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98 Cards in this Set
- Front
- Back
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the right side of the heart |
receives low oxygenated blood from the systemic circulation and pumps blood into the pulmonary circulation |
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the left side of the heart |
receives richly oxygenated blood from the pulmonary circulation and pumps blood into the systemic circulation |
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cardiovascular system needs to maintain adequate perfusion to tissues |
blood flowing through capillaries |
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atherosclerosis |
deposition of fat and fibrin in the wall of arteries which harden over |
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progression of atherosclerosis |
damaged endothelium fatty streak fibrinous plaque complicated lesion |
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damaged endothelium |
smoking, hypertension, dm, turbulent blood flow, bacteria, viruses, homocysteine |
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fatty streak |
growth factor produced stimulating smooth muscle growth lipid laden macrophages bind to endothelium LDL become oxidized this vascular lesion may be reversible with diet |
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fibrinous plaque |
fibroblasts proliferate in lesion and deposit collagen creating a more firm, rigid mass |
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complicated lesion |
instantly cause a heart attack years of progressive events with deposition of calcium. very rigid and may produce an ulcer or rupture of overlying endothelium. endothelial lesions initiate thrombus formation and can occlude lumen. |
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non-modifiable risk factors for atherosclerosis |
age sex family history race |
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modifiable risk factors for atherosclerosis |
low density lipoproteins high density lipoproteins hypertension cigarette smoking lack of exercise homocysteine creactive protein (CRP) |
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homocysteine |
amino acid derived from metabolism of methionine vitamins B6, B12 and folic acid facilitate its metabolism in the liver high levels of homocysteine increase risk of vascular disease |
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C-reactive protein (CRP) |
chronic cytokines stimulate liver to increase CRP biomarker that inflammation is in body increased CRP, increased risk of heart attack |
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hypertension |
leading cause of heart disease systolic pressure of 140mmHg or greater and or a diastolic blood pressure of 90mmHg or greater in people who are not taking antihypertensive medication |
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normal blood pressure |
less than 120, less than 80 |
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prehypertensive |
120-139 80-89 |
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stage 1 hypertension |
140-159 90-99 |
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stage 2 hypertension |
greater than or equal to 160 great than or equal to 100 |
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Primary (essential) hypertension(idiopathic) |
initiated by increased blood volume and cardiac output. maintained because vessels appear to irreversibly adapt to this new level of blood pressure despite correction of blood volume and cardiac output |
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secondary hypertension |
arises due to any underlying disease which raises peripheral vascular resistance accounts for only 5-8% of cases |
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treatment for hypertension is targeted at reducing the workload of the heart |
exercise and weight loss diuretics reduce blood volume beta blockers decrease heart rate calcium channel blockers decrease strength of heart contraction vasodilators decrease resistance to blood flow |
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ACE inhibitors |
will not let angiotension I progress to angiotension II |
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Barostim |
baroreflex activation therapy(BAT) for resistant hypertension and heart failure mechanical approach |
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ischemia |
less oxygen |
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infaction |
tissue death, heart attack |
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risk factors associated with development of coronary artery disease |
hyperlipidemia hypertension smoking diabetes mellitus genetic predisposition obesity sedentary life style loss of estrogen alcohol gender personality |
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myocardial ischemia |
transient reversible lack of oxygen to the myocardium increase anaerobic metabolism and increased production of lactic acid impaired left ventricular function due to hypoxia and lactic acid accumulation decreased contractility of myocardium decrease stroke volume and increase end diastolic volume and pressure |
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EDV |
end systolic volume the volume of blood in each ventricle at the end of diastole normal=120ml |
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normal systolic volume |
70ml |
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end systolic volume (ESV) |
120ml-70ml=50 ml |
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ejection fraction |
SV/EDV 55-70% 45% =weakened, not enough pumping out |
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clinical manifestations of myocardial ischemia |
