cardiovascular disruptions


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cardiovascular disruptions

  1. 1. Cardiovascular Disruptions
  2. 2. Objectives• Describe the normal structure, function and regulatory mechanisms of the cardiac system• Define the factors that can influence cardiac output and their significance• State the conditions/situations which can lead to the development of cardiac disruptions.• Identify the common disruptions to cardiac function and discuss each condition according to definition, pathogenesis, clinical manifestations, and medical/nursing management.
  3. 3. Normal Cardiac SystemThe heart is the pump of the circulatory system, and sits in themediastinal space of the intrathoracic cavity, in loose fittingsack called the pericardium. • The heart is suspended by the great vessels and is positioned with the wide side up, and the apex (narrower side) down and to the left. • Heart is comprised of 3 layers o Epicardium o Myocardium o Smooth Endocardium
  4. 4. Anterior view of heart and great vessels, and their relationship to lungs & skeletal structures of chest cage
  5. 5. Layers of the heart
  6. 6. Atria and VentriclesThe heart is broken up into 2 sets of 2 different chambers. • Atria: Function as a collection chamber for blood returning to the heart, and as a pump to fill the ventricle. • Ventricle: Main pumping chamber of the heart. o Right Ventricle: pumps the blood out of the heart and into the lungs through the pulmonary artery o Left Ventricle: pumps the blood out of the heart and into the body via the aorta
  7. 7. Heart ValvesThe atria and ventricles have 2 sets of valves that separate theatria and ventricles from each other, and from the systemiccirculation.The closure of these valves allows for the filling of thechambers of the heart and to allow the blood to be pumped outof the heart during systole.• Atrioventricular valves: control the flow of blood between the atria & the ventricles supported by the cordae tendonae o Tricuspid Valve (RT) o Bicuspid (Mitral) Valve (LT)• Semilunar valves: control the flow of blood out of the heart o Pulmonic Valve o Aortic Valve
  8. 8. Valvular structures of the heart.Atrioventricular valves are in an open position, semilunar valves are closed.There are no valves to control blood flow at inflow channels (vena cavae & pulmonary veins) to the heart.
  9. 9. Coronary ArteriesProvide oxygenated blood to the heart muscle.They are broken down into Right and Left Coronary Arteriesand branch directly off the aorta.• Right Coronary Artery: feeds the right side of the heart• Left Coronary Artery: breaks into 2 segments o Left anterior descending artery o Left circumflex artery
  10. 10. Coronary arteries & some of the coronary sinus veins.
  11. 11. Function/Cardiac Cycle EventsCardiac cycle is the rhythmic pumping action of the heart,which is broken into 2 events:• Systole: period during which the ventricles are contracting• Diastole: period during which the ventricles are relaxing and filling with blood.
  12. 12. Regulation of Cardiac FunctionThe conduction of heart is dependent on the depolarization ofthe nerve cells in the heart.The initial stimulus for a heartbeat originates in the SinoatrialNode (P-wave on the EKG)• P-wave  atrial contraction that moves blood  ventricles• The AV-valves close (first heart tone S1)• Ventricular pressure rises  semilunar valves open  blood is ejected from the hear• The Semilunar valves close (second heart tone S2)• Ventricular pressure < atrial pressure  AV-valves open  blood moves from the atria to the ventricle
  13. 13. Regulation of Cardiac Function:Cardiac regulation via the Sinoatrial Node (pacemaker of theheart) has some functions that make it unique in terms ofregulation of function: • Automaticity • Rhymthic • Speed of spreadThe initial depolarization in the Sinoatrial Node, is then spreadto the AV node that transmits the electrical impulse to theBundle of His that transmits it to Left/Right Bundle Branchesand ends in the Purkinje fibers
  14. 14. What can affect the regulation of thecardiac cycle?• Autonomic Nervous System: o Sympathetic Nervous System: increases the HR, speed of conduction through the AV node, and increases the force of atrial and ventricular contractions o Parasympathetic Nervous System: the vegus nerve innervation of the SA node directly allows for a slowing of SA node depolarization rate, and decrease in AV node conduction• Baroreceptors: sensitive to stretch or pressure, and when stimulated cause temporary inhibition of the sympathetic nervous system stimulation in the heart.• Chemoreceptors: present in the aorta and carotid bodies, and are stimulated by a drop in oxygen and an increase in carbon dioxide levels
  15. 15. Cardiac Output:Definition: Cardiac Output = Heart Rate x Stroke VolumeThe cardiac output can vary from person to person based on: • body size • metabolic needs o physical activity o rest/sleep • Ranges from 3.5-8 L/min
