MI complications Flashcards
quickly outline the main complications of MI
[death passing praaed close]
death
pump failure
pericarditis
rupture: myomaalcia cordis
arrhythmia
aneurysm
systemic embolism
dressler’s syndrome:pleuro-pericarditis
death
VF, LVF, CVA causing cardiac arrest
Cardiac arrest
This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.
Cardiogenic shock
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock.
This is difficult to treat.
Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture as listed below.
Patients may require inotropic support and/or an intra-aortic balloon pump.
pericarditis
Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients).
The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and
- a pericardial effusion may be demonstrated with an echocardiogram.
Features
- chest pain: may be pleuritic. Is often relieved by sitting forwards
- other symptoms include non-productive cough, dyspnoea and flu-like symptoms
- pericardial rub
- tachypnoea
- tachycardia
Causes
- viral infections (Coxsackie)
- tuberculosis
- uraemia (causes ‘fibrinous’ pericarditis)
- trauma
- post-myocardial infarction, Dressler’s syndrome
- connective tissue disease
- hypothyroidism
ECG changes
widespread ‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
Rx:
- NSAIDS- ibuprofen
- and/or echo to exclude effusion
rupture: myomalaxia cordis
Left ventricular free wall rupture
This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards.
Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).
Urgent pericardiocentesis and thoracotomy are required.
Ventricular septal defect
- Rupture of the interventricular septum usually occurs in the first week
- seen in around 1-2% of patients.
- Features: acute heart failure 9eg. raised JVP) associated with a PSM
- An echocardiogram is diagnostic and will exclude acute MR which presents in a similar fashion.
- Urgent surgical correction is needed.
Acute mitral regurgitation
- More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.
- An early-to-mid systolic murmur is typically heard.
- Patients are treated with vasodilator therapy but often require emergency surgical repair.
arrhythmias
Tachyarrhythmias
SVT :
- sinus tachy- give o2 and analgesia
- AF or atrial flutter: (compromised= DC cardioversion; otherwise rate control= digoxin + Bb)
Ventricular:
VF, is the most common cause of death following a MI.
- compromised = DC cardioversion
- else= amiodarone
- may need pacing
Other common arrhythmias including VT
- early <48hrs= reperfusion = good prog
- late >48hrs= extensive heart damage
- rx: DC shock
Bradyarrhythmias
1. Atrioventricular block is more common following inferior myocardial infarctions.= rx: pace mobitz II [has high risk of suddenly developing AVblock]
- sinus brady [esp in inf MI] rx: atropine
- ventricular brady [suggests SA + AV node damage]
Left ventricular aneurysm
LONG TERM COMPLICATION! OCCURS LATER, 4-6 WEEKS POST MI
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation.
s/s:
- LVF
- angina
- recurrent VT
- systemic emboli
ECG: persistent ST elevation and left ventricular failure.
Thrombus may form within the aneurysm increasing the risk of stroke.
Patients are therefore anticoagulated.
systemic emboli
arise from LV mural thrombosis
consider warfarin for 3mo after large anterior MI
risk of DVT + PE ===> pt’s prophalactically heparinized till fully mobile.
Dressler’s syndrome
ANOTHER LONG TERM COMPLICATION!
tends to occur around 2-6 weeks following a MI.
The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers.
It is characterised by a combination of
- fever,
- pleuritic pain,
- pericardial effusion [recurrent pericarditis
- raised ESR.
It is treated with NSAIDs. steroids if severe.
Chronic heart failure
As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.
