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Complication of MI
Transcript of Complication of MI
STAGE I :
STAGE II :
Acute PCARD – Stage I, II
Complication of MI
MECHANICAL COMPLICATION .
ARRYTHMIC COMPLICATION .
EMBOLIC COMPLICATION .
INFLAMMATORY COMPLICATION .
DRESSLER'S syndrome .
WHAT IS MI
Is the irreversible necrosis of heart muscle secondary to prolonged ischemia.
Complication of MI
INFARCT EXTINSION .
It is an inflammation of pericardial tissue overlying infarcted myocardium.
Most common cases are due to acute coronary syndrome (i.e. rupture of atheromatus plaque with thrombus formation above it ).
Clinical features : "severe central chest pain radiating to the left shoulder and upper limb, crushing in character and associated with excessive sweating, fatigue and dizziness .
It occur when an injury to the heart muscle causes blood to be present in the pericardium.
The incidence of early pericarditis after MI is approximately 10%, and this complication usually develops within 24-96 hrs.
Depend on ECG changes "persist for months " not clinical presentation "resolve by 2 weeks " .
ST elev, PR depression .
ST returns to baseline, flat T .
STAGE III :
T wave inversion .
STAGE IV :
radual resolution of T wave changes
Acute PCARD – Stage III
Echocardiography : may reveal a small pericardial effusion.
The mainstay of therapy usually includes aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs).
Colchicine may be beneficial in patients with recurrent pericarditis.
It is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium.
It is also known as post-myocardial infarction syndrome .
It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI.
The incidence of post-MI syndrome ranged
from 1-5% after AMI.
It is largely a self limiting disease that very rarely leads to pericardial tamponade.
The syndrome consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), a pericardial friction rub, and /or a pericardial effusion.
The symptoms tend to occur 4–6 weeks post myocardial infarction, but can be delayed for a few months after infarction. It tends to subside in a few days.
Management involves hospitalization and observation for any evidence of cardiac tamponade.
Treatment comprises rest, use of NSAIDs, and/or steroids in patients with recurrent post-MI syndrome with disabling symptoms.
Central nervous system or peripheral embolization
About 90% of patients who have an acute myocardial infarction (AMI) develop some form of cardiac arrhythmia during or immediately after the event .
The incidence of arrhythmia is higher with an ST-elevation myocardial infarction (STEMI) and lower with a non–ST-elevation myocardial infarction (NSTEMI).
Transmural AMI can interrupt afferent and efferent limbs of the sympathetic nervous system that innervates myocardium distal to the area of infarction resulting in generalized autonomic dysfunction that results in enhanced automaticity of the myocardium and conduction system.
Electrolyte imbalances (e.g, hypokalemia and hypomagnesemia) and hypoxia further contribute to the development of cardiac arrhythmia .
Premature ventricular contraction.
Ventricular tachycardia .
Ventricular fibrilation .
Accelerated idioventricular rhythm .
Sinus bradycardia .
AV block .
Ventricular arrhythmia is a common complication of acute MI, occurring in almost all patients, even before monitoring is possible.
It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium, as well as to irritable ischemic myocardium .
Premature ventricular contraction
Premature ventricular contractions occur in approximately 90% of patients with acute MI .
Wide QRS complex
Accelerated idioventricular rhythm
An accelerated idioventricular rhythm is seen in as many as 20% of patients who have an AMI.
Most episodes are short and terminate spontaneously .
They occur with equal frequency in anterior and inferior infarctions.
This rhythm occurs somewhat more frequently in patients who develop early reperfusion than in others .
The presence of accelerated idioventricular rhythm does not affect the patient's prognosis; no definitive evidence has shown that an untreated occurrence increases the incidence of ventricular fibrillation or death .
An accelerated idioventricular rhythm should be left untreated.
Ventricular Tachycardia and
This occurs in about 5–10% of patients who reach the hospital.
It is thought to be the major cause of death in those who die before receiving medical attention.
