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123 Cards in this Set
- Front
- Back
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Conduction pathway through the heart |
SA Node AV Node Bachmans Bundle Bundle of HIS Bundle branches Purkinje fibers Ventricular muscle |
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EKG relation Whats occurs during P-wave, PR interval, QRS, QT, T-wave |
P-wave= atrial depolarization PR interval = Atrial systole and AV node delay (normal 0.12-0.2) QRS = ventricular depolarization and atrial repolarization (Normal less than 0.12) QT= ventricular systole T-wave - Ventricular repolarization |
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Ventricular action potential cycle Phase 0-4 |
4= Resting membrane potential (-90 K determines this level), diastole 0= rapid depolarization (Na diffuses into cell) 1=transient repolarization ( K+ diffuses out and Cl diffuses in) 2= Plateau (Ca diffuses into cell) 3= Repolarization (K diffuses out of the cell) 4= Diastole (Na-K pump restores normal) |
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SA node action potential |
4 = diastole (-70) (spontaneous depolarization to threshold K out and Na in progressively, last part Ca in) 0 = slow depolarization (Ca and Na into the cell) 3 = Repolarization (K out) 4 = diastole |
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changes what phase of the action potential cycle causes HR changes |
Changing the rate of PHASE 4 depolarization leads to changes in Heart Rate |
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Ca Channel Blockers work on what part of the ventricular action potential and what part on the nodal action potential |
Ventricular action potential they work on phase 2 the plateau phase Node action potential they work on phase 4 and slow the heart rate |
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Heart Rate with EKG calculation |
count R to R interval waves occurring in 6 second and multiple by 10.
EKG trace each mm corresponds to 0.04 seconds |
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Right bundle branch how to identify it |
Rabbit ears in V1 and V6 Usually see inverted T waves in V1-V3 |
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Left Bunch branch how to identify it |
Loss of R wave in V1 and normal q wave in V6 Left ventricular depolarization will be prolonged- abnormally wide QRS |
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1st degree heart block third degree heart block |
1st- PR internal greater than 0.20 seconds. P wave and QRS have no relationship |
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2nd degree heart block type 1 or Wenckebach |
progressive increase in PR until finally a beat is dropped |
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2nd degree heart block Mobitz type 2 |
sudden appearance of a non conducted P wave P waves are normal but some don't follow ORS complex. |
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MI Subendocardial vs Transmural |
Subendocardial - produce ST depression greater than 1 mm Transmural - inverted T waves and ST elevation greater than 1 mm |
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Hypercalcemia vs Hypocalcemia EKG |
Hypercalcemia leads to shorten QT segment or short phase 2 Hypocalcemia - leads to prolonged QT segment or longer phase 2 |
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Hyperkalemia vs Hypokalemia EKG |
Hyperkalemia - Peak or tented T waves Hypokalemia - U-waves (after the T) |
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PAT - paroxysmal atrial tachycardia what is the treatment |
Rate 150-250 Vagel Give Verapamil Esmolol, propranolol, edrophonium, Dig, Phenyl Pacer or Cardioversion |
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PVC's treatment |
think low K or Low O2 Lidocaine is usually first treatment. |
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Wolf Parkinson White drugs to avoid |
AVOID DIG and Verapamil. |
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EKG Leads and wall location Posterior/Inferior Septum/Anterior Lateral |
Posterior/ Inferior wall - II, III, aVF = Right coronary artery (RCA) Septum/Anterior - V2-V5 - Left anterior descending (LAD) (widow maker) Lateral - I, aVL, V4-6 - Left circumflex |
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MAP is determine by what |
Cardiac Output and SVR |
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Cardiac output is determine by what what determines SV |
heart and SV ..... HR x SV = CO SV = preload, afterload, and contractility. |
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what hormone is most important in controlling vascular volume
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Aldosterone |
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Preload |
tension present in the wall of the left ventricle at end-diastole (immediately prior to contraction). PRELOAD= VOLUME Frank starling law of the heart |
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Afterload |
Tension in the wall of the heart at the time the aortic valve opens. Determine by SVR. |
