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Cardiology Flashcards

1
Q

What is included in acute coronary syndromes?

A

Unstable angina, NSTEMI, STEMI

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2
Q

What is the common mechanism/pathology behind ACS?

A

rupture or erosion of fibrous cap of a coronary artery atheromatous plaque with subsequent formation of a platelet-rich clot and vasoconstriction produced by platelet-release of serotonin and thromboxane A2.

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3
Q

What is the difference between NSTEMI and unstable angina?

A

NSTEMI produces myocardial damage leading to an increase in serum Troponin and Creatine Kinase. Both may have ECG changes such as T wave inversion or ST-segment depression but can also be normal

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4
Q

What is Troponin and Creatine Kinase?

A

Troponin: a protein found in the muscle unit of skeletal and cardiac muscle, which separates the Actin from the Myosin during relaxation.
Creatine Kinase: An enzyme involved in breaking down Creatine into creatine phosphate which there are three isomers: CK-MM (skeletal), CK-MB (cardiac), CK-BB (smooth/non-muscle)

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5
Q

What are the key clinical findings of a STEMI?

A

ST elevation
ECG changes
Raised Troponin and creatine kinase

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6
Q

What are the typical presenting features of ACS?

A 
chest pain (may be absent in elderly/diabetic): unrelieved by nitrates or rest, at rest, worsening pain on minimal exertion with known angina
collapse, arrhythmia or new onset HF (silent MI's)
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7
Q

What are the 3 important acute differentials for chest pain?
What are 3 other differentials?
What is the 1 key differentiating factor for each?

A

Acute:
Pulmonary embolism - sudden onset SOB,
aortic dissection - sudden tearing chest pain,
pericarditis - pain improves on leaning forward

Other: Angina - relieved by GTN, MSK pain - tender to touch, GORD - associated with eating/lying flat

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8
Q

What are the symptoms of ACS?

A 
Acute central chest pain lasting>20 mins
N+V
Sweatiness
Dyspnoea
Palpitations
Pulmonary oedema
epigastric pain 
Post-operative hypotension or oliguria
Confusion
Stroke
Diabetic Hyperglycaemic state
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9
Q

What are the clinical signs of ACS?

A 
Distress
Anxiety
Pallor
Sweatiness
increase or decrease in pulse 
increase or decrease in blood pressure
4th heart sound

Also: HF signs, pansystolic murmur, low grade fever, pericardial friction rub

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10
Q

What are the non-modifiable risk factors for ACS?

A

Age - older
Gender - male
family history or IHD - MI in 1st degree relative <55yo
Personal history of IHD

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11
Q

What are the modifiable risk factors for ACS?

A 
Smoking
HTN
DM
Hyperlipidaemia
obesity
sedentary lifestyle
cocaine use

Controversial: stress, type A personality, LVH, increase fibrinogen, hyperinsulinaemia, increased homocysteine levels, ACE genotype

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12
Q

What are the initial tests when ACS is suspected?

What does each test show in ACS

A

ECG - hyperacute T waves, ST elevation, new LBBB (within hours of transmural infarction), T wave inversion, pathological Q waves (hours to days post event)
CXR - cardiomegaly, pulmonary oedema, widened mediastinum (aortic rupture)
FBC, U+E, glucose, lipids
Troponin - T+I, acute rise and subsequent fall, repeated 6 hours after the initial test. Peaks 24-48 hours and returns to baseline over 5-14 days.
Consider Creatine Kinase and Myoglobin but less sensitive/specific than troponin

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13
Q

What is the management of ACS without ST-segment elevation?

A

Oxygen if <90% sats
Morphine 5-10mg IV + metoclopromide 10mg IV
Fondaparinux 2-5mg
GTN

Aspirin 300mg + 2nd antiplatelet agent: clopidogrel, ticragrelor or prasugrel
Beta-blocker - metoprolol 50mg/12hr if HTN

Consider ACE-inhibitor and statins (lipid management)

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14
Q

What scoring system can be used to assess a patients mortality risk in ACS without ST-segment elevation?