Nonsustained ventricular tachycardia occurring more than 48 hours after infarction in patients with LV systolic dysfunction (LV ejection fraction < 0.40) poses an increased risk for sudden cardiac death
electrophysiologic testing and appropriate therapy are indicated in these patients.
Sustained polymorphic ventricular tachycardia after an AMI is associated with a hospital mortality rate of 20%.
Emergency treatment of sustained ventricular tachycardia is mandatory because of its hemodynamic effects and because it frequently deteriorates into ventricular fibrillation.
wide bizzare QRS
The incidence of primary ventricular fibrillation is greatest in the first hour after the onset of infarct (4.5%) and declines rapidly thereafter .
Secondary or late ventricular fibrillation occurring more than 48 hours after an MI is usually associated with pump failure and cardiogenic shock .
No P wave , Bizarre QRS
Treatment for ventricular fibrillation is unsynchronized electrical countershock with at least 200-300 J (or biphasic energy equivalent) administered as rapidly as possible. Each minute after the onset of uncorrected ventricular fibrillation is associated a 10% decrease in the likelihood of survival .
Antiarrhythmics, such as intravenous amiodarone and lidocaine :
Facilitate successful electrical defibrillation and help prevent recurrent or refractory episodes.
After ventricular fibrillation is successfully converted :
Antiarrhythmic therapy is generally continued as a constant intravenous infusion for 12-24 hours.
Sinus bradycardia is a common arrhythmia in patients with inferior or posterior acute myocardial infarctions (AMIs). The highest incidence, 40%, is observed in the first 1-2 hours after AMI.
May be protective mechanism (reduce myocardial oxygen demand) .
Flat P wave ,Tented T wave , Wide QRS
No treatment is required other than observation .
If bradycardia sever or symptomatic (hemodynamic compromise) ,atropine may helpful in increasing HR.
A cardiac pacemaker may be required if bradycardia persists .
The rate of atrial fibrillation is 10-15% among patients who have AMIs.
The onset of atrial fibrillation in the first hours of AMI is usually caused by :
ischemic injury to the atria.
Pericarditis and all conditions leading to elevated left atrial pressure in association with an AMI.
Absent P waves.
Normal QRS shape.
Immediate electrical cardioversion is indicated for the patient in unstable condition, such as one with new or worsening ischemic pain and/or hypotension.
Synchronized electrical cardioversion to treat atrial fibrillation begins with 200 J (or the biphasic equivalent).
Conscious sedation (preferred) or general anesthesia is advisable prior to cardioversion.
For patients in stable condition, controlling the ventricular response is the immediate objective.
If the atrial fibrillation does not respond to cardioversion, IV amiodarone] or IV digoxin (in patients with LV dysfunction or heart failure) can be used to achieve ventricular rate control.
For patients who do not develop hypotension, a beta-blocker can be used. For example, metoprolol may be given in 5-mg intravenous boluses every 5-10 min, with a maximum dose of 15 mg .
Atrial flutter occurs in less than 5% of patients with AMI.
Atrial flutter is usually transient and results from sympathetic overstimulation of the atria.
Synchronized electrical cardioversion (beginning with 50 J, or the biphasic equivalent) may be needed relatively promptly because of a decrease coronary blood flow and/or hemodynamic compromise.
For patients whose atrial flutter is refractory to medical therapy, overdrive atrial pacing may be considered.
First-degree AV block
First-degree AV block is characterized by prolongation of the PR interval to longer than 0.20 seconds.
This type of block occurs in approximately 15% of patients who have an acute myocardial infarction (AMI), most commonly an inferior infarction.
Almost all patients who develop first-degree AV block have conduction disturbances above the His bundle
First-degree AV block
Prolonged PR interval
In these patients, the progression to complete heart block or ventricular asystole is rare.
No specific therapy is indicated unless associated hemodynamic compromise is present.
Second-degree AV block
Mobitz type I, or Wenckebach, AV block occurs in approximately 10% of patients who have an AMI and accounts for 90% of all patients who have an AMI and a second-degree AV block.
A second-degree AV block is associated with a narrow QRS complex and is most commonly associated with an inferior MI.
It does not affect the patient's overall prognosis.