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Concentric Hypertrophy vs Eccentric Hypertrophy |
Concentric = Pressure overload (left ventricular chamber is not changed) AS, untreated HTN, Coaraction Eccentric = Volume overload. (left ventricular of the heart is substantially increased) Chronic MR or AR and Obesity Both of these use Laplaces Law |
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Left Ventricular Pressure Volume Loop When does Systole begin? When diastole begin |
Systole between B and D Diastole between D and B |
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Left Ventricular Pressure Volume loop what occurs |
A (bottom left) - Mitral valve opens between A and B - diastolic filling B Mitral valve close between B and C = isovolumic contraction C aortic valve opens Between C and D = Ejection D = Aortic valve closes Between D and A = isovolumic relaxation |
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Preload changes in Pressure volume loops LV |
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What happens with changes in afterload - increase or decrease |
Increase afterload - the heart empties less so the SV decrease and both end-diastolic volume and end-systolic volume increase .. Loop up and to the right Decrease afterload - the heart empties more completely. SV increase. Both end-diastolic volume and end-systolic volume decrease .... Loop down and to the left |
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What happens to the flow loop when contractility decreases or increases |
When contractility increases - the ventricle empties more completely. End-diastolic volume decrease, but not as much as end-systolic volume, so SV increases.. loop up and to left When contractility decreases - the ventricle empties less completely. End-diastolic volume increases and so does end-sysotlic volume(increases more than diastolic) SV decreases... loop down to right |
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IHSS pressure volume loop |
Idopathic hypertrophic subaortic stenosis. smaller volumes and large pressure (due to outflow obstruction) |
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Chronic Aortic Stenosis |
Concentric Hypertrophy LV to generate greater pressures, but LV volumes remain the same. |
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Mitral Stenosis Pressure flow loop |
LV filling is diminished |
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Acute Aortic Insufficiency pressure loop |
The volume in the LV increases during early diastole. relaxation phase not isovolumetric Small Pressure loop |
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Chronic aortic insufficiency pressure loop |
Eccentric hypertrophy. LV dilates - the pressure loop is large SV is too |
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Acute Mitral Regurgitation |
The volume in LV decreases during early systole. volume loop is not isovolumetic Pressure volume loop is small |
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Chronic Mitral Regurgitation |
LV hypertrophies - eccentric. LV chamber dilates. PV-loop is large |
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Formula for SV
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CO/HR = 60-90ml normal |
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Formula for SI |
Stroke Index = Stroke volume/Body surface area normal 40-60ml/m2 |
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Formula for SVR |
(80) (MAP-CVP)/CO Normal 900-1500 dynes sec cm |
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PVR formula |
(80) (PAP-PCWP)/CO Normal 50-150 dynes sec cm |
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Treatment of Intraoperative ischemia whats the goal |
Return to slow small perfused state |
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Control of Blood pressure Baroreceptor |
Afferent action potentials of the baroreceptor comes from the aortic arch via vagus nerve and the carotid sinus via the herrings nerve (branch of glossopharyngeal) Carotid baroreceptors more important to minimizing acute blood pressure alterations |
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Cardiac output with thermal dilution |
CO is inversely proportional to the area under the thermodilution curve - the smaller the area under the curve the greater the cardiac output |
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Determinants of myocardial oxygen supply and demand Heart Rate, o2 content, diastolic b.p, and coronary vascular resistance |
Supply Heart Rate and Demand Heart Rate O2 content (Hct) = Afterload Diastolic b/p = preload Coronary vascular resistance = contractility |
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Arterial pressure waveform what happens to the pulse pressure when you move from central to peripheral ? Where is the most accurate mean arterial pressure taken from |
Pulse pressure greatest in dorsal is pedis. -farther away the greater the pulse pressure. Superimposition principle. the most accurate MAP is taken from under the aortic pressure curve. (area under curve divided by time yields MAP) |
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Direct Acting Vasodilators |