A

GRACE score: age, heart rate, SBP, serum creatinine, cardiac arrest, ST-segment deviation, abnormal cardiac enzymes, Killip class (signs/symptoms)

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15
Q

What further treatment should be considered in a high mortality risk patient with none ST-segment elevated ACS?

A

Infusion of GPIIb/IIIa antagonist such as Tirofiban

Refer for angiography as inpatient

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16
Q

What is the management of ACS with ST-elevation (STEMI)?

A

12 lead ECG
IV access, FBC, U+E, glucose, cardiac enzymes, lipids

Morphine 5-10mg IV +metoclopramide 10mg IV
Oxygen if <95% sats
Nitrates - GTN
Aspirin 300mg

PCI if within 120mins of chest pain onset

If not -> fibrinolysis with Alteplase, Reteplase, Tenecteplase with heparin

Long term:
beta-blocker - bisoprolol 5mg
ACE-inhibitor - lisinopril 2.5mg if SBP>120
2nd antiplatelet - ticagrelor, prasugrel, clopidogrel
High risk: Tirofiban

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17
Q

What is the definition of preload?

A

the volume of fluid after filling, prior to contraction. It produces an initial pressure which stretches the ventricle. Linked with but not the same as end-diastolic volume

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18
Q

What is the definition of contractility?

A

the ability of the ventricles to contract. Expressed on the Frank-Starling curve

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19
Q

What is the definition of afterload?

A

the force at which the ventricles must overcome in order to eject blood. Not the same as blood pressure!!

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20
Q

What is the definition of end-diastolic volume?

A

the volume in the ventricles prior to contraction (systole)

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21
Q

What is the definition of end-systolic volume?

A

the volume of blood in the ventricles at the end of systole just prior to filling

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22
Q

What links preload with end-diastolic volume and afterload with arterial pressure? Explain the link with the Frank-Starling law

A

Laplace’s law. Explains the eventual decline of ventricular contractility as seen with increasing EDV on the Frank-Starling. Shows that as ventricular volume increases it becomes more inefficient until this surpasses the added force of contraction in the myocytes

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23
Q

What are the commonest causes of heart failure n the developed world and Africa?

A

Developed world: IHD

Africa: HTN

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24
Q

What is the pathology behind IHD heart failure?

A

Damaged myocardium causes ventricular dysfunction (decreased contractility) and decreased cardiac output so myocardial work increases in order to maintain the cardiac output.

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25
Q

What is the pathology behind valvular causes of heart failure?

A

valvular disease increases the resistance to ventricular outflow (increased afterload) leading to hypertrophy and ultimately ventricular compliance and contractility are affected. This leads to either a diastolic or systolic dysfunction.

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26
Q

What is the pathology behind myopathic causes of heart failure?

A

Cardiomyopathy causes thinning of the ventricle walls or restriction of ventricular relaxation. Depending on the exact cause, either the ventricle contractility may be affected or the compliance can be affected.

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27
Q

What is the pathology behind systemic hypertension causing heart failure?

A

causes an increase in afterload leading to hypertrophy, which eventually reduces ventricular compliance (dilated ventricle) and contractility (Frank-Starling).

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28
Q

What is the pathology behind Cor Pulmonale leading to heart failure?

A

Chronic pulmonary hypertension causes increased afterload in the right ventricle which causes right ventricular hypertrophy and eventually right heart failure due to decreased compliance and contractility.

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29
Q

What are the 5 main mechanisms which contribute to compensating for heart failure?

A

activation of sympathetic nervous system, renin-angiotensin system, natriuretic peptides, ventricular dilatation, ventricular remodelling.

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30
Q

What are two equations that equal cardiac output?

A

HRxSV

MAP/TPR

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31
Q

What does activation of the sympathetic nervous system cause as a consequence?

A

Improved ventricular function by increasing HR and contractility: constriction of peripheral venous vessels leads to increased central venous flow, which increases preload, which increases ventricular function via the Frank-Starling mechanism

Also causes arteriolar constriction which increases afterload, which eventually causes a decrease in cardiac output due to the increased afterload

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32
Q

What does the activation of the renin-angiotensin system cause?

