-
heart
- located in mediastinum of thoracic cavity between vertebral column and sternum
- flanked by lungs
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pericardium
- protects and anchors, prevents overfilling
- fibrous: outer layer
- parietal: middle fluid layer
- visceral: inner layer
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heart wall
- epicardium: covers entire heart and great vessels
- myocardium: middle layer, cardiac muscles
- endocardium: lines chambers and vessels
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chambers and valves
- two upper atria
- two lower ventricles
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blood flow
SVC/IVC (DOB) > RA > tricuspid > RV > pulmonary valve > pulmonary artery > lungs (DOB<->OB) > pulmonary veins > LA > mitral > LV > aortic valve > aorta (OB)
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S1 sound (lubb)
- closure of AV valves (tricuspid and mitral)
- onset of ventricular systole
- ventricular blood pushes up against AV valves and snaps them shut
- also forces open SL valves
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S2 sound (dub)
- closure of semilunar valves (pulmonary and aortic)
- onset of ventricular diastole
- blood falls down from pulm artery and aortic arch d/t gravity
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systemic circulation
- left side of heart, aorta, capillaries, venous system, vena cava
- high pressure system
- supplies blood to body tissues
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pulmonary circulation
- right side of heart, pulmonary artery, lungs, pulmonary veins
- low pressure system
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coronary circulation
L and R coronary arteries from base of aorta encircle myocardium
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cardiac cycle
- contraction and relaxation of the heart (a heart beat)
- ventricular filling -> ventricular systole (contraction) -> ventricular diastole (relaxation)
- 70-80 times per minute
-
stroke volume
- amount of blood pumped in one cardiac cycle
- 60-100mL
- how strong the heart is contracting
-
ejection fraction
- SV / end diastolic volume (amount of blood in ventricle at diastole)
- normal 50-60%
-
cardiac output
- amount of blood pumped in one minute
- SV x HR
- indicated how well heart is pumping (affects tissue perfusion)
- normal 4-8L/min
- represents amount of blood perfusing tissues
- affected by HR, preload, afterload, contractility
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HR
- increased by SNS
- decreased by PNS
- tachycardia -> increased CO
- bradycardia -> decreased CO
- very rapid HR decreases ventricular filling time -> CO decreased, coronary artery perfusion decreased (because CAs fill during diastole)
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contractility
- strength of contraction of individual cardiac fibers
- aka inotropy
- poor contractility -> decreased CO
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preload
- amount of myocardial stretch at end of diastole (just before contraction)
- increased volume = increased preload = increased SV and CO
- decreased volume = decreased preload = reduced SV and CO
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afterload
- force the ventricles must overcome to eject blood
- pressure in the arterial system ahead of the ventricles
- right ventricle afterload - PVR (pulmonary vascular resistance)
- left ventricle afterload - SVR (systemic vascular resistance)
- increased BP -> increased PVR/SVR -> increased afterload
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conduction system
- several masses of nerve tissue
- controls rate, rhythm, force of HB
- SA -> AV -> Bundle of His -> Purkinje fibers
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regulation of HR
- sympathetic fibers
- --alpha and beta receptors
- --stimulation increases HR, conduction, force of contractions
- parasympathetic fibers
- --SA node, AV node, atrial tissue
- --stimulation decreases HR, conduction, force of contractions
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coronary artery disease
- impaired blood flow to the myocardium
- usually caused by atherosclerosis
- can lead to angina, acute coronary syndrome, MI, dysrhythmias, heart failure, and death
- chronic ischemic heart disease - stable angina and Prinzmetal angina
- acute coronary syndrome - unstable angina and MI
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myocardial ischemia
- inadequate O2 supply to myocardium
- caused by
- --decreased coronary perfusion (occlusions, narrow vessels, decreased BP)
- --increased cardiac workload (increased HR, contractility, preload, afterload, metabolism)
- --decreased blood O2 content (impaired gas exchange, low RBC/Hgb)
- cellular metabolism switches from aerobic to anaerobic metabolism -> lactic acid -> cell damage -> tissue death
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CAD patho
- plaque accumulates in intimal and medial layers of CA
- plaque made of lipoproteins and fibrous tissue
- high LDLs increase risk of atherosclerosis
- damage to arteries from hyperlipidemia, smoking, infections, toxins, HTN -> inflammation
- lipids, collagen, debris calcify (atheromas)
