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patho altrd perfusio
| Question | Answer |
|---|---|
| perfusion definition | forcing blood/other fluid to flow thru vessel and into vascular bed of tissues to provide O2 and nutrients |
| layers of the heart | pericardium, myocardium, endocardium |
| pericardium | fibrous covering around the heart, provides physical protection and barrier to infection includes pericardial cavity |
| pericardial cavity | third space/layer of heart between pericardium and myocardium |
| myocardium | muscular portion of heart forming walls of atria/ventricles where heart can have infarctions (heart attack) |
| endocardium | thin 3 layered membrane lining heart where heart can have infections |
| one way valves | atrioventricular (AV) and semilunar (SL) valves |
| fibrous skeleton | provides structural support and isolating force for electrical impulses |
| what is the cardiac control center | medulla of brain regulation of HR and force on contractility |
| what are intact receptors | sense changes in body that provide feedback to cardiac control center help maintain HR/BP |
| cardiac conduction | impulse that stimulates cardiac contractility, requires adequate electrical activity |
| coronary circulation | perfusion to heart structure itself |
| V/Q | ventilation/perfusion |
| major coronary vessels | left and right arteries, branches off the ascending aorta |
| Blood pressure formula | blood pressure = (cardiac output) x (systemic vascular resistance) |
| what factors affect systolic BP | think ventricular contraction - stroke volume, heart rate and aortic resistance |
| what can DBP elevation indicate | elevated diastolic (remaining pressure in aorta during rest phase) indicates inappropriate rest between contraction |
| pulse pressure | difference in systolic and diastolic |
| what factors maintain blood pressure | LV contraction peripheral vascular resistance arterial wall elasticity viscosity/volume of blood |
| arteries are | - thick walled vessels with large amounts of elastic fibers - stretch in systole and recoil in diastole |
| arterioles are | RESISTANCE VESSELS control valves for blood released into capillaries |
| what helps determines SVR/PVR | arterial dilation/contraction |
| how does nervous system control BP/CV adaptation | medulla/pons ANS BP regulation mechanisms (baroreceptors/chemoreceptor, RAAS, kidneys) |
| BP regulation mechanisms | baroreceptors/chemoreceptors RAAS system kidneys |
| autonomic nervous BP control | sympathetic division - increase HR/BP, cardiac contractility parasympathetic division - decrease HR |
| medulla/pon | regulation and adaptation of cardiac/vascular function |
| renin | enzyme produced by kidney, convert angiotensinogen to angiotensin I |
| ACE | angiotensin converting enzyme angiotensin I to angiotensin II |
| angiotensin II | potent vasoCONSTRICTOR stimulate adrenal cortex to secrete aldosterone |
| aldosterone | increase Na/H2O retention by kidneys -> increase blood volume and venous return |
| baroreceptors | pressure sensor in blood vessel/heart, activation send signal to brainstem and activate RAAS |
| B1 receptors | receptors in the heart regulating HR/contractility, stimulated by sympathetic nervous system think beta blocker |
| normal cardiac output | 3.5-8L per minute |
| normal stroke volume | 70%, or about 50-100 mL |
| preload | pressure in ventricles after diastole need adequate myocyte stretching and adequate venous return for strong contraction |
| afterload | pressure in LEFT ventricle at end of contraction "pressure to pump against" |
| contractility | ability of heart to increase force of contraction |
| excessive preload | more blood into ventricle + heart is unable to overcome pressure in the ventricles |
| inadequate preload | less blood into ventricles + decreased cardiac output/stroke volume leads to increased HR for compensation |
| clinical manifestations of altered perfusion | cyanosis/pallor/coolness pain edema SOB/tachypnea hypotension/HTN bleeding/bruise heart murmur |
| V/Q mismatch | inadequate perfusion with adequate ventilation (ie. pulm embolism) inadequate ventilation with adequate perfusion (ie. asthma) |
| impaired circulation causes | hemorrhage (injury to vessels) obstructive cause |
| obstructive causes of circulation | thrombosis/thrombocythemia embolus/thromboembolus infarct/aneurysms venous stasis bifurcation |
| hypercoagulation causes | genetic (factor V leiden) myoproliferative dz/cancer pregnancy contraceptives |
| bifurcations | blood vessel splits into new branches = slower blood flow |
