ACS happens when a disrupted atherosclerotic plaque in the coronary artery stimulates platelet aggregation and the formation of the thrombus. It is the thrombus that forms in the tissue that prevents myocardial perfusion. In the past researchers thought that it is primarily the narrowing the coronary artery that causes a reduction in blood flow. But more recent studies indicate it is the rapture of the unstable, vulnerable plaques with associated inflammatory changes.
Cells that are found in the heart need oxygen and adenosine triphosphate to maintain contractility and electrical stability that is required for normal conduction. Recognized respiration of glycogen takes over; less ATP is produced leading to the failure of the sodium-potassium pump and the calcium pumps and accumulation of hydrogen ions and lactate, resulting in acidosis. At this point, infarction or cell death will happen unless intervention has initiated that limit or reverse ischemia.
During the ischemic phase, the cells exhibit both aerobic and anaerobic metabolism. If perfusion to the myocardial cells continues to decrease aerobic respiration stops and anaerobic metabolism is eventually extremely diminished. This phase is called the injury phase. If myocardial perfusion is not restored within 20 minutes, the death of myocardial cells results and the effects are irreversible.
Impaired myocardial contractibility is as a result of scar tissue replacing healthy tissue in the damaged area. Scar tissue formation reduces cardiac output, which limits perfusion to vital organs and peripheral tissue and ultimately contributing to signs and symptoms of shock. Clinical manifestation of ACS includes; changes in the levels of consciousness, ischemia, clammy skin, hypotension, tachycardia, and decreased urine output. Patient that have experienced MI are therefore at risk of cardiogenic shock.
In an attempt to support the vital functions, the sympathetic nervous system responds to ischemic changes in the myocardium. To start with the cardiac output and blood pressure decreases which then stimulates the release of hormones epinephrine and norepinephrine. Which is the body attempts to increase the BP, heart rate and afterload, this ultimately increases the cardiac muscle demand for oxygen. As the oxygen demand grows at the same time its supply to the heart muscle decreases, ischemic tissue can become necrotic.
Low cardiac output also leads to a reduction in renal perfusion, when this happens, it triggers the renin-angiotensin system, which leads to further constriction of the vessels. Additionally, the release of aldosterone and antidiuretic hormone promotes sodium and water reabsorption increasing preload and ultimately the workload of the heart.
Preload and Afterload
Preload is the blood volume in the ventricle at the end of diastole, increases the amount of blood that is pumped out of the ventricle. Ischemia decreases the ability of the heart to contract effectively, therefore in people with ACS an increase in preload hastens the strain on an already oxygen- deprived myocardium. This further reduces cardiac output and puts the individual at an increased risk of cardiac failure. Medication such as nitroglycerin, morphine and beta blockers acts to reduce the preload. This medication along with ACE inhibitors decrease afterload, which is the force the ventricles have to work against to eject blood out of the ventricle. In myocardial ischemia, the weakened heart muscles cannot keep up with the increased pressure that is caused by an increase in afterload.
Signs and Symptoms
The degree to which the coronary arteries are blocked typically correlates with the signs and symptoms and the variation in the cardiac markers and ECG. Angina continues to be recognized as the typical symptom of ACS. The current best practice is that if an individual presents to the hospital with chest pain, the chest pain has to be assumed as a heart attack until proven otherwise. In unstable Angina, the chest pain usually happens when the individual is at rest or with exertion. Chest pain that is associated with NSTEMI normally lasts longer and more severe than chest pain that is associated with unstable angina. In the cases, the symptoms persist unless the individual rests or GTN, the pain may last longer than 15. And the pain may occur or without radiation to the neck, arm, epigastric or back.
In addition to angina, individual with ACS may present with shortness of breath, diaphoresis, nausea, and lightheadedness. Changes in vital signs such as tachycardia, tachypnea, hypertension or hypotension, and cardiac rhythm abnormalities may also be present.
The initial therapy for patients presenting with angina includes aspirin, oxygen, nitroglycerin, and morphine sulfate. Unless contraindicated, people presenting with symptoms of ACS should be given aspirin. Aspirin inhibits the aggregation of platelets and vasoconstriction by inhibiting the production of thromboxane. Aspirin is contraindicated in people with peptic ulcer disease, bleeding disorders and allergy to aspirin.
Oxygen should be administered at 2-4 L to maintain the O2 saturation at greater than 90%. Nurses should be aware of the signs and symptoms of hypoxemia, such as confusion, agitation, restlessness, pallor and changes to the skin temperature. By increasing the amount of oxygen that is delivered to the heart, supplemental oxygen will reduce the pain associated with ischemia.
Nitroglycerin spray or tablets should be administered sublingual every five minutes up to three doses, if not in a care facility, and the is experiencing chest pain after the third doses, an ambulance should be called. GTN causes vasodilation and reduces preload and afterload. GTN can cause hypotension, so individuals should be helped to bed after administration.
If the pain has not improved after GTN, morphine sulphate may be given. Morphine causes venous and arteriolar vasodilation, thereby reducing preload and afterload. Morphine’s analgesic properties also reduce the pain that is associated with ACS. Morphine can cause hypotension and respiratory depression. That is why the patient’ vital signs must be monitored upon administration.
STEMI VS NSTEMI
ST elevation myocardial infarction is a very serious type of heart attack during which the arteries that carry blood to the heart muscle are completely blocked. On the ECG it looks like this. NSTEMI is a partial blockage of the coronary arteries, the severity of the symptoms is dependent on which of part of the coronary arteries are affected.
Signs and symptoms of a STEMI include:
- Chest pain or discomfort
- Shortness of breath
- Dizziness or light-headedness
- Nausea or vomiting
- Diaphoresis (sweatiness) unexplained by ambient temperature
- Palpitations (uncomfortable awareness of the heartbeat)
- Anxiety or a feeling of impending doom
Care of a Cardiac Condition
NOTE: ALL CHEST PAIN IS CONSIDERED CARDIAC IN ORIGIN UNTIL PROVEN OTHERWISE
- For patient complaining of chest pain, they triaged as a category 2 and commenced on a chest pain pathway.
- If looking grey, sweaty or feeling unwell, the patient should be transferred to the resuscitation bay and commerce chest pain pathway.
- ECG STAT- within five minutes
- A = Assess airway, airway adjunction PRN, suction PRN
- B= Assess the work of breaking, rate, depth, quality and use of accessory muscle, nasal flaring, tracheal tug, rib retraction, posture. The nurse should also auscultate for bilateral sounds, the presence of wheeze or stridor etc.
- Assess for the effectiveness of ventilation, skin colour especially lips
- Apply oxygen at a relevant concentration
- C = Assess for circulation, skin colour, warmth, moisture
- IV access and blood – FBC, cardiac enzymes, coags etc
- Assess for pain = PQRST symptoms assessment
- GIVE MONA and reassess for circulation
- D= assess for the levels of consciousness and reduction in GCS may indicate hypoxia
- E = Ensure that the patient is removed and in a gown PRN
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