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NURS 350 patho CV MI

Patho - ischemia, MI, cardiogenic shock

QuestionAnswer
ischemia reduction or absence of blood supply to heart
ischemia results from imbalance btw 02 supply and demand. not enough 02 to meet demands
CAD occurs under what conditions narrowing of CA >50%---artery becomes prothrombic---unable to respond to ENOX = endothelial nitric oxide, a vasoDIL
ENOX = endothelial nitric oxide. it's role potent vasoDILATOR. opposed by endothelin
what is endothelin most potent vasoCONSTRICTOR. opposed by ENOX
3 factors that increase myocardial 02 demand ventricular hypertrophy --- increased HR---increased contractility
3 examples of vetricular hypertrophy hypertensive phypertrophic cardiomyopathy---aortic valve stenosis---arortic valve regurgitation (volume overload)
5 examples of increased heart rate exercise---stress---hyperthyroidism---anemia---polycythemia---hypovolemia---pharmacology
example of increased contractility any condition that increases sympathetic response
what happens if insufficient 02 for 10 seconds---20 minutes ischemia starts --- anaerobic metabolism occurs (metabolic acidosis bwo lactic acid). If reperfusion occurs BEFORE 20 minutes, cells can survive. if not---MI ---then can only try and prevent additional cell death
angina pectoris MOA ischemia --> chest pain that can radiate ---left shoulder/arm/mid-back, jaw
angina pectoris SS diaphoresis, pallor, n
3 types of angina stable (predictalbe triggers exercise, stress)----variant (unpredictable, vasospasm at rest)---silent (non-specific discomfort, unease, fatigue--> silent MIs asymptomatic
who is most likely to experience silent angina women - 2/3 who die from CAD asymptomatic---diabetics---higher mortality rates due to underdiagnosis bwo asymptomatic
How do we evaluate MI ECG--labs (Troponin I & T , CK-MB, LDH)---stress test with or without radioactive tracers---CT---MRI---coronary angiography
Findings for ischemia ST segment will be DEPRESSED----will NOT have troponin, CK-MB markers yet because cells haven't died, lysed and released them
findings for infarction WILL have troponin, CK-MB markers---EKG alteration will indicate either---Non- STEMI or STEMI (see following slides)
if CPR has been admin, will markers be present yes, we have virtually compressed them out of cell so need to use alternate diagnostic methods
what is goal in tx of Myocardial ischemia restore balance btw 02 supply (increase) and demand (reduce consumption)
first thing we tx in ischemia first tx plaque, then alter lifestyle diet/exercise
subsequent ischemia txs PCI = percutaneous coronary intervention---CABG 'cabbage' = coronary artery bypass graft---pharmacologic tx
classes of drugs used to tx ischemia/MI nitrates--BB--CCB---ACEIs---ARBs---antiplatelets---statins---diabetic drugs
How do nitrates help restore supply/demand demand: dec sys bp/dec ven vol....also inc HR, which isn't desirable, but acceptable--------supply: inc coronary perfusion, dec coronary resistance, dec coronary spasm, inc collateral blood flow
definition of MI myocardial infarction prolonged hypoxia that results in IRREVERSIBLE myocardial cell death
3 conditions resulting in total occlusion MI which will cause cell death in all distal cells atherosclerotic plaque---rupture of said plaque---prolonged spasm at plaque site.
MOA of MI after anaerobic metab uses up ATP/glycogen anaerobic metab up to 20 min, then cell death where K+ and Ca++ lysed from cell--> insufficient contractions-----catecholamines also released---> dysrhyth--->FAs released--> disrupt pmeme
so, when K+ and Ca++ lysed from cell they cause insufficient contractions
and when catecholamines are dumped from cell, they cause dysrhythmias! finally, the dots connect
evaluating MI has angina sxs (chest/arm/jaw/back pain, n/v/diaphoresis/pallor AND the following s/s also pain>30min not relieved by nitrates, elevated markers, ST elevation (depending on type), angiography shows occlusion and/or area infarcted
MIs classified as STEMI or Non-STEMI. tell me about Non-STEMI cell death limited to tissue directly beneath endocardium (subendocardial MI)---ST INVERSION---at risk for furhter thrombus/occlusion
STEMI areas of damage/ECG transumural myocardial death (all layers) ---severe myocardial dysfunction---ST ELEVATION
ST depression indicates ischemia of myocardium
ST inversion indicates Non-STEMI
ST elevation indicates STEMI
How do we tx MI thrombolysis (clot blusters ateplase, streptokinase et al)---anti-platelets (clopidogrel, ticlopidine, prasugrel) (abcixamib, eptifibatide, tirofiban)---angioplasty/stent---CABG coronary artery bypass graft---
other tx to support MI pressors---nitrates---antiarrhythmics---analgesia---02---left. vent assist devices
what are complications of MI ---all of which leading to cardiogenic shock reperfusion injury (dysrhyth)---pericarditis---rupture (LV, septum, valves)---sudden death---LV HF
what is myocardial reperfusion when 02 is restored to heart ---which causes additional injury ---yet is necessary risk to procedures like angioplasty (most commone), bypass and transplants
What are 3 mechanisms of reperfusion injury Ca++ accumulation---endothelial activation---leukocyte accumulation
what does Ca++ accumulation cause early ventricular a/dysrhythmias---stunning (dec force of contractions)
