CAD & ACS & CHF

Question 1

Risk Factors of CAD

Answer 1

NM: age, gender, ethnicity, family HX, genetic
M: hyperlipidemia, HTN, Tobacco use, physical inactivity, obesity

Question 2

CAD: contributing factors

Answer 2

Elevated homocysteine levels
- Breakdown of AA
DM
Metabolic syndrome
- Increased waist circ
- HTN
- abnormal serum lipids
- elevated fasting glucose
Stress
Substance abuse

Question 3

Angina

Answer 3

Clinical manifestation of REVERSIBLE myocardial ischemia

Question 4

MI (Myocardial infarction)

Answer 4

IRREVERSIBLE necrosis caused by abrupt decrease or cessation of coronary blood flow

Question 5

Assessment of chest pain

Answer 5

location
duration
quality
radiation
precipating factor
medication relief
EKG changes

Question 6

Gender differences in cardiac disorders

Answer 6

Prodromal symtoms
women:
-fatigue, SOB, indigestion, anxiety

Question 7

Core measures: ACS

Answer 7

ST elevation or new BBB
- thrombolytic ( clot busting drugs) within 30 mins of hospital arrival
- PCI within 45-90 mins of hospital arrival
ASA within 24-hours of hospital arrival
Admission to CCU within 30 mins after initial EKG (STEMI)
smoking cessation education
Discharge RX
- B-Blockers
- ACE1/ARB for EF less than 40%
- ASA
Cardiac Phase I activity standards

Question 8

Medical management of UA or NSTEMI w/ negative markers & on-going angina

Answer 8

-ASA
-heparin (IV or LMWH)
- glycoprotein inhibitor (Integrillin)
- Angio w/ PCI when stable

Question 9

Medical management of STEMI or NSTEMI w/ positive markers

Answer 9

reperfusion therapy
- emergent PCI
- Fibrinolytic therapy
- Surgical revascularization

Question 10

Creatine Kinase (total CK)

Answer 10

used to support Dx of myocardial injury, neurologic or skeletal muscle disease
levels rise 6-hours after injury, peak 18-hours, normalize in 2-3 days

Question 11

Isoenzymes

Answer 11

CK-MM 100% (all circulating CK, muscle injury)
CK-MB 0% (specific for cardiac cells)
- usually do NOT rise with angina, PE, CHF
- Rise 3-6 hours, peak 12- 24 hours, normalize 12- 48 hours
- quantify degree of MI & timing of onset
Shock, malignant hyperthermia, myopathy, myocarditis
- rise in unstable angina signifies increased risk of MI
Determine appropriateness of thrombylotic therapy

Question 12

Troponins

Answer 12

Specific indicator of cardiac injury
determines if chest pain is caused by cardiac ischemia
helps predict risk of future events
- elevate sooner & remain elevated longer ( 7-14 days)
Diagnosis MI

Troponin T: less than .2 ng/ml
Troponin I: less than .3 ng/ml

Question 13

Medical management of CAD/Angina

Answer 13

Restoration of blood supply
Precutaneous coronary intervention

Question 14

Nursing management of CAD

Answer 14

modifiable risk factor reduction

Question 15

Sex activity CAD

Answer 15

7-10 days without complications

Question 16

Complications of AMI/ACS

Answer 16

Dysrhythmias
cariogenic shock
papillary muscle dysfunction or rupture
pericarditis (pericardial friction rub)
- Dressler syndrome= pericarditis + effusion + fever
Venticular aneurysm
- thrombi= lead to stroke
Ventricular rupture

Question 17

Pathophysiology of HF

Answer 17

Ventricular dilation
Increased SNS stimulation
Stimulation RAAS
De-compensated HF
- Pulmonary edema

Question 18

Left-ventricular Failure

Answer 18

Back-up to LA into pulmonary veins leads to increased pulmonary pressure leads to pulmonary congestion, pulmonary edema

