Myocardial Infraction pathology 20130000

Occurs when there is a sudden and total
occlusion or near-occlusion of blood
flowing through an affected coronary
artery to an area of heart muscle
Results in ischemia injury and necrosis of
the area of myocardium distal to the
occlusion
Most often associated with atherosclerotic
heart disease (ASHD)
Acute Myocardial Inlerction

More than 1,000 000 people suffer from an MI
each year and 500 00 die each year from
CAD.
Mortality usually occurs within the first several
hours of onset and at home.
Factors that have been implicated in the
pathogenesis of MI include atherosclerotic
rupture and spasm:
Acute intracoronary thrombosis
Arterial spasm

Both are potentially reversible.
Intervention should be early and
aggressive.
The time period from the onset of
symptoms to initiation of therapy is the key
determinant of success.

Infarction produces major changes in
myocardial cell function:
Electrical depolarization
Contractility
Complications of AMI are caused by one or
both of these events.
The amount of infarcted tissue is a critical
factor in determining prognosis morbidity and
mortality.

Arrhythmias in AMI are another concern
the most frequent arrhythmias are:
Tachyarrhythmias and ventricular ectopy
caused by the electrical differences between
adjacent areas of normal and ischemic
myocardium.
Bradyarrhythmias and atrioventricular blocks
are due to either increased vagal tone or
infarction directly affecting the conduction
system.

Impaired contractility results in:
Left Ventricular Pump Failure
25”o mpaired results in heart failure
40”o rTlpaired results in cardiogenic shock
Papillary Muscles (mitral valve) impaired will
result in:
Acute mitral regurgitation which may cause acute
pulmonary edema and hypotension.

Coronary Artery Disease (CAD)
Common cause of CAD is
arteriosclerosis.
Definition: a degenerative disease of the
arteries that causes thickening loss of
elasticity and hardening of the walls from
calcium.
Most common type of arteriosclerosis is
atherosclerosis.

A disease process characterized by
progressive narrowing of the lumen of
medium and large arteries (e.g. the aorta
and its branches cerebral arteries
coronary arteries).
Results in the development of thick hard
atherosclerotic plaque called atheromas or
atheromatous lesions which are most
commonly found in areas of turbulent
blood flow.

Usually occurs with aging.
It is often linked to overweight
hypertension and diabetes.

• Hypertension • Diet
• Cigarette smoking • Obesity
• Diabetes
• Elevated cholesterol
• Sex male being at
higher risk
• Lifestyle • Family history
• Type A personality

Gradual process that continues to obstruct
the coronary arteries.
As obstruction continues other vascular
pathways enlarge collateral coronary
circulation.
These arteries serve as an alternate route
for blood flow around the obstructed artery
to the myocardium.

Two major effects on blood vessels:
The disease disrupts the intimal surface
causing a loss of vessel elasticity and an
increase in thrombogenesis
The atheroma reduces the diameter of the
vessel lumen and thus decreases the blood
supply to tissues

The classic symptom is severe anginal
pain lasting longer than 15 to 30 minutes.
The pain often radiates to the jaw neck
shoulders and arms.
The pain is described as crushing
pressingconstrictingoppressive or
heavy.

Less common presentation is high
epigastric discomfort which may be a
manifestation of myocardial ischemia and
may be dismisses as indigestion.
Any prolonged or unusual indigestion
should raise suspicion particularly in a
high-risk individual.

Pain is similar to anginal pain and may radiate to
the arms neck jaw or back
Dyspnea
Anxiety Agitation
Syncope
Sense of impending doom
Nausea and vomiting
Diaphoresis
Cyanosis
Palpitations

Less common symptoms incIude•
CVA
Pulmonary edema
Shock
Ventricular tachycardia
The out-of-hospital morality in AMI is
almost entirely due to arrhythmias:
primarily ventricular fiórillation.

Treatment is based on patient history and
presenting symptoms.
Anormal ECG cannot be relied on to
exclude the diagnosis of AMI.

Oxygen: preferablywith a NRM•if not tolerated a
nasal cannula (4-6 łpm) is acceptable.
ECG Monitoring
Bradycardias occur in up to one third of patients
ínferior wall MI).
Atrial dysrhythmias occur in 10- 5“o (atrial fibrillation)
and are usually due to significant left ventricular
dysfunction.
Ventricular dysrhythmias of some type occur in almost
100”o of patients with MI.

IV access should be established as soon
as possible:
18 gauge catheter with crystalloid solution or
saline lock
May need a route for medication
administration

Relief of Pain
When a patient presents with chest pain
sublingual nitroglycerin is tried first unless
the patient is hypotensive. If the chest pain
and ECG changes resolve promptly
infarction is less likely.
Morphine Sulfate —Only to be used if SL
NTG is not successful in relieving pain.
Relief of pain alleviates anxiety and, thus
excretion of catecholamines.