A

decreased renal perfusion leads to activation of the RAAS which then causes salt and water retention via increasing aldosterone and also vasoconstriction by the increase in angiotensin II. Both of these lead to increased BP.

Fluid retention leads to increased venous pressure, and hence increased preload. Eventually, the fluid retention leads to peripheral and pulmonary oedema. The oedema leads to dyspnoea

The arteriolar constriction caused by the angiotensin II leads to increased afterload

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33
Q

What does the release of natriuretic peptides cause?

A

Have diuretic, natriuretic and hypotensive properties. This causes decreased cardiac load by decreasing preload and afterload

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34
Q

What causes the dilatation of the ventricles?

A

decreased ejection of blood during systole leads to increased end-diastolic volume, which then increases the stretch of the myocardial fibres. This increases the contractility of the ventricle up to a point.

At this point, the tension required in the myocardium to contract exceeds the myocytes ability so venous pressure increases causing pulmonary and peripheral congestion and oedema

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35
Q

What are the 3 parts of ventricular and remodelling and what do they collectively cause?

A

Hypertrophy
Loss of myocytes
increased interstitial fibrosis

Leads to decreased contractility of the ventricles

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36
Q

ISCHAEMIC HEART DISEASE

What is the presentation of angina caused by?

A

transient myocardial ischaemia

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37
Q

What differentiates stable and unstable angina?

A

stable: brought on by exertion, relieved by rest
unstable: increased frequency/severity, minimal exertion or at rest

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38
Q

How does angina present typically?

A

central chest tightness or heaviness which may radiate to one/both arms, neck, jaw or teeth.

Associated with dyspnoea, nausea, sweatiness or faintness.

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39
Q

What can precipitate an angina attack?

A

emotion, cold weather, heavy meals

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40
Q

What are the types of angina?

A

stable - induced by effort, relieved by rest
unstable - increased frequency/severity, induced by minimal effort or at rest, increased the risk of MI
decubitus - associated with lying flat
Variant/Prinzmetals - coronary artery spasm

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41
Q

What is the gold standard test for angina?

A

CT coronary angiography

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42
Q

What is the most common cause of angina? What are 4 of the other causes?

A

Atheroma

Anaemia, aortic stenosis, tachyarrhythmias, HCM, arteritis/small vessel disease

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43
Q

What additional tests to CT angiography would you request in angina and why?

A

ECG - normal/ST depression, T wave inversion
FBC - ?anaemia
U&E’s - prior to ACE inhibitors
LFT’s - prior to statins
Lipid profile
Thyroid function test - ?hypo/hyperthyroid
HbA1c and fasting glucose - ?diabetes

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44
Q

What is an acronym to remember the management of angina? What does each letter stand for?

A 
RAMP
R - Refer to cardiology if unstable
A - advise them about diagnosis, management and when to call the ambulance
M - medical treatment
P - procedural/surgical intervention
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45
Q

What are the three main aims of the medical management of angina

A

immediate symptom relief
long term symptom relief
secondary prevention

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46
Q

What is given for immediate symptom relief of angina?

A

Glyceryl Trinitrate (GTN) spray/sublingual tablets

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47
Q

What is the management for long term symptom relief of angina?

A 
beta blockers (bisoprolol 5mg OD) or calcium channel blockers (amlodipine 5mg OD) first line
second line: beta blocker and calcium channel blockers combined

others: isosorbide mononitrate, ivabradine, nicorandil, ranolazine

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48
Q

What is used for the secondary prevention of angina?

A

Aspirin 75mg OD
Atorvastatin 80mg OD
ACE inhibitor - ramipril etc

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49
Q

What are the two procedural/surgical interventions offered for angina treatment?

A

Percutaneous coronary intervention - balloon dilatation or stent
Coronary artery bypass graft - from great saphenous vein

50
Q

What are 5 of the 7 causes for mitral stenosis?

A 
rheumatic heart disease, 
congenital, 
mucopolysaccharides, 
endocardial fibroelastosis, 
malignant carcinoid
prosthetic valve
infective endocarditis
51
Q

How does mitral stenosis usually present?