| atherosclerosis | abnormal thickening/hardening of artery/aorta (plaque) |
| cause of thickening/hardening in atherosclerosis | accumulation of lipid laden macrophage in arterial wall (HLD cause) |
| risk factor for atherosclerosis | smoking HTN FHx age (M >45, F >55) homocysteine and CRP levels |
| clinical manifestation of atherosclerosis | possible ischemia acute vessel obstruction dt plaque thrombosis/emboli formation due to vessel endothelium damage (ulceration) aneurysm formation |
| major complication of atherosclerosis | ischemic heart disease stroke peripheral vascular disease |
| thrombus | blood clot attached to vessel wall such as DVT |
| embolus | matter in blood circulation air/blood/amniotic fluid/fat |
| Virchow's Triad | 3 major factors causing embolus endothelial damage (ie. ulceration) hypercoagulability venous stasis |
| aneurysm | dilation/outpouching of vessel wall |
| true aneurysm | fusiform aneurysm (widening of the blood vessel) saccular aneurysm (looks like sac on blood vessel) |
| false aneurysm | aka pseudoaneurysm extravascular blood (vessel wall isn't damaged/slightly damaged) |
| dissecting aneurysm | tear in all layers of blood vessel |
| monitoring/treatment for aneurysm | under 5 cm - monitoring/medical management 5+ cm - surgical intervention d/t 6 cm or greater = high chance of rupture |
| aortic aneurysm/dissection | acute life threatening condition |
| management of aortic aneurysm/dissection | BP/HR control low stress |
| inadequate cardiac output | d/t change in blood impaired ventricular pumping structural conduction defect change to SVR |
| HTN pathophysiology | - progressive CVS dz leading to increased BP and/or organ damage -increased CO or PVR -impairment to BP regulatory mechanisms |
| primary vs secondary HTN | primary = unknown cause secondary = manifestation of other illness (CKD, OCP, primary aldosteronism) |
| risk factor for HTN | FHx age obesity/sedentiary DM/sodium/EtOH/smoking/nutrition black race |
| shock pathophysiology | impaired cellular metabolism (oxygen/glucose use) cause anaerobic metabolism and lactic acid production bodily compensation - SNS + RAAS simulation -> shunt blood to heart/brain |
| lactate | increase indicates hypoperfused tissue metabolic acidosis cause |
| lactate values | normal under 2 severe over 4 |
| shock manifestations (all types of shock present like this) | - tachycardia/tachypnea - cyanosis/pallor, cool/clammy extremities, peripheral pulse - decreased BP (decompensation) - alter mental/restlessness/apprehension - poor urine output/dark urine |
| labs for chock | ABG w/ lactate full labs cardiac enzymes (troponin/CRP) procalcitonin blood culture |
| hypovolemic shock | low intravascular volume (acute loss of 15-20% blood) d/t hemorrhage, burn, dehydration/GI loss |
| treatment for hypovolemic shock | resuscitation control underlying cause |
| hypovolemic shock presentation | tachycardia/hypotensive cool/clammy hands + poor skin turgor dec urine output |
| cardiogenic shock | inadequate perfusion (heart unable to pump) |
| causes of cardiogenic shock | MI sustained arrythmias heart surgery severe heart failure |
| diagnosis for cardiogenic shock | cardiac POCUS/TTE swan ganz catheter (tells you CO/CVP) |
| clinical manifestations for cardiogenic shock | hypotension decreased CO cold/wet |
| tx for cardiogenic shock | improve CO/contractility w/ inotropes reduce workload/O2 needs of myocardium regulate volume (diuretics) if due to MI tx with PCI/CABG/fibrinolytic therapy |
| distributive shock | loss of blood vessel tone and displacement of vascular volume away from heart/central circulation |
| types of distributive shock | neurogenic anaphylactic septic (also d/t alternate complication of prolonged and severe HTN 2/2 hemorrhage) |
| Neurogenic shock | decreased SNS control of blood vessel tone d/t defect of vasomotor center in brain stem or sympathetic outflow to blood vessels VERY RARE SHOCK |
| possible causes of neurogenic shock | SCI spinal anesthesia (epidural?) drug depressant action |
| clinical manifestations of neurogenic shock | hypotension bradycardia |
| treatment for neurogenic shock | vasopressors |
| anaphylactic shock | IgE mediated -> excessive vasodilators (ie histamine) causing increased arteriole/venule vasodilation and increased cap permeability |
| clinical manifestations of anaphylactic shock | bronchospasm + laryngeal edema wheezing/chest tightness dyspnea apprehension |
Created by:
sleepingbear
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