Question 19

Right-ventricular failure

Answer 19

back up to RA & venous circulation leads to systemic congestion leads to Jugular vein distention, hepatomegaly, splenomegaly, GI vascular congestion, Peripheral edema

Question 20

Complication of HF

Answer 20

Pleural effusion
Dysrhythmias
LV thrombus
Hepatomegaly
Renal failure

Question 21

Diagnostics of HF

Answer 21

ANP/BNP
Echocardigram
Doppler flow
Chest X-Ray
EKG
ABG analysis
Liver enzymes
BUN/Cr

Question 22

Atrial natriuretic peptide (ANP)

Answer 22

22-77pg/ml
Synthesized in cardiac muscle

Question 23

Brain natriuretic peptide (BNP)

Answer 23

100 less pg/mL
main source cardiac ventricle
d/t atrial / ventricular stretch causing
- vaso-relaxation
- inhibition of adrenal aldosterone secretion
- inhibition of RAAS
Implications of HTN, CHF, Atherosclerosis

Ventricular peptide

Question 24

Management of HF

Answer 24

Improve ventricular (pump) performance
Reduce workload
Reduce fluid retention
Reduce stress & risk of injury

Medications
- diuretics
- vasodilators
- Morphine
- Positive Inotropes
- digoxin (LV function)
- loading dose; not for initial treatment
Surgical:
- transplantation

Question 25

Nursing management of HF

Answer 25

Interventions to address:
- Activity intolerance
- Decreased CO
- Excess fluid volume (fluid restriction)
- Fatigue
- Impaired gas ex
- Ineffective health maintenence
- Fear

Question 26

Functional Classification of Heart Disease

Answer 26

Class I
- no limit of physical act
Class II
- Slight limitation of physical activity, no symptoms at rest, ordinary physical activity results in fatigue, dyspnea, palpations, or angina
Class III
- Limits of physical act, comfortable at rest. Ordinary physical activity causes fatigue, dyspnea, palpations, or angina
Class IIII
- Inability to carry on any physical activity w/o discomfort. symptoms of cardiac insufficiency or of angina may be present even at rest. If any physical activity is undertaken, discomfort is increased

Question 27

Mitral valve prolapse

Answer 27

Physio
- Valve leaflet prolapse or “buckle” back into LA during systole
- Usually benign

Manifestation
-Palpitations d/t dysrhythmias
- PVCs, PSVT, VT
- +/- chest pain
- Prophylactic antibiotics

Question 28

Mitral stenosis

Answer 28

adult causes from rheumatic heart disease

obstruction
increase left atrial pressure and volume
hypertrophy of pulmonary vessels
chronic LA pressure elevation

Physio
Increase in LA pressure/volume
Increased pulmonary pressure
Hypertrophy of pulmonary vessels

Manifest
Exceptional dyspnea
Fatigue
Palpitations (AFib)
Hoarseness
- LA pressing on laryngeal nerve
Chest pain
Seizure/stroke

Question 29

Mitral regurgitation

Answer 29

Causes
MI
Chronic rheumatic heart disease
Mitral valve prolapse
Ischemic papillary muscle dysfunction
Infective endocarditis

Physiology
Incomplete valve closure during systole
Blood flows backward from LV to LA

LV & LA work harder to maintain C.O. (Chronic)
LA enlargement
LV hypertrophy
Decrease in C.O.

Symptoms
Weakness
Fatigue
Palpitations
Dyspnea gradually progresses to
Orthopnea
Paroxysmal nocturnal dyspnea
Peripheral edema

ACUTE manifestations
Thready pulses
Cool, clammy extremities
Low C.O. may mask murmu

Sudden – Pulmonary edema & cardiogenic shock
CHRONIC manifestations
May be asymptomatic for years until development of some degree of LV failure
Weakness / fatigue
Palpitations
Progressive dyspnea

