Cardiac--CAD, ACS, CHF

Question 1

how does blood flow through the heart

Answer 1

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

Question 2

risk factors for CAD

gender differences:

Answer 2

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

Question 3

angina vs. mi

Answer 3

angina is reversible ischemia (coronary ischemia)
mi is IRREVERSIBLE necrosis caused by abrupt disease of a cessation of coronary blood flow

Question 4

types of angina

Answer 4

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)

Question 5

Assessing chest pain

Answer 5

location, duration, quality, radiation, precipitating factors, medication relief, EKG changes

Question 6

Core measures for ACS

Answer 6

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

Question 7

discharge Rx after event

Answer 7

unless contraindicated: one of these plus aspirin
beta blocker
ACE inhibitor & ARBs (both for EF of <40%)
Aspirin

Cardiac phase I activity standards

Question 8

Medical Management

UA, NSTEMI, STEMI

Answer 8

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

Question 9

Medical Management

CAD and Angina

Answer 9

restoration of blood supply
PCI
PCA (balloon angioplasty)
directional coronary atherectomy
intra-coronary stents
laser ablation
trans myocardial revascularization

address modifiable risk factors

Question 10

sex activity after a cardiac event

Answer 10

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)

Question 11

Complications of AMI and ACS

Answer 11

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

Question 12

CABG

Answer 12

bypassing blocked artery
traditional: stereotomy incision, coronary-pulmonary bypass

Question 13

Isoenzymes and Ck-Mb

Answer 13

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)

Question 14

Pathophysiology of HF

Answer 14

ventricular dilation (less blood flow)
increased sympathetic nervous system stimulation
stimulation of RAAS
decompensated heart failure (pulmonary edema)

Question 15

troponins

Answer 15

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

Question 16

clinical manifestations of heart failure

Answer 16

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

Question 17

diagnostics for HF

Answer 17

ANP and BNP, echocardiogram, doppler flow, chest X ray, EKG, ABG analysis, liver enzymes, BUN and creatinine

Question 18

Natriuretic peptides

Answer 18

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

Question 19

Natriuretic peptides part two

Answer 19

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

Question 20

management of HF

What do you address?

Answer 20

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

Question 21

valvular heart disease

Answer 21

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

Question 22

mitral stenosis

Answer 22

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)

Question 23

mitral regurgitation

Answer 23

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

Question 24

Aortic stenosis
**NITROGLYCERIN IS CONTRAINDICATED

Answer 24

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

Question 25

Aortic Regurgitation

Answer 25

may result from disease of aortic valve leaflets, aortic root, or both.
causes: infective endocarditis, trauma, aortic dissection

chronic causes: rheumatic heart disease, congenital bicuspid aortic valve, syphilis, chronic rheumatic heart conditions

physiology: retrograde blood flow from ascending aorta to left ventricle (volume overload)–> left ventricle compensates by dilation and hypertrophy, myocardial contractility eventually declines, and pulmonary hypertension and right ventricular failure develop

acute manifestations: sudden manifestations of CV collapse, severe dyspnea and chest pain, hypotension (LV failure, cardiogenic shock)

chronic manifestations: may be asymptomatic for years, but progressive exertional dyspnea, “water hammer” pulse (strong, quick, but collapses immediately)

Question 26

clinical manifestations of sudden CV collapse

Answer 26

left ventricle is exposed to aortic pressure during diastole

sx/sx: sudden weakness, severe dyspnea, chest pain, hypotension
MEDICAL EMERGENCY

Question 27

collaborative care

Answer 27

prevention: exacerbations of HF, pulmonary edema, thromboembolism, recurrent endocarditis

Tx depends of valve involved and severity of disease

Question 28

amurmurs

Answer 28

timing, shape, location, radiation, intensity, pitch quality
grade 1 (very soft) to grade 6 (hear it with stethoscope off

diagnostics: H+P, chest X ray, ECG, cardiac cath, doppler, imaging, stress test, direct valvular heart disease, identify and quantify pericardial fluid

drug therapy: digoxin, vasodilators, diuretics, beta blockers, anti-coagulants, low sodium diet

collaborative care: valve repair or replacement

Question 29

assessment

Answer 29

abnormal heart sounds, tachycardia, dysrhythmias, hypotension, hepatomegaly, diaphoresis, peripheral edema, ascites, crackles, wheezes, hoarseness