Cardiovascular Dysfunction & Disorders PDF - Samuel Merritt University

Cardiovascular Dysfunction & Disorders N111 Pathopharmacology 1 Samuel Merritt University  Cardiac Output  Systemic AND/OR Vascular (CO) = HR x SV Afterload...

Cardiovascular Dysfunction & Disorders N111 Pathopharmacology 1 Samuel Merritt University  Cardiac Output  Systemic AND/OR Vascular (CO) = HR x SV Afterload Resistance (SVR)  Heart Rate (HR)  Vessel Diameter  β1 Stimulation (SNS) α1 Stimulation HTN RAAS  Stroke Volume (SV)  Blood viscosity  Preload Hematocrit  Myocardial contractility Smoking  BP Regulation Receptors Baroreceptors Chemoreceptors  Located in carotid sinus & aorta  Located in specific areas of the  Respond to changes in small aorta & the carotid arteries muscle fiber length  Respond to changes in oxygen,  Activation   BP pH, and carbon dioxide in   CO arterial blood   SVR   oxygen/pH   BP Regulation of Blood Pressure (cont’d)  Hypertension (HTN)  SBP > 140 mmHg and/or DBP > 90 mmHg  On two separate occasions  HTN  Isolated systolic HTN  SBP 140, DBP 120 mmHg  End-organ damage  Cerebral edema/dysfunction  Immediate intervention required  IV antihypertensives CORONARY HEART DISEASE  Coronary Heart Disease (CHD)  Atherosclerosis  Ischemia  Coronary syndromes  Angina pectoris  Cardiac arrest  Chronic ischemic cardiomyopathy  Coronary Heart Disease (CHD) Ischemic heart disease (IHD) & coronary artery disease (CAD)  Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries  Arteriosclerosis  Abnormal thickening/hardening of vessel walls  Smooth muscle cells and collagen fibers migrate to the tunica intima  Atherosclerosis  Thickening/hardening due to lipid engulfed macrophages  Leads to Narrowing of the arterial lumen Inadequate perfusion Ischemia Necrosis  Atherosclerosis Risk Factors  Hyperlipidemia  Dyslipidemia  Diabetes  Smoking  Hypertension  Atherosclerosis Etiologies Chronic Inflamm hemodynamic cytokines wall stress Cigarette smoke Lipids toxins Artery endothelium injury Pathogenesis Atherosclerosis Atherosclerosis (cont’d)  Atherosclerosis Pathogenesis Damage endothelial & sm muscle cells Permeable LDLs enter into Oxidized LDLs Artery endothelium the intima endothelium injury Macrophage Leukocytes migration recruited Inflamm. Lipid core/ mediators/ Complicated Fibrous Sm muscle Foam cells fatty streak growth plaque plaque proliferation form formation factors released  Plaque Cellular waste products Cholesterol Calcium Fatty substances Plaque Fibrin  Plaque Types Vulnerable Plaque Stable Plaque  Large lipid core  More collagen &  Thin cap fibrin  High shear stress  Stable cap  May rupture/ become eroded  clot formation  Atherosclerosis Complications Cardiac ischemia Narrowing of the arterial lumen + Thrombus formation Coronary vasospasm Endothelial cell dysfunction  Angina pectoris  Chest pain associated with intermittent myocardial ischemia  Burning, crushing, squeezing, choking or referred pain  No permanent myocardial damage  Types  Stable angina  Unstable angina  Prinzmetal variant  Stable Angina  Stenotic atherosclerotic coronary vessels  Onset predictable & elicited by similar stimuli Relieved by rest and nitroglycerin  Prinzmetal Variant Angina  Characterized by  Vasospasms  Hypercontractility  Abnormal calcium flux in vascular sm muscle  Unpredictable attacks of anginal pain  Ca-channel blockers Myocardial Ischemia Myocardial Infarction  Myocardial Infarction (cont’d)  Manifestations:  Sudden severe chest pain; may radiate  Nausea, vomiting  Diaphoresis  Dyspnea  Complications:  Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability Myocardial Infarction (cont’d) Angina or MI?  Relevant biomarkers Biomarker Normal Implication of abnormal Myoglobin  85 ng/ml Heart/skeletal mm damage  5-6x  norm. Troponin I < 10 µg/L Heart mm damage  4- 6x  norm. Troponin T  0.1 µg/L Heart mm damage  elevated Creatine kinase Very low, Heart mm damage  (CKMB) undetectable elevated ACS algorithm Myocardial Infarction (cont’d)  Endocardial disorders Rheumatic heart disease Infective endocarditis  Rheumatic heart disease  Etiology: group A β-hemolytic streptococci Pathogenesis:  Antibodies against the streptococcal antigens damage connective tissue in joints, heart, skin  Infective endocarditis  Etiology:  Streptococcus  Staphylococcus Pathogenesis  Invasion and colonization of endocardial structures by microorganisms with resulting inflammation  vegetation  Cardiac Performance  Cardiac output  