Cardiac PDF

elastic arteries — absorb energy & stretch muscular arteries — can contract (vasoconstrict) & relax (vasodilate) veins — don't recall as quickly as arteries; muscle pump (pushes blood back to heart) capillaries — junctions between endothelial cells; blood flow into capillary beds controlled by contr...

elastic arteries — absorb energy & stretch muscular arteries — can contract (vasoconstrict) & relax (vasodilate) veins — don't recall as quickly as arteries; muscle pump (pushes blood back to heart) capillaries — junctions between endothelial cells; blood flow into capillary beds controlled by contraction & relaxation of smooth muscle bands (precapillary sphincters) at the junctions between metarterioles & capillaries endothelium roles — transportation of substances, coagulation, antithrombogenesis & fibrinolysis, immune system function, tissue growth & wound healing, vasomotion (contraction & relaxation of vessels), performance of these vital functions through synthesis & release of vasoactive chemicals mediastinum — above diaphragm & lungs; where heart is located heart wall: epicardium — outer smooth layer myocardium — thickest layer of cardiac muscle endocardium — innermost layer pericardium — double-walled membranous sac parietal — surface layer visceral — inner layer; also called epicardium pericardial cavity — space between parietal & visceral layers; contains pericardial fluid (20ml) CHAMBERS OF THE HEART thickness of each chamber depends on pressure or resistance it must overcome to eject blood atria separated by interatrial septum ventricles separated by interventricular septum GREAT VESSELS superior & inferior venae cavae — bring deoxygenated blood from the systemic circulation to right atrium R & L pulmonary arteries — transport unoxgynated blood from right heart to right & left lungs; branch into pulmonary capillaries pulmonary veins — carry oxygenated blood from lungs to left side of heart aorta — delivers oxygenated blood to systemic vessels that supply body one contraction & one relaxation; makes up one heartbeat diastole — relaxation/ventricles fill systole — contraction/blood leaves ventricles PHASES 1. Atrial systole /ventricular diastole 2. Isovolumetiric ventricular systole 3. Ventricular ejection (semilunar valves open) 4. Isovolumetric ventricular relaxation caortic valve closes) 5. Passive ventricular filling (mitral & tricuspid valves open) pumps blood thru lungs (pulm. circulation) delivers blood to lungs for oxygenation low pressure system pumps oxygenated blood to body (syst. circulation) delivers metabolic waste products to lungs, kidneys, & liver high pressure system ensure one way blood flow atrioventricular valves (AVs) atria to ventricles tricuspid valve — 3 leaflets or cusps bicuspid/mitral valve — 2 leaflets or cusps semilunar valves ventricles to either pulmonary artery or aorta pulmonic semilunar valve aortic semilunar value no sound when values open; heart sounds are result of value closure & vibration of surrounding fluids under certain pressure changes S1 — low pitch, long-lasting; closure of AV values S2 — rapid snap; closure of semilunar values S3 — low pitch; inrushing blood into ventricles S4 — hard to rear except in HTN pt with thick L ventricle; a triple contraction late in diastole Time between corresponds to diastole… AUTOMATICITY — property of generating spontaneous depolarization to threshold; all heart cells capable of spontaneous depolarization RHYTHMICITY — regular generation of action potential by heart's conduction system; SA node depolarizes spontaneously 60 - 100x/min AUTONOMIC NERVOUS SYSTEM — influences rate of impulse generation (tiring), depolarization, & depolarization; influences strength of atrial & ventricular contraction; produces changes in heart & circulatory system faster than metabolic or humoral agents sympathetic stim causes increased HR & increased contractility; norepinephrine & epinephrine parasympathetic (vagus) stim decreases HR markedly & decreases cardiac contractility slightly; acetylcholine increases electrical conductivity & strength of myocardial contraction; releases norepinephrine at sympathetic ending causes increase sinus node discharge; increases