  16. 16. Influencing factors on cardiac output• Preload• Afterload• Cardiac contractility• Heart Rate
  17. 17. Influencing factors on cardiac outputPreload: Afterload: • This represents the • This represents the volume workload of the pressure or tension work heart of the heart to move blood • Determined by the amount from the left ventricle into of blood that the heart has the aorta/pulmonary artery. to pump with each beat. o largely comprised of the • Largely determined by the venous return to the systemic arterial blood heart pressure for the left o diuretics have an affect ventricle on the preload • Pulmonary arterial pressure determines afterload for the right ventricle
  18. 18. Influencing factors on cardiac outputCardiac Contractility: Heart Rate:• This is the ability of the • this determines the heart to change the frequency with which blood strength of its contraction is ejected from the heart. without changing its o increased heart rate can resting length increase CO to a point, o increased extracellular however, the quicker the contraction can increase heart needs to eject contractile strength blood, the shorter time it o decreased ATP from has to fill with blood to ischemia can cause eject. decreased contractility
  19. 19. Overview of Alterations in the Cardiac System 1. Lack of Blood Supply 2. Infections of the heart 3. Immune mediated inflammatory conditions 4. Cardiomyopathy
  20. 20. Consequences of decreased blood flowto the myocardium (heart muscle)Lack of blood supply or perfusion to the myocardium can resultin ischemia, anginal pain, cardiac arrhythmias, myocardialinfarction (heart attack), conduction defects, heart failure andsudden death.Conditions that cause this "ischemic heart disease" are asfollows:1. Atherosclerosis of the coronary arteries2. Thrombus within the coronary arteries3. Vasospasm of the coronary arteries4. Hypovolemia
  21. 21. Atheroscelrosis of the CoronaryArteriesThis disease process of the coronary arteries is the directcause of many cases of myocardial ischemia and infarction.The manifestations of atherosclerosis in the coronary arteriesinclude:1. Angina pectoris (myocardial ischemia)2. Myocardial ischemia (heart attack)3. Sudden cardiac death
  22. 22. Stages in development of atherosclerosisDeveloping atherosclerosis in the coronary arteries is a slowlyprogressing process, that occurs over many years. Symptomsoften dont occur until the vessel is 75% occluded, which is thepoint at which collateral circulation or compensatoryvasodilation cannot keep up with myocardial muscle oxygenneeds.1. Fatty Streak2. Fibrous Plaque3. Complicated lesion
  23. 23. Angina PectorisAngina comes from a Latin word meaning: "to choke"• Symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia• precipitated by situations that increase the work demands of the heart o physical exertion o exposure to cold o emotional stress• Pain is described at constricting, squeezing, or suffocating sensation located in the precordial or substernal area of the chest
  24. 24. Areas of pain due to angina.
  25. 25. Myocardial Infarct: Heart AttackAn acute myocardial infarct is characterized by ischemic deathof the myocardial tissue associated with atherosclerotic diseaseof the coronary artery.Area of infarction is determined by the coronary artery that isaffected:• 30-40% Right Coronary Artery• 40-50% Left Anterior Descending Artery• 15-20% Left Circumflex Artery
  26. 26. Manifestations of an MIOnset of an MI can be abrupt or it can progress from unstableangina. • pain, usually severe and crushing • pain substernal radiating to the left arm, neck or jaw • pain prolonged, not relieved by nitroglycerin • associated with a feeling of impending doom • Atypical presentations: o Women have more atypical ischemic like discomfort o Elderly people often have more shortness of breath • Tachycardia, anxiety, restlessness • pale, cool, moist skin
  27. 27. Diagnosing an MI• EKG changes o T-wave Inversion o T-wave Elevation o ST segment changes  ST depression (injury confined to the subendothelium)  ST elevation (injury to the heart is transmural)• Serum Markers o myoglobin o Creatinine Kinase MB (CK-MB) o Troponin 1 and Troponin T o C-reactive protein o B-cell natriuretic peptide (BNP)
  28. 28. Top:A.Normal ECGB.ST elevation with acute ischemiaC.Q wave with acute MIBottom: current of injury patterns with acute ischemiaA.With predominant subendocardial ischemia, resultant ST segment is directed toward inner layer of the affected ventricle &ventricular cavity. Overlying leads therefore record ST-segment depression.B.With ischemia involving the outer ventricular layer (transmural/epicardial injury), the ST vector is directed outward. Overlying leadsrecord ST-segment elevation.
