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UA Pathophysiology (Lachel Story) Ch. 4 - Cardiovascular System
Pathophysiology at University of Alabama's Capstone College of Nursing UA Pathophysiology (Lachel Story) Ch. 4 - Cardiovascular System
Terms in this set (88)
Sac surrounding the heart to provide protection and support
The cardiac muscle of the heart
Inner structures of the heart, including the valves
Outer surface of the heart
Blood flow through the heart to lungs
Systemic circulation blood enters superior/inferior vena cava into the right atrium; through the tricuspid valve to the rt ventricle; through the pulmonic valve to the pulmonary arteries to the lungs for gas exchange.
Blood flow from the lungs through heart
Pulmonary circulation blood enters the heart from the pulmonary veins into the left atrium; through the mitral valve to the left ventricle; through the aortic valve to the aorta to the rest of the body
Sympathetic nervous system
Creates the fight or flight response; increases BP and heart rate
Parasympathetic nervous system
Calms the body down; lowers BP and heart rate
Ability of cells to respond to electrical impulses
Ability of cells to conduct electrical impulses
Ability to generate an impulse to contract with no external nerve stimuli
Impulses start from SA (sinoatrial) node high in the rt atrium at 60-100 bmp, through the rt and left atrium causing them to contract; then impulse travels to the AV (atrioventricular) node low in the rt atrium by the atrial septum (can create 40-60 bpm if SA fails which lowers CO); then through the bundle of His, rt and left bundle branches, Purkinje fibers causing ventricular contraction (ventricles can make 20-40 bpm if SA and AV fails, which lowers CO).
The actual contraction; increase in electrical charge via cellular ion exchange.
Relaxation; cellular recovery via ions returning to the cell membrane to prepare for depolarization.
Elements of an EKG (electrocardiogram)
P-wave: atrial depolarization (no P-wave means atrial rhythm); QRS complex: ventricular depolarization (atrium relaxes here); T-wave: ventricular REpolarization
Electrical activity when impulses come from SA node
Abnormal electrical activity which can result from issues like MIs and electrolyte imbalances (Na, K+, Ca), meds, drugs
Electrolytes help initiate cardiac cycle; medulla monitoring: autonomic nervous system, endocrine system, chemoreceptors, baroreceptors
Rate of electrical conduction
Rate of contraction
Strength of contraction
Force that blood exerts on walls of blood vessels; shows how hard heart is working; normal is 120/80; as afterload and preload increase so does BP
Top number of BP; cardiac working hardest
Bottom number of BP; cardiac rest phase. Worrisome if high bc heart should be resting and not pumping.
Should be ~40 btwn the systolic and diastolic numbers; reflects force of each contraction
Cardiac Output (CO)
Amount of blood the heart pumps in one minute
Peripheral vascular resistance (PVR)
Opposing force the heart needs to pump against in the peripheral circulation (SNS and PNS/vasodilation and vasoconstriction and arterial elasticity impacts PVR); increases as blood vessels constrict
Stroke volume (SV)
Amount of blood ejected with each heart contraction
To increase Cardio Output
Increase stroke volume or heart rate or both
Pressure needed to eject blood out of heart into the aorta (blood viscosity, volume, and PVR effect afterload); higher afterload means harder to eject blood which decrease SV.
Amount of blood returning to the heart (blood volume and venous return effect preload); as preload increases so does BP
Increases water reabsorption in kidneys which increases volume and BP; it's a vasoconstrictor which increases PVR
Signaled by decreased kidney perfusion; angiotensin II is a strong vasoconstrictor so the kidney holds on to fluid; aldosterone is also secreted
Layers of blood vessels
Tunica intima: inner layer; tunica media: middle muscular layer; tunica adventitia: outer elastic layer
Returns excess interstitial fluid/lymph to circulation; includes lymph nodes, spleen, thymus, and tonsils
Inflammation of pericardium; fluid accumulates around heart causing pericardial effusion; the swollen tissue creates audible friction.
Cardiac compression from excessive fluid accumulation which reduces CO bc heart can't fill during diastole/rest; life threatening; CM: falling arterial pressure, rising venous pressure, narrowing pulse pressure, muffled heart sounds. Complications: heart failure, shock, death
Pericardium loses elasticity resulting from chronic inflammation; becomes thick and fibrous and adheres to heart; restricts cardiac filling which reduces CO. CM: audible friction rub; sharp sudden chest pain that worsens w/ deep inspiration and eases when sitting up and leaning forward; dyspnea; tachycardia; edema; flulike symptoms (fever and chills). Diag: CBC, EKG, x-ray, echocardiogram, CT, MRI. Treat: treat underlying infection, NSAIDs, glucocorticoid agents, pain meds, bed rest, O2 therapy, pericardiocentesis, pericardectomy.
