Cases in general internal medicine 1 Flashcards
Investigations for suspected MI
- ECG
- Troponin (perhaps 6hr or 12hr after)
(if troponin +ve then coronary angiography, if -ve exercise tolerance test) - Echocardiography
Classify the causes of chest pain
Cardiac: IHD, aortic dissection, pericarditis
Resp: PE, Pneumonia, Pneumothorax
GI: gastritis, eosophagitis, eosophageal spasm
MSK: costochondritis
Aortic dissection pain
Pericarditis pain
Aortic dissection: Tearing pain radiates to the back
Pericarditis: pleuritic pain worse on inspiration
What from an examination might help you tell if there is aortic dissection
difference in BP between two arms
What problem could a patient on steroids have with chest pain (rare case)
Possibly candidasis (fungal infection) due to immunosuppression due to steroids
First line for STEMI
PCI (percutaneous coronary intervention)
Clotbusters not first line now
What leads would show changes in:
- Anterior MI
- Lateral MI
- Inferior MI
- Posterior MI
And which artery is affected in each case
When does troponin peak with MI?
What enzymes peak much earlier than troponin
Best cardiac biomarker for assessment of reinfarction during an MI admission
• Anterior MI – LAD – V1‐V4 • Lateral MI – Circumflex – V5, V6, I, aVL • Inferior MI: – RCA – II, III, aVF • Posterior MI: – Posterior descending artery – ST depression in V1-4
It rises around 4-6 hours after, peaks at 18-24hrs. Then falls over the next 5 days for a large MI. For a small MI might only be a small increase
Myoglobin and CK isoforms will peak much sooner. and are cleared sooner.
CK-MB returns to normal within about 72hrs compared to 5-7 days for trop, so it can be useful to assess reinfarciton
DDx of collapse
- Hypoglycaemia
2. Cardiac • Vasovagal • Arrhythmia • Outflow obstruction (aortic stenosis, HOCM, pulmonary embolism) • Postural Hypotension
- Neurological
• Seizure
What investigations/what might you see on examination if you suspect the following:
- Arrhythmias
- Outflow obstruction
- Postural hypotension
- Arrhythmias- ECG (? Long QT), cardiac
monitor, 24 hour tape - Outflow obstruction (see below)- Low volume/slow rising
pulse, ESM, Echocardiogram - Postural hypotension- Lying/standing BP
Cause of long QT syndrome
Abnormal ventricular repolarization
Congenital e.g. mutations in K+ channels
Acquired: low K+/ Mg2+, drugs
What might you find in family history of patient with long QT syndrome
• FH of sudden death
How to distinguish between mitral and tricuspid regurg murmurs
Both pansystolic murmurs, RILE. Right louder on inspiration and left louder on expiration
DDx of raised JVP
- R heart failure
- Tricuspid regurgitation
- Constrictive pericarditis and cardiac tamponade
What might cause right sided failure
– Secondary to L heart failure (CCF)
– Pulmonary HTN (PE, COPD etc.)
What might cause truscupid regurg
– Valve leaflets
– R ventricle dilatation
What might cause constrictive pericarditis
– Infection e.g. TB
– Inflammation: CTD e.g. lupus
– Malignancy
What are the types of tachycardia on ECG
What heart condition is most likely with chest infection
Sinus tachycardia, SVT, AF, VT and VF
Atrial fibrillation (legionnaires in particular is likely to present with AF)
DDx for Sinus tachycardia
Sepsis,
hypovolaemia,
endocrine (thyrotoxicosis,
phaeochromocytoma)
DDx for SVT
Re‐entry circuit
DDx for Atrial fibrillation
Thyrotoxicosis, alcohol
Heart: ischaemic heart disease, muscle, valve (mitral stenosis), pericardium
Lungs: pneumonia, PE, cancer
DDx for VT
ischaemia, electrolyte
abnormality, long QT syndrome
Management of SVT
- Vagal maneuvers
- Adenosine (cardiac monitor)
- DC cardioversion if evidence of haemodynamic compromise
Management of new onset AF
-risk stratification?
