Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome (ACS)

• ACS develops when myocardial ischemia is prolonged and not immediately reversible
• It includes unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI)
• ACS nomenclature reflects relationships among pathophysiology, diagnosis, prognosis, and interventions for these disorders
• Suspected ACS requires immediate hospitalization

Etiology and Pathophysiology

• ACS is associated with deterioration of an atherosclerotic plaque
• Plaque ruptures expose the intima to blood, stimulating platelet aggregation and local vasoconstriction, leading to thrombus formation
• Unstable lesions may be partially occluded by a thrombus (UA or NSTEMI) or totally occluded (STEMI)
• Systemic inflammation is thought to contribute to the instability of coronary plaques

Manifestations of Unstable Angina (UA)

• Chest pain is new in onset, occurring at rest, or worsening, and is called unstable angina (UA)
• UA is unpredictable and represents an emergency, unlike chronic stable angina
• Patients describe a significant change in the pattern of angina, with increased frequency that is easily provoked
• Women with UA symptoms seek medical attention more often than men
• Prodrome symptoms in women include fatigue, shortness of breath, indigestion, and anxiety, with fatigue being the most prominent

Myocardial Infarction (MI)

• MI results from sustained ischemia causing irreversible myocardial cell death
• 80-90% of acute MIs occur secondary to thrombus formation
• Perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis and stopping contractile function
• Most MIs affect some portion of the left ventricle, but the acute MI process takes time
• Cardiac cells can withstand ischemic conditions for approximately 20 minutes before cellular death begins
• The subendocardium is the innermost layer of tissue in the cardiac muscle, and this tissue is the first to become ischemic
• If ischemia persists, the entire thickness of the heart muscle becomes necrotic in approximately 5 to 6 hours
• Descriptions of infarctions are based on the location of damage (e.g., anterior, inferior, lateral, or posterior wall infarction)
• Location of the infarction correlates with the involved coronary circulation: -Inferior wall infarctions result from occlusions in the right coronary artery -Anterior wall infarctions result from occlusions in the left anterior descending artery -Occlusions in the left circumflex artery usually cause MIs in the lateral or posterior wall or both

Collateral Circulation and Severity of Infarction

• Pre-established collateral circulation influences the severity of infarction
• Individuals with a history of CAD may have well-established collateral circulation
• Younger individuals with MI often experience more serious impairment than older individuals with the same degree of occlusion

Clinical Manifestations of MI Pain

• Hallmark of an MI is severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
• Pain described as heaviness, pressure, tightness, burning, constriction, or crushing sensation
• Common locations are substernal, retrosternal, and epigastric areas, with radiation to the neck, jaw, arms, or back
• Pain may occur at any time but commonly occurs in the early morning hours, lasting 20 minutes or more and is more severe than usual anginal pain
• Epigastric pain may be mistaken for indigestion; symptoms may include "discomfort," weakness, or shortness of breath
• Women may experience atypical discomfort, shortness of breath, or fatigue
• Patients with diabetes are more likely to experience silent (asymptomatic) MIs

Sympathetic Nervous System (SNS) Stimulation

• During the initial phase of MI, catecholamines (norepinephrine and epinephrine) are released
• Increased SNS stimulation results in release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels
• Physical examination reveals ashen, clammy, and cool skin

Cardiovascular Manifestations

• Initially, BP and HR may be elevated due to catecholamine release
• Later, BP may drop due to decreased cardiac output (CO)
• Profound hypotension can decrease renal perfusion and urine output
• Crackles may be noted in the lungs, suggesting left ventricular dysfunction
• Jugular venous distention, hepatic engorgement, and peripheral edema may indicate right ventricular dysfunction
• Careful auscultation may reveal a third heart sound (S3) or fourth heart sound (S4), suggesting ventricular dysfunction
• A loud holosystolic murmur may indicate a septal defect or mitral valve dysfunction
• Nausea and vomiting can result from reflex stimulation or vasovagal reflexes
• Fever may occur within 24 hours, up to 38-39°C, lasting up to 1 week