Common cause is Streptococcus and Staphylococcus infections; vegetation forms on inner heart structures forming thrombi; microemboli are dislodged causing microhemorrhages. Risk factors: IV drug use, valve disorders, prosthetic heart valves, rheumatic heart disease, coarctation of the aorta, congenital heart defects, Marfan syndrome. CM: flulike symptoms, embolization, heart murmur, petechiae, splinter hemorrhages under nails, hematuria, Osler's nodes/wart-like lesions on fingers/toes. Diag: blood cultures, CBC, urinalysis, serum rheumatoid factor, erythrocyte sedimentation rate, electrocardiogram, echocardiogram. Treat: treat underlying infection, bed rest, O2 therapy, antipyretics, valve repair, valve replacement.
Inflammation of myocardium, uncommon. Organisms, blood cells, toxins, and immune substances invade and damage heart muscle. Complications: heart failure, cardiomyopathy, dysrhythmias, thrombus formation. CM: may be asymptomatic, flulike symptoms, dyspnea, dysrhythmias, palpitations, tachycardia, murmurs, chest pain, cardiac enlargement. Diag: blood cultures, EKG, cardiac enzymes, CBC, erythrocyte sedimentation rate, x-ray, echocardiogram, myocardium biopsy. Treat: treat cause, antipyretics, anticoagulants, antidysrhythmics, immune suppressive agents, bed rest, lower activity, limit fluids
Narrowing of heart valve vessel so less blood can flow through valve which causes blood to backup. Lowers CO, increases heart workload, and hypertrophy.
Insufficient valve closure so blood flows in both directions; decreases CO, increases heart workload, hypertrophy, and dilation.
Stenosis and regurgitation. Causes: congenital defects, infective endocarditis, rheumatic fever, MI, cardiomyopathy, heart failure. CM: vary based on valve involved, would reflect change in blood flow through the heart. Diag: heart catheterization, x-rays, echocardiogram, EKG, MRI. Treat: diuretics, antidysrhythmics, vasodilators, angiotensin converting enzyme inhibitors, beta-adrenergic blockers (lower SNS response), anticoagulants, O2 therapy, low-sodium diet, valve repair or replacement.
Group of conditions that weaken and enlarge the myocardium which makes it less effective. Three groups: dilated, hypertrophic, and restrictive.
Most common; cardiomegaly and ventricular dilation damages heart muscle resulting in lower CO and blood stagnation. Causes: chemo, alcoholism, cocaine abuse, preg, infections, thyrotoxicosis, diabetes mellitus, neuromuscular diseases, hypertension, coronary artery disease, hypersensitivity to meds. CM: appear as compensatory mechanisms fail, dyspnea, fatigue, nonproductive cough, orthopnea, paroxysmal nocturnal dyspnea, dysrhythmias, angina, dizziness, activity intolerance, BP changes, tachycardia, murmurs, abnormal lung sounds, tachypnea, peripheral edema, ascites, weak pedal pulse, cool/pale extremities, poor capillary refill, hepatomegaly, jugular vein distension. Diag: echocardiogram, EKG, x-ray, heart catheterization, nuclear studies. Treat: angiotensin converting enzyme inhibitors, diuretics, digoxin (Lanoxin), beta blockers, antidysrhythmics, pacemaker, cardioversion, valve repair, heart transplant, low-fat/low-sodium diet, quit smoking, exercise, abstain alcohol.
Affects diastolic function; ventricle walls become stiff and unable to relax during ventricular filling; most common in men and sedentary; risk is higher w/ hypertension, obstructive valvular disease and thyroid disease. CM: dyspnea on exertion, fatigue, syncope, orthopnea, angina, activity intolerance, dysrhythmias, left ventricle failure, MI. Diag: echocardiogram, EKG, x-ray, heart catheterization, nuclear studies. Treat: beta-blockers, calcium channel blockers, removal of excess myocardium, antidysrhythmics, avoid strenuous activity.
Rigidity of ventricles leading to diastolic dysfunction. Causes: amyloidosis, hemochromatosis, radiation to chest, connective tissue diseases, MI, sarcoidosis, cardiac neoplasms. CM: many are asymptomatic, fatigue, dyspnea, orthopnea, abnormal lung sounds, angina, hepatomegaly, jugular vein distension, ascites, murmurs, peripheral cyanosis, pallor. Diag: echocardiogram, EKG, x-ray, heart catheterization, nuclear studies. Treat: treat underlying cause, dysrhythmias and heart failure, may need heart transplant.