A

dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis, chronic bronchitis-like picture, new-onset AF

52
Q

Describe what is heard on auscultation in mitral stenosis?

A

mid-diastolic, low pitched (rumbling) murmur heard best with the patient lying on their left side on expiration
may have an opening snap prior to murmur
loud S1

53
Q

What is the cause of the malar flush that may be seen in mitral stenosis?

A

the back pressure of blood into the pulmonary system causes a rise in CO2 and vasodilation

54
Q

What structural changes take place as a result of mitral stenosis?

A

left atrial hypertrophy

55
Q

What tests are most useful in suspected mitral stenosis and what would they show?

A

ECG - p-mitrale (if sinus), RVH, progressive right axis deviation
CXR - LA enlargement (double shadow in right cardiac silhouette), pulmonary oedema, mitral valve calcification
Echo - diagnostic: valve orifice <1cm2/m2 body surface area

56
Q

When is cardiac catheterisation indicated in mitral stenosis?

A

previous valvotomy, signs of other valve diseases, angina, severe pulmonary hypertension, calcified mitral valve

57
Q

What is the management of mitral stenosis?

A

rate control + warfarin if in AF
diuretics (decrease preload and pulmonary venous congestion)

balloon valvoplasty

open mitral valvotomy/valve replacement

58
Q

What additional measures should be taken in managing mitral stenosis with suspected infective endocarditis or subacute bacterial endocarditis?

A

prophylactic antibiotics: amoxicillin+gentamicin

59
Q

What additional measures should be taken in managing mitral stenosis with suspected rheumatic heart disease?

A

oral penicillin in rheumatic in order to avoid recurrent rheumatic heart disease,

60
Q

What are the complications associated with mitral stenosis?

A

pulmonary hypertension
emboli
pressure from LA on local structures - hoarseness (recurrent laryngeal nerve), dysphagia (oesophagus), bronchial obstruction, (?)infective endocarditis

61
Q

What are five of the six main causes of mitral regurgitation? What are three of the remaining causes?

A 
functional - LV dilatation
annular calcification - elderly
rheumatic fever
infective endocarditis
mitral valve prolapse
IHD - ruptured chordae tendinae, papillaru muscle dysfunction/rupture

connective tissue disorders - Ehlars-Danlos syndrome, Marfan’s syndrome
cardiomyopathy
congenital
appetite suppresants - fenfluramine, phantermine

62
Q

How does mitral regurgitation present?

A

dyspnoea, fatigue, palpitations, infective endocarditis-like picture, congestive cardiac failure-like picture

63
Q

What is found on auscultation in mitral regurgitation?

A

pansystolic, high pitched
radiates to the left axilla

may hear an S3, loud P2, soft S1

Also a displaced, hyperdynamic apex beat
RV heave

64
Q

What 3 tests are useful in mitral regurgitation? What would each test show?

A

ECG - AF, p-mitrale if in sinus rhythm, LVH
CXR - big LA and LV, mitral valve calcification, pulmonary oedema
Echo - assesses LV function, trans-oesophageal = severity+suitability for repair instead of replacement, doppler = size+site of regurgitant jet

65
Q

What test/intervention confirms the diagnosis of mitral regurgitation?

A

Cardiac catheterisation

66
Q

What is the management of mitral regurgitation?

A

if AF: control rate and warfarin
diuretics
Surgery repair/replace

67
Q

What can mitral valve prolapse occur with?

A

ASD, PDA, cardiomyopathy, Turner’s syndrome, Marfan’s syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, WPW

can occur alone

68
Q

What is the typical presentation of mitral valve prolapse?

A

asymptomatic
or atypical chest pain + palpitations
some have autonomic dysfunction as well - anxiety, panic attack, syncope

69
Q

Describe what is heard on auscultation in mitral valve prolapse?

A

mid-systolic click or late systolic murmur - the timing of click varies with standing or squatting etc.

70
Q

What are the complications associated with mitral valve prolapse?

A

mitral regurgitation, cerebral emboli, arrhythmias, sudden death

71
Q

What are the tests that should be ordered for specifically for mitral valve prolapse? what would they show?

