Coronary Artery Disease

 

Epidemiology

Ischemic Heart Disease due to Coronary Artery Disease is the leading cause of death in the United States.  It accounted for more than 500,000 or 1 in 5 deaths in 1997.  The American Heart Association estimates the cost of treating coronary artery disease to be about $118.2 billion.

 

Pathology

Coronary atherosclerosis is the most common cause of coronary artery disease.  That is the accumulation of lipid and fibrous tissue within the coronary artery, progressively narrowing the lumen of the vessel.  Additionally, there is the development of atheromas, complex atherosclerotic plaques consisting of lipid, fibrous tissue, collagen, calcium, cellular debris and capillaries.  As the lumen narrows, resistance to flow increases and myocardial blood flow is compromised.  The final steps in the process producing the insult can occur like this:

  1. Progressive luminal narrowing by plaque enlargement.
  2. Hemorrhage into the atheromatous plaque.
  3. Thrombus formation initiated by platelet aggregation.
  4. Embolization of a thrombus or plaque fragment.
  5. Coronary artery spasm.

 

Ischemia

Oxygen demand in excess of capacity of coronary vessels can deliver results in localized ischemia.  When tissue becomes ischemic, loss of function occurs within minutes.

Transient ischemia causes reversible changes at cellular and tissue level.

Lack of oxygen causes shift from aerobic to anaerobic metabolism, which causes an increase in lactic acid production, decreasing cellular pH and increasing the hydrogen ion concentration.  This impairs left ventricular function, causing reduction of emptying on systole, decreasing cardiac output: Increases LVEDP and Increases PCWP.

Clinically the patient has an increase in BP and heart rate prior to the onset of pain. This is a sympathetic compensation in response to the depression of myocardial function.  With pain, there is also an increase in catecholamine release.  The resultant ECG changes are T wave inversion and ST elevation.  Ischemic attacks subside within minutes if the imbalance between supply and demand is corrected

 

Determinants of Myocardial Oxygen Demand

ü      Heart Rate                   

ü      Wall Tension

ü      Contractile force          

ü      Muscle Mass               

ü      Intraventricular pressure

ü      Ventricular radius

 

Infarction

Prolonged ischemia, of over 30-40 minutes causes irreversible cellular damage and necrosis, loss of contraction and alteration of conduction.  Myocardial infarction is ischemic death of myocardial tissue associated with obstruction of a coronary vessel.  This area of infarction becomes necrotic due to an absolute lack of blood flow.  The necrotic cells are inactive electrically and their cell membranes rupture releasing their cellular contents into the interstitial spaces.  Potassium release by these cells causes a relative hyperkalemia to the surrounding cells, and interferes with their electrical activity. (Arrhythmias- usually PVCs)

Infarct is surrounded by an area of injury and an ischemic zone. 

Some of the cells in the injured area will recover.  The ischemic zone has relatively viable tissue. The boundaries of these zones may change post infarction and will the relative success of measures to restore blood supply.

The ultimate size of the infarct is dependent upon this ischemic zone. Reversal of ischemia, will decrease the amount of necrosis. It can be reduced by decreasing myocardial oxygen consumption and by increasing oxygen delivery to the tissues.

The location of the infarct is important.  For instance inferior wall infarctions, usually occur from right coronary artery occlusions, and can be associated with variable degrees of heart block.  (Usually the AV node receives its blood supply from the same vessel that nourishes the inferior wall)

It appears that most episodes of myocardial ischemia leading to an acute myocardial infarction occur in the early morning hours.  This may be related to diurnal rhythms of catecholamines and cortisol levels as well as enhanced platelet aggregation.

 

ECG Changes

Dead tissue produces Q or QS waves as a result of the absence of polarization in the cells.  Dead cells leak K+.  The ECG lead reflecting the site of the infarct will show Q waves of greater amplitude.  QS waves persist after recovery because cardiac tissue does not regenerate but is replaced by scar tissue, which is not capable of repolarization.

Injured tissue produces ST segment shifts.  Injured muscles cannot become fully polarized.  Na+/K+ pump may not work because energy requirements are not met.  ST changes disappear since cells either live or die.

Ischemic tissue produces inverted T waves.  Repolarization occurs in an altered sequence and more slowly in ischemic tissue.  T wave inversion tends to disappear with adequate perfusion.

 

 

Infarcted Muscle (healing)

1.   Bruised, cyanotic from stagnation of blood.

2.   Cellular edema and inflammatory response with the mobilization of WBC's beginning within 24 hours.

3.   Cardiac enzymes are released

4.   Tissue degradation and removal of necrotic debris begins on the second or third day.  Necrotic wall is relatively thin.

5.   10 days, scar formation and revascularization begins

6.   Scar finished by third week

 

Sequelae

1.   Reduced contractility

2.   Abnormal Ventricular wall motion

3.   Altered Ventricular wall compliance

4.   Decreased stroke volume

5.   Decreased ejection fraction

 

All of these are dependent upon

1.   Infarct size

2.   Infarct location

3.   Residual or uninvolved myocardium

4.   Collateral circulation

5.   Cardiovascular compensatory mechanisms

 

Clinical Presentation

The abrupt on set of symptoms with pain is the most significant presenting symptom.  The pain is described as severe, crushing, suffocating.  There is usually some radiation of the pain from the substernal area to the neck, shoulders and arms.  Unlike angina, the pain from an MI is not relieved by NTG or rest.  The patient is often, anxious, restless, pale and diaphoretic.  Although, many ignore their symptoms and are likely to deny that they are having any significant discomfort.

 

Complications

Congestive Heart Failure is the most common complication following an MI.  Left ventricular dysfunction causes pulmonary vascular congestion, while right ventricular dysfunction results in systemic vascular congestion.  Left sided heart failure is the most common.  As left ventricular function is compromised, ventricular emptying is decreased.  Left ventricular pressures rise, transmitting backwards into the pulmonary vasculature.  As these pressures increase, fluids leak into the interstitial spaces, causing pulmonary edema as fluid leads into the alveoli.

Clinically the patient presents with dyspnea, oliguria, weakness, fatigue, pallor, weight  gain.  Physical exam reveals rales, and a third heart sound due to dilation and non-compliance of the ventricle during diastole.

 

Pericarditis is another common complication.    It usually appears 2-3 days after the infarct.  The patient typically describes pain that is increased on inspiration.  It is caused by the injured myocardium rubbing against the pericardial sac.  Occasionally is friction rub is heard.

 

Arrhythmias are a major complication of an MI.  These can be due to enhanced automaticity, re-entry phenomena, or alterations in repolarization.

 

Treatment

1.   Relief of pain                                      

  1. promotion of oxygenation                   
  2. Prevent further occlusion
  1. Promote improvement of circulation
  2. Prevent complications

 

MSO4

Usually given IV 1-2 mg/3-4 min till pain is relieved

***Decreases work of breathing and reduces metabolic demand for oxygen

Sedative to relieve pain, anxiety and promote relaxation

Depresses respiratory center, decreasing rate and work of breathing

Peripheral vasodilating effect, which contributes to relief of pulmonary edema

***MSO4 – triggers histamine release;  reduces preload by increasing venous capacitance thereby decreasing venous return.

Result - Decreased LVED volume, and myocardial oxygen consumption is reduced.

 

NTG

Direct effect on vascular smooth muscle resulting in generalized vasodilation,, reduced venous return, and decreasing cardiac output reducing the myocardial oxygen demand

Reduced venous return, decreased LVEDP and improves blood flow to subendocardial layers of the myocardium.  Increases collateral coronary blood flow.

 

ã JPFrizzell 2000

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