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Core Conditions - Cardiovascular > Cardiac Shortness of Breath > Flashcards

Cardiac Shortness of Breath Flashcards

1
Q

What causes breathlessness?

What are the 3 reasons why this might occur?

A

breathlessness is caused by insufficient oxygen delivery to respiring tissues

  • not enough oxygen reaching the lungs
    • e.g. asthma, COPD, anaphylaxis
  • not enough oxygen getting into the blood
    • ​e.g. issues with exchange surfaces leading to V/Q mismatch
    • e.g. pulmonary oedema, pulmonary fibrosis
  • not enough oxygen reaching the rest of the body
    • ​e.g. due to issues with the heart, anaemia or shock
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2
Q
A

C - right heart failure secondary to tricuspid regurgitation

  • infective endocarditis is a common reason for someone younger presenting with a HF picture
  • swelling of the ankles / face and raised JVP are signs of RIGHT HF
  • pansystolic murmur is associated with tricuspid regurgitation
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3
Q

What is the definition of heart failure?

A
  • the failure of the heart to maintain the cardiac output required to meet the body’s demands
    • CO = the volume of blood pumped by the heart in one minute
  • this means that not enough oxygen reaches the rest of the body
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4
Q

What are the 3 different ways in which heart failure can be classified?

A
  • acute or chronic
  • left or right
  • high output state or low output state
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5
Q

What is cardiac output measured relative to?

A

cardiac output is measured relative to the body’s metabolic demands

  • sometimes CO can be normal, but there is still HF present as it is not enough to meet the body’s demands at that time
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6
Q

How is chronic and acute heart failure defined?

What causes acute HF?

A

Chronic heart failure:

  • long term condition in which the heart fails to maintain an adequate circulation for the needs of the body

Acute heart failure:

  • rapid onset symptoms and signs of heart failure, which require urgent management
  • this is caused by acute coronary syndrome OR a decompensation of chronic HF
  • the patient is usually gasping for breath
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7
Q

What are the only 2 causes of acute heart failure?

A
  • acute coronary syndrome
    • e.g. an MI that damages the myocardium
  • decompensation of chronic heart failure
    • ​chronic heart failure suddenly gets worse for some reasion
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8
Q

Why is it important to distinguish right and left heart failure from each other?

What is congestive heart failure?

A
  • the signs and symptoms of HF depend on which side of the heart is affected
  • congestive heart failure occurs when BOTH LHF + RHF are present
  • in CHF, the patient usually has LHF to begin with, pressure then backs up into the pulmonary circulation and into the right heart, leading to subsequent RHF
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9
Q

What is the difference between low output state and high output state heart failure?

A

Low output state:

  • the heart fails to pump in response to normal exertion
  • this leads to reduced cardiac output

High output state:

  • cardiac output is normal, but the body has higher metabolic demands
  • e.g. pregnancy, anaemia, hyperthyroidism
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10
Q

What are the 3 different aetiologies of chronic left HF?

What are examples of these?

A

Valvular:

  • there is a problem with the aortic or mitral valves
    • aortic stenosis
    • aortic regurgitation
    • mitral regurgitation

Muscular:

  • the heart muscle is not performing properly, which reduces CO
    • ​ischaemic heart disease
    • cardiomyopathy
    • myocarditis
    • arrhythmias (AF)

Systemic:

  • hypertension
  • amyloidosis
  • drugs - e.g. cocaine, chemo
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11
Q

How can hypertension eventually lead to chronic left HF?

A
  • the left heart pumps blood into the aorta
  • if there is systemic hypertension, there is increased pressure within the aorta
  • there is increased afterload, which can cause pressure to back up into the left heart and eventually cause HF
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12
Q

What are the 2 possible categories of causes of chronic right HF?

What are examples of each?

A

Lungs:

  • pulmonary hypertension (cor pulmonale) is the main cause of RHF
  • it can also be caused by pulmonary embolism and chronic lung disease
    • e.g. cystic fibrosis or interstitial lung disease

Valvular:

  • problems with the tricuspid and pulmonary valves
    • ​tricuspid regurgitation
    • pulmonary valve disease
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13
Q

What mnemonic can be used to remember the causes of chronic high output HF?