A

Echo - diagnostic, visualise mitral valve prolapse

ECG - may show T wave inversion in inferior leads

72
Q

What is the management for mitral valve prolapse?

A

beta blockers for chest pain and palpitations

surgery may be needed in severe mitral regurgitation

73
Q

What are the 3 main causes of aortic stenosis?

A

senile calcification, congenital (bicuspid valve, William’s syndrome), rheumatic heart disease

74
Q

What is the classic triad in which aortic stenosis usually presents?

A

angina, syncope and dyspnoea

75
Q

what other symptoms besides the classical triad can present in aortic stenosis?

A

dizziness; faints; systemic emboli; sudden death

76
Q

What are the clinical signs of aortic stenosis besides the murmur?

A

slow rising pulse with a narrow pulse pressure
heaving/LV heave
non displaced, heaving apex beat
aortic thrill

77
Q

what is heard on auscultation in aortic stenosis?

A

ejection systolic murmur, high pitched, possible ejection click
crescendo-decrescendo character
heard at the base, left sternal edge and aortic area
radiates to the carotids
S4 may be heard - due to a stiff ventricle causing firmer atrial contraction

78
Q

What tests should be done in aortic stenosis and what would each show?

A

ECG - p-mitrale, LVH with strain pattern, poor R wave progression, LBBB or complete AV block
CXR - LVH, calcified aortic valve, post-stenotic dilatation of ascending aorta
Echo - diagnostic, doppler estimates gradient across the valve which approximates severity

Cardiac catheter - assess gradient, LV function, coronary artery disease but increased risk of emboli

79
Q

What is an important differential when considering aortic stenosis?

A

hypertrophic cardiomyopathy

80
Q

What is the management of aortic stenosis?

A

surgical repair with valve replacement

81
Q

What is aortic sclerosis and how does it differ from aortic stenosis?

A

senile degeneration of the valve

ejection systolic murmur but with no carotid radiation and normal pulse and S2

82
Q

What are the acute causes of aortic regurgitation?

A

infective endocarditis, ascending aortic dissection, chest trauma

83
Q

What are 10 of the 12 chronic causes of aortic regurgitation?

A

congenital, connective tissue disorders (Marfan’s, Ehlers-Danlos), rheumatic fever, Takayasu arteritis, rheumatoid arthritis, SLE, pseudoxanthoma elasticum, appetite suppressants, seronegative arthritides (ank spond, Reiter’s syndrome, psoriatic arthropathy), HTN, osteogenesis imperfecta, syphilitic aortitis

84
Q

How does aortic regurgitation present?

A

exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea

also: palpitations, angina, syncope, CCF

85
Q

What are the clinical signs of aortic regurgitation?

A

collapsing pulse, wide pulse pressure, displaced hyperdynamic apex beat

high pitched early diastolic murmur - heard best on expiration with the patient sat forward

86
Q

What specific signs are seen in aortic regurgitation that would suggest a hyperdynamic circulation?

A

Quincke’s sign - capillary pulsation of nail beds
De Musset’s sign - head nodding with each heartbeat
Duroziez’s - femoral systolic murmur heard when pressure applied 2cmm proximally
Traube’s - ‘pistol shot’ sound over femoral arteries
Corrigan’s - carotid pulsation

87
Q

What tests would you order in aortic regurgitation and what would each show?

A

ECG - LVH
CXR - cardiomegaly, dilated ascending aorta, pulmonary oedema
Echo - diagnostic

Cardiac catheter - assess the severity of the lesion, the anatomy of aortic root, LV function, CAD, other valve diseases

88
Q

What is the management of aortic regurgitation?

A

main goal is to decrease systemic HTN
ACE-I
echo every 6-12 months
Surgery for valve replacement ideally prior to singificant ventricular dysfunction

89
Q

What valvular diseases typically cause ventricular or atrial hypertrophy?

A

mitral stenosis - left atrial

aortic stenosis - left ventricular

90
Q

What valvular diseases typically cause ventricular or atrial dilatation?

