Interactive Cases 1 - Cardiology Flashcards
Musculoskeletal causes of CP?
Costochondritis, Tietze’s syndrome
STEMI: V1-4
Anterior MI, Left anterior descending
STEMI: V5-6, I, aVL
Lateral MI, left circumflex artery
STEMI: II, III, aVF
Inferior MI, Right coronary artery
Collapse? what do you ask to determine cause
Before: was there any warning/aura?
During: tongue biting, incontinence, jerky movements
After: confusion
Low volume, slow rising pulse, ESM
AS
Investigation of arrhythmia
ECG for tachy/brady and long QT syndrome, this will predispose to VT
Postural hypotension investigation
BP lying and standing
Classification of long-QT syndrome?
predisposes to VT
Abnormal ventricular repolarisation
Congenital: mutations in K channels (depolarisation problems), FH of sudden death.
Acquired: low K/Mg, drugs.
Draw a line between two R waves. The t wave should finish before the half-way point.
How are the symptoms of hypoglycaemia classified?
Neuroglycopaenic: confusion, drowsy, aggressive, coma
Adrenergic: tachycardia, sweating
May be due to insulinoma if hypo early in the morning, but more commonly due to a DM having taken insulin but not eaten food
45M fever, malaise, IVDrugUser, PSM louder on inspiration, fever 38C, raised JVP, hepatomegaly
tricuspid regurgitation
What are the features of tricuspid regurgitation?
Raised JVP
PSM at the left lower sternal edge louder on inspiration
What are the differential diagnoses of a raised JVP?
- RHF - secondary to LHF (CCF) or pulmonary HTN*
- TR - valve leaflets (IE), RV dilatation (AR)
- Ventricular septal defect (congenital)
- Constrictive pericarditis - fibrosis thickening of pericardium, calcification due to constriction seen on CXR (infection TB, inflammation CTD lupus/sarcoid, malignancy)
A person presents with chest pain. How should they be investigated?
- ECG (STEMI/NSTEMI)
- Troponin; if +ve (=STEMI/NSTEMI) PCI coronary angiography (X ray looks ate coronary arteries), if -ve exercise tolerance test (angina pectoris)
- Echo (ventricular dysfunction)
Gastro causes of CP?
Oesophageal spasm, oesophagitis, gastritis (acid in mouth, Retrosternal pain, alcohol xs is a Rx)
Causes of sudden breathlessness within seconds?
Foreign body obstruction, pneumothorax, PE
What are the cardiac differentials for CP?
IHD especially associated with nausea and sweating, aortic dissection can lead to AR EDM, pericarditis associated with post-viral illness
What are the respiratory differentials for CP?
Pneumonia (cough, sputum, temp), pneumothorax (SOB sudden), PE (haemoptysis, pleuritic CP, sudden SOB, swollen leg)
Symptoms of IHD
CP radiation to jaw, left arm, pressure-like pain, associated symptoms: sweating, nausea
Cardiac History: what do you look out for in PC
1) symptoms
2) associated symptoms
3) DDx/risk factors
1) symptoms - SOCRATES
2) associated symptoms - nausea, sweating, CP, SOB, dizziness, ankle swelling
3) DDx - DM, HTN, cholesterol, BP, FH, previous history of clots
Case - Hx:
60 yo man, chest pain, tight, 4h, nausea and sweating, HTN, DH: amlodipine.
O/E:
temp 37, S1 + S2, BP 120/80 (L), 118/75 (R), clear chest, abdomen SNT
MI
O/E of aorta dissection
difference in BP between arms
collapsing pulse
auscultate ask pt to lean forward, on expiration, left sternal edge hear EARLY DIASTOLIC MURMUR echo with S2 (AR murmur)
What is ACS?
Acute coronary syndrome is a spectrum.
1) MI (STEMI/NSTEMI) (+ve troponin as damage to myocardium)
2) unstable angina (CP at rest due to clot forming and dissolving) (may not be considered ACS as troponin MAY not be elevated)
NB. angina pectoris is pain on exertion (-ve troponin and +ve ETT)
Why is there ST elevation on an ECG?
dead myocardium provides window for electrodes to see spread of depolarization
PC of pericarditis
Pleuritic: worse on breathing in, sharp
Relieved leaning forward
maybe Flu like illness recently
Risk factors: young person with no other risk factors
Tx for STEMI and NSTEMI
Morphine O2 Nitrates Aspirin
STEMI: aspirin, clopidogrel (irreversible platelet aggregation inhibitor) and PCI
NSTEMI: aspirin, clopidogrel, fondaparinux ( ATIII-mediated selective inhibition of Factor Xa, decreased clot formation), thrombolyse (tPA or streptokinase stops clot formation)
Rx of PE
smoking, female, FH, OCP, long-haul flight, Marfans syndrome
Causes of pleuritic pain
PE (D-dimer is useful to exclude a PE, when positive not very useful) Pericarditis Pneumonia Pneumothorax Sub-diaphragmatic pathology
ECG can tell you..
