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NURSING 3PA2 Final: Alterations in Cardiovascular Function Module Summary

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Kirsten Culver

Alterations in Cardiovascular Function Module Summary PATHOPHYSIOLOGY OF ATHEROSCLEROSIS ATHEROSCLEROSIS REVIEW Endothelial cell injury Endothelium is smooth with tight junctions between cells. It can be injured due to factors such as smoking, mechanical stress due to HTN, elevated LDL levels or mechanisms of the immune system. Endothelium suffers an injury or high cholesterol levels  monocytes become sticky and attach themselves to the endothelium in response to expression of adhesion molecules. The endothelium then loses some of its ability to produce antithrombotic and vasodilating cytokines. Monocyte Emigration Endothelial injury  monocytes move into intimal layer of endothelium, squeezing through cell junctions. Monocytes are then transformed into macrophages and free radicals are released. Macrophages consume any oxidized LDLs that are present, transitioning them into foam cells. Foam cells release growth factors and inflammatory cytokines that worsen endothelial injury. LDL Oxidation LDLs make their way through the intact endothelium and are oxidized into proinflammatory lipids. Oxidized LDLs serve as an attractant to monocytes in the endothelium, causing further migration of monocytes into the subendothelium. Smooth Muscle Proliferation Platelets in blood are exposed to the subendothelium  aggregate and adhere to the site of injury This process is then followed by proliferation of smooth muscle. Smooth muscle proliferation causes the endothelial layer to pouch out, making the lumen of the vessel smaller. Formation of a Fatty Streak Fatty streaks are thin, flat, yellowish discolourations that enlarge over time, occluding the vessel lumen. They consist of macrophages and smooth muscle cells that are distended with lipid to form foam cells. Formation of Lipid Core (Plaque) Lipids accumulate beneath the endothelial layer and form a hard, lipid core. Enzymes eat away at protective fibrous cap  atherosclerotic plaque becomes vulnerable to rupture Plaque Hemorrhage Plaque begins to rupture  prothrombogenic mediators are released which help platelets floating by adhere to the lesion forming a thrombus. Thrombus forms  blood flow to the myocardium is compromised or obstructed  infarction ZONES OF TISSUE DAMAGE Interruption of blood flow to an area of the myocardium  some areas called the ‘zones of infarct, injury and ischemia’ become infarcted with areas of still-viable cells surrounding the necrotic tissue. Infarct means that cell death and necrosis has occurred. It is depicted by the presence of pathological Q waves on the ECG and cells are eventually replaced with scar tissue (zone of infarction). Injury to myocardial cells occurs when blood flow is interrupted, but the cells remain viable for a time. As long as flow is restored to this area, the cells will recover. If not, they will go onto infarct. Injury on an ECG is seen as elevation of the ST segment. Ischemia means perfusion to area is decreased but if blood flow is restored, no serious damage occurs Ischemia is depicted by the presence of ST depression or inverted T waves on the ECG. ISCHEMIA Ischemia  condition that occurs when perfusion of the myocardium is compromised due to some imbalance between myocardial oxygen supply and/or demand. Oxygen supply is regulated by the patency or size of the lumen of the coronary vessel, the ability of the ventricular wall to compress and the amount of time the ventricle spends in diastole.  Demand is dependent upon myocardial contractility, heart rate, and amount of ventricular wall stress.  If preload (volume in ventricle before it contracts) or afterload (amount of resistance the ventricle must overcome to contract) is too high or low, this adds stress to the heart and increases demand for oxygen.  Normal heart  increased demand for oxygenated blood is met by increased supply and supply decreases as the demand decreases  Non-healthy heart  increased demand may not be met with additional supply of oxygenated blood  Supply ischemia – an abrupt or acute reduction in blood flow to the myocardium caused by thrombosis, coronary vasospasm, or platelet aggregation.  Sometimes the supply of oxygenation blood is less than what is required, even at rest. This is often caused by either a blockage within the coronary artery or by spasm of that artery.  Whether demand outweighs the supply or supply just can’t meet the requirements, the end result is ischemia, or decreased perfusion of oxygenated blood to the myocardium.  Demand ischemia – an increase in need for oxygen and nutrients due to exercise or stress. With coronary artery disease, increased demand causes an imbalance.  It is reversible if blood flow is restored before permanent cellular damage occurs. If blood flow isn’t restored in good time, injury, and infarction can occur and necrosis (cell death) becomes permanent.  