Second-degree AV block
Prolonged PR interval ,progressive lengthening /2 beats then a drop .
A Mobitz type I block does not necessarily require treatment.
If the heart rate is inadequate for perfusion, immediate treatment with atropine 0.5-1 mg administered intravenously is indicated.
Transcutaneous or temporary transvenous pacing is rarely required.
Second-degree AV block
A Mobitz type II AV block accounts for 10% of all second-degree AV blocks (overall rate of < 1% in the setting of AMI).
A Mobitz type II block is characterized by a wide QRS complex, and it is almost always associated with anterior infarction. This type of block often progresses suddenly to a complete heart block.
Third-degree AV block
Occurs in 5-15% of patients who have an AMI and may occur with anterior or inferior infarctions.
In most patients, the level of the block is supranodal or intranodal, and the escape rhythm is usually stable with a narrow QRS and rates exceeding 40 bpm.
In 30% of patients, the block is below the His bundle, where it results in an escape rhythm with a rate slower than 40 bpm and a wide QRS complex.
Third-degree AV block
both compartments (atriums and ventricles )work independently
no relationship between P wave and QRS complexes.
Second degree(type 2)and thrid degree block:
Prognosis is dire in the setting of an anterior MI : emergent placement of temporary pacemaker( with later placement of permanent pacemaker).
In inferior MI prognosis is better, and IV atropin may be used initially. If conduction is not stored ,temporary pacemaker is appropriate .
A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.
The Killip classification is used to assess patients with heart failure
Killip I – no crackles and no third heart sound
Killip II – crackles in < 50% of the lung fields or S3.
Killip III – crackles in > 50% of the lung fields
Killip IV – cardiogenic shock.
Is a state in which inadequate tissue perfusion results from cardiac dysfunction.
Clinically defined by decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.
CAUSES OF CS
The downward spiral of Cardiogenic Shock
hemodynamic criteria and clinical presentation:
Sustained hypotension (systolic blood pressure < 90 mm Hg for at least 30 min) .
Reduced cardiac index (< 2.2 L/min/m2).
Elevated pulmonary capillary wedge pressure (>15 mm Hg).
Absence of hypovolemia, and presence of clinical signs of poor tissue perfusion (sinus tachycardia, low urine output, and cool extremities).
Establish the cause for the shock by doing ECG and Echocardiograph.
Admission to ICU.
Fluid resuscitation to correct hypotension.
Intubation and mechanical ventilation are commonly required.
Pharmacological therapy to maintain blood pressure and cardiac output (aspirin, heparin, norepinephrine, epinephrine).
Early and definitive restoration of coronary blood flow is the most important intervention (through thrombolytic therapy, IABP, CPI, CABG, etc..).
Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis.
ventricular free wall
VFWR is the most serious complication of AMI.
VFWR is usually associated with large transmural infarctions and antecedent infarct expansion.
It is the most common cause of death, second only to LV failure, and it accounts for 15-30% of the deaths associated with AMI.
VFWR leads to acute hemopericardium and death from cardiac tamponade.
advanced age greater than 70 years.
no previous MIs.
Q waves on ECG.
hypertension during the initial phase of STEMI.
corticosteroid or NSAID use, and fibrinolytic therapy more than 14 hours after STEMI onset.
ECG signs of impending VFWR have limited specificity but include sinus tachycardia, intraventricular conduction defect, and persistent or recurrent ST-segment elevation.
Echocardiography is the diagnostic tool of choice. The key diagnostic finding is a moderate-to-large pericardial effusion with clinical and echocardiographic signs of impending pericardial tamponade.
surgical repair after hemodynamic stability.
Patients may first need intravenous fluids, inotropic agents, and emergency pericardiocentesis.
Ventricular septal rupture
VSR is an infrequent but life-threatening complication of AMI.
Despite optimal medical and surgical treatment, patients with VSR have a high in-hospital.
The bimodal distribution of VSR is characterized by a high incidence in the first 24 hours, with another peak on days 3-5 and rarely more than 2 weeks after AMI.
