2212 Unit 3

• epicardium (outer)
• myocardium (middle, muscle)
• endocardium (inner)

• 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

• between atria & ventricles
• closed during contraction
• Tricuspid: Right side (3 leaflets)
• Mitral: Left side (2 leaflets)

• open during contraction; prevents blood flowing back to ventricles during contractoin
• Pulmonary: R ventricle & pulmonary artery
• Aortic: L ventricle & aorta

• watch for damage of these areas after MI

• 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

• 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

• 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)

• 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)

• One complete heart beat
• systole & diastole

• 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

• AV valves open; period of rapid filing (70%)
• Atrial kick: forces last 30% into ventricles in late diastole
• ventricle wall expands

• = stroke volume x heart rate
• volume of blood ejected by heart per minute

• 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

• volume of blood ejected with each contraction of L ventricle
• effected by: preload / afterload / contractility

• 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

• amount of tension required by L ventricle to open aortic valve during systole and ejection fo blood
• increased tension -> decreased stroke volume

• influences force of contraction (inotropic state)
• generated by myocardium regardless of preload
• Sympathetic = increase
• metabolic abnormalities = decrease

• resistance of systemic vascular bed
• increased: vasoconstriction (shock, L CHF)
• decreased: vasodilation (sepsis/septic shock, neurogenic shock, meds decrease afterload)

• Normal: distention when supine
• 30^o or >: no distention
• 45-90^o : 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

• 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

• L recumbent position
• 5th intercostal space midclavicular line @ apex
• pulsation / ventricular thrust normal
• if located towards L = heart enlargement

• 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

• closure of mitral & tricuspid valve
• begining of systole
• 5th intercostal space midclavicular
• corresponds with carotid artery pulse / ventricular ejection

• closure of aortic & pulmonic valves
• begining of diastole
• R & L sternal border 2nd intercostal space

• S1: normal in young children adults <40
• S2: normal inspiration; expiration = R ventricular failure

• 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

• 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

• 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

• aortic stenosis; valvular prolapse; prosthetic valves
• High pitched (heard with diaphragm)

• high pitch grating sound
• inflamed cardiac tissues rubbing together r/t pericarditis, MI, after cardiac surgery

• radial < apical
• decreased C.O.; blockage, poor circulation
• (can be pedal pulses too)

• 20 points difference in supine & standing B/P
• d/t dehydration, poorly controled HTN, CVA, or aortic disease

• observe ischemic changes during normal activity 24-48 hours
• uses symptom diary
• no showering / bathing during

• 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

• Ejection fracture
• Stress: dobutamine (increases force & rate)
• Transesophageal: swallow transmitter

• 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)

• 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

• L side heart pressure; C.O. pulmonary artery pressure
• Balloon: inflated floats into pulmonary artery; pressure measured; balloon deflated

• 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

• Injection of thrombolytic (clot busters) medications at site of clot (tPa, streptokinase)
• Percutaneous transluminar coronary artery angioplasty (PTCA)
• stent placement

• 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

• 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

• 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

• 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

• 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)

• 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

• 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)

• 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

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

• 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

• 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

• 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

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

• 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

• 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

• 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

• 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

• Heparin / LMWH (Lovenox, frafmin)
• Used: w/ fibrinolytics
• Anticoagulants: prevent clot from getting larger
• S/E: Bleeding
• Nursing: teach S&S of bleeding

• Meds: ReoPro, Integrelin; Aggrastat
• Used: in combo with ASA for pt @ high risk for unstable angina; usually given after PCI & Stent placement

• Meds: Colace
• Used: post MI to prevent constipationd/t bedrest & opiod meds; prevents straining during BM wich causes vagal stimulation l/t bradycardia

• 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

ABC's, high flow O2(NRB), assist w/ intubation if needed; IV acces; NS; draw labs; indwelling cath; NG tube

• 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

• simpathomimetic; B1 adrenergic
• MOA: increase Hr, contractility, SV, & CO (positive inotrope) decrease SVR
• Dose: 2-20mcg/kg/min

• Vasodilator: decrease afterload & preload
• decrease BP
• Nursing: BP can decrease dramatically in a matter of mins.

• 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

• 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

• 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

• 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

• 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