Infarction develops distally to the occluded
artery
Size of the infarct determined by:
Metabolic needs of the tissue supplied solely
or predominantly by the occluded vessel
Presence of collateral circulation
Duration of time until flow is reestablished

Emergency care is directed at:
Increasing oxygen supply by administering
supplemental oxygen
Decreasing the metabolic needs and in
providing collateral circulation
Reestablishing perfusion to the ischemic
myocardiumas quickly as possible after the
onset of symptoms

Most AMIs involve the left ventricle or
interventricular septum which is
supplied by either of the two major
coronary arteries
Some patients sustain damage to the right
ventricle

Anterior, lateral or septal wall infarction is
usually the result of left coronary artery
OCClUSlOn
Inferior wall infarction (of the inferior-
posterior wall of the left ventricle) is
usually the result of right coronary artery
occlusion

Infarction can be classified into one of
three ischemic syndromes based on the
rupture of an unstable plaque in an
epicardial artery:
Unstable angina
Non-ST-elevation myocardial infarction
ST-elevation myocardial infarction

Unstable Angina
The early thrombus has not completely
obstructed corona y flow
Causes an intermittent ischemic episode that
may eventually result in complete occlusion
and AMI
Non-ST-elevation MI
Evident only with ST-segment depression or
T-wave abnormalities

ST-elevation MI
Diagnosed by development of abnormal Q waves
Pathologic0 waves sign of old infarct
Greater than 5 mm in depth Or greate than .04 sec in
duration in two or more contiguous leads

When blood flow to the myocardium ceases
cells switch from aerobic to anaerobic
metabolism
This contributes to produce ischemic pain (angina}
As cells lose their ability to maintain their
electrochemical gradients they begin to swell
and depolarize
If collateral flow and reperfusion are inadequate,
much of the muscle distal to the occlusion dies

YouTube - What causes a heart attack?

Rationale:
Evidence that AMI is most often caused by the
formation of a thrombus superimposed on a
chronic atherosclerotic lesion in a major
corona y artery.
Reperfusion therapy with a fibrinolytic agent can
successfully reopen the occluded artery and
restore blood flow to the distal myocardium,
thereby salvaging myocardium that is not yet
irreversibly damaged.

Myocardial cell death is not an
instantaneous process but actually takes
place over a period of hours. Because of
this fibrinolytic therapy initiated within this
time interval can accomplish reperfusion.

Major benefits and Risks
Reduction in Infarct-Related Mortality
Bleeding complications:
Primary concern is the possibility of intracranial
bleeding and stroke
Careful screening of patients for
contraindications and precautions can minimize
this complication.

Indications for Fibrinolytic Therapy
Recent onset of chest pain (less than 6 hours)
that is not relieved by nitroglycerin.
ST-segment elevation (greater than or equal to
1 mm) in two or more associated lead. Only
true absolute indicator.
Tall o peaked T waves in two or more
associated leads
New onset Bundle Branch Block

• History of CVA • Current treatment
aneurysm with an anticoagulant
• Intracranial or spinal • Active internal bleed
surgery or trauma within 10 days
within 2 months • Significant surgical or
biopsy procedure
• Severe uncontrolled
hypertension within the last 8
• Known bleeding weeks
diathesis • Suspected pregnancy

Dependent on the Fibrinolytic agent
selected.

May be indicated by resolution of chest
pain and or degree of resolution of acute
ECG changes.
Patient may develop perfusion
arrhythmias (ventricular tachycardia
accelerated idioventricular rhythm
bradycardia), which suggest improved
coronary blood flow.

Lidocaine and atropine should be readily
available.
It may be advisable to initiate prophylactic
lidocaine with the initiation of thrombolytic

Deł'inition: Surgical procedure
performed to open coronary vessels in
hopes of reperfusing myocardial tissue.
Potentially advantageous because it is
effective in reducing the degree of residual
stenosis in the infarct related artery and
because it may open stenotic vessels when
other therapies have failed.

Intervention may not be suitable for all
patients. There may be a significant risk of
dissection of the artery.
There has been a high incidence of
restenosis or reocclusion after angioplasty
This intervention is limited and should be
performed only at centers that have cardiac
surgical backup.

Fibrinolytic therapy should be the first line of
intervention with angioplasty as the backup.
AHA recommends that all patients receive
fibrinolytic therapy followed by angioplasty
(combined has longer duration of effect).

Coronary Artery Bypass Grafting (CABG)
Definition: As open heart surgery to relieve a
blocked heart artery. An artificial tube or part ot a
blood vessel is attached to the diseased coronary
artery. it is then connected to the aorta bypassing
the damaged artery. Surge y with imp ove the blood
supply to the heart muscle ease the work oł the
heart and help anginal pain.

Significant improvement, has been demonstrated. in
lett /entricular function after CABG in AMI.
Because there are no clear indications as to which
patients would benefit compared to those that would
be harmed by this surgery. it is not practical for
widespread use in AMI.

