Cardiology 🫀 Flashcards
when is surgery recommended for AAA
when the abdominal aorta diameter is greater than 5.5cm
what does the term acute coronary syndrome cover
an umbrella term covering a number of presentation of ischaemic heart disease:
STEMI
NSTEMI
unstable angina
what does the term ischaemic heart disease mean
synonymous with coronary heart disease and coronary heart disease
it describes the gradual build up of fatty plaques within the walls of coronary arteries co
modifiable risk factors of ACS
smoking
diabetes
hypertension
hypercholesterolaemia
obesity
unmodifiable risk factors of ACS
increasing age
male gender
family history
presentation of ACS
chest pain - most typical presentation
others include
dyspnoea
sweating
nausea and vomiting
how does the chest pain in ACS present
SOCRATES
site - central/left-sided
onset - sudden
character - crushing
radiation - jaw, neck and left arm
associated sx - nausea, sweating, clamminess, sob
timing - constant
exacerbating/relieving factors - exercise and GTN spray
severity - extreme
diagnosis depends on a combination of clinical, ECG and biochemical findings
what would you find for unstable angina
cardiac chest pain
abnormal/normal ECG
normal troponin
diagnosis depends on a combination of clinical, ECG and biochemical findings
what would you find for NSTEMI
cardiac chest pain
abnormal/normal ECG
raised troponin
diagnosis depends on a combination of clinical, ECG and biochemical findings
what would you find for STEMI
cardiac chest pain
persistent ST elevation
no need for troponin
when should you test troponin levels
3 hours at least after pain started
may need to be repeated 6-12 hours after start of pain if result is ambiguous - mildly raised
but ECG ALWAYS first - if STEMI present then troponin is irrelevant
mx of STEMI
300MG ASPIRIN
if <2 hours - PCI
if >2 hours - thrombolysis
why is IV morphine/diamorphine prescribed in STEMIs and NSTEMIs
causes vasodilation so reduces preload on heart
when do you prescribe primary precutaneous coronary intervention
for STEMI
patients who present within 12 hours of onset of pain AND are <2 hours since first medical contact
mx of NSTEMI
BATMAN
beta blocker
aspirin 300mg
ticagrelor 180mg
morphine
anticoagulant -LMWH
nitrates - GTN
describe the procedure of percutaneous coronary intervention
blocked arteries are opened up using a balloon following which a stent may be deployed to prevent artery occluding against
done via a catheter inserted into radial or femoral artery
mx of unstable angina
MONA
Morphine IV
Oxygen
Nitrates GTN
Aspirin
post successful PCI how long do you wait to drive a car
1 week
no need to inform DVLA
post unsuccessful PCI or no PCI and MI how long to wait to drive a car
4 weeks
no need to inform DVLA
post unsuccessful PCI or no PCI and MI how long to wait to drive a bus/lorry
6 weeks and must inform DVLA
post successful PCI how long to wait to drive a BUS/LORRY
6 weeks and must inform DVLA
difference between stable and unstable angina
stable angina is triggered usually whereas there is no trigger for unstable
what does an U wave represent on ECG
hypokalaemia
what does saw tooth baseline show
atrial flutter
what does tall-tented T waves mean
hyperkalaemia
what does upward-sloping QRS complex mean
wolf parkinson white syndrome
these are called delta waves
sx of pericarditis
pleuritic chest pain relieved by sitting forwards + pericardial rub
ix pericarditis
ECG/troponin/ECHO
saddle shaped ST elevation
raised troponin!