Can affect CO and BP. Causes: acid-base imbalances, hypoxia, congenital heart defects, connective tissue disorders, degeneration of conductive tissues, drug toxicity, electrolyte imbalances, stress, myocardial hypertrophy, myocardial ischemia or MI. CM: palpitations, fluttering sensation, skipped beats, fatigue, confusion, syncope, dyspnea, abnormal heart rate. Diag: EKG, invasive electrophysiologic studies. Treat: antidysrhythmics, cardiac defibrillators, pacemaker, cardioversion, defibrillation, ablation, avoid triggers.
Weakening of an artery due to high pressures, plaque, infections. Common in abdominal aorta, thoracic aorta, and the cerebral, femoral, and popliteal arteries. Rupture=exsanguination. Risk factors: congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, elderly, trauma, infection. CM: may include pulsating mass, pain, respiratory difficulty, neurologic decline. Diag: physical exam, x-ray, echo, CT, MRI, arteriograph. Treat: eliminate or manage cause, and surgery.
Affect all three vessel layers.
Bulge on side of vessel
Bulge of entire circumference
Doesn't effect all layers of vessel and is iatrogenic/caused by med staff or procedure.
Occurs in inner layers of vessel
Abdominal aortic aneurysm
CM: abdominal pain first; if it pops it becomes back pain and most likely death.
High lipid levels in blood which increases risk of many chronic diseases. CM: asymptomatic until it develops into other diseases. Diag: cholesterol screening and lipid panels. Treat: diet changes, weight loss, exercise, quit smoking, lipid-lowering meds, complication mngmt.
Low-density lipoproteins (LDL)
Delivers cholesterol to body; bad cholesterol. 70-100 is safe level.
High-density lipoproteins (HDL)
Removes cholesterol from the blood; good cholesterol.
Chronic inflammation disease characterized by thickening and hardening of arterial wall. Triggered by vessel wall injury. Lesions dev on vessel wall and calcify over time. Complications: peripheral vascular disease, coronary artery disease, thrombi, hypertension, stroke. CM: asymptomatic until complications dev. Diag: identify contributing factors and complications. Treat: angioplasty, bypass, laser procedures, artherectomy, diet changes, weight loss, exercise, quit smoking, lipid-lowering meds, complication mngmt.
Peripheral vascular disease
Narrowing of peripheral vessels caused by atherosclerosis, thrombus, inflammation, vasospasms. CM: pain, intermittent cramping, numbness, burning, non-healing wounds, skin color changes, hair loss, impotency. Diag: ankle/brachial index, treadmill exercise test, angiography, ultrasounds, MRI. Treat: reduce contributing factors, angioplasty, bypass procedures, laser procedures, atherectomy, antiplatelet meds, anticoagulants, thrombolytics, lipid-lowering meds.
Inflammatory condition of the arteries.
Vasospasms of arteries, usually in hands, because of sympathetic stimulation. Raynaud's phenomenon is assoc w/ an autoimmune disorder.
Coronary artery disease
Atherosclerotic changes of the coronary arteries that impairs myocardial tissue perfusion. Causes: atherosclerosis, vasospasms, thrombus, cardiomyopathy. Complications: MI, heart failure, dysrhythmias, sudden death. CM: angina, indigestion-like feeling, nausea, vom, clammy extremities, diaphoresis, fatigue. Diag: exercise stress test, echo, EKG. Treat: nitrates, beta blockers, calcium channel blockers, O2, angioplasty, bypass, laser procedures, artherectomy, diet changes, weight loss, exercise, quit smoking, lipid-lowering meds, complication mngmt.
Chest pain from myocardial ischemia. O2 supply can't meat demand. Stable= goes away w/ demand reduction. Unstable= increased intensity or freq, doesn't go away w/ demand reduction or occurs at rest.
Necrotic damage to the myocardium.
Stationary blood clot. CM: depends on location. Diag: arteriography, ultrasound, echo, MRI. Prevention: increase mobility, hydration, antiembolism hose, sequential compression devices, antiplatelet meds, anticoagulants. Treat: thrombolytic meds and embolectomy.
Endothelial injury, sluggish blood flow, and increased coagulopathy; all promotes thrombus formation.
Traveling body that may be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and foreign substances. Can become lodged in places like lung, brain, and heart.
Engorged veins resulting from valve incompetency. Can cause stasis pigmentation, subcutaneous induration, dermatitis, thrombophlebitis (vein inflamm from thrombus). Risk factors: genetic predisposition, pregnancy, obesity, prolonged sitting/standing, alcohol abuse and liver disorders (esophageal varices) and constipation (hemorrhoids). CM: bulging veins, pedal edema, fatigue, aching in legs, shiny pigmented hairless skin on legs and feet, skin ulcers. Diag: phys exam, Doppler ultrasound, venogram. Treat: rest w/ affected leg elevated, compression stockings, avoid standing/sitting for long, exercise, sclerotherapy, surgical removal.
