3. Ventricular dysfunction
• After STEMI, LV undergoes a series of
changes in shape, size and thickness in both
infarcted and non infarcted regions.
• This is called ventricular remodeling :
generally precedes CHF in months to years.
3
4. • Acutely, ventricle begins to dilate, which
results from the expansion of the infarct, i.e.,
slippage of muscle bundles, disruption, of
normal myocardial cells & tissue loss within
the necrotic region resulting in
disproportionate thinning and elongation of
infarct zone.
4
5. • Later, lengthening of the non infarcted segments
occurs as well.
• Overall chamber size enlarges.
• Greater the dilation of anterior wall and ape of
LV, more marked hemodynamic impairment ,
more frequent heart failure and poor prognosis.
• Mx- ACE inhibitors, ARBs, and other
vasodilators (nitrates) should be started
5
6. Hypovolemia
• It may be secondary to previous diuretic use,
to reduced fluid intake during early stages of
illness, or due to vomiting associated with pain
or medications.
• Consequently hypovolemia should identified
and corrected.
6
7. • Central venous pressure should be monitored
but usually reflects RV filling
• Optimal level should be reached ~ 20 mmHg
with cautious fluid administration.
7
8. Congestive heart failure
• Management is very similar to acute heart
failure secondary to other heart diseases.
• Diuretics- extremely effective as they diminish
pulmonary congestion.
• LV pressures fall and orthopnoea , PND
improves.
8
9. • Nitrates decrease preload and congestive
symptoms
• Oral isosorbide dinitrate, topical nitroglycerine
ointment and iv nitroglycerine, all have
advantage over diuretics of lowering preload
through venodilation without decreasing total
plasma volume.
• ACE inhibitors are ideal class of drug for
management of ventricular dysfuction after
STEMI.
9
10. Cardiogenic shock
10
• Acute MI with LV dysfunction remains the most
frequent cause of Cardiogenic shock.
• Although incidence is declining due to increasing
use of early mechanical reperfusion theraapy for
MI.
• A profound depression of myocardial contractility
results in a reduced cardiac output,low BP, &
ongoing myocardial ischemia.
11. 11
Among pts of of cardiogenic shock
on admission
during hospitalization
course
12. • Causes of Cardiogenic Shock secondary to
Acute MI
-Left Ventricular Failure
-Ventricular Septal Rupture
-Papillary muscle/Chordal rupture-severe MR
-Ventricular free wall rupture
-Other conditions complicating large
myocardial infarctions
12
13. Right ventricular infarction
• 1/3rd of inferior wall MI patients have minor
degree of RV necrosis.
• Occasionally patients with inferoposterior LV
infarction also has extensive RV infarction.
• Signs of RV failure- raised JVP, hepatomegaly,
kussmaul’s sign
• Volume expansion to maintain adequate RV
preload.
13
14. Venticular Septal Rupture(VSR)
• VSR occurs a median of 24hr after infarction
but may occur upto 2weeks later.
• Incidence of infarction related VSR without
perfusion was 1-2% but has decreased to 0.2%
in the era of reperfusion.
• Current guidelines recommend immediate
surgical VSR closure,irrespective of patient’s
hemodynamic status.
• For patient ineligible for surgery interventional
percutaneous VSR umbrella device closure has
been developed 14
15. Mitral Regurgitation
• Acute severe MR due to papillary muscle
dysfunction or rupture may complicate MI &
result in cardiogenic shock.
• Afterload reduction with IABP and,if tolerated,
vasodilators to reduce pulmonary edema is
recommended as a bridge to surgery or
interventional treatment.
• MV repair or reconstruction is the definitive
therapy.
15
16. ARRHYTHMIAS
• Arrhythmia after MI is a common clinical
problem requiring promt recognition and
treatment.
• TYPES:-
1.Ventricular Arrhythmia
2. Supraventricular Arrhythmia
16
17. VENTRICULAR ARRHYTHMIA
A. Accelerated idioventricular rhythm:-
• It is a common arrhythmia seen in peri-infarct
period & is generally considered a merker of
reperfusion.
• Rhytm is benign & self limited and No
treatment is recommended.
17
18. B. Premature Ventricular Contractions :-
• It may be a marker of cardiac electrical
instability.
• PVC have long been identified as a risk factor
for sudden cardiac death(SCD).
• The mainstay of treatment remains beta
blockers.
18
19. C. Non-sustained Ventricular Tachycardia :-
• Defined as at least 3 consecutive tachycardic
ventricular beats self-terminating in less than
30secs.
• Mainstay of therapy in the period shortly after MI
is similar to that of PVCs and includes beta
blockers and other anti-arrhythmic drugs if
appropriate.
19
20. D. Ventricular Tachycardia & Ventricular Fibrillation
:-
• Approximately 6% of patients with acute MI will
develop VT or VF and is associated with increased
in-hospital and long-term mortality.
• Treatment of Ventricular Arrhythmia depends on
clinical stability.
• Pulseless VT and VF should be treated according
to ACLS guidelines including defibrillation and
CPR.
• Antiarrhythmic drugs like amiodarone may be
indicated when defibrillation attempts are
unsuccessful or in recurrent VA.
20
21. • In acute setting , IV anti-arrhythmic drugs like
amiodarone and lidocaine can suppress unstable
ischemic Ventricular arrhythmias.
21
22. Supraventricular Arrhythmias
A. Sinus Bradycardia :-
Occurs in 15-25% of patients after MI especially
involving the inferior wall.
Sinus bradycardia associated with AMI resolves
within 24hr and is associated with worse outcomes.
Medical treatment with IV atropine or
temporary/permanent pacing is indicated when there
is associated hemodynamic instability.
22
24. B. Sinus Tachycardia:-
• Occurs in upto 40% of patient with AMI.
• It is non-specific and may reflect
catecholaminergic surge ,pain ,hemodynamic
compensation, medication effects.
• Importantly, because sinus tachycardia may reflect
compensatory process, caution should be used in
initiating treatment including use of beta blockers.
24
25. C. Atrial Fibrillation/Atrial Flutter :-
• 6-21% of patient with MI develop Atrial
Fibrillation.
• Importantly, more than 90% of patient with
recorded AF were asymptomatic.
• AF causing hemodynamic compromise requires
standard ACLS guideline treatment including
emergent cardioversion or pacing and infusion of
anti-arrhythmic & rate control drugs.
• Otherwise mainstay of therapy follows standard
management strategies,in combination with stroke
risk management.
25
27. PERICARDITIS
• Pericardial rubs and pericardial pain are frequently
encountered in patients wit STEMI involving
epicardium.
• Complain of pain radiating to either trapezius
muscle is typical of pericarditis.
• Usually managed with aspirin(650mg four times a
day).
27
28. THROMBOEMBOLISM
• Thromboembolism is considered to be an
important contributing cause of death in 25%
patient with STEMI.
• Thromboembolism typically occurs in association
with large inafrcts(especially anterior), CHF.
• It often presents as a major complication such as
hemiparesis(cerebral circulation) or
hypertension(renal circulation).
• Systemic anticoagulation should be undertaken as
the incidence of embolic complications markedly
decreases.
28
29. LEFT VENTRICULAR ANEURYSM
• LV aneurysm occurs in full thickness infarct that
has been replaced by fibrous tissue.
• Most of LV aneurysm are asymptomatic however
large symptomatic aneurysm can cause heart
failure, ventricular tachyarrhythmias & sudden
cardiac death.
• LV aneurysm managed through medical treatment
directed towards its complications with
anticoagulation.
• Surgical resection in a large aneurysm ,valvular
dysfunction or worsening complications. 29