angina pectoris: chest pain caused by myocardial ischemia |
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stable angina |
ischemic episodes occur during exertion and the pain is relieved by rest and nitrates. the more nitroglycerin tables needed to relieve pain indicates progression of the disease |
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nitroglycerin |
potent vasodilator converted to nitric oxide and works to promote relaxation of vascular smooth muscle works on the veins decrease volume, decrease pressue |
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preload |
tension in muscle before it contracts |
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afterload |
tension during systole |
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unstable angina |
ischemic events occur frequently and often while at rest indicates advanced heart disease and may be sign of impeding infarction grave sign of advanced heart disease |
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subendocardia ischemia |
ST segment depression T wave inversion |
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transmural ischemia |
ST segment elevation can indicate myocardial infarction |
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possible treatments for myocardial infarctions |
1.decrease workload on the heart to decrease rate of oxygen consumption of myocardium 2. coronary artery bypass graft 3. percutaneous transluminal coronary angioplasty 4. stents- metal device guided by a wire through coronary artery and inflate balloon. |
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acute myocardial infarction (MI) |
heart attack end point of coronary artery disease prolonged ischemia causes irreversible hypoxic injury to cells and cell death and tissue necrosis |
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causes of myocardial infarctions |
atherosclerotic plaque formation in coronary vessels hemorrhage into a plaque embolism caused by thrombus coronary spasm |
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myocardial infarctions can lead to the following changes of the heart |
1. decreased cardiac contractility 2. altered left ventricle compliance 3. decreased stroke volume 4. decreased ejection fraction 5. increased left ventricle end-diastolic pressure 6. sino-atrial node malfunction |
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24 hour response to myocardial infarction |
leukocyte infiltration into inflamed and necrotic area proteolytic enzymes degrade necrotic tissue catecholamines release from damages cells (pseudo-diabetic state)- increased blood sugar caused from release of adrenaline |
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2 week response to myocardial infarction |
increase insulin release weak collagen matrix formed which is mushy and vulnerable |
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6 week response to myocardial infarction |
strong scar tissue develops this tissue does not contract/relax or conduct decrease amount of pump power, muscle tissue abnormal EKG |
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signs and symptoms of myocardial infarction |
sudden and severe chest pains pain not relieved by nitrates sympathetic activation causing profuse sweating, cool and clammy skin from peripheral vasoconstriction, reflexive increase in heart rate and blood pressure detection of cardiac iso-enzymes which act as markers of MI from damaged myocardial cells initial drop in blood pressure abnormal extra heart sounds-murmur |
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cardiac iso-enzymes and other biomarkers to aid in diagnosing myocardial infarction |
creatine kinase lactate dehydrogenase serum glutamic oxaloacetic transaminase myoglobin troponin T; troponi I myeloperoxidase |
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biomarkers |
naturally inside cardiac muscle cells, once cells die, biomarkers are released and spike in the biomarkers |
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creatine kinase-myocardial band (CK-MB) |
CK-MB2 higher than CK-MB1 most MI CK levels should be checked every 8 hours for the first day CK rises within 6-8 hours, peaks at 24 hours, returns to normal by 36-48hours normally CK-MB1=CK-MB2 post-MI CK-MB1<CK-MB2 |
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lactate dehydrogenase (LDH-1) |
LDH peaks at day 3-4 and is normal within 14 days LDH-1 higher than LDH2 post MI normally LDH1<LDH2 post-MI LDH1>LDH2 |
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serum glutamic oxaloacetic transaminase (SGOT) |
SGOT levels rise within 8-12 hours, peak at 18-36 hours, and return to normal within 14 days SGOT is not referred to as alanine aminotransferase (AST) |
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Thallium 201 imagine |
graphically demonstrates distribution of blood flow to normal or ischemic tissue more sensitive/ specific than stress EKG look for cold spots, tissue that did not take up radioactive material, this shows tissue death |
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subendocardial myocardial infarction |
myocardial injury limited to tissue just under the endocardium |
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transmural myocardial infarction |
myocardial injury extending across entire width of heart muscle wall from the endocardium to the pericardium |
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therapy goals for MI |
to relieve pain, minimize mass of infarcted tissue, prevent/ treat arrhythmias and mechanical complications |
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standard initial therapy for MI |