There are three possible outcomes then: injury, apoptosis or ‘cell removal’ or cell death (necrosis). COMMON CAUSES OF ISCHEMIA  Common causes of ischemia  blockage of coronary artery (thrombus), spasm of coronary artery, and coronary artery obstruction (formation of plaque).  This particular module will be focused on ischemia caused by formation of a thrombus. CELLULAR EFFECTS OF ISCHEMIA  Ischemia develops when the supply of oxygen and nutrients is inadequate to meet myocardial demands.  Myocardial cells start to become ischemic within 10 seconds of a blood flow interruption and contractility is depressed within a minute which is why ischemia is so detrimental.  Oxygen not available in sufficient quantities  cellular metabolism shifts from aerobic to anaerobic  Aerobic metabolism  provides 36 molecules of ATP and converts waste products to CO 2nd water  Carbon dioxide is eliminated through the pulmonary system and water via the renal system  Anaerobic metabolism  inefficient, produces only 2 molecules of ATP and creates lots of pyruvic and lactic acids, both of which are toxic to our cells  ATP is important because it provides cells with energy that is needed to function. Without enough ATP, the sodium potassium pump becomes inefficient and electrical impulses become uncoordinated.  Without enough oxygen, inflammatory mediators and free radicals accumulate causing cell toxicity. These are reasons why cells are very reliant on oxygen.  Inadequate oxygen and ATP in myocardial cells  irreversible cell injury and death if continues  Inadequate supply of oxygen and nutrients and accumulation of waste products result in alteration of cell membrane, cell edema, arrhythmias, cell death, and failure of contraction. HEMODYNAMIC EFFECTS OF ISCHEMIA  Larger the area of ischemia, injury or infarct, the less ventricular muscle is available to contract effectively. The walls of the heart may then contract poorly (hypokinesis) or not at all (akinesis).  Ventricular walls become less compliant and lose elasticity so they can’t accommodate incoming volume  We end up with a decrease in cardiac output as a result of low stroke volume. The sympathetic nervous system then initiates the sympathetic response in the form of increased HR and BP to restore balance.  Hemodynamic effects of ischemia  reduced contractility, abnormal wall motion, changes in wall compliance, decreased cardiac output and stroke volume, reduced LV emptying, compensatory stimulation of the SNS, increased HR and BP. ACUTE CORONARY SYNDROME  Acute coronary syndrome  continuum that begins with plaque rupture within a coronary artery and results in infarction of myocardial tissue if perfusion is not restored in good time.  Normal artery and vessel wall: blood flows easily through this vessel  Lipids accumulate in the intima forming an ‘atheroma’: some development of atherosclerosis occurs but blood is still able to flow through and provide enough oxygenated blood to prevent symptoms.  Formation of fatty fibrous lesion with a lipid core and fibrous cap – stable angina: lumen has significant amount of vessel narrowing from the growing atherosclerotic plaque. In this condition, the patient will have some symptoms when demand for oxygenated blood increases. Supply of oxygenated blood is decreased due to narrowed lumen. This is called stable angina because the patient can predict when it will occur and is able to control it with medication or rest.  Rupture of fibrous cap allows leaking of lipids and platelet aggregation – unstable angina: an atherosclerotic plaque has been disrupted and platelets travelling by begin to stick to it. The plaque is now ‘unstable’. Patient develops symptoms without warning and is not able to control symptoms with meds or rest. The individual cannot predict or control symptoms and is said to have ‘unstable angina’.  Clot formation – NSTEMI (ACS): a new thrombus forms as the plaque has ruptured, with hemorrhage. The lumen becomes even more occluded with clot, and the patient suffers some infarction to a part of the myocardium. Because the damage does not involve the full thickness of the ventricle, there are no changes to the ECG and the patient is said to have suffered a ‘non ST elevation MI’ or “non-STEMI”.  Thrombus causes occlusion of vessel – acute STEMI: if the clot blocks the entire lumen, the myocardium suffers a significant infarct with changes on ECG. The patient has had an ‘ST elevation MI’ or “STEMI”.  Unstable angina, NSTEMI and STEMI are the three disease states classified as acute coronary syndrome. The Normal ST Segment  There’s a P wave, Q wave, R wave, S wave, and a T wave. For now, we will focus on the QRS and T waves.  The QRS represents ventricular depolarization. The T wave represents ventricular ‘repolarization’.  