Preload  Left ventricular end-diastolic volume  Laplace law  Frank-Starling law of the heart  Afterload  Load muscle must move after it starts to contract  Determined by system vascular resistance in aorta, arteries, and arterioles Cardiac Performance (cont’d) Cardiac Performance (cont’d)  Heart rate  Cardiovascular control center  Cardioexcitatory and cardioinhibitory centers  Neural reflexes  Bainbridge and baroreceptor reflexes  Atrial receptors  Hormones and biochemicals Heart Rate Cardiac Output Normal Intracardiac Pressures HEART FAILURE  Heart failure (HF) Insufficient CO Left-sided heart failure Right-sided heart failure  Ejection Fraction (EF)  measurement of the percentage of blood leaving your heart each time it contracts.  Normal: 55-70%  HF Dysfunction Systolic Diastolic  Etiology: commonly MI  Etiology: CAD & HTN   contractility  loss  Poor ventricular filling of myocytes &  ATP  ineffective production ventricular filling Clinical Manifestations Clinical Manifestations  EF < 40%   CO  Normal EF  Congestion  Edema  HF pathogenesis Impaired contraction/relaxation of heart Congestion of systemic/pulmonary circulation Unable to increase CO to meet demands  HF clinical manifestations   CO  Forward failure = insufficient cardiac pumping  Confusion, fatigue, tachycardia, reduced urine output, and poor peripheral circulation  Congestion  Backward failure = congestion of blood behind the pumping chamber HF: Compensatory mechanism  HF: Compensatory mechanism  Current management of HF directed toward reducing the harmful consequences of these compensatory responses:  SNS activation  Increased preload  Myocardial hypertrophy  HF: Hypertrophy & Remodeling Chronic  myocardial wall tension  hypertrophy of remaining cells  myocyte loss  interstitial fibrosis Left Heart Failure: Pathogenesis & Clinical Manifestations  Dyspnea  Dyspnea on exertion (DOE)  Orthopnea  Paroxysmal nocturnal dyspnea  Cough  Crackles  Hypoxemia  cyanosis  Fatigue  Oliguria  Confusion/anxiety   HR Right Heart Failure: Pathogenesis & Clinical Manifestations  Edema, ascites  weight gain  Jugular vein distention  Impaired mental function  Hepato- & spleno-megaly  Fatigue  Oliguria  Confusion/anxiety   HR  HF Clinical Manifestations   B Natriuretic Peptide (BNP) Normal < 100 pg/ml Evident during acute/exacerbation events  HF Treatment Implications   preload/afterload  Diuretics  ACE inhibitors   fluid/Na  Improve contractility  Digitalis  Improve effectiveness of the pump  Inhibit SNS effects  β-blockers DYSRHYTHMIAS  Atrial Fibrillation (A-Fib) Atria quiver Ineffective atrial contraction Disorganized/ Blood pools/ irregular atrial stagnates in atria rhythm Treatment prevent Thrombi thrombus formation— formation blood thinners Ventricular Fibrillation (V-Fib) Ventricles quiver  Treatment implications Ineffective  Defibrillation ventricular contraction  CPR  Antiarrhythmic EKG: rapid & eratic, no QRS medication complexes Death in minutes Which of the following is an accurate statement regarding blood flow through the heart? A. Blood flows from the left ventricle through the bicuspid valve. B. Blood flows from the right atrium through the aortic valve to the right ventricle. C. Blood flows from the right ventricle through the pulmonic semilunar valve. D. Blood flows from the left atrium through the tricuspid valve to the left ventricle. A client is diagnosed with increased systemic vascular resistance. What will be the effect on the heart? A. Left atrium will be required to pump harder. B. Right atrium chamber will become enlarged. C. Left ventricle will be required to pump harder. D. Right ventricle will become ineffective because of increased pressure. Which plaque is most prone to rupture? A. Contains significant collagen and fibrin B. Has a large lipid core with a thin cap C. Contains high-density lipoproteins D. Has areas of ischemia and necrosis A client is complaining of having intermittent “chest pain” after exercise. This is most likely caused by? A. Unstable angina B. Infective endocarditis C. Inflammation of the pericardium D. Atherosclerotic plaque leading to stable angina Which of the following is a finding unique to left-sided heart failure? A. Decreased urine output B. Increased heart rate C. Peripheral dependent edema D.Shortness of breath Which patient should the nurse assess first? A patient with A. ventricular fibrillation. B. atrial fibrillation. C. unstable angina. D.an ejection fraction of 30%.