (exercise), diet (reduce salt intake)

41
Q

Medical Mx of chronic HF (4)

A

ACE inhibitors (enalapril): should be given to ALL pts with LV dysfunction as it improves survival and slows down progression.
BBs (carvedilol, bisoprolol): reduce O2 demand on the heart. All patients with CHF should receive a BB once established on an ACEi – improve survival & synergistic effects with ACEi.
Diuretics (furosemide, chlorothiazide, spironolactone): use if evidence of fluid retention, monitor electrolytes (spironolactone can cause hyperkalaemia)
Digoxin: +inotrope (increases heart contractility), helps improve symptoms but does NOT increase overall survival.

42
Q

What can lead to acute decompensation of chronic heart failure (5)

A

MI, Arrhythmias, Infection, Hypo/hyperthyroidism, Uncontrolled HTN

43
Q

What are the 2 ways of getting acute HF

A

Decompensation of previous chronic HF

Acute Coronary Syndrome

44
Q

What additional heart sound is present with what rhythm in acute HF

A

S3 gallop rhythm

45
Q

What is heard in the lungs in acute HF

A

Fine end inspiratory crackles

46
Q

What is pulses alternans

A

is alternating strong and weak pulses. In left ventricular systolic failure, the ejection fraction is low, which causes a reduced stroke volume and an increased end-diastolic volume. The high end-diastolic volume, following one weak contraction, stretches the ventricular muscle fibres which, by Starling’s law, leads to a stronger subsequent contraction.

47
Q

Acute HF Mx

A

Sit patient up
High-flow Oxygen via non rebreathe mask (Target SpO2 = 94-98%)
Furosemide 40-80mg IV
(GTN infusion evidence of pulmonary oedema AND SBP > 90mmHg)
Consider CPAP (if sats are dropping)
Treat cardiogenic shock if BP < 90mmHg with positive inotropes (e.g. dobutamine)

48
Q

What is the target SpO2 when managing acute HF

A

94-98%

49
Q

Which mask do we use when managing acute HF

A

Non-rebreathe

50
Q

What do you need to monitor and why when giving furosemide during acute HF

A

Monitor U & Es bc you can get hypokalaemia

51
Q

When is GTN indicated in acute HF

A

GTN infusion evidence of pulmonary oedema AND severe hypertension or angina

52
Q

When is CPAP indicated in acute HF

A

Consider CPAP (if sats are dropping)

53
Q

How do you treat cardiogenic shock if BP < 90mmHg in acute HF

A

with positive inotropes (e.g. dobutamine)

54
Q

Complications of HF (4)

A

Pleural effusion
Renal failure (long standing HF can lead to hypoperfusion)
Acute exacerbations
Death

55
Q

Prognosis of HF

A

50% of severe HF pts die within 2 years

In AHF, in hospital mortality: 2-20%

56
Q

Define cardiomyopathy

A

A group of diseases in which the myocardium becomes structurally and functionally abnormal (in the absence of coronary artery disease, valvular disease and congenital heart disease)

57
Q

What is the difference between primary and secondary cardiomyopathy

A

Primary: Confined to myocardium

Secondary: Part of a systemic disease

58
Q

What are the 4 types of cardiomyopathy

A

HCM = Hypertrophic cardiomyopathy, DCM = Dilated cardiomyopathy, ARVC = Arrhythmogenic right ventricular cardiomyopathy, RCM = Restrictive cardiomyopathy

59
Q

History of a cardiomyopathy (3 (+4 specific symptoms))

A 
Symptoms of HF
SOB on exertion
Fainting 
Dizziness
Fatigue

Sudden death often 1st presentation
Family History

60
Q

What is dilated cardiomyopathy associated with (5)

A 
Alcohol
Post viral
AI
Haemochromatosis
genetic
61
Q

Symptoms of dilated cardiomyopathy (6)

A

HF (dyspnoea, fatigue,

arrhythmias, ankle swelling, ascites)

62
Q

Signs of dilated cardiomyopathy (5)

A

↑ JVP
TR, MR murmur
S3
Displaced apex beat

63
Q

Which valvular pathology is seen in dilated cardiomyopathy

A

TR, MR murmur

64
Q

What extra heart sound is heard in dilated cardiomyopathy

A

S3

65
Q

What Ix for dilated cardiomyopathy

A

CXR

Echo

66
Q

What happens in hypertrophic cardiomyopathy

A

The heart thickens inwards. The
thickened ventricle may block the
Blood flow out of the ventricle

67
Q

What happens in dilated cardiomyopathy

A

the Ventricles enlarge, become dilated,
Weaken and can’ t contact
effectively.

