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52 Cards in this Set
- Front
- Back
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what causes HT failure
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inability to maintain adequate CO
CO = SV x HR due to: myocardial disease, valvular HT disease, congenital HT disease Increased Pressure Work: HBP, aortic coartation Increased Vol Work: arteriovenous shunt, xs IV fluid Increased Perfusion Work: Anemia, Thyrotoxicosis |
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when using compensatory mechanisms to avoid HT Failure what happens to the renal blood flow?
a) increase b) decrease |
Renal blood flow decreases -> triggers retention of water/Na to increase vascular vol/SV
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when using compensatory mechanisms to avoid HT Failure what happens to the vascular volume?
a) increase b) decrease |
increases due to salt/water retention
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what is the short term compensatory mechanism for HT failure
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symp activation
increase HR Increase Cardiac Contractility Increase peripheral resistance -> improved cardiac reserve |
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when using compensatory mechanisms to avoid HT Failure what happens to the peripheral resistance?
a) increase b) decrease |
increase- (vasoconstriction)
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T/F
during HT failure the afterload decreases |
F
afterload increases |
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decompensated Ht Failure causes
a) overfilling of ventricles b) increased peripheral resistance c) increased vascular volume d) ALL |
overfilling of ventricles
(other options apply to compensatory mechanism) |
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what happens to diastolic filling time during decompensated HT Failure
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decreases
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T/F
peripheral and pulmonary edema is a result of compensatory HT Failure |
False
decompensated |
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T/F
during HT failure the afterload decreases |
F
afterload increases (decompensated) |
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decompensated Ht Failure causes
a) overfilling of ventricles b) increased peripheral resistance c) increased vascular volume d) ALL |
overfilling of ventricles
(other options apply to compensatory mechanism) |
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what happens to diastolic filling time during decompensated HT Failure
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decreases
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T/F
peripheral and pulmonary edema is a result of compensatory HT Failure |
False
decompensated |
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Which of the following is not a compensatory mechanism of HT Failure
a) Frank Starling b) Activation of Parasymp c) Renin Angiotensin d) Myocardial Hypertrophy e) All of the above |
activation of parasym is not a compensatory mechanism
Symp is activated to increase peripheral resistance, HR, contractility |
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The Frank Starling mechanism compensates for HT Failure by
a) increase vascular volume b) increase peripheral resistance c) increase retention of Na d) none |
increases vascular vol to increase SV
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T/F
Anemia can cause Congestive HT Failure |
True: anemia causes increased perfusion work
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T/F
Lo output congestive HT failure is treatable |
F
symptm management only - end stage failure |
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Hi output failure is caused by ____
Lo output failure is caused by ____ |
hi- xs need/demand for CO (but HT is still working)
lo- disorder impairing pumping abilities of HT |
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T/F
Systolic HT failure is due to increased cardiac contractility and ejection fraction |
F-
Decreased strength of contraction (contractility/ejection fraction) |
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what causes diastolic congestive ht failure
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impaired ventricular filling
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Pulmonary edema is caused by blood being congested in the pulmonary system due to
a) Rt side HT failure b) Systolic Ht Failure c) Lft side HT Failure d) none of the above |
Left Sided failure
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All of the following are consequences of Rt sided Ht Failure except
a) increased venous pressure b) lower limb edema c) ascites d) all of the above |
All- due to back up of systemic venous system
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which is not a manifestation of congestive HT failure
a) malnutrition b) confusion c) sob d) nausea e) orthopnea |
nausea (manifestation of MI)
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List manifestations of congestive HT failure
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SOB, dyspnea/nocturnal, orthopnea
edema fatigue, weakness confusion, poor memory, restless cachexia, malnutrition cyanosis |
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What is the appropriate method for diagnosis of congestive HT failure
a) EKG b) catherterization c) CVP d) all e) none e) |
All
also: echocardiography, xray |
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T/F
During acute pulmonary edema congestion of alveoli us due to a lack of pressure in the pulmonary capillaries |
F
hi pressr is pulmonary capillaries pushes fluid into alveoli causing stiffness, impaired gas exchange, cyanosis |