  29. 29. Acute MI – X-section of ventricles infarct(death few days after onset of severe angina pectoris) • LV transmural infarct in posterior & septal regions. • Necrotic myocardium is soft, yellowish, and sharply demarcated. LV transmural infarct in posterior & septal regions
  30. 30. Consequences of AMI• Damage to the muscle wall of the heart o ventricular aneurysms• Damage to the conduction system of the heart o arrhythmias• Heart failure o decreased cardiac output
  31. 31. Treatment of AMI• Administration of Oxygen• Administration of analgesics• Aspirin• Beta-adrenergic blockers• Nitrates• If ECG evidence of infarction, Immediate Reperfusion therapy should be initiated: o Thrombolytic Therapy o Revascularization Interventions
  32. 32. Sudden Cardiac DeathUnexpected death from cardiac causes, usually within 1 hour ofan MI, can occur up to 24 hours post MI. • coronary artery disease accounts for 80% of cases o decreased blood flow causes an acute ventricular dysrhythmia o less frequently, the SCD can result from primary left ventricular outflow obstruction issues  aortic stenosis  hypertrophic cardiomyopathy • abrupt disruption in cardiac function, that produces an abrupt loss of cardiac output and cerebral blood flow • Biggest risk factors: left ventricular dysfunction (EF<30%) and ventricular dysrhythmias following MI
  33. 33. Conditions that disrupt blood flow in theheartThrombus within the coronary arteries: • Areas that have complicated lesions of atherosclerosis can cause the formation of thrombi. • The smooth muscle and foam cells in the lipid core contribute to the expression of tissue factor in unstable plaques, which leads to the activation of the extrinsic coagulation cascade and formation of thrombin and the deposition of fibrin = Red thrombi • If a plaque is disrupted, the endothelium is damaged and platelets bind there = white platelet containing thrombi
  34. 34. Vasospasm of the Coronary ArteriesThis is a spasm of the coronary arteries causing an acutedecrease in coronary blood flow, and ischemia • occurs most often during rest, or with minimal exercise • most frequently between midnight and 8am • can precipitate life threatening arrhythmias, and patient is at high risk for SCD • Causes (not totally known) o hyperactive sympathetic nervous system o defects in the management of Ca influx into vessel smooth muscle cells o alteration in nitric oxide production o imbalances between endothelium derived relaxing and contracting factors
  35. 35. HypovolemiaLack of circulating blood flow throughout the whole body canlead to a generalized ischemia in the heart due to the overalldecrease in oxygen carrying capacity. Hypovolemia is alsoassociated with electrolyte abnormalities that can causecardiac problems • Hypokalemia: K+ levels below 3.5 mEq/L • Hyperkalemia: K+ levels >5.5 mEq/L • Hypocalcemia: Ca++ levels <8.5 mg/L • Hypercalcemia: Ca++ levels >12 mg/dL
  36. 36. Infections of the HeartInfections in the pericardium, epicardium, myocardium,endocardium and the valves • Result in a decrease in the cardiac output • Can also cause a backward flow of blood into the ventricles (due to diseased valves) that can cause congestion of blood flow
  37. 37. Infective EndocarditisThis was previously known as bacterial endocarditis, but otherinfectious agents can cause endocarditis. Most common causeis bacterial though: • Staphylococcus aureus (can be MRSA) • Streptococcus viridansArise from infections somewhere else in the body, that allowsthe infectious organism into the blood stream. • blood flow turbulence in the heart allows the infective agent to infect previously damaged heart valves or other endothelial surfaces • the infectious agents attach the heart surfaces and form vegetations of infectious agent, platelets, fibrin, and leukocytes
  38. 38. Infective Endocarditis• The vegetations are very friable, they can break apart easily and "embolize" o 22-50% of patients with IE will experience systemic emboli from the vegetations  left side heart vegetations cause emboli to the brain, kidneys, spleen, or the limbs  right side of heart vegetations cause emboli to the lung• The infective vegetations can also cause damage to the valves and supporting structures
  39. 39. Infective EndocarditisAcute Bacterial Subacute BacterialEndocarditis: Endocarditis: • Usually affects those with • Affects those who have healthy valves preexisting valve disease • presents as an acute, • Clinical course may extend rapidly progressing illness over months Although this classification system was in historical use, now clinicians classify IE based on the cause, or the site of involvement
  40. 40. What does endocarditis look like?