Hydralazine - Arterial Dilator Diazoxide - Arterial dilator (watch for hyperglycemia) Nitroprusside - Arterial and Venous dilator Nitroglycerin - Venous Dilator |
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Ca Channel Blockers |
Verapamil and Diltiazem - arterial dilator and decrease HR Nifedipine - Arterial Dilator (poss increase in HR reflex) |
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ACE inhibitors |
Captopril (capoten) and Enalapril (vasotec) = Arterial Dilator |
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PDE - phosphodiesterase inhibitors |
Inamrinone and Milrinone(primacor) - block the breakdown of cAMP; increase myocardial contractility and decrease SVR |
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Adenosine |
Endogenous nucleotide occurring in all cells in the body Slow conduction of AV node, interrupt reentry pathway, restore NSR with PSVT (including WPW) give 6-12 mg IV as rapid - will convert within one minute. no hemodynamic effects and half time is less than 10 seconds. |
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What causes the 1st heart sound and what causes the 2nd heart sound |
1st = closure of the mitral and tricuspid valve at the beginning of systole 2nd = closure of aortic and pulmonic valve at the beginning of diastole |
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3rd heart sound why might you hear it and when |
Hear it during mid diastole and usually from CHF |
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How much is lost when you lose your atrial kick |
25-40% |
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What is Ejection fraction |
its the ratio of stroke volume (end-diastolic volume minus end-systolic volume) EF = (EDV-ESV)/EDV normal range is 60-80% |
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Name the VRG and there percent of CO |
Liver 25% Heart 5% Brain 15% Kidney 20% Lungs 100% 75% of total cardiac output goes to VRG which only account for 10% of total body mass |
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What are the determinants of arterial blood pressure and what law applies |
SVR and CO determine arterial blood pressure Ohms Law |
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In what segment of the systemic circulation is resistance the greatest |
Arterioles account for about half the resistance |
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Bainbridge reflex |
Venous baroreceptors - located in right atrium and great veins. produce in increase in HR when right atrium or great veins are stretched by increased vascular volume. Vagus nerve carries the signal |
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With Inspiration and Expiration what happens to HR and BP
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HR increases with inspiration and BP decreases with inspiration HR decreases with expiration and BP increases with expiration |
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Arterial system contains what percent of blood and what about venous
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Arterial 13% Capillaries (exchange O2, Nutrients, fluid, hormones, etc..) 7% 64% venous Capillary exchange uses Fick's law of diffusion |
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Whats the oxygen consumption rate of the heart |
8-10 ml o2/100g/min |
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IHSS how to treat |
increase preload, increase afterload, normal HR range, NSR is crucial, slightly depressed contractility. 1st Treatment IS VOLUME then Give patient Phenylephrine then Esmolol, Propranolol, and Volatile agents. Aline maybe bifid (bisferiens pulse) |
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What drugs to avoid with IHSS |
avoid Vasodilators, Positive inotropes, beta adrenergic agonists, and diuretics. |
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How long to postpone elective surgery after an MI |
6months biggest risk within 1st month highest risk surgeries are intra-thoracic and intra-abdominal lasting longer than 3 hours |
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Whats Becks triad... Cardiac Tamponade |
Hypotension, JVD, and distant muffled heart sounds occurs with cardiac tamponade- decrease in CO due to reduced SV Tx is pericardiocentesis - if u need to induce use ketamine |
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Takayasus disease |
pulseless dx. absence of palpable pulses. usually young asian females. decreased organ perfusion Tx with corticosteroids |
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CVP whats the A wave C wave and V wave? Whats the X descent and Y descent? |
A wave= right atrial contraction C wave = slight elevation of the tricuspid valve into right atrium X descent - ventricular systole - atrial relaxation (downward displacement of tricuspid) V -wave = blood flow in the right atrium before tricuspid opens Y descent = represents early ventricular filling through the opening of the tricuspid valve |
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In a A-line what does the dicrotic notch represent |
Closure of the aortic valve |