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define shock
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vascular failure with decreased peripheral perfusion and inadequate oxygenation of vital organs/cells
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which is not true about physiologic shock
a) intravascular fluids enter interstitium b) blood pressure increases c) arterioles and venules contract d) a,b e) b,c |
blood pressure DROPS
arterioles and venules RELAX |
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the compensatory mechanism for shock includes
a) increased excretion of Na b) activation of adrenal medulla c) activation of parasymp d) a, b d) a, c |
activation of adrenal medulla (and sympathetic)
(renin-angiotensin/aldosterone, ADH activation RETAINS Na/Water as a compensatory mech) |
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as a result of shock what are the cellular changes that occur
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1. reduced production of ATP- malfunction of Na/K pump
2. lactic acid accumulation 3. cell death due to rupturing of lysosomal enzymes |
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list the forms of circulatory shock
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hypovolumetric
obstructive |
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T/F
hypovolumetric shock causes a decrease in CO/BP due to an acute loss of 10-15% of Blood/Fluid volume |
F- 15-20% loss
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list the manifestations of hypo-volumetric shock
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thirst
cool/moist skin lo body temp tachycardia oliguria restless, apprehensive apathy, stupor |
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T/F
Obstructive shock is due to an mechanical blockage of blood through the peripheral circulation |
F
blockage of central circulation/pulmonary causes increase in Rt HT pressure/impaired venous return |
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what is not true about obstructive shock
a) can be caused by pulmonary embolism b) impairs venous return c) increases pressure in left heart d) all are true |
increases pressure in Rt Heart
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loss of vascular tone causes
a) distributive shock b) obstructive shock c) hypo-volumetric shock |
distributive shock = loss of vascular tone -> increased compartment size and shift of vascular volume away from HT/Central Circulation
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list the forms of distributive shock
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neurogenic
anaphylactic septic toxic |
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Slow HR with dry and warm skin is a manifestation of
a) neurogenic shock b) anaphylactic shock c) septic shock d) toxic shock |
neurogenic shock
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Fever and hyperventilation are manifestations of
a) neurogenic shock b) anaphylactic shock c) septic shock d) toxic shock |
septic shock
also: vasodilation, warm flushed skin abrupt changes in personality |
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fever is a manifestation of
a) neurogenic shock b) anaphylactic shock c) septic shock d) toxic shock |
septic and toxic shock
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list the manifestation of toxic shock
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hi fever
lo bp confusion rash conjunctivitis vomit peeling skin of soles/palms |
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chest tightness and itching are manifestations of
a) neurogenic shock b) anaphylactic shock c) septic shock d) toxic shock |
anaphylactic shock
also: wheezing, apprehension, bronchial spasm |
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sever infection can cause
a) neurogenic shock b) anaphylactic shock c) septic shock d) toxic shock |
septic shock - esp due to gram (-) backteria
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inflammatory response is the mechanism of
a) neurogenic shock b) anaphylactic shock c) septic shock d) obstructive shock |
septic shock
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what is the mechanism behind neurogenic shock
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defect in vasomotor cntr of brain or sympathetic outflow
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vasodilation is the main mechanism for ____ which is caused by _____
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anaphylactic shock- vasodilation caused by histamine
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list the causes of neurogenic shock
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depressnt drugs
CNS injury lack glucose general anesthesia severe pain |
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vasodilation is the mechanism for ______ but a manifestation for ______
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anaphylactic shock - mechanism
septic shock- manifestation |
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list the possible complications of shock
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-Shock LU (ARDS)
-Acute Renal Failure -GI Dysfnctn -DIC- disseminated intravascular coagulation -Organ Dysfnctn |
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increased permeability of pulmonary capillaries causes
a) Congestive HT Failure b) ARDS c) Pulmonary Edema d) a,b e) a,c |
ARDS - LU shock
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what is the mechanism for acute renal failure
a) vasoconstriction, lo BP b) vasoconstriction, Hi BP c) vasodilation, Hi BP d) vasodilation, lo BP |
vasoconstriction, lo BP
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DIC is characterized by ____________
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small clots-> abnormal bleeding
complication of septic shock |
