2212 Unit 3

  1. Cardiac tissue layers
    • epicardium (outer)
    • myocardium (middle, muscle)
    • endocardium (inner)
  2. Drop of blood through heart
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  3. Pericardium
    • Parietal: outer barrier to infection from surrounding structures
    • Visceral: thin layer closely adheres to heart
    • Space: holds 5-20ml fluid; lubricates surfaces as they slide together, cushions heart against external trauma
  4. AV valves
    • between atria & ventricles
    • closed during contraction
    • Tricuspid: Right side (3 leaflets)
    • Mitral: Left side (2 leaflets)
  5. Semilunar Valves
    • open during contraction; prevents blood flowing back to ventricles during contractoin
    • Pulmonary: R ventricle & pulmonary artery
    • Aortic: L ventricle & aorta
  6. Papillary muscle & Chordee tendinae
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    • watch for damage of these areas after MI
  7. Coronary circulation
    Coronary arteries
    • perfused by pressure; branch off aorta above aortic valve
    • RCA: R atrium, ventricle, inferior portion L ventricle, posterior septum wall, SA & AV node
    • LCA: divided into LAD & Cirdcumflex
    • LAD: anterior & apex L ventricle; ant. ventricular septum; bundle branches
    • Circumflex: L atrium & posterior L ventricle
    • 75% during diastole
  8. Electrophysiology
    • Depolarization: inside becomes less (-) K+ & Cl- leave cell; Na+ & Ca+ enter cell; muscle cell contraction occurs
    • Re-polarization: cell returns to baseline becomes more (-); K+ moves back into cell, Na+ leaves cell; relaxation of muscle cell occurs
    • Prolonged refractory period (resting period): short time cell cannot be stimulated to contract
  9. Physiologic Properties of Myocardial Cells
    • Automaticity: ability to initiate pulse w/o external control
    • Conductivity: ability to transmit electrical impulses along & across cell membranes (allows heart to work as a unit)
    • Contractility: respond with pumping action
    • Excitability: respond to impulse occurs as result of ion exchange (Na+, K+, Mg+)
    • Rhythmicity: sequence of depolarization/re-polarization regular & predictable intervals
    • Refractoriness: inability to respond to new stimulus while still in a state of contraction from previous stimuli (0.25-0.3 seconds)
  10. Cardiac Conduction System
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    • SA: Pacemaker 60-100 (parasympathetic (increase) & sympathetic (decrease) effect)
    • AV: 40-60; takes over w/o SA
    • AV bundles (Bundle of His): 15-40
    • Purkinji Fibers: wave of depolarization spreads from inside to outside; repolarization occurs in reverse order (last cell depolarized = 1st to re-polarize)
  11. Cardiac Cycle
    • One complete heart beat
    • systole & diastole
  12. Systole
    (Ventricular contraction )
    • increased ventricular pressure forces semilunar valves open
    • 60% ejected into lungs & body 1st 1/4 cycle
    • Ventriculars begin to relax -> aoritc & pulmonic pressures exceed ventricular pressure -> semilunar valves close
  13. Diastole
    (Ventricular Relaxation)
    • AV valves open; period of rapid filing (70%)