Ischaemia (ST elevation/depression) Conduction problems (e.g. AF) Structural problems (e.g. LVH)
On an ECG: ST elevation V1-V4 (anterior) V5/6 and I + aVL (lateral)
Anterolateral STEMI
Evidence of ischaemia
ST depression in other leads = reciprocal changes
ST elevation in II, III, aVF
right coronary artery
inferior STEMI
Case Hx:
30 year old man
Collapse
HPC
Before: No warning
During: No tongue biting, incontinence, jerk-like movements
After: not confused
FH: brother died at a young age
O/E: HS1 + 2 + 0. BP120/80 (lying), 115/75 (standing). Vesicular sounds. SNT abdomen.
CNI-XII: NAD, Normal I, T, P, R, C, S, G.
Tachyarrhythmia (and FH sudden death). No postural hypotension from BP, no risk factors for PE, neurological exam in normal.
before: No warning suggests cardiac cause with VT (brady or tachyarrhthmia). Prodromal aura suggests seizures
after: (after VT) drowsy/confused after seizure
Cardiac causes of collapse
VAOP
Vasovagal – P’s: posture, prodrome, provoking factors - standing up in hot environment, cough reflex, micturition reflex (fainting when getting up to go to the loo) associated with increased vagal activity slowing down the heart.
Arrhythmia: either brady or tachy
Outflow obstruction: aortic stenosis, HOCM (congenital left side - narrowing of the outflow due to septum thickening); PE (if big and blockage of pulmonary artery; right side)
Postural hypotension
and HYPOGLYCAEMIA!!! (check capillary glucose
Tx of collapse
ABC resuscitate
check capillary glucose
non cardiac causes of collapse
Ask for the CBG - capillary blood glucose
Fast pt 72 hrs - Insulinoma
= tumour secretes insulin collapse first thing in the am because as fasted overnight.
NB. usual cause is in T2DM taking insulin and not eating.
Symptoms of hypoglycaemia = Neuroglycopenic and
Adrenergic
neurological causes of collapse
seizure
O/E and Ix of DDx of collapse:
1) arrythmia
2) Outflow obstruction
3) postural hypotension
1) ECG (tach/brady, long QT), cardiac monitor to catch episode, 24 hr tape
2) low volume/slow rising pulse (thrill under fingers on the carotid pulse - like a car struggling up a hill), ESM (AS)
3) lying/standing BP
Case Hx: 45 year old man Fever, Malaise,IV drug use O/E:Temp 38 High JVP to earlobes, High JVP HS: I, II, PSM: louder on inspiration Hepatomegaly
Tricuspid regurgitation
Valve leaflets damaged (IE) or dilatation of the root of the valve (R ventricle)
TR (PSM, louder on inspiration at L lower sternal edge, high JVP)
Likely organism: Staph aureus (IVDU)
(hepatomegaly due to backlog and congestion)
DDx systolic murmur
whoosh whoosh
- AS (louder on exp, radiates to neck) Slow rising pulse (thrill under thumb in neck), soft S2
- MR (louder on exp in mitral area, radiates to axilla, displaced apex beat
- TR (louder insp, Pulsatile liver, high JVP
- VSD (congenital)
Case Hx:
65 yr male, breathlessness, palpitations, PMH: HTN, DH: Bendroflumethiazide
O/E: temp 38, PR 160, irregular, BP 110/80, dull percussion note and coarse crackles L lung base
AF
due to pneumonia (crackles)
Features of sinus tachycardia
Causes of sinus tachycardia
Narrow QRS, regular, p waves seen
Sepsis → hypotension (reflex tachy)
Hypovolemia (caused by bleeding)
Endocrine: thyrotoxicosis, phaeochromocytoma
Features and causes of SVT
Reentry circuit: re-entrant tachycardias No p wave, Fast and regular Narrow QRS complex < 3 s sq Treat with ADENOSINE - if a slurred QRS upstroke develops pt has AVNRT not AVRT Causes: AVNRT, AVRT
Pathophysiology of AVRT (SVT)
AVRT: Wolff Parkinson White
Accessory pathway (AP) Bundle of Kent.
Depolarisation gets to AVN, travels down the septum and then back up the AP to reach the AVN again
If the patient is in sinus rhythm, resting ECG shows:
Short PR interval (p wave present), Delta wave (slurred upstroke as 2 depolarisation conduction pathways -> risk of AVNRT so accessory pathway is ablated.
Problem when direction of the depolarisation changes conduction directed back UP to the AVN via AP.
Pathophysiology of AVNRT (SVT)
Reentry circuit at the AV node: conducted down and goes round in circles
No p wave (depolarisation comes from AVN not SAN)
Normal ECG after it has resolved - no slurred upstroke (as no Bundle of Kent AP)
Features of AF on ECG
Irregular
No p waves
Narrow QRS
Features of atrial flutter on ECG
Chaotic atrial activity
No p waves (p waves is SAN initiating depolarisation)
Saw-tooth baseline
Causes of AF
Metabolic: Thyrotoxicosis, alcohol
Heart (by layer): pericarditis, muscle (CM, IHD, HTN, myocarditis), valves (MS, MR)
Lungs: pneumonia, PE, cancer
How would you differentiate AF and SVT on an ECG?