- decreased lumen size -> decreased blood flow
- atheromas ulcerate or rupture -> thrombosis/embolus
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LDL
- low density lipoproteins
- bad cholesterol
- carry cholesterol from liver to peripheral tissues
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HDL
- high density lipoproteins
- carry cholesterol from peripheral tissues to liver
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CAD risk factors
- non modifiable: genetics, ethnicity, age, gender
- men > 45, women > 55 (estrogen is heart-protective)
- modifiable:
- diet - fruits, veggies, grains, unsaturated fats are protective
- inactivity - exercise increases O2 to heart, decreases BP
- smoking - CO damages arterial lining, nicotine increases BP, HR, and vasoconstricts
- obesity - increased rates of HTN, diabetes, hyperlipidemia
- HTN - damages lining of arteries, stimulates plaque development
- diabetes - increases lipid levels, damages lining of arteries
- hyperlipidemia - LDL deposits cholesterol on arterial wall
- emerging: inflammation
- women: oral contraceptives, premature menopause, hormone replacement therapy
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metabolic syndrome
- group of metabolic risk factors
- truncal obesity
- hyperlipidemia
- HTN
- elevated BGL
- clotting
- inflammation
- insulin resistance
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CAD dx
- lipid profile:
- CHO < 200
- HDL > 60
- LDL < 130
- triglycerides < 150
- C-reactive protein: inflammatory mediator (> 3 = risk for CAD)
- ankle-brachial index < 0.9 = PAD, > risk for CAD
- exercise ECG: detect myocardial ischemia, chest pain, fatigue, dysrhythmias
- EBCT: CT scan of heart and CA
- myocardial perfusion imaging: eval myocardial blood flow and perfusion at rest and under stress
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CAD risk factor management
- quit smoking
- change diet: low cholesterol, healthy fats, veggies, fiber
- exercise
- manage HTN and DM
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CAD meds
- statins
- bile acid sequestrants
- nicotinic acid
- fibrates
- low dose aspirin
- ACE/ARBs
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statins
- lower LDL by inhibiting a liver enzyme
- monitor LFTs
- s/e: muscle pain, tenderness, brown urine (myopathy - muscle breakdown)
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bile acid sequestrants
- lower LDL by binding bile acids in intestine (prevent reabsorption)
- s/e: GI upset
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nicotinic acid (niacin)
- lowers LDL, total cholesterol, and triglyceride levels
- s/e: flushing, increased HR
-
fibrates
lower serum triglyceride levels
-
complementary therapies
- diet and exercise
- vitamins
- omega 3
-
CAD nursing dx
- imbalanced nutrition (more) r/t obesity
- ineffective health maintenance r/t risk factors
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angina pectoris
- chest pain r/t reduced coronary blood flow which causes temporary imbalance between supply and demand
- imbalance r/t CAD, atherosclerosis, vessel constriction, anemia, heart failure, ventricular hypertrophy, pulmonary disease
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exercise, hyperthyroidism, stimulant abuse, stress increase also demand
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angina patho
- lack of O2 causes temporary, reversible myocardial ischemia
- reduced O2 causes anaerobic metabolism -> lactic acid buildup -> pain
- three types:
- --stable
- --unstable
- --Prinzmetal
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stable angina
- predictable r/t increased cardiac workload s/t physical exertion, stress, cold
- relieved by rest and nitrates
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Prinzmetal angina
- aka variant angina
- chest pain at night, unrelated to activity
- caused by vasospasm
- tx: calcium channel blockers
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unstable angina
- unpredictable
- increasing frequency, severity, duration
- occurs with stress or at rest
- risk for MI
-
angina manifestations (stable)
- chest pain - tightness, pressure, squeezing, burning, radiates to jaw or left arm
- --lasts < 15 minutes
- --relieved by rest
- indigestion, nausea, vomiting, upper back pain (women)
- unstable: dyspnea, pallor, tachycardia, anxiety, fear
-
angina dx
- EKG - 1st test - cardiac conduction changes with ischemia
- stress EKG
- radionuclide testing - eval myocardial perfusion and L ventricular function
- coronary angiography
- --aka cardiac cath
- --gold standard for coronary artery eval
- --cath into femoral or brachial artery
- --dye injected to visualize CA branches
-
angina meds
- goal: reduce O2 demand and increase O2 supply
- nitrates
- beta blockers
- calcium channel blockers
- aspirin
-
nitrates
- dilates veins and arteries to decrease myocardial work and O2 demand
- vasodilation reduces preload and afterload
- SL, IV, transdermal, PO (Indur)
- s/e: HA, hypotension (r/t systemic dilation)
- at home: take one, sit down, if no relief in 5 min call 911
- at hosp: check BP, O2, give nitro, wait 5 min, repeat x 3 then get EKG and call MD
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beta blockers