rate of conduction of impulse; increases force of contraction in atria & ventricles stimulation of both β1 & β2 — increases HR (chronotropy) & force myocardial contraction (inotropy) if HR is affected the effect is called chronotropy negative chronotropy — decreases HR positive chronotropy — increases HR if heart contraction is affected the effect is called inotropy negative inotropy — decreases force of contraction positive inotrophy — increases force of contraction β1 — normal heart activation leads to increases in contractile force & HR; located on pacemaker, myocardium, salivary gland ducts, scribe & apocrine sweat glands; norepinephrine & epinephrine β2 — vascular & nonvascular smooth muscle regulatory; inverse response ( stimulation = decreased activity or muscle tone); activation leads to vascular & nonvascular smooth muscle relaxation; located on smooth muscle (GI tract, bladder, some coronary arteries) causes hyperpolarization of cardiac pacemaker cells because of increased k+ permeability in response to acetylcholine; this causes decreased transmission of impulses reducing HR or temporarily stopping HR FACTORS AFFECTING CARDIAC OUTPUT Heart rate Average heart rate in healthy adults: ~70 beats/minute Cardiovascular control center Activation of sympathetic system: Increases heart rate Activation of parasympathetic system: Decreases heart rate; controls resting heart rate Neural reflexes Sinus arrhythmia Baroreceptor reflex: when blood pressure falls, heart rate increases and arterioles constrict Bainbridge reflex: changes in heart rate from IV infusions Atrial receptors Hormones and biochemicals Epinephrine, norepinephrine, thyroid hormone, GH Myocardial contractility Stroke volume — volume of blood ejected during systole Determinants of the force of contraction Changes in the stretching of the ventricular myocardium, caused by changes in ventricular volume (preload) Alterations in nervous system input to the ventricles Adequacy of myocardial oxygen supply Positive inotropic agents: Increase the force of contraction. Norepinephrine from the sympathetic nerves supplying the heart Epinephrine from the adrenal medulla. Thyroid hormone and dopamine Negative inotropic agents: Decrease the force of contraction. Acetylcholine released from the vagus nerve Hypoxia: Decreases contractility. degree of cardiac contractility heart rate venous return to the heart blood volume patency of venous system degree of arteriolar dilation differential pressure skeletal muscle pump respiratory pump Greater resistance, lower blood flow More stretch = force of contraction smaller chambers, and thicker chamber walls equal increased contraction force ventricular dilation the force needed to maintain ventricular pressure lessens available contractile force Excess K+ decreases contractility Cause heart to become dilated and flaccid, slows heart rate Rise to just 2-3 times normal (8-12mEq/L) can lead to death Excess Ca causes spastic contraction, and low Ca causes cardiac dilation. Arterial pressure — effects of cardiac output CO = MAP (when no decrease in peripheral resistance) CO = drop in MAP and flow rate Neural control of resistance Baroreceptors — reduce blood pressure to normal by decreasing cardiac output and peripheral resistance; also BP when needed. Arterial receptors: Chemoreceptors — sensitive to oxygen, carbon dioxide, or pH. Regulate blood pressure. Decrease in PaO2 or increase in PaCO2 causes increase in HR, SV, and BP LYMPHATIC SYSTEM special vascular system picks up excess fluid and returns it to the venous circulation moving lymphocytes & leukocytes between different components of the immune system is another important function has lymph nodes & vessels valves allow one way flow lymphatic fluid is made up of primarily water & small amounts of dissolved proteins, mostly albumin. cross-bridge cycling — attachment of acting into myosin at cross bridge; causes thin filaments to slide past thick filaments (contraction) calcium — enters myocardial cell from ISF after electrical excitation; diffuses towards myofibrils where it binds with troponin excitation contraction coupling — calcium-troponin complex facilitates contraction process myocardial