AF no p waves, AVRT (pre-SVT) has p waves and delta wave. AVNRT no p waves
SVT regular, AF irregular
Features of VT on an ECG
Broad QRS complexes - you can see pink paper between the two limbs of complex
Regular
Causes of VT
Ischaemia (collapse with MI due to arrhythmia) Electrolyte abnormality (check K, Mg) Congenital: long QT congenital (look at old ECGs)
What is management of SVT pt with BP 120/80?
Vagal manoeuvres: Immerse face in cold water, Valsalva Adenosine with cardiac monitor (Contraindications = asthma) DC cardioversion (synced defib) -> if haemodynamically compromised (hypotension)
What is the management of AF?
Manage cause e.g. pneumonia and infection (Abx / fluid)
Manage- Complications (stroke) anticoagulation warfarin, CHA2DS2-VASC
Rate control - beta blocker, digoxin (not in infection)
Rhythm control - onset >48h, anticoagulate for 3-4 weeks before cardioversion (as stroke risk)
What is the management of VT?
IV amiodarone (anti arrhythmic) if no haem compromise Treat underlying cause (e.g. electrolyte imbalance) Implantable cardiac defibrillator Pulseless VT: defibrillate
ECG: deep S wave V1/2 and tall R wave V5/6
Sum of large squares >7
LVH by voltage criteria*
DDx: HT due to e.g. AS
*need echo to diagnose as it’s gold standard
ECG changes in
1st degree heart block
2nd degree heart block
3rd degree heart block
1st degree: Prolonged PR interval (> 1 large sq) lead 1?
2nd degree: missed QRS after p waves (pacemaker!)
3rd degree heart block: no assocation between p and QRS, broad QRS (pacemaker!)
Pathologies suggested by ECG
Ischemic: ST, T inversion (NSTEMI), Q (old infarct) Arrhythmias/conduction defects: Rate, rhythm PR, QRS, QT Ventricular strain or hypertrophy Axis (R/L sided), R, S waves
Case Hx: 65 y/o. SOB - Onset over few hours. Orthopnea. PMHx: 2 x MI. DH: aspirin, simvastatin, ramipril, bisoprolol.
O/E: Temp 36.5, High JVP, HSI+II+III. Fine chest crackles. Peripheral oedema.
CCF
not sudden onset
Orthopnea - breathless on lying flat
3rd heart sound is very close & just after S2.
Heart sounds Closure of mitral valve Closure of aortic valve Atrial septal defect Fixed wide splitting of Associated with ventricular filling Associated with ventricular hypertrophy
Closure of mitral valve S1
Closure of aortic valve S2
Atrial septal defect Fixed wide splitting of S2
Associated with ventricular filling S3 (3rd heart sound/gallop rhythm is very close & just after S2)
Associated with ventricular hypertrophy S4 (4th heart sound is just before S1, 4-1-2)
How to differentiate split S2 and S3?
S3 - listen with bell, light pressure, low pitched.
Atrial septal defect - listen with diaphragm.
S4 - atria contraction against stiff ventricle.
What is the management of acute HF?
Sit up
60-100% O2
GTN infusion - venodilators, reduces preload
Diamorphine
Furosemide (IV) - (not for diuresis, venodilator as well)
( IV as if they have gut oedema they will not absorb the drug orally)
Daily weights needed
Treat the underlying cause e.g. MI
Management of Chronic HF
Heart cannot meet demands: SOB, reduced exercise tolerance etc.
Beta blocker: blocks sympathetic nervous system.
ACEi & spironolactone (activation of RAAS causes cardiac remodelling).
(NOT IN EXAM)
VF on ECG? Management?
asystole on ECG?
VF - broad QRS, irregular (hence not VT). Mx = CPR ONLY
asystole - flat line
Causes of cardiac arrest
Hypoxia
Hypothermia
Hypovolaemia
Hypo/hyperkalaemia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins / metabolic disorders: drugs, therapeutic agents, sepsis
ALS algorithm
for VF/pulseless VT
Shock
CPR for 2 minutes…
Re-assess rhythm
Adrenaline every 3-5 minutes
Metabolism slows down when the patient is cold. Do not give Adr as normal because otherwise the drug will build up and could be toxic.
Correct reversible causes
for Asystole/Pulseless Electrical Activity - ECG looks fine but pt has no pulse!
CPR+ Correct reversible causes. No drugs!
Case Hx: 30 y/o woman. URTI. Pleuritic chest pain. Better when leaning forward.
ECG: ST elevaion in all leads
Pericarditis
ST elevation (cannot be ischaemic because not confined to territories).
What are non-acute causes of breathlessness?
HF, pneumonia, arrhythmias, MI