AICD —
Automatic Internal Cardioverter
Defibrillator
Developed fo ambulatory patients at risk of sudden
death from ventricular fibrillation
The defibrillałors monitor the ECG continuously
recognize ventricular fibrillation and ventricular
tachycardia and defibrillate or cardiover with 10-20
Y
O
UUS.
The charge is derive ed by two cup electrodes
surgicallyapplied over the apex and base of the
hea t.

Congestive Heart Failure
Left VentricularPump Failure
Cardiogenic Shock
Acute Mitral Regurgitation
Ventricular Septal Rupture

Definition: A condition in which the heart
cannot pump sufficient blood to meet the
metabolic needs of the body.
Usually occurs following an AMI.
Circulatory congestion which often results
from fluid overload is not CHF.

Myocardial failure results in reduction of stroke
volume
Sympathetic stimulation compensates to
estore stroke volume
Causes tachycardia and systemic vasoconstriction
Tachycardia is an inotropic stimulus
Increases myocardial oxygen demands
Systemic arteriolar vasoconstriction produces
increased afterload
Increases myocardial oxygen demands

Venous constriction produces increased left
ventricular filling pressure and end-diastolic
volume (preload) and acts to restore stroke
volume through the Frank Starling mechanism
The compensatory mechanisms in CHF are all
potentially detrimental to myocardial function.

History will usually determine the cause of
myocardial failure:
AMI MI
Hypertension
Patient will present with dyspnea
With effort' progressing to a rest
Usually worsens in the supine position
Patient will sit bolt upright to breath
Pulmonary rales can extend to the lung apices

If Right Ventricular Failure
Peripheral pitting edema is present
Sacral edema
Distended jugular veins
These occur especially if the patient has been at
bed rest
If Left Ventricular Failure:
Pulmonaryedema
Disłended jugular veins

CPAP!
Reduce preload and relieve pulmonary edema
Reduce afterload (vasodilators) to enhance
stroke volume and enhancement of contractile
function
Preload reduction is accomplished by IV
diuretics and nitrates
Furosemide •g' Lasix
Nitroglycerin • ' Sublingual

Define: a condition in which the left
ventricle Iails to contract forcefully enough
to maintain a normal output of blood.
Clinical manifestations will depend on the
extend of damage. A classification of
pump dysfunction that is based on clinical
criteria is the /¢iIIip-KimhaII
Classification.

Uncomplicated infarction
Negative evidence of heart failure
30’o incidence
5 % mortality

Mild-to-moderate heart failure (rales in the
lower hall of the lung field)
40’o incidence
15-20 oMortality

Severe left ventricular failure or pulmonary
edema
10’o incidence
40% mortality

Cardiogenic Shock
Systolic BP < 90 mmHg
Pulmonary vascular congestion
20% incidence
80% or greater mortality

Current managementof LV dysfunction is based
on the underlying hemooynamicderangement
Treatment depends on which Class you are
clinicallyviewing at the time
Classes 1 2 and 3 are primarily treated with
CPAP vasodilators, morphine and diuretics
Class 4 will require vasopressor agents

Define: pump failure. Can result from
pump failure, dysrhythmias mechanical
factors and obstruction flow.
Patients with shock usually have 40% or
more of their left ventricle myocardium
infarcted.

Left ventricular performance is
determined by preload afterload and
contractility
For a given preload the lower the
afterload the larger the stroke volume.
Ascontractility increases, the stroke
volume increases at the same loading
conditions.

The compensatorymechanism of
tachycardia and vasoconstriction are
detrimental
Tachycardia increases myocardial
oxygen consumption
Vasoconstriction W increases afterload on
the heart which also increases myocardial
oxygen demand

The oxygen demand cannot be met by the
available coronary artery supply resulting
in aggravation of the existing

Right Ventricular Infarction
Suspected in patient with inferior infarction
Hypotension
Distended neck veins
Treatment
Judicious fluid therapy
Dopamine
Vasodilators should be avoided

Left Ventricular Pump Failure
Hypotension
Oliguria
Cardiogenic Shock
Pulmonary vascular congestion
Decreased level of consciousness

Definition: refers to the loss of integrity
or separation of any portion of a cardiac
valve and can involve the leaflet annular
attachment chordae tendinea or
muscular support.
Potentially life-threatening if the aortic or
mitral valves involved.

Types:
Acute Tricuspid Regurgitation
Acute Mitral Regurgitation
Acute Aortic Regurgitation
Prosthetic Valve Dehiscence
Regurgitation will be discussed in greater
detail in Valvular Disease Lecture.

Delínintíon: Separation of a surgical incision
May result from technical problems or from
undermining of the suture lines owing to
infection or necrosis in surrounding tissue
Result is the same as acute regurgitant lesions
in natural valves
Dehiscenceof the aortic valve is the most
common and serious: surgical replacement is
necessary

Occurs during the course of an MI when a
necrotic intraventricular septum ruptures
Shock syndrome develops that is confused with
acute mitral regurgitation
Shock symptoms with pulmonary congestion
Initial treatment is similar to that of acute mitral
regurgitation
Vasodilators
Surgical intervention is necessary

Myocardial Infraction pathology 20130000

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