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What is the appropriate size of the bladder width and length for a bp cuff What about obese people and forearms |
40% of the circumference of the extremity encircle atleast 80% of the length Forearms overestimate bp |
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Wheres the phlebostatic axis located |
right atrium 4th intercostal space midanteroposterior level. |
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Most sensitive indicator for air embolus
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#1 TEE #2 doppler |
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Aortic Regurgitation how to treat |
Fast Forward Flow HR sinus. Maintain preload and contractility. Decrease afterload. minimal symptoms if less than 40% of SV Severe symptoms if greater than 60% |
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Mitral Regurgitation |
Chronic due to rheumatic fever or valve incompetent Acute - MI, chest trauma, or infective endocarditis Fast Forward Flow |
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Aortic Stenosis |
Maintain Low HR SR -important Maintain preload, contractility, and afterload. Normal valve 2-3cm, critical valve 0.5-0.8, severe 0.8-1.0 systolic murmur heard at right 2nd intercostal space w/transmission into the neck (aortic arch) NO SPINALS/EPIDURALS WITH SEVERE |
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Mitral Stenosis |
Maintain slow HR and sinus Preload - maintain (excess cause pulm edema) Afterload - maintain Contractility maintain Possibly rheumatic fever. |
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Platelets lifespan? where do they sequester and what percent |
Platelet lifespan 8-12 days Sequester 33% in the spleen |
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Steps in primary hemostasis |
Adhesion of platelets to damage vascular wall activation of platelets Aggregation of platelets Production of fibrin |
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where is Von Willberands factor manufactured and what does it promote |
vWF - promotes platelet adhesion and its manufactured by the endothelial cells |
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vWF |
vWF- Most common inherited dx DDAVP is standard treatment. If DDAVP doesn't work give cyro or factor VIII concentrate |
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What does Cyro contain |
Factor VIII, I(fibrinogen), and Factor XIII |
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Thrombin activates what |
Thrombin (Factor II or IIa) activates platelets. The activated platelets synthesizes and release thromboxane A and ADP. Both of these promote platelet aggregation by binding to receptors and activating signal transduction |
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What does Fibrinogen do |
Fibrinogen (Factor 1) - aggregates platelets |
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Aspirin |
COX is rendered non-functional Cyclooygenase is the rate limiting enzyme in conversion of arachidonic acid to thromboxane A2 The acetylation of platelet cycloyxgenase persists for the life of the platelet 8-12days |
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NSAIDS |
Ketorolac and Ibuprofen - same effects as aspirin but temporarily, only 24-48 hours. |
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Antiplatelet drugs |
Plavix= 7 days lifetime of platelet Ticlopidine - 14 days Anti-fibrinogen GP IIb/IIIa = 24-72 hours. |
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Vitamin K dependent factors |
2, 7, 9, 10 |
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Which Factors are not made in the liver |
III =(tissue Factor or thromboplastin-vascular wall and extra vascular cells) IV (calcium =diet), VIII:vWF(Endothelial cells) |
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Name these factors I, II, III, IV, VIII, IX, X, XIII |
I - Fibrinogen II Prothrombin III Tissue factor IV -Ca VIII- vWF IX - Christmas X- Stuart power XII - Hageman XIII - Fibrin Stabilizing Factor |
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Coagulation Cascade Extrinsic pathway |
III TF to VII Proconvertin to To V (proaccelerin) with X (stuart factor) Only 3 and 7 |
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Intrinsic pathway |
XII Hagmen to XI Plasma thromboplastin to IX (christmas) & VIII vWF to X Stuart Factor Only 12,11,9,8 |
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Common Pathway |
V and X to
II - prothrombin to I fibrin to XIII Fibrin Stabilizing |
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What does heparin work on and what does Coumadin work |
Coumadin interferes with the extrinsic pathway, lab values INR and PT Heparin interferes with the intrinsic pathway, lab values PTT and ACT |
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Hemophilla A |
VIII deficiency usually a male disease 2nd most common disorder Treatment FFP and Cyro - both contain VIII, Preferred tx is VIII concentrate |
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Whats the only acceptable reason for giving PRBC |
increase oxygen carrying capacity |