A
  • caused by conditions that require a higher CO, which puts a strain on the heart
  • NAP MEALS
  • N - nutritional (B1 / thiamine deficiency)
  • A - anaemia
  • P - pregnancy
  • M - malignancy
  • E - endocrine (hyperthyroidism)
  • A - AV malformations
  • L - liver cirrhosis
  • S - sepsis
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14
Q

Why can anaemia and hyperthyroidism lead to chronic high output heart failure?

A
  • in anaemia, the blood is not carrying enough oxygen so the heart needs to pump harder to compensate for this
  • in hyperthyroidism, there is an increased basal metabolic rate, which increases metabolic demands of the body
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15
Q

What types of symptoms result from left and right HF and why?

A

LHF:

  • fluid accumulates in the lungs, leading to respiratory symptoms

RHF:

  • fluid accumulates in the peripheries, leading to swelling signs
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16
Q

What are the respiratory symptoms associated with LHF?

A
  • dyspnoea
    • paroxysmal nocturnal dyspnoea (PND)
    • exertional dyspnoea
    • orthopnoea
  • nocturnal cough (+/- pink frothy sputum)
    • ​pink frothy sputum is more associated with acute left HF
  • fatigue
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17
Q

What are good questions to ask for assessing SOB, orthopnoea and PND?

A

Shortness of breath:

  • How far are you able to walk before getting breathless?
  • How many flights of stairs?

Orthopnoea:

  • Have you noticed anything making the SOB worse?
  • What about lying down?

PND:

  • Do you ever wake up at night gasping for air?
  • How many pillows do you sleep with at night? Has this changed recently?
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18
Q

What are the heart signs associated with LHF?

A
  • increased HR and RR
  • irregularly irregular heartbeat
  • pulsus alternans
  • displaced apex beat
  • S3 gallop rhythm
  • S4 in severe heart failure
  • murmur in AS, MR and AR
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19
Q

What is pulsus alternans?

A

a physical finding on arterial pulse waveform that shows alternating strong and weak beats

it indicates left ventricular systolic impairment

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20
Q

What are the lung signs associated with LHF?

A
  • fine end-inspiratory crackles at the lung bases which suggests pulmonary oedema
  • wheeze which suggests cardiac asthma
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21
Q

What are the symptoms of RHF?

A
  • fatigue
  • reduced exercise tolerance
  • anorexia
  • nausea
  • nocturia
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22
Q

What are the signs associated with RHF?

A
  • facial swelling
  • elevated JVP
  • increased HR and RR
  • ascites and/or hepatomegaly
  • ankle and sacral pitting oedema
  • there may be a murmur present if there is an underlying valve disorder
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23
Q

What are the bedside, bloods and imaging investigations performed in HF?

A
  • ECG is performed at the bedside
    • this rules out more acute causes, like MI
  • FBC, U&Es, LFTs, TFTs and BNP
    • FBC rules out anaemia
    • TFTs rule out hyperthyroidism
  • imaging involves CXR and transthoracic echo (TTE)
    • TTE is the gold standard for diagnosing HF
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24
Q

Is BNP sensitive or specific?

How is it used in diagnosing HF?

A
  • if BNP is low then HF is very unlikely
  • if BNP is high then a TTE is performed to diagnose HF
  • BNP is sensitive but not specific
    • it is not specific as it can be raised by other heart conditions
    • HF can only be diagnosed by TTE
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25
Q

What is the diagnostic test for HF?

A

transthoracic echocardiogram (TTE) coupled with doppler

doppler allows you to visualise blood flow

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26
Q

Why can TTE with doppler be used to diagnose HF?

A
  • visualising the structure and function of the heart may show the cause of HF
    • e.g. underlying valve abnormalities
  • can calculate the ejection fraction (EF)
    • ​this is the % of blood present in the LV that gets pumped during systole
    • normal is 50-70%
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27
Q

What type of HF is present if ejection fraction (EF) is < 40%?

What does this indicate?

A

HF with reduced ejection fraction

(previously known as systolic HF)

this indicates the inability of the ventricle to contract normally

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28
Q

What type of heart failure is present when EF > 50%?