The ST segment is the relationship between the S and the T wave, measured from the end of the QRS to the onset of the T wave and it represents the end of ventricular depolarization and the beginning of repolarization. Normally it should be somewhat flat on the ECG.  Any elevation or depression of this segment of 1 mm or more is considered worthy of attention. Unstable Angina  Unstable angina  plaque has been disrupted, exposing the now-injured endothelium to platelets and coagulant factors. It leads to transient episodes of vessel occlusion at the site of plaque disruption.  The thrombus is labile and vulnerable, but perfusion is usually restored before necrosis occurs.  Unstable angina involves atherosclerotic plaque disruption, platelet aggregation, hemostasis (clot formation), pain is persistent and severe, can occur at rest, and difficult to relieve. The ST Segment in Unstable Angina  Unstable angina is often seen on an ECG as ST segment depression and T wave inversion during the period of pain. Contractility may be somewhat abnormal on an echocardiogram.  Cardiac enzymes such as creatinine kinase, lactic dehydrogenase and troponin, are usually negative. Non ST Elevation MI (NSTEMI)  In non-STEMI, necrosis of myocardial tissue occurs, but because the full thickness of the ventricle is not involved, electrical activity is not disrupted and there are no obvious changes on the ECG.  The patient complains of severe and abrupt pain and has difficulty obtaining relief.  Cardiac biomarkers in serum are the only way to determine if an infarct has occurred. Increased levels of myocardial enzymes (CK-MB and troponin).  Creatinine Kinase (CK): an enzyme found in the heart, brain and skeletal muscle and is released when these cells are damaged. Found in all muscle cells. Elevation confirms that muscle damage has occurred.  In order to determine if the muscle damage is cardiac in origin, we must look at the isoenzyme, CK-MB.  After an infarct, total CK levels begin to rise in 6 hours, peak in 18 hours and return to normal levels in 2-3 days. CK-MB levels rise in 3-6 hours post infarction, peak in 12-24 hours and return to normal levels in 12- 48 hours. An increase in CK-MB of > 5% of the total CK, supports a diagnosis of MI.  This positive finding helps diagnose MI in the absence of ST changes on ECG, hence termed ‘non STEMI’.  Troponin: Troponin is a protein that is found in skeletal and cardiac muscle fibres. With myocardial infarction, troponin T and troponin I levels rise very quickly. The ST Segment in NSTEMI  NSTEMI is not accompanied by changes in the ST segment. Thus, the ECG appears normal. ST Elevation MI (STEMI)  In STEMI, arterial occlusion is complete, resulting in necrosis of the full thickness of the ventricle, which alters electrical conduction. This alteration is seen as ST elevation on the ECG.  STEMI involves death of tissue, full thickness of ventricular wall, obstruction of artery, severe and abrupt pain, no relief and is diagnosed by history, pain, biomarkers and ECG changes. The ST Segment in STEMI  The ST segment has changed dramatically and is elevated indicating that injury to myocardial cells has occurred. MYOCARDIAL INFARCTION PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION (MI)  Blood flow impeded by a thrombus or plaque  ischemia results  new blood vessels form in a process called ‘angiogenesis’ to form a detour around the blockage. These new blood vessels are able to ‘bypass’ the occlusion, restoring flow to myocardial tissue. This is referred to as collateral circulation and is lucky.  If perfusion to myocardial tissue is prolonged, necrosis of the full thickness of the ventricle can occur.  Remember that necrotic or ‘dead’ cells can never again participate in contraction, so that part of the ventricle is either hypokinetic or akinetic. Some part of ventricular function is then lost.  Infarct causes the area to become bruised and cyanotic and cardiac enzymes are released.  The area is then infiltrated by neutrophils and inflammatory cytokines. The complement and coagulation cascades begin. The area becomes reddened, edematous, and painful.  For patients with long standing atherosclerosis, angiogenesis has likely already begun. The blood vessel that precedes the blockage sprouts new branches to form collateral arteries to bypass the obstruction.  Inflammation and angiogenesis leads to a process called ventricular remodelling.  Myocardial cells release catecholamines  stimulate increase in blood glucose levels needed for energy  Liver and skeletal muscles makes stored glucose available  serum glucose ↑, stops release of insulin  Coronary vasoconstriction occurs in the area of infarct. Embolization of thrombi and death of myocytes  stimulates production of toxic free radicals that further plug coronary capillaries, decreasing blood flow to the area.  Location and size of infarct is dependent on vessel that becomes occluded.  Right coronary artery supplies right ventricle so occlusion of this artery leads to right ventricular infarct.  