TREAT REVERSIBLE CAUSE
-Haemodynamically unstable:
DC cardioversion
-Haemodynamically stable with left thrombus:
RATE control with b-blocker/CCB (or digoxin/amiodarone if HF)
+
Anticoagulate
+
DC or pharmacological cardioversion 3-4 weeks later
-Haemodynamically stable, no left atrial thrombus, symptom onset <48hrs: CHADVASC SCORE 0-1: -Rate control with b-blocker/CCB \+ -DC or pharmacological cardioversion CHADVASC SCORE >2: -Rate control with b-blocker/CCB \+ -DC or pharmacological cardioversion AND heparin \+ -Anticoagulation
Haemodynamically stable without left atrial thrombus, but symtpom onset >48hrs:
CHADVASC SCORE 0-1:
-Rate control with b blocker/CCB
-Give heparin
-Electrical or pharmacologic cardioversion once heparin established
CHADVASC SCORE >2
- Rate control with b blocker/CCB
- Anticoagulate
- Electrical or pharmacological cardioversion follwoing 3-4 weeks of anticoagulation
Then, risk stratification for future stroke:
C - Congestive heart failure (or Left ventricular systolic dysfunction)
H- Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)
A2-Age ≥75 years
D-Diabetes Mellitus
S2-Prior Stroke or TIA or thromboembolism
V- Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)
A- Age 65–74 years
Sc- Sex category (i.e. female sex)
Low-risk patients can be managed with aspirin, and high-risk patients require anticoagulation with warfarin.
Management of VT
If no haemodynamic compromise: IV Amiodarone
• Look for & treat underlying cause
• ICD
Pulseless VT: defibrillate
How does digoxin, adenosine and amiodarone work?
…….
What is LVH by voltage criteria in ECG
Deep
S in V1/2
• Tall
R in V5/6
S in V 1 + R in V 5 or V 6 (whichever is larger) ≥ 7 large squares
ECG changes due to ischaemia?
• ST elevation, T wave inversion, Q waves (suggest old MI)
What might be affected by arrhythmia or conduction defects on ECG
- Rate, Rhythm
* Look at intervals: PR, QRS, QT
What might be affected by ventricular strain or hypertrphy on ECG
What would indicate strain on the right heart and what could cause that
Axis, R, S
Prominent R waves (i.e. upstroke) in V1 is suggestive of a strained right heart (PE, COPD etc.)
What are the following heart sounds associated with:
S1, S2, S3, and S4
Closure of mitral valve= S1
Closure of aortic valve= S2
Associated with ventricular filling (i.e. during heart failure) =S3 (very closely follows 2nd heart sound)
Associated with ventricular hypertrophy (i.e. during HTN) =S4 (very closely before the 1st heart sound)
What heart sound with atrial septal defect
Fixed wide splitting of S2
Management of acute HF
- Sit up
- Oxygen
- Furosemide (IV)
- (GTN infusion)
- Treat the underlying cause
Management of MI
STEMI: aspirin, clopidogrel, cath lab
NSTEMI: aspirin, clopidogrel, LMWH
Management of:
VF
Pulseless VT
Asystole
PEA
You can’t shock or give adrenaline if hypothermia
ALS ALGORITHM
-VF/pulseless VT
Shock, 2 min CPR, assess rhythm, adrenaline every 3-5 mins, amiodarone after 3 shocks, correct reversible causes
-Asystole/PEA (NOT shockable rhythm)
2 mins CPR, adrenaline every 3-5 min, correct reversible causes
30 yr old woman • URTI • Pleuritic chest pain • Better when leaning forward
What is the differential
Pericarditis
DDx of pleuritic chest pain
Pericarditis
PE
Pneumonia
Pneumothorax
Pleural pathology
Sub‐diaphragmatic pathology
Pericarditis, give some associated symptoms (system) to ask about
Viral- pericarditis commonly follows a viral infection so ask about flu like symptoms, fever etc.
What are reciprocal ECG changes?
Reciprocal change is a very important ECG finding, not only supporting the diagnosis of STEMI but also indicating a high-risk patient.
Reciprocal change is defined as ST-segment depression occurring on an ECG which also has ST-segment elevation in at least 2 leads in a single anatomic segment. (e.g. elevation in III and depression in aVL)
Causes of outflow obstruction from left side (aorta) and right side (pulmonary trunk)
LEFT: aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM)
Right: PE
What should you ask the patient if they had a collapse without warning and came around quickly after
Ask about sudden death (QT syndrome!)
Differentiate AVNRT and AVRT, as types of supraventricular tachycardia
AVNRT:
AVRT:
NGL kind of baffling me rn…. use osmosis
Basically….
Fast, no p wave and regular: SVT
Fast, no pwave and irregular: AF
What type of QRS complex in sinus tachy, SVT, AF and vf
All narrow QRS complexes apart from VF which is broad
What would you think of if there was a deep S in v1/v2 and a tall r in v5/v6?
LVH by voltage critera:
S in V1 + R in V5 or V6 (whichever is larger) > or equal to 7 sqaures is LVH by voltage criteria (need to do echo to check)
Most common cause of LVH is hypertension, so this would suggest HYPERTENSION
Causes of VF
4Hs:
-Hypoxia, hypothermia, hypovolaemia, hypokalaeamia
4Ts:
Tension pneumothorax, tamponade, toxins and thrombosis
What causes the right heart failure in COPD
There is chronic hypoxia leading to vasoconstriction in the pulmonary vasculature
So the pressure goes up and there’s increased pressure for the heart to pump against