1.continuos EKG monitoring for arrhythmias 2.control of pain with either morphine sulfate and or nitroglycerin 3. supplemental oxygen by nasal cannula to maintain 02 above 70mmHg 4. low-dose heparin and aspirin 5. acute repercussion via thrombolytic therapy to enzymatically degrade thrombus 6. intravenous streptokinase or tPA(tissue plasminogen activator (Activase)) may be given within 4 hours of chest pain onset. no benefit with later administration |
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blood thinners |
viscosity does not change, prevent blood from getting thicker (coagulation) |
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complications associated with myocardial infarction |
1. dysrhythmias 2. left ventricular failure 3. pericarditis 4. rupture of heart structures 5. rupture of wall of infarcted ventricle 6. systemic thromboembolism 7. sudden death |
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disorders of the heart wall |
epicardium-visceral layer of the pericardium myocardium endocardium |
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disorders of the pericardium |
acute pericarditis pericardial effusion |
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acute pericarditis |
inflammatory condition of pericardium most commonly cause by infection produces friction rubs and severe chest pain especially with respiratory movements |
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pericardial effusion |
the accumulation of fluid in the pericardial cavity normally 10-30 cc of serous fluid gradual and rapid accumulation |
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gradual accumulation |
can accommodate up to 1000cc of fluid in the pericardial space |
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rapid accumulation |
50-100 cc usually blood referred to as cardiac tamponade- can't expand heart, not filling properly, filling of chambers, decrease volume and pressure, can't feel pulse, mechanical problem, not electrical, normal EKG notice signs of right heart failure first: 1.distention of jugular veins 2. edema 3.hepatomegaly 4. pulseless electrical activity (PEA) no pulse but normal EKG mechanical impedance cardiac output decreases remove fluid, pericardalcentisis |
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dilated cardiomyopathy |
decreased cardiac contractility decreased systolic performance increased EDV decreased stroke volume walls getting thinner, cells dying cells don't get replaced causes: 1. idiopathic 2. alcholism-enthanol toxic 3. post-partum-hormal reactions 4.following previous infection-rheumatic heart diesease |
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hypertrophic cardiomyopathy |
hypertrophy of inter ventricular septum myocardium becomes noncompliant treatment: beta blockers, calcium channel blockers, surgical resection cells increase in size, increase in proteins decrease in performance of heart controlled heart attack. 100% ethanol to kill off muscle tissue |
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restrictive cardiomyopathy |
infiltrative disease: 1.amyloid 2.hemochromatosis 3.gylcogen storage disease eventually the myocardium become non compliant. stiff-heart syndrome fibrosis |
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endocardium: valvular stenosis |
valve orifice is constricted and narrowed-outflow obstruction. stiff chamber behind valve has increased workload myocardial wall becomes hypertrophied aortic semilunar valve and bicuspid valve(left side of heart) most commonly affected causes include: rheumatic heart disease, congenital malformations, calcifications. |
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endocardium: aortic semilunar valve stenosis |
hypertrophy of left ventricle decreased stroke volume and cardiac output leading to decreased tissue perfusion narrowed pule pressure (systolic-diastolic) increase work load blood pressure: 110/90 |
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endocardium: left a-v valve stenosis (bicuspid or mitral valve) |
left atrial hypertrophy decrease cardiac output increased blood volume and pressure backs up into pulmonary circulation: pulmonary congestion not as much blood can flow through winded very quickly increase workload, degeneration of cells thrombus risk increases, causing stroke water filled alveoli, hard to breathe, water replaces air, dyphea balloon-tipped, swan ganz catheter for measuring pulmonary capillary wedge pressure wedge pressure= pulmonary capillary hydrostatic pressure pulmonary hypertension, pulmonary edema, right sided heart failure |
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endocardium: valvular regurgitation |
valve leaflets fail to shut completely retrograde flow of blood occurs increased blood volume in chamber, increased workload of chamber, hypertrophy, failure |
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aortic regurgitation |
retrograde flow of blood in left ventricle end diastolic volume increases increases stroke volume widened pulse pressure which creates a "water-hammer pulse"on the limbs and corriganspulse on the carotid blood pressure 130/70 systolic-more volume more pressure diastolic: blood is going forward and backward. decrease volume and pressure |
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mitral regurgitation |
retrograde flow of blood into left atrium causing dilation and hypertrophy left ventricle hypertrophies for compensation but eventually fails pulmonary hypertension right ventricular failure, increase workload on right side increase wedge pressure |
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mitral valve prolapse |
cusps billow excessively up into left atrium common in young women minimal morbidity and mortality often asymptomatic but related to: tachycardia, palpations, anxiety, panic attacks can lead to: 1. rupture of chordae tendineae 2. ventricular failure 3. systemic emboli 4. sudden death treatment: directed at the associated symptoms and not necessarily the prolapsed valve, if serious surgical repair or valve remplacement |