Healing Process

• The body responds to cell death via inflammation, with leukocytes infiltrating the area within 24 hours
• Enzymes released from dead cardiac cells are important diagnostic indicators
• Proteolytic enzymes remove necrotic tissue by the second or third day
• Collateral circulation improves areas of poor perfusion
• Catecholamine-mediated lipolysis and glycogenolysis allow anaerobic metabolism of oxygen-depleted myocardium
• Serum glucose levels are frequently elevated
• ECG changes (e.g., ST-segment elevation, pathological Q wave) and nuclear scanning identify the necrotic zone
• Neutrophils and monocytes clear the necrotic debris, and the collagen matrix for scar tissue is laid down
• After 10-14 days, scar tissue is still weak, making the myocardium vulnerable to increased stress
• By 6 weeks, scar tissue has replaced necrotic tissue, but the scarred area is less malleable, leading to uncoordinated wall motion, ventricular dysfunction, or pump failure
• Ventricular remodeling involves compensatory hypertrophy and dilation of normal myocardium
• Remodeling can lead to late heart failure, especially in individuals with atherosclerosis

Complications of Myocardial Infarction Dysrhythmias

• Dysrhythmias are the most common complication
• 80% of patients who have had an MI will have this complication
• Primary cause of death in patients in the prehospitalization period
• Dysrhythmias are caused by conditions that affect the myocardial cell's sensitivity to nerve impulses
• Such as ischemia, electrolyte imbalances, and sympathetic nervous stimulation
• Intrinsic rhythm of heartbeat is disrupted: -Fast HR (tachycardia) -Slow HR (bradycardia) -Irregular heartbeat
• Each adversely affect the ischemic myocardium
• Life-threatening dysrhythmias happen with anterior wall infarction, heart failure, or shock
• Ventricular fibrillation is a common cause of sudden cardiac death (SCD)
• Lethal dysrhythmia most often occurs in the first few hours after the onset of pain
• Ischemia causes cardiac cells to lack in oxygen and become depolarized
• This causes an alteration in impulse formation or conduction
• Premature ventricular contractions (PVCs) may precede ventricular tachycardia and fibrillation

Heart Failure (HF)

• Heart failure is a complication of MI in which the pumping action of the heart has diminished
• Heart failure occurs initially with subtle signs: -Mild dyspnea -Restlessness -Agitation -Slight tachycardia
• Other signs: -Pulmonary congestion -S3 or S4 heart sounds -Crackles -Jugular vein distension

Cardiogenic Shock

• Cardiogenic shock is a condition in which inadequate oxygen and nutrients are supplied to the tissues because of severe left ventricular failure
• Mortality rate is high
• Aggressive management is necessary: -Control of dysrhythmias -Intra-aortic balloon pump (IABP) counterpulsation therapy to maintain perfusion -Vasoactive medications to improve contractility
• Goal of therapy is to: -Maximize oxygen delivery -Reduce oxygen demand -Prevent complications such as acute kidney injury

Papillary Muscle Dysfunction

• Papillary muscle dysfunction occurs if the infarcted area includes or is adjacent to the papillary muscle that attaches to the mitral valve
• Causes mitral valve regurgitation
• Increases the volume of blood in the left atrium
• Aggravates an already compromised left ventricle by reducing CO
• Papillary muscle rupture is a rare but life-threatening complication
• Massive mitral valve regurgitation
• results in dyspnea, pulmonary edema, and decreased CO

Ventricular Aneurysm

• Results when the infarcted myocardial walls become thin and bulges during contraction
• The patient may experience refractory Heart Failure, dysrhythmias, and angina
• Ventricular aneurysms harbor thrombi, which can cause an embolic stroke

