Pathophysiology

Heart Physiology 

Figure 4. Normal Heart Blood Flow (Pediatric Heart Specialists, 2019)

Deoxygenated blood travels from the superior vena cava or the inferior vena cava to the right atrium of the heart. Blood can also travel to the right atrium through the coronary veins and enter the right atrium through the coronary sinus.  During diastole, when the heart relaxes, blood travels through the tricuspid valve into the right ventricle. The right ventricle the contracts and pushes blood through the pulmonary valve and into the pulmonary arteries, which carry blood to the left and right lungs. The blood is oxygenated in the lungs and returns to the heart’s left atrium via pulmonary veins. This completes the pulmonary circulation. Systemic circulations begins with the blood in the left atrium passing through the mitral valve into the left ventricle during heart relaxation. The left ventricle contracts and sends blood through the aortic valve into the aorta. The aorta carries the blood to the rest of the organs and tissues throughout the body. Oxygen is exchanged at the organs and tissues for carbon dioxide. The blood is now deoxygenated and travels back to the right atrium via the inferior and superior vena cava (Osmosis, 2017).

Pathophysiology of Myocardial Infarction

What is myocardial infarction?

Otherwise known as a “heart attack,” myocardial infarction is diagnosed when evidence of myocardial necrosis exists. Myocardial infarction is a sudden blockage of blood flow to cardiac cells caused by a blood clot within a coronary artery, commonly caused by atherosclerotic plaque rupture and thrombus formation. A thrombus/atherosclerotic plaque can form on a coronary artery vessel wall and eventually cause an obstruction. Also, an embolus (a dislodged thrombus) can travel to the heart and get lodged in a coronary artery, which prevents oxygen-rich blood from flowing to the areas of the heart that the blood vessel supplies. Cardiac cells have a very large oxygen demand. A decrease in oxygen-rich blood flowing to the heart can cause ischemia. If not aggressively treated and reversed, it only takes 20 minutes for tissue necrosis and cellular death to occur (McCance & Huether, 2019).

Risk Factors

Figure 5. Risk Factors for Heart Attack (Cardiac Wellness Institute, 2018)

Diagnosis

  • Troponin– When necrosis occurs in myocardial tissue, troponin (a cardiac intracellular enzyme) is released from cell membranes into the interstitial spaces. As these enzymes are carried through the lymphatics and bloodstream, it’s elevation can be recognized during serological testing. Otherwise known as cTnI, cardiac troponin is the most precise indicator of myocardial infarction and can be detected 2-4 hours after onset of symptoms. Other markers such as CPK-MB and LDH are released by damaged cardiac cells and laboratory findings with finding these changes during serologic testing (McCance & Huether, 2019).
  • ECG/EKG– Electrocardiogram to check for electrical activity changes
  • Nuclear Medicine Scan– Used to assess the flow of blood to the heart muscle
  • Angiography- Used to look for blockages or to rule out other causes of symptoms

Figure 6. Myocardial Infarction Symptoms at Onset (Carmie Frost, 2019)

Zones of Injury

The extent of injury to the cardiac tissues may not appear for several hours. Injuries due to these ischemic conditions create three zones. A zone of ischemia, zone of infarct and zone of hypoxic injury.  The period in which cardiac cells are ischemic determines the size and character of the infarction. The zone of infarction is the area of the myocardium that was completely deprived of oxygen which resulted in cellular death. The area directly surrounding the zone of infarction is called the zone of hypoxic injury, which will return to normal, progress to necrosis or undergo the formation of scar tissue (remodeling). Remodeling can be limited and even reversed if rapid restoration of oxygen-rich blood can be restored through aggressive treatment and medications. The zone of ischemia is usually reversed once these treatments are provided. (McCance & Huether, 2019)

Figure 7. Figure 33.23 (McCance & Huether, 2019)

STEMI vs. Non-STEMI

  Most myocardial infarctions can be classified as being one of 2 types, depending on the extent of the injury caused by necrosis.

