Cardiology Flashcards
1
Q
What is included in acute coronary syndromes?
A
Unstable angina, NSTEMI, STEMI
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.
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
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)
5
Q
What are the key clinical findings of a STEMI?
A
ST elevation
ECG changes
Raised Troponin and creatine kinase
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)
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
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
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
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
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
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
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)
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)
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
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
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
18
Q
What is the definition of contractility?
A
the ability of the ventricles to contract. Expressed on the Frank-Starling curve
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!!
20
Q
What is the definition of end-diastolic volume?
A
the volume in the ventricles prior to contraction (systole)
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
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
23
Q
What are the commonest causes of heart failure n the developed world and Africa?
A
Developed world: IHD
Africa: HTN
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.
25
What is the pathology behind valvular causes of heart failure?
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.
26
What is the pathology behind myopathic causes of heart failure?
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.
27
What is the pathology behind systemic hypertension causing heart failure?
causes an increase in afterload leading to hypertrophy, which eventually reduces ventricular compliance (dilated ventricle) and contractility (Frank-Starling).
28
What is the pathology behind Cor Pulmonale leading to heart failure?
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.
29
What are the 5 main mechanisms which contribute to compensating for heart failure?
activation of sympathetic nervous system, renin-angiotensin system, natriuretic peptides, ventricular dilatation, ventricular remodelling.
30
What are two equations that equal cardiac output?
HRxSV
| MAP/TPR
31
What does activation of the sympathetic nervous system cause as a consequence?
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
32
What does the activation of the renin-angiotensin system cause?
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
33
What does the release of natriuretic peptides cause?
Have diuretic, natriuretic and hypotensive properties. This causes decreased cardiac load by decreasing preload and afterload
34
What causes the dilatation of the ventricles?
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
35
What are the 3 parts of ventricular and remodelling and what do they collectively cause?
Hypertrophy
Loss of myocytes
increased interstitial fibrosis
Leads to decreased contractility of the ventricles
36
ISCHAEMIC HEART DISEASE
What is the presentation of angina caused by?
transient myocardial ischaemia
37
What differentiates stable and unstable angina?
stable: brought on by exertion, relieved by rest
unstable: increased frequency/severity, minimal exertion or at rest
38
How does angina present typically?
central chest tightness or heaviness which may radiate to one/both arms, neck, jaw or teeth.
Associated with dyspnoea, nausea, sweatiness or faintness.
39
What can precipitate an angina attack?
emotion, cold weather, heavy meals
40
What are the types of angina?
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
41
What is the gold standard test for angina?
CT coronary angiography
42
What is the most common cause of angina? What are 4 of the other causes?
Atheroma
Anaemia, aortic stenosis, tachyarrhythmias, HCM, arteritis/small vessel disease
43
What additional tests to CT angiography would you request in angina and why?
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
44
What is an acronym to remember the management of angina? What does each letter stand for?
```
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
```
45
What are the three main aims of the medical management of angina
immediate symptom relief
long term symptom relief
secondary prevention
46
What is given for immediate symptom relief of angina?
Glyceryl Trinitrate (GTN) spray/sublingual tablets
47
What is the management for long term symptom relief of angina?
```
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
48
What is used for the secondary prevention of angina?
Aspirin 75mg OD
Atorvastatin 80mg OD
ACE inhibitor - ramipril etc
49
What are the two procedural/surgical interventions offered for angina treatment?
Percutaneous coronary intervention - balloon dilatation or stent
Coronary artery bypass graft - from great saphenous vein
50
What are 5 of the 7 causes for mitral stenosis?
```
rheumatic heart disease,
congenital,
mucopolysaccharides,
endocardial fibroelastosis,
malignant carcinoid
prosthetic valve
infective endocarditis
```
51
How does mitral stenosis usually present?
dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis, chronic bronchitis-like picture, new-onset AF
52
Describe what is heard on auscultation in mitral stenosis?