    • Atrial kick: forces last 30% into ventricles in late diastole
    • ventricle wall expands
  14. Cardiac Output (C.O.)
    • = stroke volume x heart rate
    • volume of blood ejected by heart per minute
  15. Cardiac Index (C.I.)
    • cardiac output in terms of L/min over body surface area (CO/body surface area)
    • takes into account differences in body size
    • describes how well tissues perfused
  16. Stroke volume
    • volume of blood ejected with each contraction of L ventricle
    • effected by: preload / afterload / contractility
  17. Preload
    • myocardial fiber lenght L ventricle @ end-diastole; ventricle full of blood just before contraction
    • Frank-Starling's Law: increase length / stretch -> increased force of contraction
    • larger preload = larger stroke volume
    • Increased: fluids given
    • Decreased: diuresing pt
  18. Afterload
    • amount of tension required by L ventricle to open aortic valve during systole and ejection fo blood
    • increased tension -> decreased stroke volume
  19. Contractile state
    • influences force of contraction (inotropic state)
    • generated by myocardium regardless of preload
    • Sympathetic = increase
    • metabolic abnormalities = decrease
  20. Systemic Vascular Resistance (SVR)
    • resistance of systemic vascular bed
    • increased: vasoconstriction (shock, L CHF)
    • decreased: vasodilation (sepsis/septic shock, neurogenic shock, meds decrease afterload)
  21. Cardiac Assessment
    Head to Toe
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  22. Neck Vein Distention
    • Normal: distention when supine
    • 30o or >: no distention
    • 45-90: abnormal increase in fluid volume
    • r/t R chf or obstructed flow in superior vena cava
    • Hepato-Jugular Reflex: supine, press on liver.  Distention + indicates increased fluid
  23. Palpitation
    • Symmetry
    • Thrills: palm of hand / Tremor w/ murmur
    • Heave: sustained lift of chest wall in precordial area (between apex & sternum) Ventricular enlargement
    • Pulsations: normal in epigastric region (either side of mid-line below xyphoid)
    • Aneurysm - pulsating mass L of periumbilical areal
  24. Point of Maximum Intensity (PMI)
    • L recumbent position
    • 5th intercostal space midclavicular line @ apex
    • pulsation / ventricular thrust normal
    • if located towards L = heart enlargement
  25. Location of Heart sounds
    • Aortic: R sternal border 2nd intercostal
    • Pulmonic: L sternal border 2nd intercostal
    • Tricuspid: L sternal border 5th intercostal
    • Mitral: midclavicular line 5th intercostal
    • Erbs Point: L of sternum 3rd intercostal
  26. S1
    • closure of mitral & tricuspid valve
    • begining of systole
    • 5th intercostal space midclavicular
    • corresponds with carotid artery pulse / ventricular ejection
  27. S2
    • closure of aortic & pulmonic valves
    • begining of diastole
    • R & L sternal border 2nd intercostal space
  28. Splitting
    • S1: normal in young children adults <40
    • S2: normal inspiration; expiration = R ventricular failure
  29. S3
    Ventricular Gallop
    • pathologic in adults: CHF, HTN, volume overload, mitral valve regurgitation
    • Normal in childrein & young adults
    • end of diastole (after S2)
    • vibration occur during rapid filling of dilated ventricles
    • Ken tuc KY
  30. S4
    Atrial Gallop
    • may be heard in adult > 40
    • Pathological: CAD; cardiomyopathy; HTN
    • end of diastole before S1
    • vibration d/t atrial contraction & push of blood into non-compliant ventricle
    • TEN nes see
  31. Murmur
    • location:
    • pitch: (bell= low; diaphragm = high)
    • timing: systole / diastole
    • Position:
    • Characteritistics:
    • Radiation:
    • Grading: I(barely audible)-IV (heard w/o stethoscope): ex: I/VI; IV/VI
    • Systole: produced in some valve disorders may occur in healthy heart
    • Innocent: commoin in children, adults >50, pregnancy
    • Diastole: pathologic produced by valvular disease
  32. Clicks
    • aortic stenosis; valvular prolapse; prosthetic valves
    • High pitched (heard with diaphragm)
  33. Friction Rubs
    • high pitch grating sound
    • inflamed cardiac tissues rubbing together r/t pericarditis, MI, after cardiac surgery
  34. Pulse Deficit
    • radial < apical
    • decreased C.O.; blockage, poor circulation
    • (can be pedal pulses too)
  35. Orthostatic Hypotension