  41. 41. Immune Mediated InflammatoryConditionsThese conditions primarily infect the valves, which results incongestion within the ventricles and in the lung and viseralcirculation• Rheumatic heart disease is a prime example of this o sequela to group A (beta hemolytic) streptococcal (GAS) throat infection o decreased incidence in the US because of antimicrobial treatment of GAS infection• Thought that the untreated GAS leads to antibody formation, which can affect the heart, joints, CNS and skin.• the myocardium develops Aschoff Bodies that are nodules with swelling and fragmentation of the collagen fibers that become more fibrous as we age
  42. 42. Rheumatic Heart DiseaseType III hypersensitivity: antibodies against the strep areformed, and there is a complex of strep and strep antibodiesthat are deposited in the heart, activates complement.• These complexes can also be deposited into the joints, but the effects on the joints are reversible• effects on the myocardium are permanent
  43. 43. CardiomyopathyA group of disorders that affect the heart muscle, which candevelop as primary or secondary disorders. Often lead tocardiomegaly and heart failure (dilitation of the heart muscle,hypertrophy of the the heart, or stiffening of the ventricles).Primary: Result of disease in the heart muscle itself, butusually an unknown causeSecondary: from a secondary disease, like a myocardialinfarction
  44. 44. Types of Cardiomyopathy1. Dilated2. Hypertrophic3. RestrictiveEach of these types of cardiomyopathy have their own etiology,presentation, pathophysiology and treatments.General Causes of Cardiomyopathy: Toxins such as alcohol,cocaine, chemotherapy agents, excess thyroid hormone,uremic disorders, metabolic abnormalities and familialtendencies
  45. 45. Dilated CardiomyopathyCharacterized by progressive cardiac hypertrophy and dilationand impaired pumping ability by one or both ventricles. Atriaare also enlarged. • because of wall thinning that occurs, the hypertrophied ventricles are thinner than one would expect. • mural thrombi are common and may be source of microemboli • Stasis of blood in the left ventricle • Causes: o Alcoholism o familial condition o toxic agents (chemotherapy)Most common form of cardiomyopathy.
  46. 46. Hypertrophic CardiomyopathyAbnormality that causes excessive ventricular growth orhypertrophy. Involvement of the interventricular septum tendsto be disproportionate, which produces intermittent leftventricular outflow obstruction and impaired relaxation of theheart. • Genetic disorder identified in many of the cases o mutation in one of the 10 genes coding for the cardiac sarcomeres o found to have myofibril disarray on microscopic evaluation of the heart • most common cause of SCD in the young • need to screen 1st degree relatives once discovered in an individual
  47. 47. Restrictive CardiomyopathyVentricular filling is restricted because of excessive rigidity ofthe ventricular walls, although the contractile properties of theheart remain relatively normal.• Endemic in parts of Africa, India, South and Central America, and Asia• In the U.S., the number 1 cause is amyloidosis, or amyloid infiltrations of the heart• Symptoms include: dyspnea, PND, orthopnea, peripheral edema, ascites, fatigue and weakness.Least common cardiomyopathy in the U.S.