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NURS 350 patho CV MI
Patho - ischemia, MI, cardiogenic shock
| Question | Answer |
|---|---|
| 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
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