    • 20 points difference in supine & standing B/P
    • d/t dehydration, poorly controled HTN, CVA, or aortic disease
  36. Holter Monitor
    • observe ischemic changes during normal activity 24-48 hours
    • uses symptom diary
    • no showering / bathing during
  37. Stress Test
    • ECG; checks if O2 demands > supply from heart
    • exercise on treadmill / given Dipyridamole (Persantine)
    • Pre-care: no beta blockers / caffeine 24 h before; no smoking/eating 3 hours before; may have "light" breakfast; comfortable clothes & shoes
    • during: make sure pt advises of pain/ discomfort; test can be stopped at any time
    • Post-care: no hot bath/shower 2 hours after d/t hypotension
  38. Echocardiagram
    • Ejection fracture
    • Stress: dobutamine (increases force & rate)
    • Transesophageal: swallow transmitter
  39. Muclear Cardiology
    • inject radioactive isotope
    • Thallium / Cardiolyte: healthy cells pick up isotope; Dipyridamole (persantine) vasodilator given to increase blood to well perfused coronary arteries
    • Technetium 99 phosphate: injured cells pick up isotope (7-10 days after MI)
  40. Central Venous Pressure (CVP )
    • normal 4-10cm/H2O
    • measures pressure in superior vena cava / R atrium (R ventricular filling pressure / preload; R ventricular end-diastole pressure)
    • guide to fluid volume replacement (dehydration / overhydration)
    • Phlebostatic Axis: 4th intercostal space midaxillary line (R atrium); zero point of manometer
    • Increased (>10): R CHF; constrictive pericaditis; cardiac tamponade; valvular stenosis; pulmonary HTN; increased circulating volume; vasoconstriction; HTN
    • Decreased (<4): early LVF; decreased circulating volume (hypovolemic shock); vasodialtion / peripheral pooling; dehydration
    • Complications: air emboli; pulmonary emboli; fluid overload; dysrhtyhmias; infection
  41. Pulmonary Artery Pressure
    Pulmonary Wedge Pressure
    Swan Ganz
    • L side heart pressure; C.O. pulmonary artery pressure
    • Balloon: inflated floats into pulmonary artery; pressure measured; balloon deflated
  42. Coronary Artery Catheterization
    • Before: check allergies (iodine / shellfish); consent; NPO; local; feel warm & fluttering sensation; nausea; may instruct to cough / deep breathe
    • After: monitor VS (HR, arrhythmia, resp distress); supine 6-8 hours w/ pressure dressing; sensation distal q15 for 1h then decrease; Check dressing (swelling, bleeding, bruising)
    • Post-op teaching: push fluids 1st 24h; S&S infection/bleeding; no tub baths (24-48 hours) may shower; avoid strenuous exercise for several days; Tylenol for pain(not aspirin; ibuprofen)
    • Complications: bleeding (place supine; remove dressign & apply pressure above insertion site; fluid replacement; notify physician) infection
  43. Coronary Catheterization Procedures
    • Injection of thrombolytic (clot busters) medications at site of clot (tPa, streptokinase)
    • Percutaneous transluminar coronary artery angioplasty (PTCA)
    • stent placement
  44. Atherosclerosis
    Coronary Artery Disease (CAD)
    • fat deposits that harden with age in coronary arteries.
    • C-reactive Protein (CRP): nonspecif marker of inflammation; predictor of future cardiac events; chronic exposure triggers rupture of plaques
    • Collateral circulation: normal to have some arterial anastomoses with coronary circulation; greater chance of adequate circulation when CA occurs slowly
  45. Factors for CAD
    • Modifiable: Serum lipids:•Total cholesterol >200 mg/dL•Triglycerides ≥150 mg/dL*•LDL cholesterol >160 mg/dL•HDL cholesterol <40 mg/dL in men or <50 mg/dL in women*  Blood pressure - ≥140/90 mm Hg* Diabetes mellitus Tobacco use Physical inactivity  Obesity - Waist circumference ≥102 cm (≥40 in) in men and ≥88 cm (≥35 in) in women* Fasting blood glucose ≥100 mg/dL* Psychosocial risk factors (e.g., depression, hostility and anger, stress) Elevated homocysteine levels
    • Non-midifiable: Increasing age Gender (men > women until 65 yr of age) Ethnicity (whites > African Americans) Genetic predisposition and family history of heart diseas
  46. Decreasing CAD risk factors
    • HTN: meds; decrease salt; reduce weight; regular physical activity
    • Elevated serum lipids: reduce fat intake; reduce animal (saturated) fat intake; meds; increase complex carbohydrates & vegetable protein 
    • Tobacco Use: cessation; change daily routine; substitute other activities; support
