Cardiac--CAD, ACS, CHF Flashcards
how does blood flow through the heart
inferior vena cava to right atrium through the tricuspid valve to the right ventricle to the pulmonary artery to the lungs to the pulmonary vein to the left atrium through the bicuspid valve to the left ventricle to the aortic valve to the aorta and out to the body through the…right subclavian, common carotid, and left subclavian artery
risk factors for CAD
gender differences:
non-modifiable: age, gender (male), ethnicity, family hx, genetic
modifiable: elevated homocysteine levels, metabolic syndrome, stress, substance abuse
gender differences: prodromal symptoms: early manifestations: women: fatigue, SOB, indigestion, anxiety
angina vs. mi
angina is reversible ischemia (coronary ischemia)
mi is IRREVERSIBLE necrosis caused by abrupt disease of a cessation of coronary blood flow
types of angina
stable angina (predictable and FIXED lesions)
unstable angina (more intense, occurs during rest)
variant angina (coronary artery spasm)
silent ischemia (EKG evidence but patient reports no symptoms)
Assessing chest pain
location, duration, quality, radiation, precipitating factors, medication relief, EKG changes
Core measures for ACS
ST elevation or new BBB: thrombolytic within 30 minutes of hospital arrival
PCI within 45 to 90 minutes of hospital arrival
Aspirin given immediately (WHY? to thin blood so no clots form)
STEMI: admission to CCU within 30 mins after initial EKG
smoking cessation education
discharge Rx after event
unless contraindicated: one of these plus aspirin
beta blocker
ACE inhibitor & ARBs (both for EF of <40%)
Aspirin
Cardiac phase I activity standards
Medical Management
UA, NSTEMI, STEMI
UA or NSTEMI with negative markers and ongoing angina:
aspirin
heparin
glycoprotien inhibitors (WHY?)
angina with PCI–if pt. is stable
STEMI OR NSTEMI with positive markers:
reperfusion therapy
emergency PCI
fibrinolytic therapy
surgical revascularization
Medical Management
CAD and Angina
restoration of blood supply
PCI
PCA (balloon angioplasty)
directional coronary atherectomy
intra-coronary stents
laser ablation
trans myocardial revascularization
address modifiable risk factors
sex activity after a cardiac event
stable patients can resume within 7-10 days
according to AHA, if they can engage in moderately vigorous activity (walking up stairs), they are generally healthy enough for sex)
Complications of AMI and ACS
dysrhythmias, cardiogenic shock, dysfunction/rupture of papillary muscles
pericarditis (pericardial friction rub)
Dressler syndrome (pericarditis, effusion, and fever)
ventricular aneurysm (may harbor thrombi and lead to stroke
ventricular rupture
CABG
bypassing blocked artery
traditional: stereotomy incision, coronary-pulmonary bypass
Isoenzymes and Ck-Mb
looking at them can support a dx of myocardial injury, neurologic or skeletal disease. Levels rise 6 h after injury, peak at 18 hours, and normalize in 2-3 days
ck-mm 100% (all circulating ckm muscle injury)
ck-mb (cardiac specific) (usually do NOT rise with angina, PE, and CHF)
rise 3-6 hours, peak 12-24 hours, normalize 12 (24?) -48 hours
quanitfy degree of MI timing and onset
ck-bb=0% (brain, lung)
Pathophysiology of HF
ventricular dilation (less blood flow)
increased sympathetic nervous system stimulation
stimulation of RAAS
decompensated heart failure (pulmonary edema)
troponins
Specific indicator of cardiac injury
Determines if chest pain is caused by cardiac ischemia
Helps predict risk of future events
Nearly always normal in non-cardiac diseases
Elevate sooner (3-hours) & remain elevated longer (7 – 14 days) than CK-MB
Troponin T: < 0.2 ng/mL
Troponin I: < 0.03 ng/mL
clinical manifestations of heart failure
left ventricular failure:
back up into LA into pulmonary veins leads to increased pressure pulmonary efema which leads to pulmonary congestion and edema
right ventricular failure:
back up to RA and venous circulation leads to systemic congestion which leads to JVD, hepatomegaly, splenomegaly, GI vascular congestion, peripheral edema
diagnostics for HF
ANP and BNP, echocardiogram, doppler flow, chest X ray, EKG, ABG analysis, liver enzymes, BUN and creatinine
Natriuretic peptides
Neuroendocrine peptides used to identify & stratify patients with CHF
Atrial natriuretic peptide (ANP)
22 – 77 pg / mL
Synthesized in atrial cardiac muscle
Brain natriuretic peptide (BNP)
< 100 pg / mL
Main source cardiac ventricle
Continuously released d/t atrial / ventricular stretch causing: Vaso-relaxation, Inhibition of adrenal aldosterone secretion, Inhibition of renal renin secretion, Natriuresis & reduction of blood volume
Rate increased by hemodynamic load, regulation of preload & afterload
Implicated in HTN, CHF, Atherosclerosis
Natriuretic peptides part two
BNP: good marker for CHF, correlates well with left ventricular pressures
differential diagnosis of SOB: higher levels: severity of CHF
dyspena with elevated BNP: CHF
dyspena with normal BNP: pulmonary origin
**if BNP remains elevated with TX: increased risk of mortality
management of HF
What do you address?
HF: improve ventricular performance
reduce workload, fluid retention, stress and risk of injury
medications: diuretics, vasodilators, morphine,
digoxin
address: activity intolerance, decreased CO, excess fluid volume (fluid restriction), fatigue, impaired gas exchange, ineffective health maintenance, fear
valvular heart disease
stenosis: value or orifice restricted (forward flow impaired)
pressure gradient is created across valve (gradient differences are related to the degree of stenosis)
regurgitation: incomplete closure of the valve leaflets which results in backward blood flow
mitral valve prolapse: valve leaflets prolapse “buckle back” in LA during systole. usually benign, but manifestations include palpitations d/t dysrhythmias–PVCs, PSVT, VT, + or - chest pain
prophylactic antibiotics
mitral stenosis
caused mostly by rheumatic heart disease
scarring of leaflets and chordae tendineae
contractures and adhesions between commissures
obstruction, increased left arterial pressure and volume, hypertrophy of pulmonary vessels.
physiology: increase in LA pressure and workload, increased pulmonary pressure, hypertrophy of pulmonary vessels
manifestations include: exertional dyspena, fatigue, palpitations, hoarseness, chest pain, seizure, stroke (slide 38 has more)
mitral regurgitation
causes: MI, chronic rheumatic heart disease, mitral valve prolapse, ischemia papillary muscle dysfunction, infective endocarditis
physiology: incomplete valve closure during systole, blood flows backward from LA to LV, causing LA and LV to work harder to maintain CO, LA enlargement, LV hypertrophy, DECEASED CO
Acute sx/sx: thready pulses, cool/clammy extremities, low CO may mask murmur
**pulmonary edema and cardiogenic shock
Chronic: sx/sx: weakness, fatigue, palpitations, dyspnea, orthopnea, paroxysmal nocturnal dyspnea leading to peripheral edema
Aortic stenosis
**NITROGLYCERIN IS CONTRAINDICATED
congenital, isolated, non-rheumatic
obstruction of flow from LV to aorta during systole, leading to reduced CO and decreased tissue perfusion leading to pulmonary HTN –> HF
effects: LV hypertrophy, increased myocardial o2 consumption d/t increased mass, decreased CO and pulmonary HTN.
clinical manifestations: angina, syncope, exertional dyspnea