relaxation — troponin release of calcium begins myocardial relaxation Cardiac Alterations Hypertension ○ Consistent elevation of systemic arterial blood pressure ○ JNC 8 Guidelines ○ < 150/90 is the goal; unless underlying comorbidities, DM, Renal disease then 140/90. Primary (essential) hypertension – no known cause; is 95% of those with hypertension. Secondary hypertension – caused by altered hemodynamics from an underlying primary disease or drugs. ○ Caused by systemic disease that raises peripheral vascular resistance and/or cardiac output ○ Renal artery stenosis, renal parenchymal disease, pheochromocytosis, and drugs are examples. Complicated hypertension – hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling Malignant hypertension ○ Rapidly progressive hypertension ○ Diastolic pressure is usually >140 mm Hg ○ Can lead to encephalopathy Aneurysm complication – aortic dissection ○ Tear in intima of aorta, into which blood flows furthering the tear. ○ Devastating complication that involves the aorta (ascending, arch, or descending); can disrupt the flow through the arterial branches. ○ Surgical emergency Deep venous thrombosis (DVT) ○ Thrombus: Clot ○ Detached thrombus: Thromboembolus; can lead to pulmonary emboli ○ Clot in a large vein ○ Obstruction of venous flow leading to increased venous pressure ○ Factors: Virchow triad Venous stasis Venous endothelial damage Hypercoagulable states ○ Postthrombotic syndrome Atherosclerosis – form of arteriosclerosis. Thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall; plaque development; leading cause of coronary artery and cerebrovascular disease. Coronary Artery Disease – any vascular disorder that narrows or occludes the coronary arteries. Results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients. Reversible myocardial ischemia or irreversible infarction may result. Most common cause: Atherosclerosis Dyslipidemia – an indicator of coronary risk. ○ Increased LDL: Play a role in endothelial injury, inflammation, and immune responses that are important in atherogenesis. ○ Low levels of HDL: Are responsible for “reverse cholesterol transport,” which returns excess cholesterol from the tissues to the liver. ○ Elevated serum VLDL (triglycerides) ○ Increased lipoprotein (a) Types of Myocardial Ischemia (coronary blood cannot meet the demand of the myocardium for oxygen and nutrients) ○ Stable angina: predictable chest pain. ○ Prinzmetal angina (variant): unpredictable chest pain. ○ Silent ischemia: no detectable symptoms. ○ Angina pectoris: transient substernal chest discomfort. Acute Coronary Syndromes – sudden coronary obstruction because of thrombosis formation over a ruptured atherosclerotic plaque ○ Examples: Unstable angina, MI ○ Most common complications: Dysrhythmias, congestive heart failure, and sudden death Myocardial Infarction – prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis). ○ Myocardial stunning – temporary loss of contractile function that persists for hours to days after perfusion has been restored. ○ Hibernating myocardium – tissue that is persistently ischemic undergoes metabolic adaptation to prolong myocyte survival. ○ Remodeling – process that occurs in the myocardium after an MI. ○ Repair – consists of degradation of damaged cells, proliferation of fibroblasts, and synthesis of scar tissue Myocardial Infarction ○ Individuals experiencing MI at highest risk for complications are those with ST segment elevations (STEMI) on the ECG; this requires immediate intervention. ○ Smaller infarctions not associated with ST segment elevations (non-STEMI) suggest that additional myocardium is still at risk for recurrent ischemia and infarction. ○ Clinical manifestations: sudden severe chest pain, N/V, Diaphoresis, Dyspnea, ECG changes, Troponin I: Most specific (elevates in 2 to 4 hours), Creatine phosphokinase–MB (CPK-MB), LDH, Hyperglycemia ○ Complications: dysrhythmias, cardiogenic shock, pericarditis, Dressler (postinfarction) syndrome, organic brain syndrome Thromboangiitis obliterans (Buerger disease) ○ Occurs mainly in young men who smoke. ○ Is an inflammatory disease of the peripheral arteries. Digital, tibial, plantar, ulnar, and palmar arteries ○ Obliterates the small- and medium-sized arteries. Lesions accompanied by thrombi and vasospasm of arterial segments ○ Pain and tenderness develop in the affected part. Hair loss in affected area ○ Sluggish blood flow, rubor, and cyanosis result. ○ Can often lead to gangrenous lesions Raynaud phenomenon and Raynaud disease Episodic vasospasm (ischemia) in the arteries and arterioles of the fingers; less commonly in the toes Clinical manifestations: Changes in skin color and sensation caused by ischemia ○ Pallor, cyanosis, cold, and pain Raynaud phenomenon: Secondary to other systemic diseases or conditions Raynaud disease: Primary vasospastic disorder of unknown origin ○ Tends to affect young women ○ Vasospastic attacks triggered by brief exposure to cold or emotional stress Rheumatic fever ○ Abnormal immune response to the M proteins that cross react with normal tissues ○ Fibrinoid necrotic deposits: Aschoff bodies ○ Clinical manifestations Carditis: Murmur Polyarthritis: Large joints mainly affected Chorea: Sudden, aimless, irregular, involuntary movements Erythema marginatum: Truncal rash Valvular stenosis – valve orifice is constricted and narrowed ○ Forward blood flow impeded ○ Increased workload of chamber with affected valve ○ Intraventricular or atrial pressure increases ○ Leads to myocardial hypertrophy ○ Aortic & Mitral valves Valvular regurgitation ○ Also called insufficiency or incompetence ○ Valve leaflets, or cusps, fail to shut completely ○ Blood flow continues even when valve is closed ○ Increase volume of blood that heart must pump because of leaking back through valve ○ Increased volume lead to dilation ○ Increased workload leads to hypertrophy ○ Aortic, Mitral, & Tricuspid valves Aortic regurgitation ○ Inability of the aortic valve leaflets to close properly during diastole ○ Clinical manifestations: Widened pulse pressure as a result of increased stroke volume and diastolic backflow, diastolic murmur Mitral regurgitation ○ Most common causes: Mitral valve prolapse and rheumatic heart disease ○ Permits backflow of blood from the left ventricle into the left atrium ○ Results in LV hypertrophy because of increased volume in LA entering the ventricle. ○ Systolic murmur, pansystolic murmur ○ Presence of S3 Tricuspid regurgitation ○ Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure ○ Systolic murmur that increases with inspiration Tricuspid Stenosis ○ Patho essentially the same as MS, except that it occurs on the right side of the heart ○ Diastolic murmur Mitral valve prolapse syndrome ○ Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole ○ Clinical manifestations: Asymptomatic ○ Affected valves at greater risk of developing infective endocarditis Pulmonic Stenosis ○ Result of congenital anomaly ○ Systolic murmur Pulmonic Regurgitation ○ Seen with pulmonary hypertension ○ Diastolic murmur Infective Endocarditis – inflammation of the endocardium from infectious agents ○ Clinical manifestations: Osler nodes: Painful erythematous nodules on the pads of the fingers and toes Janeway lesions: Nonpainful hemorrhagic lesions on the palms and soles Constrictive pericarditis ○ Pericardium becomes rigid and impairs filling ○ Signs and symptoms similar to right and left sided heart failure. ○ Kussmaul’s sign Pericardial effusion ○ Accumulation of fluid in pericardial sac ○ Tamponade Severe restriction of cardiac motion Fatal if not resolved s/s hypotension, increased JVP, distant heart sounds Hypertrophic (asymmetric) cardiomyopathy ○ Hypertrophic obstructive cardiomyopathy ○ Common inherited heart defect of a thick septal wall ○ Clinical manifestations: Angina, syncope, palpitations, diastolic heart failure Hypertensive or valvular hypertrophic cardiomyopathy ○ Hypertrophy of the myocytes – attempts to compensate for increased myocardial workload. ○ Clinical manifestations: Asymptomatic or may complain of angina, syncope, dyspnea on exertion, and palpitations. Dilated (congestive) cardiomyopathy ○ Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure ○ Causes: MI; diabetes; alcohol; Valvular regurgitation ○ Clinical manifestations: Dyspnea and fatigue, systolic dysfunction Restrictive cardiomyopathy ○ Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. ○ Clinical manifestations – right heart failure occurs with systemic venous congestion. Congestive (left) heart failure ○ Systolic heart failure or diastolic heart failure Cardiac output – depends on the heart rate and stroke volume ○ Stroke volume – contractility, preload, and afterload ○ MI – the most common cause of decreased contractility. ○ Preload – increased when decreased contractility or excess plasma volume is present. ○ Increased afterload: most commonly from increased peripheral vascular resistance. Systolic heart failure - ejection problem ○ Inability of the heart to generate adequate cardiac output to perfuse tissues ○ LVEF 40% Systolic heart failure ○ Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation ○ Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema ○ Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or hypertension Diastolic heart failure ○ Heart failure with preserved ejection fraction ○ Decreased compliance of the left ventricle and abnormal diastolic relaxation which leads to increased end diastolic pressure ○ Higher end diastolic left ventricular pressure transmitted to pulmonary circulation leads to pulmonary congestion ○ Causes: HTN, Ischemia, HR, Afib, ventricular hypertrophy, aging ○ Clinical manifestations non-specific; dyspnea, exercise intolerance, fatigue, weakness Clinical manifestations of R heart failure: ○ Pedal edema, ascites, enlarged liver, elevated JVP, sacral edema, nocturia, and even jaundice and coagulopathy. Staging Heart Failure A At high risk for heart failure but without structural heart disease without structural heart disease or symptoms of heart failure or symptoms of heart failure B Structural heart disease but without signs/symptoms of heart failure C Structural heart disease with current or past symptoms of heart failure D Refractory heart failure requiring specialized interventions High output failure ○ Occurs when CO is higher than normal ○ Underlying patho = reduced systemic vascular resistance ○ Is the inability of the heart to supply the body with bloodborne nutrients, despite adequate blood volume and normal or elevated myocardial contractility. ○ Common causes – Anemia, septicemia, hyperthyroidism, and beriberi Heart Blocks Multifocal atrial tachycardia (MAT) ○ Tachyarrhythmia starts at multiple sites ○ Occurs in pt’s with pulmonary disease ○ Multiple P wave morphologies Atrial flutter ○ Reentrant circuit in atrium; EKG with saw-tooth appearance of P waves Atrial fibrillation ○ Reentrant circuits ○ EKG wavy, chaotic, disorganized baseline without recongizable P waves ○ Rate >300 ○ Risk of thrombus, emboli, stroke, mesenteric ischemia Pre-excitation syndromes – Wolff-Parkinson-White and Lown-Ganong-Levine ○ Congenital presence of accessory pathways (bundle of Kent and Mahaim fibers) conducts very rapidly and bypasses the AV node. ○ Cause early ventricular depolarization in relation to atrial depolarization – PR shortened, Delta wave ○ Supraventricular tachycardia ○ Complications with AFib – sudden cardiac death Classifications of Pediatric Hypoxemia – based on blood flow ○ Lesions increasing pulmonary blood flow Defects that shunt from high-pressure left side to low-pressure right side with pulmonary congestion; acyanosis ○ Lesions decreasing pulmonary blood flow Generally complex with right-to-left shunt and cyanosis ○ Obstructive lesions Right- or left-sided outflow tract obstructions that curtail or prohibit blood flow out of the heart ○ Mixing lesions Desaturated blood and saturated blood mix in the chambers or great arteries of the heart Patent ductus arteriosus (PDA) ○ Vessel located between junction of main and left pulmonary arteries ○ Failure of the ductus arteriosus to close results in persistent patency of the ductus arterisus ○ PDA allows blood to shunt from the aorta to pulmonary artery causing left-to-right shunt ○ Hemodynamic effect is increased pulmonary blood flow, resulting in increased pulmonary venous return to the LA and LV with increased workload on the left side of the heart ○ Clinical manifestation Continuous, machinery-type murmur Risk for bacterial endocarditis Atrial septal defect ○ Abnormal opening between