    • Physical inactivity: 30 mins of moderate physical activity / day; increase activities to a fitness level
    • Psychological state: awareness; set goals; reassess priorities; stress management; professional help; rest & sleep
  47. Clinical Manifestation of CAD
    • Chronic Stable Angina:
    • Acute Coronary Syndrome:
    •    - unstable angina (partial occlusion)
    •    - non-STEMI (partial occusion with necrosis)
    •    - STEMI (total occlusion)
    • Sudden Cardiac Death: abrupt disruption in cardiac function l/t loss of CO & cerebral blood flow; death w/i 1 hour onset of MI symptoms; most often caused by ventricual dysrhythmias
  48. Chronic Stable Angina
    • Patho: reversible (temperary) Myocardial ischema ( angina) d/t narrowing of CA r/t atherosclerosis; O2 demand > O2 supply
    • S&S: intermittent chest pain (long period with same pattern of OPQRST); lasts 3-15 minutes (subsides when precipitating factor is relived) pain relived by rest & NTG
    • Types: silent ischemia (associated w/ DM & HTN) Nocturnal angina (only @ night not necessarily during sleep) Angina decubitus (only while laying down relived by sitting / standing) Prinzmetal's Angina ( @ rest, spasm occur in absent of CAD, REM sleep; relieved with moderate exercise tx: Calcium channel blocker / nitrates)
    • DX: H&P; 12-lead; ECHO; CHEST xray; stress test; cardiac cath; nuclear imaging; lipid profile;
    • TX: Short / long acting nitrate; (prophylactic 5-10 min before activity) beta blockers (calcium channel blockers if beta poorly tolerated); ACE inhibitors; coronary revascularization (PCI / sent placement)
  49. Unstable Angina
    • Patho: ischemia is prolonged and not immediately reversible
    • S&S: new in onset (@ rest, sleep, worsening pattern) Women (SOB, fatigue, anxiety, indigestion) S&S d/t catecholamines (epi & norepi)
    • Dx: H&P; 12-lead; ECHO; CHEST xray; stress test; cardiac cath; nuclear imaging; lipid profile; cardiac markers; ECG conduction change will show which ardtery is occluded
  50. Non-STEMI / STEMI
    • Patho: d/t sustained ischemia (>20 mins) causing irreversible myocardail cell death (necrosis); necrosis of entire thickness takes 4-6h
    • S&S: depends of area & size; pain d/t lactic acid build up (severe immobilizing chest pain not relived by rest, position change or nitrates) diaphoresis ; increase HR, then BP, then lower BP, crackles, JVD, S3/S4 sounds, new murmur; N/V, fever (>100.4 may last for a week)
    • Complications: dysrhythmias (most common); HF (crackles, edema); cardiogenic shock; papillary muscle dysfunction ( mitral valve regurgitation); ventricular aneurysm; acute pericarditis (2-3 days post-MI chest pain different than MI may l/t HF); Dressler Syndrome (pericarditis with effusion 4-6 weeks post-MI)
  51. Treatment Unstable Angina / MI
    • Emergency Management: VS, O2 (2-4L) ECG, Chew ASA, SL/IV nitro (if IV nitro does not work, morphine to dilate and decrease anxiety)
    • goal is to open vessle within 90 mins of ER arrival
    • Emergency PCI: (tx of choic for confirmed MI: balloon angio & drug eluting stents
    • Fibrolytic therapy: tPa, ateplase, (bleeding complication) (watch for re-perfusion dysrhythmias)
    • Drug tx: ASA, IV nitro, Morphine, beta blockers, antidysrhtyhmic, cholesterol lowering, stool softeners
    • nutrition: NPO until stable -> low salt, fat, cholesterol
    • Medical management fails: coronary surgical revascularization (PCI failed or not candidate) in ICU 24-36 hours   - CABG, minimally invasive CAB, off pump CAB, transmyocardial laser revascularization
    • Home Care: teaching, cardiacl rehab, resumption of sexual activity, prophylactic use of nitro before activity
  52. Anti-Platelet Agents
    Meds: ASA 325mg, then 81-325mg/day chewed (for faster absorption); Clopidogrel (Plavix) (alternative to ASA) loading dose then 75mg/day

    Indication: Suspected ACS

    MOA: inhibits Platelet aggregation

    • *often first med given when ACS is suspected*
    • Contraindicated: active peptic ulcer disease; hepatic disease; bleeding disorders; aspirin allergy
  53. Anti-Anginal:
    Immediate onset
    • Tridil (IV NTG)
    • Used: acute MI, unstable angina, acute/severe CHF
    • MOA:dilates peripheral veins -> decreased SVR -> increased venous pooling in periph veins -> decrease blood return to heart = decreased preload, SV, workload & O2 demand;  Dilates healthy CA -> incread blood flow to ischemic area -> increased myocardial O2 supply