Swelling due to lymph obstruction. Secondary lymphedema: caused by med procedures, infection, injury. CM: hyperpigmentation, ulcerations, thickening of skin. Diag: MRI, CT, Doppler ultrasound, nuclear imaging. Treat: sequential compression devices, compression stockings, exercise, massage, antibiotics, benzopyrone meds (promote edema fluid reabsorption), diuretics, surgery.
Prolonged elevation of BP that wears on our vessels and causes elastic changes in them. Excessive cardiac workload due to increased afterload and vasoconstriction. Risk factors: elderly, ethnicity, history, obesity, physical inactivity, smokers, high sodium diet, low K+ diet, high Vit D intake, excessive alcohol intake, stress. CM: silent killer, fatigue, headache, malaise, dizziness. Complications: atherosclerosis, aneurysms, heart failure, stroke, hypertensive crisis, renal damage, vision loss, metabolic syndrome, memory problems. Diag: multiple BP readings, EKG, lab tests to find complications. Treat: based on JNC7 standards, early detection and mngmt is key to prevent complications.
Most common form that develops over time.
More sudden and sever; caused by renal disease, adrenal gland tumors, some congenital heart defects, some meds, illegal drugs.
Intensified form that doesn't respond well to treatment. Will kill if not controlled quickly.
Pregnancy induced hypertension
First seen in pregnancy. Indicators: high BP, proteinuria, edema. Risk factors: renal disease, diabetes mellitus, multiple fetuses, maternal age <20 or >40. Complications: seizures, miscarriages, poor fetal dev, placental abruption. Treat: bed rest and Mg sulfate.
Myocardial infarction (MI)
Death of the myocardium due to blocked blood flow of coronary artery bc of atherosclerosis, thrombus, or vasospasms. CM: some are silent; angina, fatigue, nausea, vom, shortness of breath, diaphoresis, indigestion, elevation in cardiac markers, EKG changes. Complications: heart failure, dysrhythmias, cardiac shock, thrombosis, death. Diag: EKG, cardiac markers, stress testing, nuclear imaging, angiography. Treat: MONA= Morphine (vasodilates), Oxygen, Nitrates (vasodilate), Aspirin (thins blood) and thrombolytics.
Decreased contractility leads to decreased CO
Worse; decreased filling due to abnormal myocardial relaxation.
Left-sided heart failure
Affects left ventricle, leads to low CO, crackles sound (fluid in lungs) bc the blood backs up into the lungs. Fluid settles in the posterior lung. Causes: left ventricle infarction, hypertension, aortic/mitral valve stenosis. CM: short of breath, lung congestion, activity intolerance.
Right-sided heart failure
Blood backs up in systemic circulation. Causes: pulmonary disease, left-sided failure, pulmonic/tricuspid valve stenosis. CM: edema and weight gain.
Decreased blood volume or circulatory stagnation from inadequate tissue or organ perfusion. Stages: Compensatory= SNS and renin-angiotensin-aldosterone system activated. Progressive= compensatory mechanisms fail, tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, metabolic acidosis develops. Irreversible= organ damage occurs. Complications: respiratory distress, renal failure, disseminated intravascular coagulation, cerebral hypoxia, death. CM: thirst, tachycardia, restlessness, irritability, tachypnea to Cheyne-Stokes breathing, cool/pale skin, hypotension, cyanosis, decreased urine. Diag: CBC, cultures, coagulation studies, cardiac markers, ABGs, x-ray, hemodynamic monitoring, EKG, echo. Treat: underlying cause, maintain breathing, heart monitoring, rapid fluid replacement.
Vasodilation causes hypovolemia.
Loss of vascular sympathetic tone and autonomic function lead to massive vasodilation.
Bacterial endotoxins create immune rxn. CO decreases leading to multi-system failure.
Excessive allergic rxn.
Left ventricle can't maintain adequate CO.
Venous return reduces bc of blood volume loss.
Inadequate pumping leads to decreased cardiac output, increased preload, increased afterload. Activates compensatory mechanisms: SNS, renin-angiotensin-aldosterone system, ventricular hypertrophy. CM: appear as compensatory mechanisms fail, indications of systemic or pulmonary fluid congestion. Diag: x-ray, ABGs, echo, EKG, brain natriuretic peptide presence. Treat: angiotensin-converting enzyme inhibitors, diuretics, beta blockers, calcium channel blockers, pacemaker, intraaortic balloon pump, heart transplant.
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