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Pathophysiology- Cardiovascular System

by: Shelby Stephens

Pathophysiology- Cardiovascular System NUR 305

Shelby Stephens
GPA 3.5

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This 0 page Study Guide was uploaded by Shelby Stephens on Wednesday December 9, 2015. The Study Guide belongs to NUR 305 at University of Alabama - Tuscaloosa taught by Owings in Fall 2015. Since its upload, it has received 28 views. For similar materials see Pathophysiology in Nursing and Health Sciences at University of Alabama - Tuscaloosa.

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Date Created: 12/09/15
Cardiovascular Functions 0 Delivers vital oxygen and nutrients to cells 0 Removes waste products 0 Transports hormones Branches 0 Systemic Carries blood throughout the body to meet the body s needs and remove waste products Includes arteries veins and capillaries Works with the lymphatic system 0 Pulmonary Carries blood to and from the lungs for gas exchange Heart 0 Pericardium Surrounds the heart to provide protection and support 0 Myocardium Cardiac muscle 0 Endocardium Inner structures including the valves 0 Four Chambers Two Atria receiving chambers Liquot39l mmn f i IIHE39 IJrE zri EiIfi 39 H39s quotlamamil ri39i39anI i39 IWWE39 5s n ELIJE39i39HZIDquotE39 ntJDJI 39 n n LEE39Z39E wingr ghii l m l aai j J i quot 7 j minhm A 39 LEquot manian R Hi l gummyi HIE quotan WENquotwarquot 1 ji39lhll39l ill l ga y m E EmiIEIuIIia E39Ii3939u39 maili39 lf i39ihili39 IIII HIEIJIE39AI39J39E INEI arl J fl E Siramid We a Lqu unduean IdiFl i39leil39ixllFEquotl iil Emgm H 3 phihr quot39m illlliilT39FEHIHILKIh39iI I l39 Two Ventricles pumping chambers Blood flow through the Heart Systemic Blood from the systemic circulation enters from the superior vena cava and the inferior vena cava Blood empties directly into the right atrium From the right atrium blood travels through the tricuspid valve to the right ventricle The right ventricle pumps blood through the pulmonic valve to the pulmonary arteries To arteries of heart and arms Superior vena cava from upper body Right pulmonary artery to right lung iRigtit pulmonary veins from right quot Icing to left atrium LEFTATRIUM Aortic naive Mitral waive LE FT VENTRICLE Epicardiuirn quotVisceral pericardium Pericardiizal space Peri etal pericardium Descending aorta to tower badly Endocardium Unoxygeinated blood My cardium E ny39geinatedi blood Capfr igmc39a 2010 2006 2002 by Saunaere an Imprint or Eleevier Inc The pulmonary arteries carries blood to the lungs for gas exchange Blood flow through the Heart Pulmonary Blood from the pulmonary circulation enters from the pulmonary veins Blood empties directly into the left atrium Blood leaves the left atrium through the mitral valve to the left ventricle The left ventricle then pumps blood through the aortic valve to the aorta From the aorta the blood is carried the rest of the body Conduction System gtiltgtiltgtilt Organizes electrical impulses in the cardiac cells Involves Excitability ability of the cells to respond to electrical impulses Conductivity ability cells to conduct electrical impulses Automaticity ability to generate an impulse to contract with no external nerve stimulus Mechanical contractility FOLLOWS electrical conduction One cannot eXist Without the other PM lt Conduction Pathway Impulses originate in the sinoatrial SA node PACEMAKER high in the right atrium at a rate of 60 100 bpm Im ulses travel throu h the ri ht and l i 7 M p g g Flow of carlalc lmpulse Spread Dfmmduction 1 impulses from SA node to left altl39llU m left atrium internodal pathways SA node Ilnltemodlall causing atrial contraction pathways Impulses then travels to the 7 Left bundle atrloventrlcular AV node 1n the branch right atrium adjacent to the septum Impulses are delayed in the AV node to allow for complete ventricular AV Ode filling Bundle oinls 39 V 39 Anterosupelrlorfasclcle Flight bundle of left bundle branch bra nc h Impulses then move rapidly through the bundle of His right and left bundle branches and Purkinje P urkin39e