PR depression
mx pericarditis first line - viral
NSAIDs + restrictive exercise
adjunctive: colchicine
ax of myocarditis
proceeding viral illness 2-3 weeks prior
sx myocarditis
chest pain
dyspnoea
pulmonary oedema
palpitations
raised JVP
bibasal crackles
ix myocarditis
ECG: sinus tachycardia with non-specific ST
segment/ T wave inversion
prolonged QRS/QT
raised troponin
ax infective endocarditis
staph aureus/strep.viridans
risk factors infective endocarditis
IVDU
poor dentition and dental infections
tricuspid valve disease
male sex
sx infective endocarditis
fever + pansystolic/early diastolic murmur
janeway lesions
oslers nodes
features of heart failure
night sweats
ix of infective endocarditis
Duke’s criteria + transthoracic ECHO
3x sets of blood cultures
septic screen
what is duke’s criteria
classify cases into definite IE, possible IE and rejected IE
definite IE - 2 major criteria, 1 mqajor +3 minor or all 5 minor criteria
tx Infective endocarditis
long term antibiotics
staph -> flucloaxcillin
strep -> benzylpenicillin
surgical replacement
what would indicate surgery for an infective endocarditis patient
PR interval prolongation
what shows on an ECG in a patient with AF
absence of P waves
narrow QRS complex tachycardia
irregularly irregular ventricular rhythm
sx of AF
palpitations
SoB
syncope
symptoms of associated diseases
Tx of AF
assess haemodynamic stability
unstable -> immediate DC cardioversion
Stable - rate control - over 48 hours
rhythm control - less than 48 hours
causes of AF
SMITH
sepsis
Mitral valve pathology
Ischaemic heart disease
Thyrotoxicosis
HTN
rate control how is it done
- beta blocker e.g atenolol or CCB e.g diltiazem (contraindicated in heart failure)
- digoxin
rhythm control how is it done
electrical cardioversion
pharmacological cardioversion
examples of medication used in pharmacological conversion
flecainide - younger patients
amiodarone - older
sotalol - beta blocker with rhythm control action
components of CHA2DS2-VASc
Congestive heart failure
HTN
Age >75V (2)
Diabetes
Stroke/TIA (2)
Vascular disease
Age 65-74
Sex (female)
what score of CHA2DS2-VASc do you consider anticoagulation
0: none
1: consider
2+ : offer it
ix heart failure NTproBNP
NT-proBNP
- >2000 bnp = urgent 2WW +ECHO
- 400-2000bnp = 6WW +ECHO
ix heart failure ECHO
ECHO
ejection fraction -
<40% = heart failure with reduced ejection fraction
greater than 40% but raised BNP = heart failure with preserved ejection fraction
ix heart failure CXR what are you looking for
Alveolar oedema - batwing appearance
kerley B lines
Cardiomegaly
upper lobe Diversion
pleural Effusion
Fluid in horizontal fissure
firs line treatment heart failure
ABAL + annual flu vaccine
Ace inhibitor
Beta-blocker
Aldosterone antagonist
Loop diuretics
also consider MRAs if symptoms persist
what is cor pulmonale
right-sided heart failure caused b y pulmonary hypertension stemming from underlying lung disease
symptoms of cor pulmonale
peripheral oedema
raised JVP
hepatomegaly
SoB
exertion dysponea + syncope
cyanosis
hypoxia
how many days before surgery to stop warfarin
5 days
signs and symptoms of aortic stenosis
ejection systolic murmur (2nd ICS right sternal edge) louder on expiration radiates to carotids
slow rising pulse
narrow pulse pressure
syncope
heart failure
angina
signs and symptoms of mitral regurgitation
pan-systolic murmur (5th ICS,MCL) louder on expiration which radiates to the axilla
SoB
exertional dyspnoea
signs and symptoms of aortic regurgitation
early diastolic soft murmur (2nd ICS R sternal edge)
collapsing pulse
widened pulse pressure
signs and symptoms of mitral stenosis
mid-diastolic low pitched “rumbling” murmur (5th ICS MCL) which radiates to axilla
acute causes of aortic regurgitation
infective endocarditis
aortic dissection
chronic causes of aortic regurgitation
marfans syndrome
rheumatic heart disease
infective endocarditis
which leads on an ECG would be affected by RCA
II, III, aVF
What is heart failure
Heart failure is result of an inability of the heart to maintain adequate cardiac output
What is heart failure commonly secondary to
Ischaemic heart disease
Hypertensive heart disease
What is heart failure characterised by
SoB
Fluid overload
Fatigue
What re the common causes of acute heart failure
Acute myocardial dysfunction
Acute valvular
Pericardial tamponade
Describe systolic heart failure
Reduction in left ventricular ejection fraction
Other words; heart is pumping out a proportion of the blood that fills the ventricles during diastole
The increase in blood at the end of systole leads to ventricular stretch, dilation and eccentric remodelling
Describe diastolic heart failure
Refers to impaired ventricular filling or relaxation
LVEF is preserved as systole is not affected
Ventricular hypertrophy tends to develop
Characterised by concentric remodelling
Describe low output heart failure