What does this indicate?

A

HF with preserved ejection fraction

(previously called diastolic HF)

this indicates the inability of the ventricle to relax and fill normally

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29
Q

What are the A - E signs of heart failure on CXR?

A
  • A - alveolar oedema
  • B - Kerley B lines
  • C - cardiomegaly
  • D - dilated upper lobe vessels + diverted upper lobe
  • E - effusion (transudative pleural effusion)
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30
Q

What criteria are used to make a clinical diagnosis of HF?

A
  • clinical diagnosis can be made using the Framingham Criteria
  • there must be 2+ majors OR 1 major + 2 minors
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31
Q

What are the 4 stages involved in the management of chronic HF?

A
  • treat the underlying cause
  • treat the exacerbating factors
  • lifestyle modifications
    • smoking cessation
    • reduced salt diet
    • increased exercise
  • drugs (ABD):
    • ​ACE inhibitors
    • beta-blockers
    • diuretics
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32
Q

When are ACE inhibitors given to patients?

What are examples and what can be done if they are not tolerated?

A
  • given to all patients with LV dysfunction
  • enalapril, perindopril, ramipril
  • can switch to ARBs if they are not tolerated
    • this is usually due to a chronic cough
33
Q

Why are beta-blockers given in heart failure?

What are examples?

A
  • they slow down the heart and reduce the oxygen demand
  • e.g. bisoprolol, carvedilol
  • they are particularly useful when someone has a coronary artery disease that has resulted in heart failure
34
Q

When are diuretics given in heart failure?

What are the different types?

A
  • these are given when there is evidence of fluid retention
  • loop diuretics - e.g. furosemide
  • aldosterone antagonists - e.g. spironolactone
35
Q

What medication is considered in Afro-Caribbean patients with HF?

A

hydralazine + nitrates

36
Q

What is cardiac resynchronisation therapy?

A

it aims to improve the timings of contraction of the atria and ventricles

37
Q

What are the 5 steps in the emergency management of acute HF?

A
  • sit the patient upright
  • give 60 - 100% oxygen
  • give IV diamorphine 2.5 - 5 mg
  • GTN infusion
  • give IV furosemide 40 - 80 mg
    • this is a loop diuretic which causes massive diuresis and helps get rid of fluid
38
Q

What mnemonic can be used to remember the stages of treatment of acute HF?

A

DMONS

  • D - diuretics
  • M - morphine
  • O - oxygen
  • N - nitrates
  • S - sit-up

(not in order)

39
Q

What are the potential complications of acute HF?

A
  • respiratory failure
  • renal failure (due to hypoperfusion)
  • acute exacerbations
  • death
40
Q

What is the prognosis like for acute heart failure?

A
  • prognosis is very poor and worse than most malignancies
  • 50% of patients with severe HF die within 2 years
41
Q
A

E - alveolar oedema

this is due to LHF causing pulmonary oedema

42
Q

What is the definition of cardiomyopathy?

Who tends to be affected?

A
  • a group of diseases in which the myocardium becomes structurally and functionally abnormal
  • in the absence of coronary artery diease, valvular disease and congenital heart disease
  • it can affect young people
43
Q

What is the difference between primary and secondary cardiomyopathy?

A
  • primary is confined to the myocardium
  • secondary is part of a systemic disease
44
Q

What are the 4 types of cardiomyopathy?

A
  • normal
  • dilated
  • hypertrophic
  • restrictive
45
Q

What happens in dilated cardiomyopathy?

A
  • the ventricle becomes larger
  • the ventricle walls become thinner and weaker
  • the dilated ventricle is less effective at pumping blood
46
Q

What happens in hypertrophic cardiomyopathy?

A
  • cardiac muscle has hypertrophied and become thicker
  • the thickened myocardium is stiffer and less effective at pumping blood
  • the excess cardiac muscle also invades into the ventricle and blocks it off slightly
47
Q

What happens in restrictive cardiomyopathy?