bers network of bers caus1ng ventricular l Semi contraction The AV node can initiate impulses if the SA node fails 40 60 bpm The ventricles can initiate impulses if the SA and AV nodes fail 20 40 bpm which may be inadequate Electrical Activity Depolarization Increase in electrical charge Accomplished through cellular ion exchange Generates cardiac contraction Repolarization Cellular recovery Ions returning to the cell membrane in preparation for depolarization Can be read by an electrocardiogram P wave atria depolarization QRS compleX ventricular depolarization T wave ventricular repolarization Sinus rhvthm Electrical activity when impulses originate in the SA node Dysrhythmias Abnormal electrical activity Can result from issues such as myocardial infarctions and electrolyte imbalances Conduction Control Electrolyte signals Sodium potassium and calcium Medulla monitoring Autonomic nervous system endocrine system chemoreceptors and baroreceptors Effects Chronotropic rate of electrical conduction Dromotropic rate of contraction Inotropic strength of contraction Blood Pressure vs The Cardiac Cycle Blood Pressure Force that blood exerts on the walls of blood vessels Re ects the how hard the heart is working Represented as a fraction Systolic top number cardiac work phase Diastolic bottom number cardiac rest phase Example 13282 Pulse pressure 40 difference between the two numbers Re ects force of each contraction The Cardiac Cycle Electrocardiogram r r Systole f Ileart sounds I I I I In uences on Blood Pressure BP C0 X PVR Cardiac output CO Peripheral vascular resistance PVR Sympathetic nervous system Parasympathetic nervous system Arterial elasticity Cardiac Output CO CO SV X HR 0 CO THE VOLUME OF BLOOD EXPELLED FROM THE LEFT VENTRICLE OVER A MINUTE The cardiac output is the gold standard measure of the heart s effectiveness The heart is a PUMP A normal CO is 5 6 L per minute 0 What determines the CO Stroke volume SV The volume of blood eXpelled with each left ventricular contraction Heart rate HR How many times the left ventricle contracts in a minute What factors influence cardiac output 0 Preload the volume of blood in the left ventricle prior to contraction 0 Afterload the resistance the left ventricle has to pump against to push blood into circulation 0 Contractility the force of the left ventricular contraction Frank Starling s Law 0 A phenomenon that occurs when the heart muscle works HARD over a period of TIME Blood Vessels 0 Arteries carry blood away 0 Veins carry blood back 0 Capillaries site of exchange 0 Three layers Lymphatic System 0 Works to return excess interstitial uid lymph to the circulation 0 Plays a role in immunity 0 Includes lymph nodes the spleen the thymus and the tonsils Pericarditis 0 In ammation itis of the pericardium 0 Fluid accumulates pericardial effusion Swollen tissue creates friction Cardiac tamponade Cardiac compression from excessive uid accumulation Life threatenin g Manifestations O 0 000000 Pericardial FRICTION RUB grating sound heard when breath is held Sharp sudden severe chest pain angina that increases with deep inspiration and decreases when sitting up and leaning forward Muf ed heart sounds Dyspnea difficulty breathing Tachycardia Edema swelling Flulike symptoms Complications heart failure shock and death Infective Endocarditis Commonly caused by Streptococcus and Staphylococcus infections Vegetation forms on internal structures and creates small clots thrombi Microemboli occur as they the vegetation is dislodged resulting in microhemorrhages Risk factors 0 O O O Intravenous drug use Valvular disorders mitral valve prolapse Prosthetic heart valves Rheumatic heart disease Myocarditis In ammation of the myocardium Uncommon Organisms blood cells toxins and immune substances invade and damage the muscle Complications Heart failure Cardiomyopathy Dysrhythmias OOOO Thrombus formation Valvular Disorders Brainstorm What is the purpose of a heart valve Disrupt blood ow through the heart Stenosis narrowing Less blood can ow through the valve Causes decreased cardiac output increased cardiac workload