Coronary Heart Disease

• located in mediastinum of thoracic cavity between vertebral column and sternum
• flanked by lungs

• protects and anchors, prevents overfilling
• fibrous: outer layer
• parietal: middle fluid layer
• visceral: inner layer

• epicardium: covers entire heart and great vessels
• myocardium: middle layer, cardiac muscles
• endocardium: lines chambers and vessels

• two upper atria
• two lower ventricles

SVC/IVC (DOB) > RA > tricuspid > RV > pulmonary valve > pulmonary artery > lungs (DOB<->OB) > pulmonary veins > LA > mitral > LV > aortic valve > aorta (OB)

• 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

• closure of semilunar valves (pulmonary and aortic)
• onset of ventricular diastole
• blood falls down from pulm artery and aortic arch d/t gravity

• left side of heart, aorta, capillaries, venous system, vena cava
• high pressure system
• supplies blood to body tissues

• right side of heart, pulmonary artery, lungs, pulmonary veins
• low pressure system

L and R coronary arteries from base of aorta encircle myocardium

• contraction and relaxation of the heart (a heart beat)
• ventricular filling -> ventricular systole (contraction) -> ventricular diastole (relaxation)
• 70-80 times per minute

• amount of blood pumped in one cardiac cycle
• 60-100mL
• how strong the heart is contracting

• SV / end diastolic volume (amount of blood in ventricle at diastole)
• normal 50-60%

• 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

• 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)

• strength of contraction of individual cardiac fibers
• aka inotropy
• poor contractility -> decreased CO

• 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

• 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

• several masses of nerve tissue
• controls rate, rhythm, force of HB
• SA -> AV -> Bundle of His -> Purkinje fibers

• 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

• 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

• 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

• 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

• low density lipoproteins
• bad cholesterol
• carry cholesterol from liver to peripheral tissues

• high density lipoproteins
• carry cholesterol from peripheral tissues to liver

• 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

• group of metabolic risk factors
• truncal obesity
• hyperlipidemia
• HTN
• elevated BGL
• clotting
• inflammation
• insulin resistance

• 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

• quit smoking
• change diet: low cholesterol, healthy fats, veggies, fiber
• exercise
• manage HTN and DM

• statins
• bile acid sequestrants
• nicotinic acid
• fibrates
• low dose aspirin
• ACE/ARBs

• lower LDL by inhibiting a liver enzyme
• monitor LFTs
• s/e: muscle pain, tenderness, brown urine (myopathy - muscle breakdown)

• lower LDL by binding bile acids in intestine (prevent reabsorption)
• s/e: GI upset

• lowers LDL, total cholesterol, and triglyceride levels
• s/e: flushing, increased HR

lower serum triglyceride levels

• diet and exercise
• vitamins
• omega 3

• imbalanced nutrition (more) r/t obesity
• ineffective health maintenance r/t risk factors

• 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

• lack of O2 causes temporary, reversible myocardial ischemia
• reduced O2 causes anaerobic metabolism -> lactic acid buildup -> pain
• three types:
• --stable
• --unstable
• --Prinzmetal

• predictable r/t increased cardiac workload s/t physical exertion, stress, cold
• relieved by rest and nitrates

• aka variant angina
• chest pain at night, unrelated to activity
• caused by vasospasm
• tx: calcium channel blockers

• unpredictable
• increasing frequency, severity, duration
• occurs with stress or at rest
• risk for MI

• 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

• 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

• goal: reduce O2 demand and increase O2 supply
• nitrates
• beta blockers
• calcium channel blockers
• aspirin

• 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

• 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

• 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

• prophylaxis
• reduce risk of platelet aggregation and thrombus formation
• prevents clots -> MI

ineffective tissue perfusion, cardiac r/t impaired cardiac blood flow

• 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)

• 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)

• CK/CK-MB - WNL or transient elevation
• troponin - elevated (myocardial damage)
• EKG - changes in cardiac conduction

• 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)

• restore blood flow and O2 to ischemic tissue
• nonsurgical:
• --PTCA
• --intracoronary stents
• surgical:
• CABG

• 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

• 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

• 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

minimally invasive coronary artery bypass

transmyocardial laser revascularization

• necrosis of myocardial cells
• loss of function -> reduced cardiac output -> cardiogenic shock

• 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

• 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

• 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

• 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

• NOMA
• nitro/O2/morphine/asa
• fibrinolytics
• antidysrhythmics
• beta-blockers
• ACE inhibitors

• bedrest 12 hours
• gradual increase in activity
• quiet environment
• cardiac diet