A
  • there is the same amount of muscle present as in a normal heart
  • the myocardium has become infiltrated with something which makes it more rigid and less effective at pumping blood
  • a stiff myocardium also has impaired relaxation, so the ventricle cannot fill with as much blood
48
Q

What are the key points to pick up in the history of someone with a cardiomyopathy?

A
  • they often have symptoms of heart failure
    • SOB on exertion
    • fainting
    • fatigue
  • sudden death is often the first presentation
  • there is often a family history
49
Q

What is a very important question to ask in the history if cardiomyopathy is suspected?

A
  • ” Is there any family history of sudden, unexplained cardiac death at a young age?*
  • i.e. under 50 “*
50
Q

What signs might be present on examination of someone with a cardiomyopathy?

A

signs of heart failure:

  • respiratory crackles
  • heart murmurs
  • S3 and S4
51
Q

What investigations are performed in someone with suspected cardiomyopathy?

A
  • there is no single diagnostic test for all types
  • ECHO is performed as this is good at visualising the structure of the heart
  • bloods can be done, including BNP
  • as well as CXR, ECG, cardiac catheterisation, stress test
52
Q

What is the pathophysiology involved in dilated cardiomyopathy?

What “Law” is relevant to explain the consequence of this?

A
  • ventricles enlarge and become dilated
  • walls of ventricles become thinner and weaker, meaning contractions are not as effective
    • cardiac output is reduced
  • the Law of Laplace states that increased radius** leads to **reduced ventricular pressure
    • reduced ventricular pressure results in reduced CO
53
Q

What are the risk factors for dilated cardiomyopathy?

A
  • alcohol
  • can occur post-viral infection
  • genetic
  • haemochromatosis
54
Q

How does someone with dilated cardiomyopathy present?

A
  • they will have signs and symptoms of heart failure
  • displaced apex beat
    • this occurs as the ventricles become larger, shifting the position of the apex
  • tricuspid regurgitation / mitral regurgitation murmur
  • S3 heart sound
55
Q

What investigations are performed in dilated cardiomyopathy and what might they show?

A
  • CXR shows a large, globular heart
  • Echo will show a dilated ventricle
56
Q

What is involved in the pathophysiology of hypertrophic cardiomyopathy?

A
  • the myocardium thickens inwards
  • increased stiffness of thicker muscle affects the pumping
  • thickened muscle disrupts electrical conduction and causes arrhythmia
57
Q

What happens if hypertrophic cardiomyopathy progresses to hypertrophic obstructive cardiomyopathy (HOCM)?

A
  • the thickened myocardium starts to obstruct the outflow of blood from the ventricle
58
Q

What is particularly important to ask about in hypertrophic cardiomyopathy?

What is the classical presentation?

A
  • family history is very important as 50% cases are familial (autosomal dominant)
  • classic presentation is of a young, healthy person who suddenly collapses and often dies
59
Q

What are the symptoms associated with obstructive cardiomyopathy?

A
  • usually asymptomatic
  • sudden cardiac death is often the first presentation
  • may have some cardiac symptoms:
    • angina
    • dyspnoea on exertion
    • palpitations
    • syncope
60
Q

What are the signs associated with obstructive cardiomyopathy?

A
  • ejection systolic murmur
    • the muscle is obstructing the outflow of blood
    • this is the same murmur as aortic stenosis as blood is struggling to leave the ventricle
  • jerky carotid pulse
  • double apex beat but not displaced
    • muscle is growing inwards, so the apex is not displaced as the position of the ventricle is not changing
  • S4 heart rhythm
61
Q

What investigations are performed in hypertrophic cardiomyopathy?

What would they show?

A

ECG:

  • Q waves
  • left axis deviation
  • signs of left ventricular hypertrophy

Echo:

  • shows ventricular hypertrophy
    • this is asymmetrical septal hypertrophy
62
Q

What is involved in the pathophysiology of restrictive cardiomyopathy?

A
  • the ventricles become abnormally rigid and lose flexibility
  • there is impaired ventricular filling during diastole
  • reduced preload leads to reduced blood flow (cardiac output) and backing up of blood
63
Q

What are the different causes of restrictive cardiomyopathy?