and hypertrophy Regurgitation insufficient closure Blood ows in both directions through the valve Causes decreased cardiac output increased cardiac workload hypertrophy and dilation 0 Causes 0 Congenital defects 0 Infective endocarditis O Rheumatic fever 0 Myocardial infarction O Cardiomyopathy 0 Heart failure Cardiomyopathy Conditions that weaken and enlarge the myocardium Classified into three groups dilated hypertrophic and restrictive Dilated Cardiomyopathy Most common type Hrma Hart DHEEEILI EE 39dilmynptath Risk higher with advancing age and African American men Cardiomegaly and ventricular dilation damages myocardium muscle fibers resulting in decreased cardiac output and blood stagnation Causes O 0000 R Ell li 7 E39EI39ITIE Cocaine abuse Pregnancy Infections Hyperthyroidism Diabetes mellitus 0 Hypertension O Coronary artery disease CAD 0 Manifestations O Appear as compensatory mechanisms fail Dyspnea difficulty breathing Dysrhythmias Angina chest pain Dizziness Activity intolerance Blood pressure changes Tachycardia fast heart rate Tachypnea fast respiratory rate Edema swelling Weak pedal foot pulses Cool and pale extremities J ugular vein distension J VD OOOOOOOOOOOO 1H ypertmiph ii Eardmmy athg Hypertrophlc enlarged muscle Cardiomyopathy mum 0 More common in men and those who are sedentary 0 Risk higher with hypertension valvular disease and thyroid disease 7 r 7 0 Ventricle wall becomes stiff and unable Mr39m39 HEW Wartm mm Ea to relax Restrictive Cardiomyopathy 0 Common in South and Central America India Asia and Africa 0 Causes 0 Radiation exposure to the chest Connective tissue diseases Myocardial infarction Sarcoidosis 0000 Cardiac neoplasms cancers Aneurysms 0 Weakening of an artery 0 Can occur in an artery Common in the abdominal aorta thoracic aorta and the cerebral femoral and popliteal arteries 0 Can rupture exsanguination 0 Risk factors 0 Congenital defect Atherosclerosis Hypertension Dyslipidemia Diabetes mellitus Tobacco Advanced age OOOOOOO Trauma 0 Infection TT iii1F 39HT III Mil TERTSM S EarI Llli39 lJ l MLLW IF1U fi39ifIlia Ii Halm Bushe H39s iUII 9 II New Ha Li Emilia mm 5 hF ill ilii39wlifigh39ti hills elatatlliiuwwu in Ilgy 5m le gm irn lllfilllL39ll39F il39i awn tri rig 5E Ih ihit idg jt wrJ39mliiwan H39IW EIH juugaJiJU Luann ml 1 himxi mull 1 In II smitea Ule in iI39IL39iI I unise aneurysm Ii d i mli l39ilg39 liraHH Imm limiting list EI139i39llia tulle I1139IIi cru Ilur I EI IHI39wIliillhilull 39I i IJLEH E 1 i I 0 True aneurysms affect all three vessel layers Saccular aneurysm bulge on the side Fusiform aneurysm occurs the entire circumference 0 False aneurysm does not affect all three layers of the vessel Dissecting aneurysms occurs in the inner layers Dyslipidemia 0 High levels of lipids fats in the blood 0 Increases risk for many chronic diseases 0 Lipids come for dietary sources and liver production 0 Dietary sources Cholesterol animal products Triglycerides saturated fats Atherosclerosis 0 Leads to vessel obstruction platelet aggregation and vasoconstriction Can occur in any artery in the bOdY Complications Peripheral vascular disease PVD Coronary artery disease CAD leading Normal artery to myocardial infarction MI Thrombi Hypertension Stroke Artery With fat buildup Plaque Artery blocked with fat Copyright 2010 2366 m by Saunders an irrp ntaf ElSE39I39IE39I Ina Peripheral Vascular Disease PVD Aorta 0 Narrowing of the peripheral vessels Causes Common Illao artery I External iliao artery 0 Atheroscleros1s lnguinal ligament artery 0 Thrombus Internal iliao hypogastric artery 0 In ammation Common femoral artery 0 vasospasms Deep femoral profunda femoris artery 0 Raynaud s dlsease vasospasms of o rt 39 It I t arteries usually in the hands because of pa 39c39a 8mm are sympathetic stimulation P plitea39 artery Raynaud s phenomenon 0 Manifestations Peroneal arteryquot 0 Pain Anterior tibial artery 0 Intermittent claud1cation Posterior tibial artery intermittent pain Numbness Burning Non healing wounds Skin color changes Hair loss Impotency Dorsalis pedie artery Copynght 8321010 2006 2002 by Saunders an Irrpnnta