Heart cannot maintain an adequate cardiac output
Results in increased systemic vascular resistance to maintain mean arterial pressure
Clinically patients have weak pulse, cool peripheries and low blood pressure
Describe high output heart failure
Characterised by high cardiac output and low systemic vascular resistance
Heart fails to meet grossly increased demands
Can occur in a healthy heart
What is stroke volume
Amount of blood pumped out of heart from each contraction
Cardiac output
Amount of blood pumped out heart in one minute
HR * SV
Preload
Stretching of cardiomyocytes at end of diastole
After load
Pressure or load against which ventricles must contract
Inotropy
Refers to myocardial contractility I.e force of muscular contractions
Sx of heart failure
SoB
Wheeze
Fatigue
Weight loss
Paroxysmal nocturnal dyspnoea
Orthopnoea
Ankle swelling
What is BNP
Protein released by cardiomyocytes in response to excessive stretching
pathophysiology of cor pulmonale
chronic lung disease makes it harder to oxygenate blood
pulmonary arteries respond by vasoconstriction
this increases resistance and therefore causes pulmonary hypertension
RV finds it harder to pump blood into pulmonary circulation as a result of hypertension
concentric hypertrophy of RV occurs -> diastolic heart failure
causes backlog of blood in venous system
dx of cor pulmonale
echocardiogram for evidence of increased pressure
spirometry for lung disease
right heart catheterization to measure lung pressures
treatment cor pulmonale
treat the underlying lung condition
define sinus tachycardia
HR>100 bpm
it is a normal physiological response when the body is put under stress
management of torsades de pointes
management is aimed at shortening the QT interval with IV magnesium sulphate
if a patient is unstable they should undergo immediate DC cardioversion
describe VF
this arrhythmia is incompatible with life and will result in loss of consciousness and cardiac arrest
VF occurs when the ventricular muscle fibres contract independently
what would you see on an ECG for VF
no coordinated electrical activity with a chaotic fibrillating baseline
A 43-year-old woman is seen on the ward following an episode of feeling her heart pounding. This came on 2 minutes
ago and is not associated with any other symptoms. She is normally fit and healthy. Her current stay in the hospital is for
elective cosmetic surgery. An ECG carried out by her nurse shows a narrow-complex tachycardia at a rate of 220 bpm.
There are no other abnormalities in the ECG.
Apart from her tachycardia, her vital signs are stable.
Which of the following represents the first-line immediate management?
A) Bilateral carotid sinus massage
B) DC cardioversion
C) Valsalva manoeuvre
D) IV adenosine
E) 2222 crash call
C) Valsalva manoeuvre
Vagal manoeuvres such as carotid sinus massage and Valsalva can be used as the first line management in stable patients with a narrow complex tachycardia
Buzz words for wolf Parkinson white syndrome
Pre-excitation
Intermittent QRS complexes
Short PR interval
Tx wolf Parkinson white syndrome
Radio frequency ablation of the accessory pathway (definitive)
Tx of VF
Shock
Describe VF
Uncoordinated electrical activity with a chaotic fibrillating baseline
Tx torsades de pointes
IV magnesium sulfate + stop offending drug + correct electrolyte imbalance
Medications that can cause torsades de pointes
Anti-psychotics
Citalopram
Flecainide
Sotalol
Amiodarone
Macrolides
Ketoconazole
What do you do with pulseless VT
Unsynchronised Biphasic shock
What do you do with pulsed VT + adverse features
Synchronised DC cardio version (up to 3 attempts)
Then IV amiodarone 300mg
What do you do with pulsed VT without adverse features
IV amiodarone
Bradycardia with adverse features
IV atropine 500 mcg
Repeat to maximum of 3g
Describe 1st degree heart block
Prolonged PR interval
describe 2nd degree type 1 heart block
Progressively prolonged PR interval until a QRS complex drops
Describe 2nd degree type 2 heart block
Same PR interval until a QRS complex drops
Describe 3rd degree heart block
Complete dissociation between P waves and QRS complexes
Causes of LBBB
Aortic stenosis
Digoxin toxicity
Hyperkalaemia
Describe what you would see on an ecg for LBBB
In V1 you’ll see a w shape
In v2 you’ll see a M shale
Causes of RBBB
normal variant
RV hypertrophy
PE
Describe what you would see on an ecg for RBBB
v1 M shape
V6 W shape
MOA amiodarone
Blocks potassium Channels
Infective endocarditis in a patient positive for IVDU most commonly affects what structure
Tricuspid valve
All valves in the heart are derived from the endocardia cushion
What is hypertrophic cardiomyopathy caused by
Aysmmetric septal hypertrophy
What is S3 (third heart sound) caused by
Caused by diastolic filling of the ventricle
Heard in left ventricular failure, constrictive pericarditis and mitral regurgitation
What is S4 (fourth heart sound) caused by