the atria; blood flows from left atria to right atria ○ Three major types: Ostium primum defect – opening found low in septum, may be associated with AV abnormalities, esp. mitral valve insufficiency Ostium secundum defect – opening in center of septum, most common Sinus venosus defect – opening is high in septum near superior vena cava and RA junction ○ Shunting from the left to right atrium because of higher pressure in left atrium and lower pulmonary vascular resistance – right atrial and ventricular enlargement ○ Clinical manifestations – often asymptomatic; diagnosed by murmur; pulmonary symptoms on exertion at later age Ventricular septal defect (VSD) ○ Abnormal communication between ventricles Shunting from the high-pressure left side to the low-pressure right side Amount of shunting dependent of size of defect and degree of pulmonary vascular resistance Small VSDs limit blood flow through defect therefore degree of pulmonary congestion is low, leading to minimal ventricular enlargement ○ Common congenital heart lesion (25% to 33%) ○ Pulmonary overcirculation accounts for symptoms associated with a large VSD ○ Clinical Manifestations – heart failure, poor weight gain, murmur and systolic thrill Tetralogy of Fallot ○ Syndrome represented by four defects 1. VSD 2. Overriding aorta straddles the VSD 3. Pulmonary valve stenosis 4. Right ventricle hypertrophy ○ Cyanosis and clubbing, feeding difficulty, squatting ○ Hypercyanotic spell or a “tet spell” that generally occurs with crying and exertion Coarctation of the aorta ○ Narrowing of the lumen of the aorta that impedes blood flow (8% to 10% of defects) ○ Is almost always found in the juxtaductal position, but it can occur anywhere between the origin of the aortic arch and the bifurcation of the aorta in the lower abdomen. ○ Directly at the insertion of the closed ductus arteriosus in the aortic arch ○ Causes condition in which there are higher pressures proximal to the site of stenosis and lower pressures distal ○ Direction of shunting depends on the pressure difference between PA and aorta and location of the ductus (always high to low pressure) ○ If blood pressure is greater in the aorta than PA = left to right shunting, resulting in increased pulmonary venous return to left side of heart, over time leading to hypertrophy of LV, and then HF ○ Clinical manifestations – newborns usually exhibit CHF. Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock. ○ Clinical manifestations – older children Hypertension in the upper extremities Decreased or absent pulses in the lower extremities Cool mottled skin Leg cramps during exercise Hypoplastic left heart syndrome ○ Left-sided cardiac structures develop abnormally. Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed. Obstruction to blood flow from the left ventricular outflow tract results in high pressure, leading to saturated blood entering the LA and then mixing with desaturated blood in the RA through atrial septal communication ○ As the ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock. ○ Fatal if left untreated Transposition of the great arteries ○ Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. ○ Results in two separate, parallel circuits. ○ Unoxygenated blood continuously circulates through the systemic circulation. ○ Oxygenated blood continuously circulates through the pulmonary circulation. ○ Extrauterine survival requires communication between the two circuits. ○ Clinical manifestations – cyanosis may be mild shortly after birth and worsen during the first day. Pediatric systemic hypertension ○ Often have underlying renal disease or coarctation of the aorta. ○ Cause of hypertension is almost always found. ○ Commonly asymptomatic. ○ Clinical manifestations – systolic and diastolic blood pressure levels are greater than the 95th percentile for age and gender on at least three occasions. Kawasaki disease – mucocutaneous lymph node syndrome ○ Is an acute, self-limiting systemic vasculitis that may result in cardiac sequelae. ○ Approximately 80% of cases occur in children under the age of 5. ○ Cause – unknown ○ Theory – immunologic response to an infectious, toxic, or antigenic substance (including superantigen)