Week 1 & 2: CAD, MI & Acute Coronary Syndrome Flashcards
How does atherosclerosis contribute to the development of Coronary Artery Disease (CAD)?
Atherosclerosis is the most common cause of CAD as it can narrow or occlude coronary arteries. Dyslipidemia is an indicator of coronary risk as there is a strong link between abnormal concentrations of lipoproteins & CAD. This results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients. Reversible myocardial ischemia or irreversible infarction may occur.
Identify the modifiable risk factors associated with the development of CAD.
- Dyslipidemia
- HTN
- Cigarette smoking
- Excessive alcohol consumption
- Diabetes and insulin resistance
- Obesity
- Diet (atherogenic)
- Physical inactivity/sedentary
Identify the non-modifiable risk factors associated with the development of CAD.
- Advanced age
- Family history (genetics & environment)
- Male sex
- Female sex - after menopause
What is Coronary Artery Disease (CAD)?
A disease of the arteries that supply the heart; most commonly a narrowing and can be related to a stable or unstable plaque.
* reduces myocardial oxygen supply
* responsible for both angina and myocardial infarction
* begins early and develops over a long period of time, often taking 40-50 years
What is Chronic Ischemic Heart Disease?
Involves the narrowing of coronary artery lumen by atherosclerosis and/or vasospasm. It is recurrent and transient episodes of myocardial cell ischemia without infarction typically caused by a stable plaque with symptoms of stable angina.
What is Acute Coronary Syndrome (ACS)?
Involves the disruption of atherosclerotic plaques and compromise of the coronary lumen before an event. Typically caused by unstable plaques that result in unstable angina, and myocardial infarction (NSTEMI or STEMI)
Discuss the pathogenesis and manifestations associated with stable angina.
Stable angina is chest pain occurring intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms. It is caused by myocardial ischemia, but may eventually develop into unstable angina.
Stable angina might occur with over exertion during activity, stress or exposure to cold, when there is an increasing oxygen demand. It is relieved by rest and nitrates. When blood flow is restored, no necrosis of myocardial cells results.
Differentiate the pathogenesis and clinical manifestations associated with ACS, including: unstable angina, non-STEMI and STEMI.
Acute Coronary Syndrome (ACS) consists of unstable angina and a STEMI or non-STEMI MI. It is sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic unstable plaque or complicated lesion. Most common complications include dysrhythmias, heart failure, and sudden cardiac death.
Unstable Angina is chest pain that is easily provoked and occurs with increasing frequency (i.e., during sleep, or at rest), has a worsening pattern, and is unpredictable. Pain is not relieved with rest.
A Myocardial Infarction is irreversible cardiac cellular death cause by sustained myocardial ischemia. Can be STEMI or non-STEMI.
NSTEMI: Non-ST Elevated Myocardial Infarction is transient thrombosis or incomplete coronary occlusion causing partial thickness damage and will show as a depression of the ST-segment on an ECG.
STEMI: ST Elevation Myocardial Infarction is a more extensive MI associated with prolonged or complete coronary occlusion that causes full-thickness damage of the heart muscle and shows elevation of the ST-segment. STEMIs require IMMEDIATE intervention.
Describe the pathophysiological processes that lead to myocardial cell injury and myocardial cell death.
When there is an imbalance between coronary oxygen supply and myocardial demand (e.g., CAD, ACS, etc.), there will be a myocardial oxygen deficit. If this deficit is less than 20 minutes, we consider it an ischemic attack; if it is greater than 20 minutes we consider it a myocardial infarction. Resulting from either an ischemic attack or an MI, abnormal or absent response to electrical pulses will be present. This might result in a failure to contract, leading to impaired cardiac pumping and ultimately heart failure OR it may lead to dysrhythmias which can lead to sudden death.
Describe structural and functional changes within cardiac tissue that occur as a result of myocardial infarction, as well as the subsequent repair of cardiac muscle.
A myocardial infarction is prolonged ischemia that causes irreversible damage to the heart muscle as well as cellular injury, leading to cellular death. Myocardial reserves are used up in 8 seconds after oxygen is cut off. Due to lack of oxygen, myocardial stunning occurs where there is a temporary loss of contractile function that persists for hours to days after perfusion has been restored. Tissues that are persistently ischemic undergo metabolic adaptation to prolong myocyte survival (they hibernate). Eventually, we will see myocardial remodeling and the infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal. Necrosis of myocardial tissue results in release of intracellular enzymes (i.e., troponin, through damaged cell membranes into interstitial spaces).
Describe the diagnostics for stable and unstable Angina, as well as MI.
Unstable Angina: no bio-markers, no cell-death
* Cardiac biomarkers (troponins, creatine, etc.) will be NORMAL; because there is no cell death, just ischemia
* ECG often reveals ST-segment depression and T-wave inversion during pain that resolves as pain is relieved
* Considered an emergency - immediate hospitalization and administration of nitrates, antithrombotics & anti-coagulants
* Once stabilized, administer beta blockers & ACE inhibitors
* Emergency PCI may be performed if condition does not improve
Myocardial Infarction: when cardiac muscle is damaged, myocardial cells necrose & die, releasing their contents including enzymes (biomarkers) into blood
* Cardiac troponin I (CTnI): primary biomarker for diagnosis of MI; rise within 2-4 hours after onset of symptoms
* Creatine phosphokinase-MB (CPK-MB): released by myocardial cells but is also in other muscle cells; used as the 2nd biomarker but has decreased sensitivity and specificity; levels exceed normal ranges within 4-8 hours of injury
* Lactate dehydrogenase (LDH): enzyme found in almost all body tissues, including heart
* Myoglobin: released quickly from infarcted myocardial tissue and elevated within 1 hour after myocardial cell death, peak levels reached within 4-8hrs
* Leukocytosis
* Elevated CRP
* Hyperglycemia
Discuss the non-pharmacological treatment for ACS.