    S/E: decreased BP, HR; diaphoresis, N/V; Dysrhythmias

    Nursing: titrate dose to relive pain (keep BP adequate); special tubing, glass bottles; taper off; if OD: decrease or stop infusion & elevate legs
  54. Anti-Anginal:
    Short Acting Nitrates
    • SL NTG or Translingual spray
    • Used: first line of defense for tx of angina
    • SL: 1 tab under tongue, if no relief after 1st tab call HCP/EMS; repat q5 mins up to 3 doses
    • Spray: 1 spray SL, pain relief in 3 mins, duration of 30-60 mins
    • S/E: orthostatic Hypotension; HA; dizinees; flushing; increased HR
    • Nursing: easy acces; do NOT combine w/ ED drugs; dark glass bottle; tingle under tongue; sit down before taking; can use prophylactically  before activity
  55. Long Acting Nitrates
    • Isordil / Imdur (PO): sustained release
    • Nitropaste: dosed by inch, avoid getting on hands, duration 3-6h, area w/o hair/scars
    • Transdermal (topial): reservoir - dose dumping if seal punctured; matrix - slow delivery, do dumping; both- steady plasma levels for 24 hours, only 1x/day opitimal levels in 2 hours
    • Used: decrease incidence of angena attacks, paste for nocturnal / unstable angina
    • S/E: pouding HA (use tylenol); hypotension; weak; dizzy; flushing; reflex tachycardia; edema; orthostatic hypotension
    • Nursing: monitor BP (esp after 1st dose); tolerance can occur (8 hour nitrate free period needed); warm of danger associated w/ alcohol
    • Patch: remove old one 1st, rotate site, do not cut/touch w/ bare hands; wash off old ointment
  56. Beta-Adrenergic Blockers
    Used: preferred drug to manage chronic stable angina, used in 1st hour of MI to decrease size of infarction & complications

    • Nonselective: Propranolol (inderal), Nadolol (Corgard), & Carvedilol (Coreg)
    • MOA: blocks both beta 1&2 causing broncho & vaso constriction

    • Selective: Metroprolol (lopressor) & Atenolol (tenormin)
    • MOA: blocks beta 1 -> decreased HR -> decreased contractility -> decreased SVR -> decreased BP -> decreasee myocardial O2 demand/consumption

    S/E: Bradycardia; decreased BP; wheezing; GI complaints; weight gain; depression; fatigue; sex dysfunction; hyperglycemia

    Nursing: avoid in pts w/ asthma; caution in pts with diabetes (can mask hypoglycemia) do NOT d/c abruptly; monitor HR & BP
  57. Calcium Channel Blockers
    • Meds: Verapamil, Diltiazem (carizem), Nifedipine, Nicardipine
    • Used: antiaginal after nitrates & betal blockers fail; tx Prinzmetal's Angina
    • MOA: prevents movement of Ca into cells -> decrease muscle contractility -> dilated coronary & peripheral vessels (decreased BP) -> decrease myocardial contractility (decreased CO) -> slows conduction (decrease HR) -> decreased workload & O2 demand of heart
    • S/E: HA; Decreased C.O. bradycardia; fatigue; dizzy; impotence; decreased BP; edema; constipation; dysrhythmias
    • Nursing: used w/ nitrates: increase probability of HA, hypotension, reflex tachycardia & edema.
    • can increase dig levels (50-70%)
    • if d/c abruptly can cause angina
    • verapamil & diltiazem: bradycardia
    • nifedipine & nicardipine: tachycardia
    • difedipine: profound hypotension
    • diltiazem (cardizem): fewer s/e
  58. Morphine
    • IVP 1-5mg 5-30 min intervals (max 15mg/4h) until pain is relieved; peaks 7mins
    • Used: chest pain not relieved by NTG
    • MOA: peripheral vasodilator -> decreased blood return to heart (decreased preload) -> decreased contractility -> decreasee BP (decreased afterload) & decreased HR -> decreased O2 demand of heart; also decreases anxiety & fear
    • *drug of choice for acute myocardial pain*
    • S/E: bradycardia; hypotension; resp depression *antidote: Nalaxone/Narcan IVP*
    • Nursing: monitor VS *esp resp*; narcan ready for emergency; frequent check pain level
  59. Angiotensin-Converting Enzyme (ACE) Inhibitors
    • Meds: Captopril (Capoten) & Enalapril (Vasotec)
    • Use: prevent ventricular remodeling & prevent / slow HF progression; decrease endothelial dysfunction
    • S/E: hypotension; dizziness; loss of taste; Cough; hyperkalemia; acute renal failure; skin rash; angiodema
    • Nursing: monitor BP&HR; K levels; monitor for cough
  60. Fribinolytic Therapy (IV)
    • Meds: rPA (Retavase); tPA (Activase); TNK-tPA (TNKase)
    • Thrombolytics: dissolve blood clots