f Elsevier Inc OOOOOO Coronary Artery Disease CAD Stages of CAD Atherosclerotic changes of the coronary arteries Impairs myocardial tissue perfusion 1 cause is AT HEROS CLEROSIS Angina intermittent chest pain resulting from myocardium ischemia Stable goes away with demand reduction Unstable increased intensity or frequency does not go away with demand reduction or occurs at rest Infarction permanent necrotic damage to the myocardium DEATH of heart tissue Complications O Myocardial infarction 0 Heart failure 0 Dysrhythmias O Sudden death Manifestations O Angina O Indigestion like sensation O Nausea O O Diaphoresis Fatigue Thrombus 0 Stationary blood clot Virchow s Triad endothelial injury sluggish blood flow and increased Emboli traveling body May be a thrombus air fat tissue bacteria amniotic uid tumor cells and foreign substances Can become lodged in places like the lungs brain and heart Varicose Veins Engorged veins resulting from valve incompetency Most common in the legs May also occur as esophageal varices and hemorrhoids Risk factors 0 Genetic predisposition Lymphedema Causes Pregnancy Obesity Prolonged sitting or standing Alcohol abuse and liver disorders esophageal varices OOOOO Constipation hemorrhoids Swelling due to a lymph obstruction Primary lymphedema Rare usually congenital Secondary lymphedema 0 Surgery Radiation O 0 Cancer 0 Infectior injury Hypertension Prolonged elevation in blood pressure Excessive cardiac workload due to increased afterload and vasoconstriction Risk factors O Advancing age Ethnicity family history Being overweight or obese Physical inactive poor diet 0000 Tobacco use and high sodium diet Primary hypertension 0 Most common form 0 Develops gradually over time Secondary hypertension 0 Tends to be more sudden and severe 9 Causes I Renal disease Adrenal gland tumors Certain congenital heart defects Manifestations 0 Silent killer 0 Include fatigue headache malaise and dizziness 0 Complications 000000 0 Atherosclerosis Aneurysms Heart failure Stroke Renal damage Vision loss Memory problems 0 Diagnosis 0 O 0 History physical examination Multiple blood pressure usually three readings at varying times of the day Laboratory tests to determine the presence of complications Myocardial Infarction 0 DEA TH of the myocardium 0 Coronary artery blood ow is blocked due to atherosclerosis Coronary Artery Disease CAD thrombus or vasospasms 0 Risk factors are the same as those for atherosclerosis 0 Complications 0000 0 Heart failure Dysrhythmias Cardiac shock Thrombosis Death 0 Manifestations O 0 Some are asymptomatic Silent MI Includes angina fatigue nausea shortness of breath diaphoresis and indigestion Heart Failure 0 Inadequate pumping 0 Leads to decreased cardiac output increased preload and increased afterload 0 Compensatory mechanisms activated Activation of the sympathetic nervous system Activation of the renin angiotensin aldosterone system Ventricular hypertrophy 0 May be acute or chronic 0 Manifestations O Depend on type 0 Fluctuates in severity O Appear as compensatory mechanisms fail 0 Includes indications of systemic and pulmonary uid congestion Left Sided Failure 0 Cardiac output falls 0 Blood backs up to the pulmonary circulation 0 Causes 0 Left ventricular infarction 0 Hypertension O Aortic and mitral valve stenosis 0 Manifestations 0 Pulmonary congestion O Dyspnea 0 Activity intolerance Right Sided Failure Blood backs up to the systemic circulation 0 Causes 0 Pulmonary disease 0 Left sided failure 0 Pulmonic and tricuspid valve stenosis Manifestations 0 Peripheral edema and weight gain Cor Pulmonale Right sided heart failure that occurs secondary to a PULMONARY conditions and long tem high blood pressure in the lungs Causes include COPD and other CHRONIC lung conditions MAP Mean Arterial Pressure 0 MAP is determined by Cardiac Output CO systemic vascular resistance SVR and central venous pressure CVP 0 MAP 2 X Diastolic systolic 3 0 Diastole counts for twice as much because 23 of the cardiac cycle is spent in diastole 0 MAP normal range 70 1 10


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