what does endothelial activation do increases adhesion molecules---radicals---enzyme release causing a/dysrhythmias---stunning---vascular damage
what does leukocyte accumaltion cause everything that endothelial activation does while also blocking blood flow in smallest vessels
pericarditis is inflamm of pericardium caused by MI---tamponade (pericardial effusion)---viral---neoplasm
cardiogenic, septic and hypovolemic are types of shock that all lead to lead to widespread impairment of cellular metabolism bwo CV unable to perfuse tissues
cardiogenic shock has a high mortality rate and this common pathophysiology inefficent pumping --> low CO
contributors to cardiogenic shock HTN---ischemia/MI---virus---congenital---dysrhyth---early sepsis
Frank Starling normal normally, heart can increase SV if EDV increases (by increasing contraction)
how does cardiogenic shock alter Frank Starling mechanism because at any given EDV there is a DECREASE in stroke volume . . . this is due to inability of failing heart to increase contraction
first step in cardiogenic shock results in decreased CO which then activates activates compensatory mechanisms ---SNS---RAAS
when does cardiogenic shock become life threatening when compensatory mechanism INCREASE myocardial 02 consumption-->further taxes the heart----tx then focuses on HF and enhancing CO
cardogenic shock triggers SNS to compensate how SNS activated by barorecptors-->vasomotor center in medulla-->SNS--->catecholamine-->vasoCON--------->ventricular remodeling over time (vicious cycle)
cardiogenic shock triggers RAAS to compensate how? kidney senses it is underperfused-->renin-->inc Angio-2, Aldosterone-->ventricular remodeling over time (vicous cycle)
ventricular remodeling: hypertrophy/apoptois MOA increased load/neurohormones activate myocyte receptors = NE, TNF, All---2nd mesengers---produce muscle-specific gene products--> hypertrophy/apoptosis
effect of hypertrophied cells they contract less efficiently---load increases---ventricular dilation--> increased wall stress and 02 supply/demand mismatch
what are ECmatrix changes during remodeling increased deposition of ---fibronectin---laminin---vimentin, (cytoskeleton)--collagen---------all this results in loss of Force transmission and fiber slippage during contraction
RAAS is activated by SNS (dec renal perfusion too)---> angiotensin which also activates THIS HORMONE I ALWAYS FORGET ABOUT ADH...ADH...ADH....(keep water)
what does elevated aldosterone contribute to short term is fine, long term contributes to fibrosis---vascular damage--baroceptor stops working---blunts NE uptake by myocardium
ANP = atrial natriuretic peptide, is produced where produced in RIGHT atrial myocytes. RELEASED when myocytes are stretched
ANP actions released in response to high bp--> reduces water/Na/adipose loads on circ system
normal physiology ANP may act as counter-regulatorly hormone causing diuresis-------which opposes RAAS and NE (SNS)
Does ANP work anymore in HF patients nope, its physiological effects are attenuated in chronic HF pts. ---------ANP is a marker for HF-----------Inc ANP indicates HF
What goes wrong in SNS response over time initial inc NE is good (inc HR, contractility, preload, vasocon perfuse tissues)-----continued release down-regulates B-adrenergic receptors-----uncouples them from adenylate cyclase---decreased responsiveness to NE---body continues to release NE-->vicous
BNP = brain natriuretic hormone, was originally identified from brain extracts, but really is secreted primarily where BNP is acutallly secreted from VENTRICLES. It acts like ANP in that it decreases bp
BNP action with respect to HF is produced in early HF in response to ventricular wall stress-----released in proportion to severity of vent. volume expansion/pressure overload
what is BNP a marker for HF bwo inciating LVEDpressure
because BNP has a short half-life, how is its measurement useful clinically if BNP is high enough can indicate hospitalization nec for HF. Conversely, if it decreases enough, indicates pt stable for dc-----called a true 'paradigm shift' in diagnosis of cardiac decompensation
the inflammatory response contributes to remodeling how TNF-alpha released (regulates immune cells)-----dec ENOX ---dec vasoDIL---myocyte apoptosis
review of compensatory mechanisms - name 4 according to book SNS----RAA---hypertrophy---interstitial remodeling
short term effect SNS compensation inc HR--contractility--bp
long term effect SNS compensation Inc myocardial 02 consumption---dec coronary perfusion---hypertrophy---arrhythmias---inc afterload---down regulation B-adrenergic receptors
short term effect of RAAS inc blood volume---increased preload---peripheral vasoCON
long term effect of RAAS pulmonary/peripheral edema---interstitial fibrosis---hypertrophy
short term effect of hypertrophy more myofibrils for cross-bridge cycline----more mito and inc ATP supply
short term effect of intersitial remodeling inc collagen formation--> may reduce ventricular dilation
long term effect of interstitial remodoeling dec compliance/diastolic dysfunction----dec force transmission through ventricular wall---fiber slippage/realignment
all forms of shock (septic, cardiogenic, hypovolemic, etc) have final pathway (3 steps) decreased CO---decreased tissue perfusuion---impaired cellular metabolism
Created by: lorrelaws