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Cardiovascular System John P. McDonough, CRNA, Ed.D., ARNP Vessels Arteries – carry blood away from the heart » oxygenated (except PA) Veins – carry blood to the heart » desaturated (except PV) Capillaries – local circulation – connects arteries to veins “Great” Vessels Vena cava – superior & inferior Pulmonary artery Pulmonary vein Aorta Blood Flow Through the Heart Rt Atrium Tricuspid valve Rt ventricle Pulmonic valve Lt atrium Mitral valve Lt ventricle Aortic valve Structure of the Heart Pericardium – visceral – parietal – pericardial fluid Myocardium – contractile heart muscle Endocardium – cavity lining Circulation to the Heart Itself Lt main coronary artery – Lt anterior descending – Lt circumflex Rt coronary artery Coronary perfusion – occurs during diastole – rate changes effect diastole only Cardiac Conduction System (electrical mechanical function) Sinoatrial (AS) node – “pacemaker of the heart” Intra-atrial conduction pathways Atrioventricular (AV) node Bundle of His Rt bundle branch Lt bundle branch – Lt anterior & posterior facicles Circulatory System 2 separate circuits, serially connected Output of one the input of the other – pulmonary, systemic Heart is functions as 2 pumps – Rt = pulmonary, Lt = systemic Arteries Veins Capillaries Adrenergic Control of Heart Rate -adrenergic receptors (generally dilates & excites) – 1 found mostly in the heart (conduction system) – 2 found mostly in the lungs (bronchi), but also in the coronary arterioles Adrenergic Control of Heart Rate -adrenergic stimulation will heart rate & dilate bronchi -adrenergic blockade will heart rate & constrict bronchi Norepinephrine binds with 1 receptors Epinephrine binds with 2 receptors Adrenergic Control of Heart Rate -adrenergic receptors – some in the heart, but mostly in vessels Stimulation causes constriction Autonomic Control of Heart Rate Sympathetic – thoracic chain ganglia – neurotransmitter = norepinephrine (NE) parasympathetic – vagus nerve (CN-X) – neurotransmitter = acetylcholine (Ach) Other Controls of Heart Rate Volume control – Barinbridge reflex Pressure control – baroreceptors Factors Effecting Cardiac Output Preload Afterload Heart Rate Contractility 1, 300, 000 Myocardial Infarctions yearly in the United States 50% are fatal Risk Factors for CV Disease Smoking Diabetes mellitus Hypertension Hyperlipidemia Risk Factors for CV Disease (con’t) Genetic predisposition Obesity Sedentary life-style Type A personality Hypertension 50 million Americans have it Diagnosed if >2 B/P measurements show: – diastolic readings >90 – average of 2 systolic >140 Mortality rates: – – – – white women white men black women black men 4.7% 6.3% 29.3% 22.5% Determinants of Hypertension Essential hypertension – stress – diet – genetic factors Secondary hypertension – – – – pheochromocytoma renal vascular disease Cushing’s syndrome thyrotoxicosis Effect of Vessel Diameter With the same 100mg/Hg pressure driving: – d=1 1 ml/min – d=2 16 ml/min – d=3 256 ml/min Complications of Hypertension Myocardial ischemia Ventricular failure Pulmonary edema Aortic dissection Intracerebral hemorrhage Common Antihypertensives Beta Blockers Propanolol, esmolol, metoprolol, atenolol ACE Inhibitors Captopril, enalapril, Calcium antagonists Nifedipine, diltiazem Blocks effect of cate. at receptors. Decreases HR & CO Dec conversion of AT-1 To AT-2 Orthostatic hypotension Inhibits Ca++ uptake, dec peripheral resistance Reflex tach, hypotension Bronchospasm, bradycardia, hypotension Cardiomyopathies Primary disorders of the muscle itself – not related to CAD, HTN or valve disorders Dilated cardiomyopathy – toxins, ETOH, infection, nutrition, Hypertrophic cardiomyopathy – usually congenital Restrictive cardiomyopathy – usually infiltrative disease process Congestive Heart Failure (a symptom complex) Each side of the heart can fail separately Left HF is a frequent cause of right HF – frequent, but the not the only S/S Left heart failure – dyspnea – pulmonary congestion S/S Right heart failure – peripheral edema – vein distention Treatment of CHF Rate control Digitalis glycosides (lanoxin) Diuretics Phosphodiesterase (PDE) inhibitors Cardiac muscle extracts the largest amount of oxygen because of the extensive work the heart does (manifested as contractility) even during rest. At rest: 8-10 ml O2/min/100g of myocardium. During exercise this can increase by a factor of 10. But what drives the contraction process in myocytes? Answer: ATP As demand goes up, inotropic response of the heart increases and the coronary vasculature adapts by vasodilating to provide an adequate oxygen supply. If, due to atherosclerotic disease, the coronary arteries are unable to sustain the myocardium, ischemia ensues and the flow is predicted by: Q = P r4/ 8 n L where r is radius of vessel, n is viscosity and L is vessel length. Factors in Supply & Demand Decreased supply – – – – reduced content reduced coronary flow increased LV pressure fixed vascular obstruction Increased demand – – – – – positive chronotropism positive inotropism increased LV volume increased wall tension increased afterload Visualization of intracellular oxygenation: Microspectrophotometry Reference: Takahashi, E. and K. Doi. Visualization of oxygen level inside a single cardiac myocyte. Am. J. Physiol. 268: H2561-H2568, 1995. Aerobic environment Happy myocytes Anoxic environment Myocytes not happy History Pain Dyspnea Palpitation Edema Syncope Fatigue & Weakness Cyanosis Hemodynamic to Formulae BP = CO x SVR CO = SV x HR SV = LVEDV - LVESV SVR = MAP - CVP x 80 / CO – normal = 800-1200 dyne/sec/cm-5 Congestive Heart Failure (diagnostic problems) Volume overload Bronchospasm Pneumonia Pulmonary embolism Ischemically mediated pulmonary edema Characteristics of Chest Pain ANGINA – retrosternal, diffuse – Lt arm, jaw, back – aching, dull, pressing, squeezing, – minutes – effort, emotion, eating cold – rest, NTG PROBABLY NOT – Lt inframam, localized – Rt arm – sharp, cutting, shooting, – seconds, hours, days – respiration, posture, motion – nonspecific Cardiac Causes of Chest Pain CAD aortic valve disease pulmonary hypertension mitral valve prolapse pericarditis IHSS Pulmonary Causes of Chest Pain pulmonary embolism pneumonia pleuritis pneumothorax Musculoskeletal Causes of Chest Pain costochondritis arthritis muscular spasm bone tumor GI Causes of Chest Pain ulcer disease bowel disease hiatal hernia pancreatitis cholecystitis Other Causes of Chest Pain Vascular – aortic dissection Emotional – anxiety – despression Common Causes of Palpitations extrasystoles tachyarrthymias bradyarrthymias drugs smoking caffeine thyrotoxicosis Common Causes of Dyspnea Cardiac – Lt failure – mitral stenosis Pulmonary – – – – obstructive disease asthma restrictive disease pulmonary HTN Emotional High altitude exposure Anemia Physical Exam of the Heart inspection blood pressure assess arterial pulse assess JV pulse percussion palpation auscultation evaluation of edema Murmur Description timing in cycle location radiation duration intensity pitch quality relationship to position relationship to respiration Grading of Murmurs (I-V/VI) I lowest intensity II low intensity III medium intensity (without thrill) IV medium intensity (with thrill) V loudest murmur with scope on chest VI loudest, heard with scope off chest Location of Murmurs within Cardiac Cycle “Shape” of Murmurs Three Most Important Survival Factors MYOCARDIAL PRESERVATION MYOCARDIAL PRESERVATION MYOCARDIAL PRESERVATION “Dead meat don’t beat!”