Caused by atrial contraction against a stiff ventricle
May be heard in aortic stenosis, HOCM, hypertension and therefore coincides with the P wave on an ecg
How does clopidogrel work
Anti-platelet agent that works by inhibiting the P2Y12 ADP receptor which in turn inhibits the activation of platelets
What is the physiological role of troponin I
Binds to actin to hold the troponin-tropomyosin complex in place
Where is the SA node found
Right atrium
Where is the AV node found
Atrioventricular septum
What is Ebstein’s anomaly
Congenital defect leading to a large right atrium and a small right ventricle which is known as “atrialisation”
Typically accompanied by tricuspid regurgitation
Describe the phases of cardiac action potential
Phase 0 - rapid depolarisation - rapid sodium influx
Phase 1 - early depolarisation - efflux of potassium
Phase 2 - plateau - slow influx of calcium
Phase 3 - efflux of potassium
Phase 4 - restoration of ionic concentrations - resting potential is restored by Na+/K+ ATPase
Pathophysiology of hypertrophic obstructive cardiomyopathy
Results in predominantly diastolic dysfunction - left ventricle hypertrophy - decreased compliance - decreased cardiac output
Characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes and fibrosis on biopsy
Features of hypertrophic obstructive hypertrophy
Often asymptomatic
Exertional dyspnoea
Angina
Syncope typically following exercise
Sudden death
ECHO findings for hypertrophic obstructive cardiomyopathy
MR SAM ASH
Mitral regurgitation MR
Systolic anterior motion SAM of anterior mitral valve leaflet
Asymmetric hypertrophy ASH
ECG findings for HOCM
left ventricular hypertrophy
Non-specific ST segment and T wave abnormalities
Deep Q waves
AF occasionally
MOA of tirofiban
glycoprotein IIb/IIIa antagonist
what is arrhythmogenic right ventricular cardiomyopathy
a form of inherited cardiovascular disease that can present with syncope or sudden cardiac death
pathophysiology of arrhythmogenic right ventricular cardiomyopathy
autosomal dominant
right ventricular myocardium is replaced by fatty and fibrofatty tissue
pathophysiology of arrhythmogenic right ventricular cardiomyopathy
autosomal dominant
right ventricular myocardium is replaced by fatty and fibrofatty tissue
presentation of arrhythmogenic right ventricular cardiomyopathy
palpitations
syncope
sudden cardiac death
management of arrhythmogenic right ventricular cardiomyopathy
sotalol
catheter ablation
implantable cardioverter-defibrillator
what’s the first line secondary prevention of stroke
clopidogrel
moa of warfarin
vitamin k antagonist
moa of aspirin
COX inhibitor
moa of heparins
activation of antithrombin II
moa of bivalirudin
reversible direct thrombin inhibitor
What should you consider for patients with recurrent proximal DVT or PE despite adequate anticoagulation treatment
Inferior vena cava filter
Where is BNP mainly secreted from
Ventricular myocardium
What conditions are associated with hypertrophic obstructive cardiomyopathy
Friedreich’s ataxia
Wolff-Parkinson white
What embryological structure gives rise to the ascending aorta
Truncus arteriosus
What is dressler syndrome
Complication of MI that can occur any time between 2 weeks to several months post MI
Symptoms include fatigue malaise pleuritic chest pain mild dyspnoea
Decreased BP on inspiration is associated with DS
Why would mitral stenosis cause an enlarged left atrium
Mitral stenosis means mitral valve has thickened that results in impaired blood flow into the left ventricle
This increases pressure in the left atrium which causes enlargement of the left atrium
Features of mitral stenosis
Dyspnoea due to increased atrial pressure causing pulmonary venous hypertension
Haemoptysis- pink frothy sputum
Mid late diastolic murmur best heard expiration
Loud S1
opening snap
Low volume pulse
Malar flush
AF
What would you see on an ECG for a posterior STEMI
ECG will show reciprocal changes e.g ST depression in leads V1-4
May also see upright t waves and tall broad R waves
Classic signs of cardiac tamponade
Becks triad
Muffled heart sounds
Raised JVP
hypotension
treating heart failure if symptoms persist after first-line medications
consider second-line treatment
ivabradine
sacubitril/valsartan
hydralazine
digoxin
dapagliflozin
treating heart failure if pt remains symptomatic after first and second line meds
ICD - poor LVEF + reasonable QoL + eps of VT/VF
CRT - only appropriate in its with prolonged QRS
LVAD - end stage HF - used as interim
transplant - also last point intervention
An 8-year-old girl is brought to the GP by her mother with a sore throat for the past five days. Incidentally, on examination, a harsh pan systolic murmur is heard during cardiac auscultation at the left lower sternal region. Echocardiogram reveals a small septal defect located apical to the aortic annulus but below the crista supraventricularis.