Question 30

Aortic stenosis

Answer 30

Congenital: Usually childhood, adolescence, or young adulthood
Later in life usually
Rheumatic fever
Fusion of commissures
Calcification of leaflets (Stiffness, retraction)
Accompanied by MV disease
Senile fibrocalcific degeneration of normal valve
Isolated AS almost always non-rheumatic
Obstruction of flow from LV to aorta during systole
Reduced C.O. – decreased tissue perfusion
Pulmonary HTN – Heart failure

Effect
LV hypertrophy
↑ myocardial oxygen consumption d/t ↑ mass
↓ CO & pulmonary HTN
Clinical manifestations
Angina
Syncope
Exertional dyspnea
Triad = LV failure
Poor prognosis
Symptoms
Obstruction not relieved
Nitroglycerin contraindicated**
Reduces preload

Question 31

Aortic stenosis

Answer 31

Congenital: Usually childhood, adolescence, or young adulthood
Later in life usually
Rheumatic fever
Fusion of commissures
Calcification of leaflets (Stiffness, retraction)
Accompanied by MV disease
Senile fibrocalcific degeneration of normal valve
Isolated AS almost always non-rheumatic
Obstruction of flow from LV to aorta during systole
Reduced C.O. – decreased tissue perfusion
Pulmonary HTN – Heart failure

Effect
LV hypertrophy
↑ myocardial oxygen consumption d/t ↑ mass
↓ CO & pulmonary HTN
Clinical manifestations
Angina
Syncope
Exertional dyspnea
Triad = LV failure
Poor prognosis
Symptoms
Obstruction not relieved
Nitroglycerin contraindicated**
Reduces preload

Question 32

Aortic regurgitation

Answer 32

May result from disease of aortic valve leaflets, aortic root, or both
Caused by
Infective endocarditis
Trauma
Aortic dissection

Chronic AR results from
Rheumatic heart disease
Congenital bicuspid aortic valve
Syphilis
Chronic rheumatic heart conditions

Acute manifestations
Sudden manifestations of CV collapse
Severe dyspnea & chest pain
Hypotension
LV failure
Cardiogenic shock
Chronic manifestations
May be asymptomatic for years
Progressive exertional dyspnea
“Water-hammer” pulse
A strong quick beat that collapses immediately

Physiology
Retrograde blood flow from ascending aorta to left ventricle
Results in volume overload
Left ventricle compensates by dilation & hypertrophy
Myocardial contractility eventually declines
Pulmonary hypertension & right ventricular failure develop

Clinical manifestations of sudden cardiovascular collapse
Left ventricle exposed to aortic pressure during diastole
Sudden weakness
Severe dyspnea
Chest pain
Hypotension
Constitutes a medical emergency

Question 33

Classification of Murmurs

Answer 33

Timing
Shape
Location
Radiation
Intensity
Pitch Quality

Grade 1 – Very faint
Grade 2 – Soft
Grade 3 – Heard all over the precordium
Grade 4 – Loud, with palpable “thrill”
Grade 5 – Very loud, with palpable “thrill”
May be heard with stethoscope partially off chest
Grade 6 – Very loud, with thrill
May be heard with stethoscope entirely off chest

Question 34

Diagnostic studies

Answer 34

History & physical exam
Chest x-ray
ECG
Cardiac catheterization

Echocardiogram & Doppler flow studies
Evaluation of cardiac wall motion (function)
Detect valvular heart disease
Stress testing
Identify / quantify pericardial fluid
Color doppler imaging demonstates direction & velocity of blood flow
TEE: Trans-esophageal echocardiography
Patent ductus arteriosus (PDA)

Question 35

Drug therapy

Answer 35

Digoxin (positive inotrope)
Vasodilators
Diuretics
-Blockers
Other drug therapies
Anti-coagulants
Anti-arrythmics
Low-sodium diet

Question 36

Nursing Assessment

Answer 36

Objective data
Abnormal heart sounds
Tachycardia
Dysrhythmias
Hypotension
Hepatomegaly
Diaphoresis
Peripheral edema
Ascites
Crackles, wheezes, hoarseness