- Percutaneous coronary intervention (PCI): is a non-surgical procedure used to treat the blockages in a coronary artery; it opens up narrowed or blocked sections of the artery, restoring blood flow to the heart
- Coronary artery bypass graft (CABG): uses healthy blood vessels from another part of the body and connects them to blood vessels above and below the blocked artery
- Minimally invasive direct coronary artery bypass (MIDCAB): This procedure uses two small incisions between the ribs on the left side of the chest to access the heart. We’ll harvest an artery from the chest, either directly or via a surgical robot, and will stitch the harvested artery to the coronary arteries.
- Gene & stem therapy for myocardial angiogenesis & spinal cord stimulation
Explain reperfusion injury and how it relates to the treatment of MI.
Ischemia and reperfusion also cause damage to the coronary circulation through endothelial injury, platelet activation, inflammation, and vasoconstriction. It involves the release of toxic oxygen free radicals, calcium flux, and pH changes that contribute to cellular death. While restoration of blood flow is crucial to reducing infarct size, reperfusion of ischemic myocardium can trigger a reperfusion injury that can add as much as 50% to overall infarct size.
Describe the pathophysiology and clinical manifestations of left versus right heart failure.
The heart becomes weak and cannot eject all the blood it receives, impacting cardiac output and systemic perfusion.
Left sided: interferes with movement of blood from pulmonary circulation to systemic circulation
* blood accumulates in the left ventricle
* wall of the left ventricle thickens in attempt to compensate for extra blood retained in chamber
* blood backs up to lungs
* manifests in cough, SOB, pulmonary congestion, edema, cyanosis, inspiratory crackle, fatigue, not good CO - lungs under back pressure, decreased urine output and edema
* kidneys are shorted blood supply
* blood accumulates in left atrium, left ventricle & pulmonary circulation - causes increase in pulmonary venous pressure
Right sided: when blood is not moved forward by the right ventricle, blood backs up and accumulates/gets congested in the systemic venous system. Will be caused by any condition that impeded blood flow into the lungs (i.e., pulmonary congestion, pulmonary HTN, COPD, severe pneumonia, PE), may also be caused by conditions compromising pumping effectiveness of right ventricle.
* blood backs up into peripheral veins
* jugular venous distention
* peripheral edema
* engorgement of organs (i.e., liver)
* hepatosplenomegaly - liver and spleen back pressure
The primary cause of right HF is left HF! the development of left HF typically translates to right HF due to increasing fluid and pressure backing up.
Treatment involves knowing where the blood is getting backed up and how this will manifest; there is no cure, we are just looking to improve QoL.
Explain how myocardial dysfunction activates the various compensatory mechanisms, and describe the short and long term effects of the compensatory mechanisms.
During heart failure, cardiac output is reduced leading to a series of responses by the body; the main goal is to return perfusion to tissues and organs but this can create long term complications:
- Increases SNS activity & releases catecholamines: is triggered by the decrease of CO, SNS will attempt to adjust the HR, force of contraction, and peripheral vascular resistance to compensate for decreased CO; however, this increases the cardiac workload and HF worsens
- Anti-diuretic hormone: results in peripheral vasoconstriction and renal fluid retention but exacerbates hyponatremia and edema (preload) & afterload, worsening HF
- RAAS mechanisms: RAAS gets activated as a result of reduced CO resulting in decreases renal perfusion and GFR but promotes vasoconstriction and volume retention, raising the BP and again adding more work for the heart
- Natriuretic peptides: secreted in response to increased volume overload & dysfunction (ANP for atria; BNP from ventricles) and cause diuresis & reverse negative effects of SNS & RAAS on heart, but chronic HF will eventually lead to their depletion
- Frank-Starling Law: increased preload causes increased stretch of myocardial fibers, the force of each contraction is increasing leading to increased cardiac output. But, as preload continues to rise it causes repeated stretching of myocardium and it doesn’t snap back as forcefully. Due to the reduced contractility, cardiac output is decreased and HF worsens.
- Myocardial hypertrophy & remodeling: when contractility decreases, SV falls and left ventricular end-diastolic-volume increases. This causes dilation of the heart and increased preload, which can improve CO initially, but as preload continues to rise, it causes stretching of the myocardium that can lead to dysfunction and decreased contractility. The heart will compensate for this increased workload by getting bigger, it will require more oxygen and we are already having a problem with oxygenation.
Describe the pathophysiology and implications of ventricular remodeling.
Within 24 hours, leukocytes infiltrate necrotic area and proteolytic enzymes from scavenger neutrophils degrade necrotic tissue. By 10 to 14 days after infarction, a collagen matrix is deposited and it is initially weak, mushy & vulnerable to reinjury. After 6 weeks, necrotic area is completely replaced by scar tissues. This tissue is strong, but unable to contract and relax like healthy myocardial tissue!
Identify common dysrhythmias which can arise as complications of MI.
- Premature Ventricular Contractions (PVCs): the ventricle contracts before it can finish filling, resulting in decreased CO. Is considered common, feels like flutters.
- Ventricular Tachycardia: the ventricle is contracting too much and too fast but is still following a sinus rhythm (typically 150-200 bpm) resulting in decreased CO from loss of atrial contribution to ventricular preload. High risk for sudden death.
- Ventricular Fibrillation: weak, quivering of the ventricles; considered cardiac arrest. The ventricles pump little or no blood and quickly starve the issues of oxygen. It is life threatening and requires immediate treatment.
- Heart block or atrioventricular conduction block: classified as first, second or third degree. impulses are stopped through the heart.