- stable angina
- prevent anginal attacks by blocking epi/norepi (which stimulate heart)
- reduce HR, myocardial contractility, BP -> reduced myocardial demand
- contraindicated asthma/COPD - bronchospasm, bradycardia
- use with caution in HF
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calcium channel blockers
- stable angina
- prevent attacks by reducing myocardial demand, increasing myocardial O2 supply
- reduce BP, contractility, HR - reduce demand
- potent coronary vasodilator - increase supply
- use with caution in dysrhythmias, HF, hypotension
-
aspirin
- prophylaxis
- reduce risk of platelet aggregation and thrombus formation
- prevents clots -> MI
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angina nursing dx
ineffective tissue perfusion, cardiac r/t impaired cardiac blood flow
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acute coronary syndrome
- unstable cardiac ischemia - acute angina and acute MI
- patho: coronary blood flow reduced but not fully occluded -> ischemia -> reduced contraction -> reduced output
- results in injured myocardial cells
- caused by:
- --plaque rupture -> blood clot
- --CA spasm
- --progressive CA obstruction
- --CA inflammation
- --increased O2 demand/decreased O2 supply (blood loss, anemia)
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ACS manifestations
- chest pain - substernal or epigastric that lasts longer than 10-20 minutes
- more severe and prolonged than angina
- dyspnea, diaphoresis, pallor, cool skin, tachycardia, hypotension (r/t decreased CO)
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ACS dx
- CK/CK-MB - WNL or transient elevation
- troponin - elevated (myocardial damage)
- EKG - changes in cardiac conduction
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ACS meds
- goal: reduce ischemia, reduce risk of clotting
- fibrinolytics - clot busters (rarely used)
- nitrates
- beta blockers
- aspirin, Plavix (antiplatelet) - bleeding/hemorrhage (bruising, petechiae, purpura, occult bleeding)
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revascularization
- restore blood flow and O2 to ischemic tissue
- nonsurgical:
- --PTCA
- --intracoronary stents
- surgical:
- CABG
-
PTCA
- percutaneous transluminal coronary angioplasty
- treats stable angina unrelieved by meds, unstable angina, acute MI, LCA stenosis, CABG stenosis
- arterial catheter guided into coronary artery
- guide wire threaded through catheter
- balloon threaded over guide wire and inflated for 30 sec to 2 mins
- compresses plaque against arterial wall, reduces occlusion
-
intracoronary stent
- cardiac cath procedure
- usually done with PTCA
- metallic stent is placed over balloon and threaded over guide wire
- after balloon inflation/removal, stent is left in artery
- Plavix for 1 year after procedure
- risk for clotting, bleeding
- monitor BP, chest pain, hemorrhage
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CABG
- coronary artery bypass graft
- surgery that uses a section of a vessel to create a bypass from aorta to coronary artery
- bypasses area of obstruction
- open heart surgery
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MIDCAB
minimally invasive coronary artery bypass
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TMLR
transmyocardial laser revascularization
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acute myocardial infarction
- necrosis of myocardial cells
- loss of function -> reduced cardiac output -> cardiogenic shock
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MI patho
- usually caused by unstable lesions that rupture -> thrombus formation
- complete blockage of blood flow -> prolonged tissue ischemia -> irreversible cell damage (> 20-45 mins)
- cellular acidosis, electrolyte imbalances, hormones -> conduction changes -> decreased contractility -> decreased SV, CO, BP, tissue perfusion
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MI manifestations
- severe, crushing chest pain - sudden onset, unrelieved by rest or nitro
- women/elderly: atypical chest pain - indigestion, heartburn, nausea, vomiting
- SNS stimulation: anxiety, tachycardia, cool, clammy skin (vasoconstriction)
- tachypnea
-
MI complications
- dysrhythmias - most frequent complication
- pump failure - reduced cardiac contractility, ventricular wall motion, compliance -> heart failure
- cardiogenic shock - impaired tissue perfusion r/t pump failure
- infarct extension and expansion - continued myocardial necrosis
- structural defects - aneurysms, valve defects
- pericarditis - r/t inflammatory response s/t tissue death
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MI dx
- serum cardiac markers - ordered on admission + 3 days
- --CK - 4-6 hours after MI
- --CK-MB > 5% = MI
- --troponin
- CBC - elevated WBC
- ESR - inflammation
- ABGs
- EKG - conduction changes
- Echo - eval cardiac wall motion and LV function (decreased contraction)
- hemodynamic monitoring
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MI meds
- NOMA
- nitro/O2/morphine/asa
- fibrinolytics
- antidysrhythmics
- beta-blockers
- ACE inhibitors
-
MI tx
- bedrest 12 hours
- gradual increase in activity
- quiet environment
- cardiac diet
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