Acute Pericarditis
- What clinical features can be seen?
- What can cause it?
- What investigations are done?
- How is it managed in idiopathic / viral cases?
- chest pain - often relieved by sitting forward, may be pleuritic
- dyspnoea
- dry cough
signs: tachypnoea, tachycardia, pericardial rub
+/- JVP increasing with inspiration
(pathophysiology: poorly compliant myocardium/pericardium exacerbated bu increase in thoracic pressure causes blood backlog therefore increase in JVP)
- malignancy, trauma, viral infection
- TB
- post MI (AKA Dressler’s syndrome)
- connective tissue disease
- hypothyroidism
- uraemia (causes fibrinous pericarditis)
mnemonic: 3 generals, then work through the systems
3. ECG - widespread ST elevation not corresponding to vascular territories - saddle-shaped ST elevation - PR depression is most specific
all patients with suspected pericarditis should get trans thoracic echo
- colchicine
- NSAIDs (naproxen, ibuprofen)
What are the reversible causes of cardiac arrest?
4Hs
- hypoxia
- hypovolaemia
- hypothermia
- hypokalaemia (and hyper), hypocalcaemia, hypoglycaemia, acidosis
4Ts
- thrombosis
- tension pneumothorax
- tamponade
- toxins
Advanced life support
- When is a single shock and then 2 minutes of CPR not carried out?
- If IV access cannot be achieved how should drugs be given?
- What drugs should be given when?
- What should happen if you suspect PE?
- if cardiac arrest in monitored patient (e.g. in coronary care ward) then give 3 shocks back to back
- Intra-osseously (IO)
- Adrenaline
- non-shockable rhythm: 1mg ASAP
- shockable: 1mg after the 3rd shock and again every 3-5 mins
Amiodarone (lidocaine can be used as alternative)
300mg after 3 shocks, another 150mg after 5 shocks
mnemonic: everything is in 3s and 5s
4. give thrombolysis (e.g. alteplase) , continue CPR for 60-90 mins
Describe the management of angina.
- aspirin
- statin
- sublingual GTN for angina attacks
beta blocker OR calcium channel blocker
- if CCB on its own use rate-limiting e.g. verapamil or diltiazem
- if with another drug use nifedipine (longer acting dihyropyridine)
if still symptomatic add another drug
if patient cannot tolerate CCB or BB add one of: long acting nitrate, ivebradine, nicorandil or ranolazine
What is the lifelong treatment guidance following the diagnosis of the following:
- ACS or PCI
- Ischaemic stroke / TIA
- PAD
- 1st line: aspirin lifelong and ticagrelor for 12 months
(can give prasurgrel for 12 months instead of ticagrelor if PCI)
2nd line: if aspirin contraindicated, give clopidogrel
- 1st line: clopidogrel
2nd line: aspirin + dipyridamole
- 1st line: clopidogrel
2nd line: aspirin
Aortic dissection CFs
- What is it associated with?
- What clinical features can be seen?
- Which symptoms may be seen with involvement of the following arteries:
a) coronary arteries
b) spinal arteries
c) distal arteries - What complications can be seen in
a) forward tear
b) backward tear
- hypertension (most important RF)
- bicuspid aortic valve
- collagens: marfans, ehlers-danlos
- turners, noonans syndromes
- pregnancy
- syphilis
- tearing chest / back pain (chest pain typically type A, back pain typically B)
- a) angina
b) paraplegia
c) limb ischaemia
4
a)
- pulse deficit: weak absent pulses, variation in pulse strength and BP between arms
- stroke
- renal failure
b)
- aortic regurgitation
- inferior MI (due to involvement of RCA)
Aortic Dissection Investigations and Management
- Define
a) stanford classification type A (DeBakey II)
b) stanford classification type B (DeBakey III)
c) DeBakey I - What is seen on investigation?
- What is the management for types
a) A
b) B
1
a) ascending aorta (2/3rds of cases)
b) descending aorta (1/3rd of cases) [rarely extends proximally but will extend distally]
c) originates in ascending extending to at least aortic arch
- CXR - widened mediastinum
CT angiography CAP - false lumen
trans oesophageal echo if patient to risky to take to CT scanner - a) surgery - control BP 100-120 before surgery
b) conservative
- IV labetalol to control BP
- bed rest
Aortic Regurgitation
- What clinical features are seen?