  1. STEMI (Transmural MI) – A STEMI is characterized by complete occlusion of the blood vessel lumen, resulting in transmural injury and infarct from the endocardium extending through to the pericardium. The acronym STEMI represents marked elevations in the ST segments during myocardial infarction as shown on ECG. It only takes 30-60 seconds of hypoxia for these cardiac changes to appear on ECG. This type is the most serious form of myocardial infarction and carries the highest risk for fatal complications. Immediate recognition and treatment is required. It is unsettling to note that 1/3 of patients present with STEMI as the first sympathetic manifestation of coronary disease (McCance & Huether, 2019).
  2. Non-STEMI (sub-endocardial MI) – A Non-STEMI occurs when persistent coronary occlusion of the cardiac blood vessels leads to myocyte necrosis of the myocardium. During a Non-STEMI, the plaque rupture and thrombus formation cause partial occlusion to the vessel. With this type of myocardial infarction, the thrombus causing the infarct may have broken up before total tissue necrosis could have extended beyond the myocardial layer of the heart. The ECG changes associated with this type of myocardial infarction show ST-depression and T-wave inversion (McCance & Huether, 2019).

Figure 8. Acute Coronary Syndrome (Sneath & Zhao, 2019)

What else happens?

Cardiac cells require very high levels of oxygen and can only withstand ischemic conditions for approximately 20 minutes before the cells begin to die. If restoration of oxygen occurs within that 20-minute timeframe the cells can remain viable. Myocytes consume so much oxygen that it only takes 8-10 seconds of decreased oxygen-rich blood flow for the myocardium to become cooler and cyanotic. After that initial 8 second timeframe, glycogen stores begin to decrease and anaerobic (without oxygen) metabolism begins. The heart’s oxygen demands are so high that even after glycolysis occurs, only 65-70% of the demands of the myocardial cell are met. Glycolysis also does not produce enough ATP to provide the heart enough energy required to maintain function (McCance & Huether, 2019).

The accumulation of lactic acid and hydrogen ions results in the sensation of chest pain and a low cellular pH, creating an acidic environment and compromising the myocytes. The resulting acidosis can make the myocardium more negatively affected by the damaging effects of lysosomal enzymes, suppress impulse conduction and contractile function which leads to the heart’s inability to pump adequately enough to supply the rest of the body with oxygen-rich blood (McCance & Huether, 2019).

The ischemia experienced in myocardial infarction is a precursor to a series of events that create an even more undesirable state within the body. As the heart is deprived of oxygen-rich blood due to a blocked artery caused by a thrombus, electrolyte disturbances involving the loss of potassium, calcium, and magnesium from cells occur. In addition, myocardial cells release catecholamine (epinephrine and norepinephrine) when deprived of oxygen. This can cause sweating, nausea, vomiting. As a result, glycogen, glucose and stored fat from other cells within the body are released into the bloodstream. This can damage the cellular membrane, elevate blood glucose levels and suppress pancreatic B-cell activity. A reduction in B-cell activity will reduce insulin secretion which results in an even higher blood glucose level. The release of these catecholamines can result in functional abnormalities, dysrhythmias and heart failure (McCance & Huether, 2019).

Another negative effect as a result of the ischemia that occurs is the release of angiotensin II, which causes vasoconstriction and fluid retention. Vasoconstriction causes the already dis-functioning heart to require more oxygen and beat harder to push the blood through the smaller vasculature. To top it off, the retention of fluid within the body gives the heart an even larger volume to circulate. These effects cause the heart to demand more oxygen in an already oxygen-deprived state. The heart has also experienced the loss of contractility when the heart is not pumping enough blood out to the rest of the body, which results in a lack of oxygen to those areas as well. The left ventricle will begin to hypertrophy, which will result in additional myocardial dysfunction (McCance & Huether, 2019).

 Figure 9. Functional Changes Post Myocardial Infarction (Carmie Frost, 2019)

Repair process

During the repair process, 3 steps occur. These steps are heavily dependent upon the availability of nutrients and hormones, for optimal recovery. These steps include:

  1. The first 24hrs Leukocytes infiltrate the damaged/necrotic area and proteolytic enzymes from scavenger neutrophils begin the process of degradation. During this time frame, the patient can also be experiencing arrhythmias and cardiogenic shock.
  2. 1-3 days Inflammation of the pericardium, triggered by cellular death. This inflammation can also lead to pericarditis.
  3. 3-14 days Proliferation of fibroblasts for scar formation. A weak and vulnerable collagen matrix is deposited. This area can easily be reinjured! Encourage stress reduction!
  4. 2 weeks + The unaffected muscles in the heart start picking up the slack and begin to grow. Which can result in left ventricle enlargement and decreased contractility which can lead to pulmonary congestion and hypoxia.
  5. 6 weeks+ Scar tissue that is less capable of contracting and relaxing, than the previous tissue, is in place.

(McCance & Huether, 2019).