CAD & ACS & CHF Flashcards
Risk Factors of CAD
NM: age, gender, ethnicity, family HX, genetic
M: hyperlipidemia, HTN, Tobacco use, physical inactivity, obesity
CAD: contributing factors
Elevated homocysteine levels
- Breakdown of AA
DM
Metabolic syndrome
- Increased waist circ
- HTN
- abnormal serum lipids
- elevated fasting glucose
Stress
Substance abuse
Angina
Clinical manifestation of REVERSIBLE myocardial ischemia
MI (Myocardial infarction)
IRREVERSIBLE necrosis caused by abrupt decrease or cessation of coronary blood flow
Assessment of chest pain
location
duration
quality
radiation
precipating factor
medication relief
EKG changes
Gender differences in cardiac disorders
Prodromal symtoms
women:
-fatigue, SOB, indigestion, anxiety
Core measures: ACS
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
Medical management of UA or NSTEMI w/ negative markers & on-going angina
-ASA
-heparin (IV or LMWH)
- glycoprotein inhibitor (Integrillin)
- Angio w/ PCI when stable
Medical management of STEMI or NSTEMI w/ positive markers
reperfusion therapy
- emergent PCI
- Fibrinolytic therapy
- Surgical revascularization
Creatine Kinase (total CK)
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
Isoenzymes
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
Troponins
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
Medical management of CAD/Angina
Restoration of blood supply
Precutaneous coronary intervention
Nursing management of CAD
modifiable risk factor reduction
Sex activity CAD
7-10 days without complications
Complications of AMI/ACS
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
Pathophysiology of HF
Ventricular dilation
Increased SNS stimulation
Stimulation RAAS
De-compensated HF
- Pulmonary edema
Left-ventricular Failure
Back-up to LA into pulmonary veins leads to increased pulmonary pressure leads to pulmonary congestion, pulmonary edema
Right-ventricular failure
back up to RA & venous circulation leads to systemic congestion leads to Jugular vein distention, hepatomegaly, splenomegaly, GI vascular congestion, Peripheral edema
Complication of HF
Pleural effusion
Dysrhythmias
LV thrombus
Hepatomegaly
Renal failure
Diagnostics of HF
ANP/BNP
Echocardigram
Doppler flow
Chest X-Ray
EKG
ABG analysis
Liver enzymes
BUN/Cr
Atrial natriuretic peptide (ANP)
22-77pg/ml
Synthesized in cardiac muscle
Brain natriuretic peptide (BNP)
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
Management of HF
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
Nursing management of HF
Interventions to address:
- Activity intolerance
- Decreased CO
- Excess fluid volume (fluid restriction)
- Fatigue
- Impaired gas ex
- Ineffective health maintenence
- Fear
Functional Classification of Heart Disease
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
Mitral valve prolapse
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
Mitral stenosis
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
Mitral regurgitation
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
Aortic stenosis
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
Aortic stenosis
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
Aortic regurgitation
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
Classification of Murmurs
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
Diagnostic studies
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)
Drug therapy
Digoxin (positive inotrope)
Vasodilators
Diuretics
-Blockers
Other drug therapies
Anti-coagulants
Anti-arrythmics
Low-sodium diet
Nursing Assessment
Objective data
Abnormal heart sounds
Tachycardia
Dysrhythmias
Hypotension
Hepatomegaly
Diaphoresis
Peripheral edema
Ascites
Crackles, wheezes, hoarseness