68
Q

What proportion of HOCM is congenital and what is its mode of inheritance

A

50% is familial (Autosomal dominant)

69
Q

Symptoms of HOCM

A

Angina, dyspnea on exertion, palpitations, syncope

Often sudden cardiac death might be the 1st presentation

70
Q

Signs of HOCM (4)

A 
Ejection systolic murmur
Jerky carotid pulse
Double apex beat
S4
Apex beat NOT displaced
71
Q

Difference between apex beat in HOCM and dilated cardiomyopathy

A

NOT displaced in HOCM and double in HOCM

72
Q

ECG findings of HOCM (3)

A

ECG findings:
Q waves
Left axis deviation
Signs of Left Ventricular Hypertrophy

73
Q

LVH by voltage criteria (3)

A

Deep S in V1/2
Tall R in V5/6
S in V1 + R in V5 or V6 ≥ 7 large squares

74
Q

Ix for HOCM

A

ECG

Echo

75
Q

What happens in restrictive cardiomyopathy

A

The
ventricles become abnormally rigid and lack the flexibility to
expand as the ventricles fill with blood

76
Q

Causes of restrictive cardiomyopathy (3)

A

Idiopathic, familial,

Systemic (e.g. infiltrative)

77
Q

What is Kussmaul’s sign

A

Kussmaul’s sign (paradoxical rise in JVP in inspiration due to restricted filling of the ventricles)

78
Q

Which cardiomyopathy has Kussmaul’s sign

A

Restrictive

79
Q

Symptoms of restrictive cardiomyopathy (4)

A

Asymptomatic or

symptoms of HF (dyspnea, fatigue)

80
Q

What is arrhythmogenic right ventricular cardiomyopathy

A

There is progressive fatty and fibrous replacement

of the ventricular myocardium.

81
Q

Aetiology of ARVC

A

inherited (AD)

82
Q

Presentation of ARVC

A

Can be asymptomatic initially or present

with symptoms of arrhythmias especially during exercise

83
Q

Define constrictive pericarditis

A

chronic
inflammation of the pericardium with
thickening and scarring

84
Q

Causes of constrictive pericarditis (6)

A

Idiopathic
Infectious (TB, Bacterial, Viral)
Acute pericarditis
Cardiac surgery and radiation

85
Q

S/s of constrictive pericarditis (4)

A

(resembles
Restrictive cardiomyopathy):
RHF symptoms (dyspnea, ↑ JVP, fluid congestion)
Kussmaul’s sign

86
Q

Ix for constrictive pericarditis (3)

A

CXR: pericardial calcification
ECHO: ↑ pericardial thickness
Cardiac CT/MRI

87
Q

What happens in constrictive pericarditis

A

the pericardium, the sac that encloses the heart becomes inflamed. There are 2 layers of pericardium (visceral and parietal). These 2 layers are normally distensible with a small space between them containing fluid. However, in constrictive pericarditis they become inflamed and they fuse.
Basically it acts as if there was a box around the heart.

88
Q

Bacterial causes of constrictive pericarditis (2)

A

staphylococci and pseudomonas

89
Q

Viral causes of constrictive pericarditis (2)

A

coxsackievirus, hepatitis

90
Q

What is myocarditis

A

Inflammation of the myocardium

91
Q

Causes of myocarditis (5)

A

Infectious, Drugs, cocaine,

metals, radiation

92
Q

What drugs have been associated with myocarditis (4)

A

penicillins, cephalosporins, digoxin antiepileptic

93
Q

Presentation of myocarditis (5)

A

Flu-like prodrome
Positional chest pain (worse when lying down)
SOB
Palpitations

94
Q

Why does CK rise in myocarditis and not pericarditis

A

Because myocarditis is inflammation of cardiac muscle

95
Q

Ix myocarditis (3)

A 
ECG: non-specific ST changes, T-wave abnormalities
Cardiac biomarkers (CK &amp; troponins)
Endomyocardial biopsy (diagnostic but not routinely performed)
96
Q

Which valvular pathologies lead to pan systolic murmur (2)

A

Tricuspid and mitral regurgitation

97
Q

Which diseases is Kussmaul’s sign usually seen in

A

Seen in constrictive pericarditis & restrictive cardiomyopathy

Y3 MedEd (34 decks)

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