Which of the following best describes the type of ventricular septal defect?
membranous ventricular septal defect
what is ventricular septal defect?
VSD is most common congenital cardiac anomaly in children
typically have a pan-systolic murmur promninently heard at left lower sternal border
diagnosing aortic dissection
CT angiogram
TOE can also be used if CT isn’t available
clinical signs on examination of aortic dissection
radio-radial delay
radio-femoral delay
blood pressure differential between arms
initial mx aortic dissection
resus if necessary
cardiac monitoring
strict blood pressure control
definitive management aortic dissection
type a - surgery
type b - normally managed conservatively
clinical features of aortic dissections
usually presents in men over the age of 50
sudden onset tearing chest pain or interscapular pain radiating to the back
symptoms of digoxin toxicity
abdominal pain, nausea, vomiting, arrhythmias and yellow-green visual disturbances
digoxin effects on ECG
downsloping ST depression
T wave changes
the morphology of the QRS complex/ST segment is variously described as resembling a reverse tick
what is brugada syndrome
genetic condition caused by sodium channelopathies
high incidence in south east asian males
clinical features of brugada syndrome
patients may be asymptomatic or present with palpitations and syncope due to arrhythmias
risk factors that can increase the risk of arrhythmia in patients with brugada syndrome
fever - biggest risk
excess alcohol intake
dehydration
medication
electrolyte abnormalities
management of brugada syndrome
definitive management is an ICD to reduce the risk of sudden death from arrhythmias
management of cardiac tamponade
first line in patients who are haemodynamically unstable is pericardiocentesis
complications of pericardiocentesis
pneumothorax - pts should have a CXR post procedure
damage to myocardium, coronary vessels
thrombus
arrhythmias/cardiac arrest
damage to peritoneum
First line investigation for carotid artery stenosis
Duplex ultrasound
what is peripheral arterial disease
narrowing of the arteries supplying the limbs and peripheries, reducing the blood supply to these areas
signs and symptoms of peripheral arterial disease
sx: walking impairment + pain in buttocks and thighs relieved at rest
signs: hair loss, pale, arterial ulcers, weak/absent pulses, poorly healing wounds
ix peripheral arterial disease
full CVS risk assessment + ABPI
treatment of peripheral arterial disease medical
atorvastatin 80mg + clopidogrel 75mg OD
what is acute limb ischaemia
severe symptomatic hypoperfusion of a limb occurring for <2 weeks
SURGICAL EMERGENCY
sx and presentation of acute limb ischaemia
6 Ps
pain
pulselessness
paraesthesia
paralysis
pallor
perishingly cold
Ix of acute limb ischaemia
handheld arterial doppler
mx of acute limb ischaemia
analgesia + IV heparin + vascular review
what is critical limb ischaemia
end point of PAD
sx of critical limb ischaemia
night pain relieved by hanging limb out of bed
resting pain >2 weeks
ulceration
gangrene
absent pulses
cold limb
management of critical limb ischaemia
- conservative
- endovascular
- open surgery
- amputation
what electrolyte abnormality is most likely seen in a patient with acute digoxin toxicity
hyperkalaemia
indications for a permanent pacemaker
severe heart failure not responding to treatment
complete heart block
mobitz type 2 heart block
symptomatic bradycardia
drug- resistant tachyarrythmias
sick sinus syndrome