A

mitral regurgitation - left atrial

aortic regurgitation - left ventricular

91
Q

What are 5 of the 6 causes of tricuspid regurgitation?

A

functional (RV dilatation), rheumatic fever, infective endocarditis, carcinoid syndrome, congenital (ASD, AV canal, Ebstein’s anomaly ie downward displacement of tricuspid valve), drugs (ergot-derived dopamine agonist, fenfluramine)

92
Q

How does tricuspid regurgitation present?

A

fatigue, hepatic pain on exertion, ascites, oedema

also, dyspnoea and orthopnoea if LV dysfunction is the cause

93
Q

What are the clinical signs of tricuspid regurgitation?

A

giant v waves and prominent y descent in JVP
RV heave
pansystolic murmur heard best at LLSE on inspiration
pulsatile hepatomegaly, jaundice, ascites

94
Q

What is the management of tricuspid regurgitation?

A

treat underlying cause
diuretics
digoxin
ACE-I

ultimately - valve replacement

95
Q

What are the causes of tricuspid stenosis?

A

rheumatic fever - the disease is not normally isolated to tricuspid
congenital
infective endocarditis

96
Q

How doe tricuspid stenosis present?

A

fatigue, ascites, oedema

97
Q

What are the clinical signs of tricuspid stenosis?

A

giant a wave and slow y descent in JVP
opening snap, mid-diastolic murmur heard at LSE on inspiration
AF can occur

98
Q

How is tricuspid stenosis diagnosed and managed?

A

echo

diuretics and surgical repair

99
Q

What are the causes of pulmonary stenosis?

A

congenital - usually (Turner’s, Noonan’s, Williams, ToF, rubella)
rheumatic fever
carcinoid syndrome

100
Q

How does pulmonary stenosis present?

A

dyspnoea, fatigue, oedema, ascites

101
Q

What are the clinical signs of pulmonary stenosis?

A 
dysmorphic faces (congenital causes)
prominent a wave in JVP, RV heave, ejection click (mild), ejection systolic murmur which radiates to left shoulder, widely split S2
102
Q

What tests should be done in pulmonary stenosis and what would they show?

A

ECG - RAD, p-pulmonale, RVH, RBB
CXR - prominent main, right or left pulmonary arteries causes by post-stenotic dilatation

cardiac catheterisation is diagnostic

103
Q

What is the management of pulmonary stenosis?

A

pulmonary valvuloplasty or valvotomy

104
Q

What are the causes of pulmonary regurgitation?

A

any cause of pulmonary hypertension can cause pulmonary regurgitation

105
Q

What is heard on auscultation in pulmonary regurgitation?

A

a decrescendo murmur in early diastole best heard at LSE

106
Q

What are the three clinical syndromes seen in heart failure? What are some causes of each?

A

Left ventricular systolic dysfunction - IHD, valvular HD, HTN

Right ventricular systolic dysfunction - secondary to LVSD, primary/secondary pulmonary HTN, RV infarct, adult congenital HD

Diastolic heart failure - (HF w/ normal ejection fraction) RCM, constrictive pericarditis, tamponade

107
Q

What are the symptoms of heart failure?

A

exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue

108
Q

What are the signs of heart failure?

A

Cardiomegaly w/ displaced apex beat, 3rd/4th heart sound, raised JVP, tachycardia, hypotension, crepitations, pleural effusion, ankle oedema, ascites, tender hepatomegaly, cool peripheries, pulsus alternans, narrow pulse pressure

109
Q

What are the four stages of the New York Heart Association?

A

I - no limitation
II - mild limitation, comfortable at rest, normal physical activity produces dyspnoea and fatigue
III - marked limitation, comfortable ay rest, minor physical activity produces marked HF symptoms
IV - symptoms at rest, exacerbated with physical activity

110
Q

What are the Framingham criteria for CCF?