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rheumatic heart disease |
cardiac involvement stemming from a groupA beta hemolytic streptococcus infection bacterial antigens bind to receptors on heart, muscle, rains, and synovial joints autoimmune response and inflammatory resonse producing arthritis and inflammation of endocardium and myocardium. the arthritis resolves following recovery repair process leads to inflammation of valve leaflets and formation of vegetation on cusps and chordae tendinease 1. vegetations (verrucae) = platelet and fibrin deposits 2. aschoff bodies= sited of fibrinoid necrosis confined to myocardium leads to incompetent valves, heart disease acute valvular involvement |
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development of rheumatic heart disease |
pharyngeal infection 3% without treatment rheumatic fever 10% rheumatic heart disease |
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dysrhythmias (arrhythmias) |
heart rate greater than 100 or less than 60rpm caused by abnormal rate of impulse generation at SA node and abnormal conduction normal rate: 70bpm ranges (60-100) normal rhythm: refers to the regular occurrence of P, ORS and T waves |
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sinus bradycardia |
heart rate less than 60bmp maintains normal rhythm |
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sinus tachycardia |
heart rate greater than 100bpm maintain normal rhythm |
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ventricular fibrillation |
caused by chaotic ventricular depolarizations very active heart muscle, rate can be greater than 300 bmp muscle cells are quivering no organized or synchronized degree of ventricular contraction, cardiac output decreases defibrillation needed to shock cells, stop depolarizations and allow SA node to reset the pace |
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heart block |
AV blocks dysfunction of the intrinsic conduction system sa node, av node, bundle of His, rt./lft. bundle branches, purkinje fibers |
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1st degree heart block |
increase in the P-R interval longer than normal >200ms |
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2nd degree heart block |
increase in the P-R ratio more p's than r's should be a 1:1 ratio |
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3rd degree heart block (complete block) |
AV node does not conduct action potentials into ventricles atria and ventricles beat independently need artificial pacemaker to remedy situation regular p waves, 70 waves are independent of p, 30-35pm |
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right sided heart failure systemic congestion (cor pulmonale) |
increased pulmonary vascular resistance increased central venous pressure(CVP) increased systemic capillary hydrostatic pressure peripheral edema |
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left sided heart failure (congestive heart failure; CHF) and pulmonary congestion |
intrinsic causes include myocardial ischemia extrinsic causes include systemic hypertension, aortic valvular stenosis, and aortic regurgitation left sided heart failure, increased pulmonary hydrostatic pressure, pulmonary edema alveoli fill with fluid orthopnea dyspnea impaired gas diffusion suffocation |
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possible treatments for heart failure |
decrease workload on heart by: correcting valvular dysfunction vasodilators to decrease resistance to blood flow diuretics to decrease blood volume and pressure intropic drugs are designed to increase force of myocardial contractility but not rate common drug is digoxin |
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diagnosis of heart failure |
measuring b-type natrutretic peptide (BNP) released by heart to osmotic diuerisis increase= trouble breathing, cardiac not pulmonary decrease= pulmonary |
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shock |
cardiovascular system fails to perfuse tissues adequately, resulting in widespread impairment of cellular metabolism. progresses to organ failure and death if untreated in positive feedback loops that maintain a downward spiral |
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cardiogenic shock |
caused by heart failure myocardial infarction coronary heart disease hypertension heart attack |
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hypovolemic shock |
decreased intravascular fluid volume hemmorrhage burns loss of blood |
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neurogenic (vasogenic) shock |
decreased vasomotor tone decreased resistance decreased blood pressure spinal cord injury |
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anaphylactic shock |
hypersensitivity reactions allergies immune reaction |
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septic shock |
reaction to disseminated infection response to bacterial endotoxins often called warm shock due to accompanying fever from the infection bacterial infection |
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adrenailine in circulatory shock |
vasoconstriction |
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arginine vasopressin for the treatment of circulatory shock |
systemic effect for vasoconstriction. last step in shock: opens potassium channels and closes calcium channels with vasopressin: opens calcium channels and smooth muscle contract and pro most vasoconstriction |
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shock |
decrease cardiac output, decrease arterial pressure, decrease capillary perfusion, decrease venous return |