Septal ruptures are most common in patients with large anterior MIs due to occlusion of the LAD artery causing extensive septal infarcts.
simple vs. complex
In simple septal rupture, the perforation is at the same level on both sides of the septum, and a direct through-and-through communication is present across the septum.
A complex septal rupture is characterized by extensive hemorrhage with irregular, serpiginous tracts in the necrotic tissue.
Echocardiography with color flow Doppler imaging is the diagnostic tool of choice for identifying a VSR.
Cardiac catheterization is usually required to confirm the diagnosis.
Define the site and size of septal rupture.
Assess the LV and RV function.
Estimate the RV systolic pressure.
Quantify the left-to-right shunt.
hemodynamic stabilization with the administration of oxygen and mechanical support with use of an intra-aortic balloon pump.
the administration of vasodilators diuretics, and inotropic agents.
Results from local and global LV remodeling.
MR typically occurs 7-10 days after an AMI.
Papillary muscle rupture resulting in MR occurs within 1-14 days.
Diagnosis of MR
Chest radiography may show evidence of pulmonary edema
Echocardiography with color flow Doppler imaging
Cardiac catheterization should be performed in all patients to determine the extent and severity of coronary artery disease
Treatment of MR
Medical management includes afterload reduction with the use of diuretics, sodium nitroprusside, and nitrates in patients who are not hypotensive.
Emergency surgical intervention is the treatment of choice for papillary muscle rupture.
Mitral valve replacement.
Coronary artery bypass grafting (CABG).
Left ventricular mural thrombus
It frequently develops after anterior infarcts of the LV wall. The incidence of LVMT as a complication of AMI ranges from 20-40% and may reach 60% in patients with large anterior-wall AMIs who are not treated with anticoagulant therapy.
Anticoagulant therapy may substantially decrease the rate of embolic events by 33% compared with no anticoagulation.
If MI is followed by LV regional wall akinesia or dyskinesia with blood stasis, injury to and inflammation of the endocardial tissue that provides thrombogenic surface, and a hypercoagulable state.
The most common clinical presentation of patients with LVMT complicating an MI is stroke. Most episodes occur within the first 10 days after AMI.
Physical findings depend on the site of embolism.
Transthoracic echocardiography remains the imaging modality of choice and is 92% sensitive and 88% specific for detecting LVMT.
Apical 2-chamber view depicts a large left ventricular apical thrombus with mobile extensions.
Early anti-coagulation (i.e., within hours of the acute event) with oral heparin or warfarin for 3 to 6 months.
Incidence of mural thrombus may be reduced in patients receiving thrombolytic therapy very early after the onset of infarction (i.0.. within 3 h).
In the survivor of a large anterior myocardial infarction with or without associated heart failure, full-dose intravenous heparin or subcutaneous should be instituted immediately.
Left ventricular aneurysm
Left ventricular aneurysm (LVA) is defined as a localized area of myocardium with abnormal outward bulging and deformation during both systole and diastole. The rate of LVAs after AMI is approximately 3-15%.
Acute transmural MI is often followed by thining and stretching of the infarcted segment, this leads to increase in the wall stress with progressive dilatation and hypertrophy of the remaining ventricle (ventricular remodeling).
Infarct expansion can occur over a few days or weeks, but remodeling can take years.
A history of MI and third or fourth heart sounds paradoxical impulse on the chest wall are all common findings from the patient's history and physical examination.
The chest radiograph may reveal an enlarged cardiac silhouette.
Is 93% sensitive and 94% specific for detection of LVA.
But cardiac catheterization remains the standard for establishing the diagnosis.
is characterized by ST elevation that persists several weeks after AMI and that appears in the same leads as those showing the acute infarct.
Patients with small or clinically insignificant aneurysms can be treated conservatively with close follow-up.
Medical therapy generally consists of the use of (ACE) inhibitors .
Anticoagulation is required when patients have severe LV dysfunction and/or thrombus in the LV or aneurysm.
Surgical resection of the LVA is indicated if severe heart failure, ventricular tachyarrhythmias refractory to medical treatment, or recurrent thromboembolism is present.