The left anterior descending artery supplies much of the anterior portion of the left ventricle and the left circumflex supplies the lateral part of this ventricle.  Catheterization of coronary circulation helps determine which vessel is occluded which helps predict the clinical manifestations that might occur in our patients.  Ex. occlusion of left anterior descending artery leads to significant issues with cardiac output  Patho of MI involves inflammation, angiogenesis, ventricular remodelling, release of catecholamines, elevation of glucose, and coronary vasoconstriction. Location of infarct depends on the vessel involved. ZONES OF MYOCARDIAL INFARCTION  Ischemia is depicted by the flipped or inverted T wave, injury by the elevated ST segment and once an infarct has become established, with death of myocardial tissue, you will then see a Q wave that is pathological. A pathological Q wave is deep and/or wide. CLINICAL PRESENTATION  Coronary artery disease (CAD) presents in many ways. Some patients have very few symptoms and an infarct is discovered by accident some time later on routine ECG analysis.  Once an infarct occurs, the pathological Q waves persist forever on an ECG.  Pain due to buildup of lactic acid during ischemic episode or myocardial stretching (irritate nerve fibers)  Sympathetic stimulation and release of catecholamines  pallor, dyspnea, anxiety and diaphoresis  Sympathetic stimulation and release of catecholamines also causes blood flow to divert to priority areas such as the brain, heart, and lungs and vasoconstricts the non-priority areas.  Dysrhythmias are often caused by movement to anaerobic metabolism in the presence of ischemia – without manufacture of enough ATP, the sodium potassium pump, and the rhythm becomes unstable.  Nausea/vomiting occur due to reflex stimulation of vomiting centers by pain fibers. DIAGNOSTICS  Diagnosis of CAD and ACS  history, identification of risk factors and complete physical assessment  The 12 lead or 15 lead ECG is very important to identify any changes.  Detection of the presence of cardiac enzymes, normally released with cellular injury, is also important.  Echocardiogram  helps identify associated damage to the myocardium and ventricle due to infarct IMMEDIATE NON-PHARMACOLOGICAL MANAGEMENT OF MI  Immediate transfer to an acute care facility, an individual should never travel in a personal vehicle.  Administration of supplemental oxygen – usually given via nasal prongs at 3 – 4 L per minute.  Oxygen saturation is monitored to ensure that patient is saturating hemoglobin for delivery to tissues.  A 12 lead ECG is done to identify the likely area of the ventricle that is being infarcted; knowing which area of the ventricle is ischemic gives us clues as to which coronary artery is the culprit.  Cardiac rhythm is continuously monitored for changes and vital signs are monitored to determine the effect of the infarct on cardiac output (low BP indicates that cardiac output is compromised).  Chest x-ray is done to examine the potential effects the infarct might have on the lungs (ex. fluid shifts)  Echocardiogram provides info on the state of the ventricle – we usually receive a report about the ‘kinetics’ or ability of the walls of the ventricle to participate in contraction.  Bed rest is recommended to preserve available energy and to decrease the demand on the heart.  History and physical examination are done to determine risk factors and effects caused by infarct.  Blood work is done to determine the presence of cardiac biomarkers, elevated white count from the inflammatory process and level of hemoglobin for oxygen carrying capacity, lipid profile to determine risk for atherosclerosis and coagulation studies to determine risk for clot as a baseline. MANAGEMENT OF MI  Morphine: used to manage pain, decreases afterload through vasodilation. Use with caution in pts with right ventricular infarct as fluid needs to return to right ventricle so it can stretch and fill.  Oxygen: it supplements oxygen supply to supplement the patient’s reserves. It is considered a drug.  Nitroglycerin: Vasodilates vascular smooth muscle, decreases afterload and myocardial oxygen demand and improves coronary artery blood flow. Given as a spray under the tongue.  ASA: Prevents platelet aggregation. ASA is given as soon as possible; in the ambulance preferably.  Beta Blockers: Block beta-receptors and decrease workload of the heart by decreasing contractility and heart rate. In essence, it reduces the myocardial oxygen demand.  Adenosine Diphosphate Receptor Antagonist (Clopidogrel): Prevents activation of the glycoprotein IIb/ IIIa complex needed for platelet aggregation. Antiplatelet med helps prevent thrombus formation.  Anticoagulant (Heparin): Accelerates action of antithrombin which prevents formation of thrombus.  Reperfusion Therapy: Fibrinolysis is achieved
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