Pericarditis

• Acute pericarditis is an inflammation of the visceral or parietal pericardium or both
• May result in cardiac compression, decreased ventricular filling and emptying, and HF
• May occur 2-3 days after an acute MI
• Characterized by chest pain: -May be mild or severe -Aggravated by inspiration, coughing, and movement of the upper body -Relieved pain by sitting in a forward position
• An assessment can reveal a friction rub over the pericardium

Dressler's Syndrome

• Characterized by pericarditis with effusion and fever that develops 4-6 weeks after Myocardial Infarction
• May be caused by an antigen-antibody reaction to necrotic myocardium
• The Patient may have pericardial pain, fever, a friction rub, pleural effusion, arthralgia
• Lab findings include: -Elevated white blood cell count -Elevated sedimentation rate
• Short-term courses of corticosteroids are used to treat this

Diagnostic Studies for Unstable Angina and MI

• ECG is the primary tool to rule out confirm UA or MI.
• Serum cardiac markers (CK and troponin) measurement
• Changes can occur in the QRS complex, ST segment, and the T wave caused by ischemia and infarction
• Compared to a previous ECG recording if possible
• Pattern of ECG changes among the 12 leads provides information on which of the coronary arteries is involved
• Important to distinguish among STEMI, UA, and NSTEMI.
• During STEMI a patient may have more extensive damage, prolonged and complete coronary occlusion and the development of ST elevation
• ST segments return to baseline, with T-wave inversion and pathological Q waves over hours or days
• The Q wave will remain forever on the ECG
• NSTEMI has transient thrombosis or incomplete coronary occlusion
• Areas of ischemia or infarction may be noted
• ECG may be normal/nondiagnostic. If nondiagnostic, serial ECGs are obtained

Serum Cardiac Markers

• After a MI, certain proteins (serum cardiac markers) are released into the blood in large quantities from necrotic heart muscle
• Cardiac enzymes and troponin
• Important in the diagnosis of MI
• An increase in serum cardiac markers that occurs after cellular death can indicate whether cardiac damage is present and the approximate extent of the damage
• CK levels: -Rise approximately 3 to 12 hours after an MI -Peaks in 24 hours -Returns to normal within 2 to 3 days -Creatine kinase(CK-MB) band is specific to myocardial cells
• Troponin: -Myocardial muscle protein is released into circulation after myocardial injury -Highly specific indicators of MI -Tests have greater specificity and sensitivity for myocardial injury -Troponin level rises as quickly as the CK level -Increase 3 to 12 hours after the onset of MI -Peaks at 24 to 48 hours -Returns to baseline over 5 to 14 days
• Myoglobin: -Released within a few hours of a MI -Lacks cardiac specificity -Rapidly excreted in urine -Blood levels return to normal range within 24 hours after the MI

Coronary Angiography

• The patient with Unstable Anging or NSTEMI undergoes coronary angiography to evaluate the extent of the disease and determine the most appropriate therapeutic modality
• PCI may be performed at this time if appropriate
• Coronary angiography is the only way to confirm the diagnosis of Prinzmetal's angina

Clinical Procedures

• Nuclear testing and echocardiography may be conducted when a patient has an abnormal but nondiagnostic baseline ECG
• Dobutamine or persantine stress echocardiography can be performed in patients unable to exercise to increase the HR to identify ischemia or cardiac wall dysfunction

Interprofessional Care for ACS

• Rapid diagnosis and treatment are extremely important so cardiac muscle can be preserved and managed properly
• Establish an access route for emergency medication therapy through an intravenous route (IV)
• Sublingual nitroglycerin/chewable ASA are administered if the patient hasn't already received them in the prehospital phase
• Morphine sulphate is given intravenously for pain unrelieved by nitroglycerin -Decrease the workload of the heart
• Administer Oxygen to maintain oxygen saturation at 90%-94%
• Receive ongoing care in a critical care unit or telemetry unit -For continuous ECG monitoring to detect dysrhythmias
• Vital signs are monitored frequently for the first few hours
• Bed rest with limited activity for 12-24 hours initially
• ASA, Heparin, and a glycol protein IIb/IIIa inhibitor is a recommended combination for patients with increasing cardiac markers and angina