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
What is the cause of the malar flush that may be seen in mitral stenosis?
the back pressure of blood into the pulmonary system causes a rise in CO2 and vasodilation
54
What structural changes take place as a result of mitral stenosis?
left atrial hypertrophy
55
What tests are most useful in suspected mitral stenosis and what would they show?
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
When is cardiac catheterisation indicated in mitral stenosis?
previous valvotomy, signs of other valve diseases, angina, severe pulmonary hypertension, calcified mitral valve
57
What is the management of mitral stenosis?
rate control + warfarin if in AF
diuretics (decrease preload and pulmonary venous congestion)
balloon valvoplasty
open mitral valvotomy/valve replacement
58
What additional measures should be taken in managing mitral stenosis with suspected infective endocarditis or subacute bacterial endocarditis?
prophylactic antibiotics: amoxicillin+gentamicin
59
What additional measures should be taken in managing mitral stenosis with suspected rheumatic heart disease?
oral penicillin in rheumatic in order to avoid recurrent rheumatic heart disease,
60
What are the complications associated with mitral stenosis?
pulmonary hypertension
emboli
pressure from LA on local structures - hoarseness (recurrent laryngeal nerve), dysphagia (oesophagus), bronchial obstruction, (?)infective endocarditis
61
What are five of the six main causes of mitral regurgitation? What are three of the remaining causes?
```
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
How does mitral regurgitation present?
dyspnoea, fatigue, palpitations, infective endocarditis-like picture, congestive cardiac failure-like picture
63
What is found on auscultation in mitral regurgitation?
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
What 3 tests are useful in mitral regurgitation? What would each test show?
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
What test/intervention confirms the diagnosis of mitral regurgitation?
Cardiac catheterisation
66
What is the management of mitral regurgitation?
if AF: control rate and warfarin
diuretics
Surgery repair/replace
67
What can mitral valve prolapse occur with?
ASD, PDA, cardiomyopathy, Turner's syndrome, Marfan's syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, WPW
can occur alone
68
What is the typical presentation of mitral valve prolapse?
asymptomatic
or atypical chest pain + palpitations
some have autonomic dysfunction as well - anxiety, panic attack, syncope
69
Describe what is heard on auscultation in mitral valve prolapse?
mid-systolic click or late systolic murmur - the timing of click varies with standing or squatting etc.
70
What are the complications associated with mitral valve prolapse?
mitral regurgitation, cerebral emboli, arrhythmias, sudden death
71
What are the tests that should be ordered for specifically for mitral valve prolapse? what would they show?
Echo - diagnostic, visualise mitral valve prolapse
| ECG - may show T wave inversion in inferior leads
72
What is the management for mitral valve prolapse?
beta blockers for chest pain and palpitations
| surgery may be needed in severe mitral regurgitation
73
What are the 3 main causes of aortic stenosis?
senile calcification, congenital (bicuspid valve, William's syndrome), rheumatic heart disease
74
What is the classic triad in which aortic stenosis usually presents?
angina, syncope and dyspnoea
75
what other symptoms besides the classical triad can present in aortic stenosis?
dizziness; faints; systemic emboli; sudden death
76
What are the clinical signs of aortic stenosis besides the murmur?
slow rising pulse with a narrow pulse pressure
heaving/LV heave
non displaced, heaving apex beat
aortic thrill
77
what is heard on auscultation in aortic stenosis?
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
What tests should be done in aortic stenosis and what would each show?
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
What is an important differential when considering aortic stenosis?
hypertrophic cardiomyopathy
80
What is the management of aortic stenosis?
surgical repair with valve replacement
81
What is aortic sclerosis and how does it differ from aortic stenosis?
senile degeneration of the valve
ejection systolic murmur but with no carotid radiation and normal pulse and S2
82
What are the acute causes of aortic regurgitation?
infective endocarditis, ascending aortic dissection, chest trauma
83
What are 10 of the 12 chronic causes of aortic regurgitation?
