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Cardiac tissue layers
- epicardium (outer)
- myocardium (middle, muscle)
- endocardium (inner)
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Drop of blood through heart
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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
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AV valves
- between atria & ventricles
- closed during contraction
- Tricuspid: Right side (3 leaflets)
- Mitral: Left side (2 leaflets)
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Semilunar Valves
- open during contraction; prevents blood flowing back to ventricles during contractoin
- Pulmonary: R ventricle & pulmonary artery
- Aortic: L ventricle & aorta
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Papillary muscle & Chordee tendinae
- watch for damage of these areas after MI
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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
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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
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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)
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Cardiac Conduction System
- 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)
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Cardiac Cycle
- One complete heart beat
- systole & diastole
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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
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Diastole
(Ventricular Relaxation)
- AV valves open; period of rapid filing (70%)
- Atrial kick: forces last 30% into ventricles in late diastole
- ventricle wall expands
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Cardiac Output (C.O.)
- = stroke volume x heart rate
- volume of blood ejected by heart per minute
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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
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Stroke volume
- volume of blood ejected with each contraction of L ventricle
- effected by: preload / afterload / contractility
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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
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Afterload
- amount of tension required by L ventricle to open aortic valve during systole and ejection fo blood
- increased tension -> decreased stroke volume
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Contractile state
- influences force of contraction (inotropic state)
- generated by myocardium regardless of preload
- Sympathetic = increase
- metabolic abnormalities = decrease
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Systemic Vascular Resistance (SVR)
- resistance of systemic vascular bed
- increased: vasoconstriction (shock, L CHF)
- decreased: vasodilation (sepsis/septic shock, neurogenic shock, meds decrease afterload)
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Cardiac Assessment
Head to Toe
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Neck Vein Distention
- Normal: distention when supine
- 30o or >: no distention
- 45-90o : 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
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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
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Point of Maximum Intensity (PMI)
- L recumbent position
- 5th intercostal space midclavicular line @ apex
- pulsation / ventricular thrust normal
- if located towards L = heart enlargement
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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
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S1
- closure of mitral & tricuspid valve
- begining of systole
- 5th intercostal space midclavicular
- corresponds with carotid artery pulse / ventricular ejection
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S2
- closure of aortic & pulmonic valves
- begining of diastole
- R & L sternal border 2nd intercostal space
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Splitting
- S1: normal in young children adults <40
- S2: normal inspiration; expiration = R ventricular failure
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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
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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
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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
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Clicks
- aortic stenosis; valvular prolapse; prosthetic valves
- High pitched (heard with diaphragm)
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Friction Rubs
- high pitch grating sound
- inflamed cardiac tissues rubbing together r/t pericarditis, MI, after cardiac surgery
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Pulse Deficit
- radial < apical
- decreased C.O.; blockage, poor circulation
- (can be pedal pulses too)
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Orthostatic Hypotension
- 20 points difference in supine & standing B/P
- d/t dehydration, poorly controled HTN, CVA, or aortic disease
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Holter Monitor
- observe ischemic changes during normal activity 24-48 hours
- uses symptom diary
- no showering / bathing during
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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
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Echocardiagram
- Ejection fracture
- Stress: dobutamine (increases force & rate)
- Transesophageal: swallow transmitter
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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)
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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
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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
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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
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Coronary Catheterization Procedures
- Injection of thrombolytic (clot busters) medications at site of clot (tPa, streptokinase)
- Percutaneous transluminar coronary artery angioplasty (PTCA)
- stent placement
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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
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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
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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
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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
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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)
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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
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Non-STEMI / STEMI
(MI)
- 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)
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Dobutamine
- simpathomimetic; B1 adrenergic
- MOA: increase Hr, contractility, SV, & CO (positive inotrope) decrease SVR
- Dose: 2-20mcg/kg/min
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Nitroprusside
- Vasodilator: decrease afterload & preload
- decrease BP
- Nursing: BP can decrease dramatically in a matter of mins.
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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
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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
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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
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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
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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
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