A
  • the infiltrative “osis” diseases:
    • sarcoidosis
    • amyloidosis
    • haemochromatosis
  • familial
  • idiopathic
  • it is rarer than dilated or hypertrophic cardiomyopathy
64
Q

What are the signs and symptoms associated with restrictive cardiomyopathy?

A
  • it is asymptomatic or has heart failure symptoms
  • often there are RHF signs:
    • raised JVP
    • S3 heart sound
    • ascites / peripheral oedema
    • hepatomegaly
  • Kussmaul’s sign is positive
    • ​this is a paradoxical rise in the JVP during inspiration
    • (usually the JVP should fall during inspiration)
65
Q

What happens in arrhythmogenic right ventricular cardiomyopathy?

A
  • there is progressive fatty and fibrous replacement of the ventricular myocardium
  • this is an inherited autosomal dominant condition
66
Q

What happens in Takotsubo cardiomyopathy?

A
  • there is sudden weakening of the heart muscle after a significant stressor
  • also known as “broken heart syndrome”
67
Q

What is constrictive pericarditis?

A
  • chronic inflammation of the pericardium with thickening and scarring
  • the pericardium is the outer sheath that acts to protect the heart
  • when it is damaged, it becomes less compliant, meaning the heart is less able to fill with blood and maintain CO
68
Q

What are the causes of constrictive pericarditis?

A
  • idiopathic
  • infectious - TB, bacterial and viral
  • acute pericarditis
  • cardiac surgery & radiation
69
Q

What are the signs and symptoms of constrictive pericarditis?

A
  • they are similar to restrictive cardiomyopathy
    • the difference is which layer of the heart is being affected
  • RHF presentation with raised JVP and oedema
  • Kussmaul’s sign present
70
Q

What investigations are performed in constrictive pericarditis and what do they show?

A
  • CXR shows pericardial calcification
    • this is not very specific as other heart diseases can cause calcification
  • Echo shows increased pericardial thickness
    • ​this can differentiate it from restrictive cardiomyopathy
  • cardiac CT / MRI
71
Q

What is the difference in the way in which restrictive cardiomyopathy and constrictive pericarditis can be “cured”?

A
  • restrictive cardiomyopathy does not have a cure
  • constrictive pericarditis can be cured via surgical removal of the pericardium in a pericardectomy
72
Q

What is myocarditis?

What can cause this?

A
  • it is inflammation of the myocardium
    • sometimes called inflammatory cardiomyopathy
    • it can affect the electrical conduction system, leading to arrhythmias

Causes:

  • infections
    • ​Coxsackie B virus is the most common cause in Europe
    • if this infection becomes severe, it can lead to dilated cardiomyopathy
  • drugs - especially cocaine
  • metals
  • radiation
73
Q

What are the signs and symptoms associated with myocarditis?

A
  • flu-like prodrome
    • relevant as a virus is the most likely cause
  • chest pain that is worse when lying down
  • shortness of breath
  • palpitations
74
Q

What investigations are performed in myocarditis and what might these show?

A

ECG:

  • this shows non-specific ST and T wave changes

Cardiac biomarkers:

  • creatinine kinase and troponin
  • these are measured to ensure it is the myocardium that is diseased and not the pericardium
    • CK and troponin will NOT be raised in pericarditis

Endomyocardial biopsy:

  • this is diagnostic but not routinely performed
    • only really performed when suspected myocarditis is not responsive to treatment
75
Q
A

B - arrhythmia

  • this is a classic example of hypertrophic cardiomyopathy, which causes obstructed blood flow from the heart
  • in HOCM with obstructed blood flow, there is usually some sort of warning symptoms
    • e.g. breathlessness on exertion / fainting
  • arrhythmia is the most common reason for death from HOCM as the thick muscle does not conduct electricity as well
    • ​the heart will start beating abnormally and then suddenly stop
76
Q
A

E - chest pain

this is an acute presentation with chest pain that is worse when lying down

77
Q
A

A - Echo

  • if a patient has features of RHF and Kussmaul’s sign, this could be either restrictive cardiomyopathy or constrictive pericarditis
  • the only way to tell the difference between these conditions is with Echo
78
Q
A

Core Conditions - Cardiovascular (6 decks)

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