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FFP contains what |
all procoagulants except for platelets |
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How much 1 unit of PRBC raise HCT and Hgb |
Raise Hct 3-4% or 1g/dL 1cc/kg RBC will increase Hct 1% |
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How much will one unit of platelets increase platelet count |
5,000-10,000 |
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Whats Massive Transfusion |
1 complete blood volume transfused within 24 hours |
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Antithrombin |
made in the liver and neutralizes the common pathway
works strongly on factor IIa and Xa and partially on IXa, XIa, XIIa Heparin binds to antithrombin III - heparin increases attachment by 1000 fold. Acquired antithrombin deficiency = cirrhosis of the liver and nephrotic syndrome |
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If you have a patient that you give heparin to and there ACT goes from 210 to 240 what else might you give to fix the ACT
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give FFP, you don't have enough antithrombin. |
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How does protamine work |
Neutralization of heparin, binds a positive charged substance with a negative charged substance |
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Coumadin what does it work on |
Vit K dependent factors. |
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Whats the normal lab values for these labs Bleeding time, PT, PTT, ACT, Fibrinogen |
Bleeding time 3-10 minutes PT 12-14 seconds PTT 25-35 seconds ACT 80-150 (Heparinization requires ACT 400) Fibrinogen > 150 |
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What breaks down a clot |
Plasminogen(made in liver) (inactive) transition to plasmin to breakdown clots tPA and uPA convert plasminogen to plasmin. Plasmin breaks down fibrin.
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How does aprotinin and Amicar work |
work by inhibiting plasmin . When plasmin is inhibited, fibrin that if formed breaks down slowly, so bleeding is decreased. |
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Disseminated Intravascular Coagulation DIC |
Manifestation of underlying process will see decreased platelets, fibrinogen, prothomrbin, factor V, VIII, XIII, and increased fibrin degradation split products. |
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Transfused blood is usually lacking what two coagulation factors |
V and VIII
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Whats the major cause of bleeding after a massive blood transfusion |
Thrombocytopenia non functional platelets |
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Normal Lifespan of a RBC |
80-120 days |
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Erythropoietin where is it made and what does it do |
Made in the Kidney (90%) and liver (10%) and stimulate bone marrow to produce and release RBCS |
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What is dosing for FFP |
10-15 ml/kg which expected to bring clotting factor levels to at least 30% of normal. 5-8ml/kg for Coumadin reversal |
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One unit of cyro has enough fibrinogen to increase its level to what
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5-7 mg/dl |
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whats virchows triad |
Endothelial injury stasis or turbulent blood flow hypercoagualability |
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Three herbal medicines that could cause anemia or associated with bleeding |
garlic, ginseng, and ginkgo stop 2 weeks before surgery |
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Protamine reactons |
Hypotension, Pulm HTN, Allergic reactions |
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What are the antidotes to Coumadin When should you stop taking coumadin |
Vit K but takes 4-24 hours (10-20mg/kg) FFP Whole blood Stop taking coumadin 3-5 days before |
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TEG - R time and how do you treat if prolonged |
reaction time- indication of how long it takes for first significant clot formation. normal 5-10 minutes tx FFP |
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TEG - K time and how do you treat prolonged |
Achievement of clot firmness or stabilization measure at the end of R time 1mm until 20 mm clot kinetics normal 3-7 minutes Tx Cyro or FFP |
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Alpha angle TEG - how do you treat |
speed of clot formation (fibrin cross linking) normal value 50-60 degrees Tx with Cyro or FFP |
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MA maximum amplitude - TEG - how do you treat |
absolute strength of the fibrin clot normal 50-60mm Low ma = give platelets |
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Lysis or Ly 30/Ly 60 - TEG - how do you treat |
measures breakdown of the clot in increments of 30 and 60 minutes. normal fibrinolysis is 300 minutes Elevated ly 30 or ly 60 - consider antifibrinolutic |
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