PCI (Percutaneous Coronary Intervention)

• Common elective procedure considered once the patient is stabilized with angina controlled or if it returns
• In patients with STEMI or NSTEMI with elevated levels of cardiac markets, reperfusion therapy may be involved
• PCI is recommended as a first line of treatment for patients with confirmed MI
• Goal is to open the affected artery
• A catheter is used to locate blockages severity, collateral circulation, left ventricular function
• Can select treatment modalities better this way
• PCI with placement of one or more stints
• Stints expand the mesh like frames (either Bare metal or Drug eluting)
• Drug eluting stints prevents intimal lining overgrowth prevent the reoccusion of the vessels
• Aggressive anti coagulation prevents the occlusion of the stints through thrombus formation
• Local anistetic
• Ambulatory
• Shorter hospital stay
• Rapid return to work

Complications with PCI

• Dissection of the newly dilated coronary artery- If damage is extensive can rupture resulting in
• Cardiac Tamponade
• Ischemia
• Infarction
• Decreased Cardiac Output and possible death
• Danger if the lesson is calcifies and a portion of the plaque becomes dislodged, occluding the vessel distal to the catheter

Fibrinolytic Therapy

• Advantages of availability and rapid administration
• Stop the infarction process by dissolving the thrombus by
• Should be given as soon as possible
• No greater than 12 hours ideally within 2-3 hours of onset of symptoms
• Guided by cost, efficancy and ease of administation
• Produces lysis of the pathological clots- other clots (post operative, trauma)
• Important to minimize bleeding
• Inclusion criteria: -Chest pain is typical of acute MI -Less than 12 hours in duration -Consistant 12 lead ECGs -No absolute contradictions
• Baseline assessments completed before fibrinolytic
• Medication may be administered to reduce bleeding in the patient
• Should see returns in ST segment
• Resolution of chest pain
• enzyme levels
• Reinfaration dysrhythmias: accelerated idioventrical

Nursing Assessments

• Major conversation with bleeding
• Should be stopped
• Nitroglycerin, ASA
• Initial medication with LMWH or UH are initial medications for choice
• ACI inhibits are recommended

CABG

• Saphenous Vein: develop intimal hyperplasia( stenosis and graft cocclusions
• Antiplatelet therapy and Statitsin after surgery improves the vein patency
• Palliative treatment not a cure
• Improves outcomes
• Complications and mortality increase when older -Women have higher rates -Later treatment and more ill -Smaller coronarty vessels and a less use of

Minimally Invasive

• MIDCAB-patients with limited disease
• Requires many small incisions
• Heart slowed
• IMA is sutured
• OPCAB- full acess or sternotomy
• Performed with a beating heart- mechanical stablaizers no CBP
• Limited disease or high risk for traditional surgery
• Robatic surgey - increases pricision, smaller incisins, decreased blood, les pain,
• TMR-laser - patients not candidate for traditional surgeries.
• nursing diagnoses

Nursing Management Actions

• Admin oxygen
• Measure Vitals
• EGC
• Pain Medication
• Auscultation
• Paitient positioning
• Promote Health
• Prevent Angin
• Avoid exposure
• Small frequent meals
• Regular exercises
• Proper usage of nitroglycerin
• Manage oxygen needs
• Medication and avoid injury

Sudden Cardiac Death (SCD)

• Unexpected death from cardiac arrest
• Teaching can help
• CPR defibrillation save lives
• Cardiac function disrupted that causes immediate loss of CO, function disrupetd
• May or maynote have history
• Often first sign
• Usually within the first hour
• Genetic
• Ventricular dysrythmias cause
• First group patients who did not have acute MI second did have -Risk factor- sex family history -Daignostic work up determine have MI -Electrophysiolgocial study -Medication with amiodione -Alernt to patients- psychosocial adaptation this sudden with “brusht with death" -“TimeBomb"
• Anxiety angry and depressed