A

> 2 major or 1 major +>2 minors

Major: paroxysmal nocturnal dyspnoea, crepitations, S3 gallop, cardiomegaly, increased CVP, weight loss >4.5kg in 5 days post tx, neck vein dilatation, acute pulmonary oedema, hepatojugular reflux

Minor: bilateral ankle oedema, dyspnoea on ordinary exertion, tachycardia >120bpm, decreased vital capacity by 1/3 from max recorded, nocturnal cough, hepatomegaly, pleural effusion

111
Q

What are the signs of heart failure seen on chest x-ray?

A

ABCDE - alveolar oedema (Bat’s wings), Kerley B lines, Cardiomegaly, Dilated prominent upper lobe vessels, pleural effusion

112
Q

What investigations should be ordered and what would each show?

A

ECG - ventricular hypertrophy

Bloods: FBC - anaemia, LFT - alteration suggests hepatic congestion, Glucose - for DM, U&E - for baseline prior to diuretics + ACE inhibitors, TFT - AF + elderly

Echo - assess ventricular systolic and diastolic function

Others - cardiac catheter, PET, MRI, CXR

113
Q

What is the treatment for chronic heart failure?

A

diuretics eg furosemide

reduced ejection fraction:
ACE inhibitor - lisinopril (ARB)
then add beta blocker - bisoprolol (start low, go slow)
add mineralocorticoid receptor antagonist - eplerenone
surgical intervention - implantable cardioverter defibrillators

if preserved ejection fraction:
loop diuretics - furosemide

114
Q

What is the treatment for acute heart failure?

A

sit patient upright + oxygen
IV access + monitor ECG + tx any arrhythmias
investigations whilst treating
diamorphine 1.25-5mg IV slowly
Furosemide 40-80mg IV slowly
GTN spray/tabs (not if SBP<90)
investigations, history and examinations
if SBP>100 - start nitrate infusion, keep SBP>90 - Isosorbide mononitrate 2-10mg/hr IV
If pt worsening - further furosemide, consider CPAP, increase nitrate infusion
If SBP<100 tx as cardiogenic shock -> ICU

115
Q

What are the clinical symptoms of acute pulmonary oedema?

A

dyspnoea
orthopnoea
pink frothy sputum

116
Q

What are the clinical signs of acute pulmonary oedema?

A

distressed, pale, sweaty, increased pulse, tachypnoea, pulsus alternans, increased JVP, fine lung crackles, triple/gallop rhythm, wheeze (cardiac asthma), usually sitting up + leaning forward

117
Q

What investigations should be ordered for acute pulmonary oedema and what will each of them show?

A

CXR - cardiomegaly, signs of pulmonary oedema: look for shadowing (usually bilateral), small effusions at costophrenic angles, fluid in the lung fissures and Kerley B lines
ECG: signs of MI, dysrhythmias
U&E, troponin, ABG
Consider echo
Plasma BNP if diagnosis in question - high negative predictive value

118
Q

How should acute pulmonary oedema be managed immediately?

A
  1. Oxygen and sit patient upright
  2. IV access and monitor ECG, treat any arrhythmias
  3. start investigations whilst continuing treatment
  4. diamorphine 1.25-5mg IV slowly, caution in liver failure and COPD
  5. furosemide 40-80mg IV slowly - larger doses required in renal failure
  6. GTN spray 2 puff s/l, don’t give if systolic <90mmHg
  7. Necessary investigations, examination and history
  8. if systolic bp >100mmHg, start nitrate infusion, aim to keep systolic above 90mmHg
  9. if the patient is worsening: further furosemide dose, consider CPAP, if systolic BP <100mmHg then treat as cardiogenic shock and refer to ICU
119
Q

How should acute pulmonary oedema be managed once the patient has been stabilised?

A

daily weights - aim for a reduction of 0.5kg/day, check obs QDS
Repeat CXR
change to oral furosemide or bumetanide
if a large dose of loop diuretic needed then consider adding in a thiazide
if LVEF <40% -> ACE-I
if LVEF <35% -> beta-blocker and spironolactone
biventricular pacing/cardiac transplantation?
consider digoxin +/- warfarin, especially in AF

120
Q

What are two common exacerbating medications of chronic heart failure?

A

NSAIDs - fluid retention

verapamil - negative inotrope

Cardiology (8 decks)

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