    • Used: to salvage as much heart tissue as possible; dissolves clot l/t reperfusion of myocardium; STEMI
    • tx begins w/in 60 mins of onset of symptoms (ideally); prefereabbly within first 6 hours
    • S/E: reperfusion dysrhythmias (heart is irritable); bleeding
    • Nursing: obtain baseline lab values; IV bolus over 30-90 mins; Heparin usually given simultaneously
  61. Unfractioned Heparin / LMWH
    • Heparin / LMWH (Lovenox, frafmin)
    • Used: w/ fibrinolytics
    • Anticoagulants: prevent clot from getting larger
    • S/E: Bleeding
    • Nursing: teach S&S of bleeding
  62. Glycoprotein / IIb/ IIIa inhibitors
    • Meds: ReoPro, Integrelin; Aggrastat
    • Used: in combo with ASA for pt @ high risk for unstable angina; usually given after PCI & Stent placement
  63. Stool Softeners
    • Meds: Colace
    • Used: post MI to prevent constipationd/t bedrest & opiod meds; prevents straining during BM wich causes vagal stimulation l/t bradycardia
  64. Cardiogenic Shock
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  65. Cardiogenic Shock:
    • Clinical Manifestations: decreased CO; myocardial ischemia; cerebral hypoxia; impaired tissue perfusion; renal circulation decreased; anaerobic metabolism w/ lactic acidosis; peripheral vascualr system collapse; SHOCK
    • S&S: dysrhythmias, chest pain; anxiety, agitation, restlessness, disorientation; decreased/absent urinary output; lactic acid accumulation in blood; tachycardia, thready, tachypnea; decreased blood pressure; narrowed pulse pressure; cyanosis, cold, moist, pale, clammy skin; decreased peripheral pulses; delayed cap refill; hypoactive bowel sounds
    • Medical Management: recognition & control of life-threatening S&S; oxygen; parenteral fluid as volume expander; drug therapy: vasopressors, inotropic cardiac glycoside, adrenergic drugs, sodium bicarbonate (combats lactic acidosis)
    • Nursing: monitor VS q5 minutes acute; qhour when stabilized; O2 as orderd; maintain bedrest (reduce myocardial workload); monitor acid-base balance; I&O; NPO; meds as ordered; comfort
  66. Inital Management of Cardiogenic Shock
    ABC's, high flow O2(NRB), assist w/ intubation if needed; IV acces; NS; draw labs; indwelling cath; NG tube
  67. Dopamine
    • Vasopressor, sympathomimetic
    • MOA: vasodilate renal & mesenteric arteries -> increased blood to kidneys, decreases preload = decrease worload on heart (increasing BP & HR)
    • Central line (d/t extravasion)
    • Antidote: Regitine
    • Doses: low (2-5mcg/kg/min) renal & mesenteric vasodilate
    • moderate (5-15mcg/kg/min) increase HR, increase contractility, increase CO, increase B/P
    • High (>15mcg/kg/min) not beneficial d/t vasoconstriction
  68. Dobutamine
    • simpathomimetic; B1 adrenergic
    • MOA: increase Hr, contractility, SV, & CO (positive inotrope) decrease SVR
    • Dose: 2-20mcg/kg/min
  69. Nitroprusside
    • Vasodilator: decrease afterload & preload
    • decrease BP
    • Nursing: BP can decrease dramatically in a matter of mins.
  70. Goal of tx in Cardiogenic shock
    • tx underlying cardiac condition (MI, pump failure)
    • thrombolytics, cardiac cath w/ angioplasty &/ stent
    • increase perfusion to all organs, esp vital organs, reduce chance of multisystem organ failure
  71. Troponin
    • myocardial muscle protein released into circulation after injury; two subtypes specific to myocardial tissue
    • detectable 4-6 hours of myocardial injury
    • peak 10-24 hours
    • detected up to 10-14 days
    • <0.034ng/ml
  72. Ck-MB
    • elevation is Specific to myocardial tissue injury
    • begin to rise 6 hours after onset
    • peak 18 hours
    • return to baseline 24-36 hours after MI
    • <2.37ng/ml
  73. Myoglobin
    • low molecular weight heme protein found in cardiac & skeletal muscle
    • elevation sensitive indicator in early myocardial injury
    • rise w/in 2 hours
    • peak 3-15 hours
    • return to basline within 24h
    • not as valuable d/t nonspecificty for MI & its brief presence
  74. Serum Lipids
    • Cholesterol: <200mg/dl (elevated considered risk for atherosclerotic heart disease)
    • Triglycerides: <150mg/dl (elevated associates with cardiovascular disease & diabetes)
    • LDL: <100; near optimal 100-129; mod risk for CAD 130-159; high risk >160
    • HDL: male >40; female > 50.  low risk CAD >60; high risk CAD <40
Card Set
2212 Unit 3
cardiac A&P, physical assessment, diagnostic, CAD, Angina, MI, Drug therapy, carcinogenic shock