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
How does aortic regurgitation present?
exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
also: palpitations, angina, syncope, CCF
85
What are the clinical signs of aortic regurgitation?
collapsing pulse, wide pulse pressure, displaced hyperdynamic apex beat
high pitched early diastolic murmur - heard best on expiration with the patient sat forward
86
What specific signs are seen in aortic regurgitation that would suggest a hyperdynamic circulation?
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
What tests would you order in aortic regurgitation and what would each show?
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
What is the management of aortic regurgitation?
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
What valvular diseases typically cause ventricular or atrial hypertrophy?
mitral stenosis - left atrial
| aortic stenosis - left ventricular
90
What valvular diseases typically cause ventricular or atrial dilatation?
mitral regurgitation - left atrial
| aortic regurgitation - left ventricular
91
What are 5 of the 6 causes of tricuspid regurgitation?
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
How does tricuspid regurgitation present?
fatigue, hepatic pain on exertion, ascites, oedema
also, dyspnoea and orthopnoea if LV dysfunction is the cause
93
What are the clinical signs of tricuspid regurgitation?
giant v waves and prominent y descent in JVP
RV heave
pansystolic murmur heard best at LLSE on inspiration
pulsatile hepatomegaly, jaundice, ascites
94
What is the management of tricuspid regurgitation?
treat underlying cause
diuretics
digoxin
ACE-I
ultimately - valve replacement
95
What are the causes of tricuspid stenosis?
rheumatic fever - the disease is not normally isolated to tricuspid
congenital
infective endocarditis
96
How doe tricuspid stenosis present?
fatigue, ascites, oedema
97
What are the clinical signs of tricuspid stenosis?
giant a wave and slow y descent in JVP
opening snap, mid-diastolic murmur heard at LSE on inspiration
AF can occur
98
How is tricuspid stenosis diagnosed and managed?
echo
diuretics and surgical repair
99
What are the causes of pulmonary stenosis?
congenital - usually (Turner's, Noonan's, Williams, ToF, rubella)
rheumatic fever
carcinoid syndrome
100
How does pulmonary stenosis present?
dyspnoea, fatigue, oedema, ascites
101
What are the clinical signs of pulmonary stenosis?
```
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
What tests should be done in pulmonary stenosis and what would they show?
ECG - RAD, p-pulmonale, RVH, RBB
CXR - prominent main, right or left pulmonary arteries causes by post-stenotic dilatation
cardiac catheterisation is diagnostic
103
What is the management of pulmonary stenosis?
pulmonary valvuloplasty or valvotomy
104
What are the causes of pulmonary regurgitation?
any cause of pulmonary hypertension can cause pulmonary regurgitation
105
What is heard on auscultation in pulmonary regurgitation?
a decrescendo murmur in early diastole best heard at LSE
106
What are the three clinical syndromes seen in heart failure? What are some causes of each?
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
What are the symptoms of heart failure?
exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue
108
What are the signs of heart failure?
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
What are the four stages of the New York Heart Association?
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
What are the Framingham criteria for CCF?
>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
What are the signs of heart failure seen on chest x-ray?
ABCDE - alveolar oedema (Bat's wings), Kerley B lines, Cardiomegaly, Dilated prominent upper lobe vessels, pleural effusion
112
What investigations should be ordered and what would each show?
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
What is the treatment for chronic heart failure?
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
What is the treatment for acute heart failure?
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
What are the clinical symptoms of acute pulmonary oedema?
dyspnoea
orthopnoea
pink frothy sputum
116
What are the clinical signs of acute pulmonary oedema?
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
What investigations should be ordered for acute pulmonary oedema and what will each of them show?
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
How should acute pulmonary oedema be managed immediately?
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
How should acute pulmonary oedema be managed once the patient has been stabilised?
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
What are two common exacerbating medications of chronic heart failure?
NSAIDs - fluid retention
| verapamil - negative inotrope