- What are the causes due to
a) valvular disease
b) aortic root disease
- nailbed pulsation (Quinke’s sign)
- collapsing pulse (wide pulse pressure)
- Headbobbing (De Musset’s sign)
- early diastolic murmur
+ heard best leaning forward, on expiration at left parasternal edge
+ intensity increased by handgrip manoeuvre
Severe AR: mid diastolic Austin-Flint murmur caused by partial closure of mitral valve due to aortic regurgitation streams
2
a)
- rheumatic fever
- endocarditis
- connective tissue disease e.g. RA / SLE
- bicuspid aortic valve
b)
- aortic dissection
- hypertension
- collagen: marfan’s, ehlers-danlos
- syphilis
- spondyloarthropathies (Ank. spond.)
THINK: many of the same causes as aortic dissection
Aortic Stenosis
- a) what clinical features can be seen?
b) What additional features can be seen in severe disease - What can cause it?
- What is the management if
a) asymptomatic
b) symptomatic
- a)
- chest pain
- dyspnoea
- pre-syncope / syncope (possibly brought on by exertion)
- ejection systolic murmur
+ radiates to carotids
+ reduced by valsalva manoeuvre
mnemonic: SAD - syncope, angina, dyspnoea on exertion
THINK: it is the systolic murmurs which radiate because this is when the heart has to create the most pressure to pump blood round the full body
NOTE: no radiation of murmur to carotids implies aortic sCLERosis over stenosis
b)
- narrow pulse pressure - slow rising pulse
- thrill
- soft / absent S2
- S4
- LV hypertrophy / failure
- degenerative calcification (>65)
- bicuspid aortic valve (<65)
- post-rheumatic disease
- supravalvular: William’s syndrome
- subvalvular: hypertrophic obstructive cardiomyopathy
3
a) observation
(and check aortic valve gradient <40mmhg otherwise consider surgery)
b) surgery: either valve replacement
(surgery if low/medum risk or transcatheter if high risk)
OR
balloon valvuloplasty (in children if no calcification or elderly wouldn’t cope with valve replacement)
Mitral Regurgitation
- What can cause it?
- What clinical features are seen?
- What investigations are done?
- MI
- rheumatic fever
- endocarditis
- congenital
- often asymptomatic until cardio defects of HF, arrhythmias or pulmonary hypertension
pan systolic murmur which radiates to the axilla
+/- quiet S1
- echo
- ECG may show large P wave indicating atrial enlargement
Mitral Stenosis
- What is almost exclusively the cause?
- What clinical features are seen?
- What can be seen on CXR?
(management as per aortic stenosis)
- rheumatic fever
- AF
- low volume pulse
- malar flush
- auscultation: loud S1, opening snap, mid-late diastolic murmur
- Left atrial enlargement
Arrhythmogenic right ventricular cardiomyopathy
- What is the pathophysiology?
- What clinical features can be seen?
- What is seen on investigation?
- How is it managed?
- What is Naxos disease?
- autosomal dominant condition where right ventricle is converted to fatty / fibrofatty tissue
- palpitations
- syncope
- sudden cardiac death
- ECG changes in V1-3 (since this is the RV!!)
- T wave inversion
- epsilon wave: positive deflection at end of QRS complex (present in about 50%)
MRI can identify fibrofatty tissue
- catheter ablation to prevent VT
- cardioverter-defibrillator implanted
- autosomal recessive ARVC with triad of: ARVC< palmoplantar keratosis, wooly hair
Atrial Flutter
- What is seen on the ECG?
- What is curative for most patients?
- sawtooth baseline with atrial rate of 300 bpm
- ventricular rate 100 or 150bpm
- radio frequency ablation of tricuspid valve isthmus
NOTE: atrial flutter can have same treatment as AF but:
- is more sensitive to cardioversion so requires lower energy levels
- medication may be less effective
Atrial myxoma
- What clinical features are seen?
- What is seen on investigation?
- mid-diastolic ‘tumour plop’
- AF - emboli
- resp: dyspnoea, clubbing
- general: fatigue, weight loss, pyrexia
- echo - pedunculated tumour attached to the fossa ovals region
Atrial Septal Defects
- What clinical features can be seen?
- There are two types. What is associated with
a) ostium secundum
b) ostium primum
- ejection systolic murmur
- fixed splitting of S2
- embolism may move from right to left side causing stroke
pathophysiology: atrium are filling during systole, pressure in the left is higher causing shunt of blood from left to right, this causes overfilled RA causing
- embolus formation
- fixed S2 splitting
2
a)
- tri-phalangeal thumbs (Holt-Oram syndrome)
- RBBB + right axis deviation
b)
- abnormal AV valves
- RBBB + left axis deviation
