Coronary Artery Disease
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Transcript Coronary Artery Disease
Oxygen Needs
Interference
with
O2 Transport
Case Study
Oxygen Needs
Interference with O2 Transport
Coronary Artery Disease
Complications
Dysrhythmias
Pulmonary Embolism
Hypertension
Complication
Congestive Heart Failure
Peripheral Vascular / Arterial Disease
Oxygen Needs
Interference with O2 Transport
Care of Patients with:
Coronary Artery Disease
Risk Factors
Myocardial Infarction
Alterations in:
Rate & Rhythm (Cardiac Conduction)
Effect on Cardiac Output
Content Approach
Anatomy & Physiology Review
Demographics/occurrence
Pathophysiology
Clinical Manifestation
Medical / Surgical Management
Nursing Process (APIE)
Assessment - Nursing Actions - Education
Anatomy & Physiology
Right Heart
Left Heart
Systole
Valve Closure:
Diastole
Valve Closure:
Cardiac Circulation
Myocardium
Anterior
Posterior
Cardiac Cycle
1. Passive Filling – preload
2. Atrial contraction – Aortic & Pulmonic semilunar
valves close – S2
3. Isovolumetric ventricular contraction – all
valves closed
4. Ejection – ventricular systole – Mitral & Tricuspid
valves close – S1 - afterload
5. Isovolumetric ventricular relaxation – all valves
closed
Cardiac Cycle Phases
Heart Sounds & Stethoscope
Placement
Coronary Arterial System
Physiology: Oxygen Supply
to the Cardiac Muscle during
the Cardiac Cycle
Coronary artery oxygen deficit
during ventricular contraction & ejection (systole)
Coronary artery filling
during ventricular filling (diastole)
What is the impact of heart rate on coronary artery filling?
Oxygen Supply to the Cardiac Muscle
during the Cardiac Cycle
The actual time available for diastole shortens significantly as the heart rate
increase
% of a Minute
70%
50%
33%
Heart Rate
60
120
188
Results: Less time for ventricular filling & coronary artery filling + as HR
increases, increased oxygen is needed each minute to eject the same volume of
blood.
Stroke volume: volume ejected in one heart beat
Cardiac Output: volume ejected in one minute
Cardiac Output = Stroke Volume x Heart Rate
Factors
Determining Myocardial Oxygen Needs
Decreased Oxygen Supply:
Noncardiac: Anemia, hypoxemia, pneumonia, asthma, COPD, low blood
volume
Cardiac: Arrhythmias/dysrhythmias, congestive heart failure (CHF), coronary
artery spasm, coronary artery thrombosis, valve disorders
Increased Oxygen Demand or Consumption:
Noncardiac: anxiety, cocaine use, hypertension, hyperthermia,
hyperthyroidism, physical exertion
Cardiac: aortic stenosis, arrhythmias, cardiomyopathy, hypertension,
tachycardia
CAD - Demographics
CAD - Demographics
Comparison of death by CV Disease and
Breast Cancer – by Women’s Age
400
300
Cardiovascular
Disease
Breast Cancer
200
100
0
35-54
55-74
>=75
Coronary Artery Disease (CAD)
Pathophysiology
ASHD, IHD, CVHD = CAD
AHA
1.1 mil Americans will have an MI in 2003
460,000 will die
About half of those deaths occur within 1 hour of the start of
symptoms and before the person reaches the hospital.
Major cause: Atherosclerosis—focal deposit of
cholesterol & lipids
CAD – Risk Factors
Unmodifiable: Age, Gender, Ethnicity, Genetic
predisposition/family history
Modifiable Major: Dyslipidemia--Elevated serum
lipids*, hypertension*, cigarette smoking, obesity—
visceral/central obesity
Modifiable Contributing: Diabetes Mellitus*,
stressful lifestyle
* may have genetic predisposition
CAD – Risk Factors
• Metabolic Syndrome:
–
–
–
–
–
–
Insulin Resistance
Hyperglycemia >110mg/dL
Hypertension - > 130/85
Increased triglycerides >110mg/dL
Decrease HDL <40 men; < 50 women
Central Obesity
• men: waist > 40” women: waist > 35”
Risk Factors
One of the Major Modifiable
Physical Inactivity
Types of Plasma Lipoproteins
HDL –
Contain more protein and less lipid
Carry lipids away from arteries to liver for metabolism
This process prevents lipid accumulation within arterial walls
Higher levels are desirable
LDL –
Contain more lipids than any other lipoproteins
Affinity for arterial walls
Increased levels correlate closely with an increased
incidence of atherosclerosis
Lower levels are desirable
VLDL
Contain of triglycerides
Correlation with heart disease is uncertain
Plasma Lipoproteins
Atherosclerosis
Elevated serum lipids
Cholesterol > 200mg/dl
Triglyceride > 200mg/dl
HDL
< 35 mg/dl – major risk
45-59 mg/dl – average risk
> 60 mg/dl – negative risk
LDL
< 130 – desirable
130 – 159 mg/dl – borderline risk
> 160 mg/dl – high risk
Progressive Atherosclerosis
Drug Therapy for Dyslipidemia
Bile Acid Sequestrants (Questran) - Binds with bile salts
Niacin - Inhibits synthesis of VLDL & LDL
Fibric Acid Derivatives (Atromid)– Decrease VLDL
HMG CoA Reductase Inhibitors (Statins - Lipitor, Pravachol,
Zocor) – Block synthesis of cholesterol
Cholesterol Absorption Inhibitor (Zetia)– Inhibits intestinal
absorption of cholesterol
Natural Lipid Lowering Agents
Niacin - < LDL levels
Omega-3 fatty acids – fish/flaxseed oil <Triglycerides & > HDL levels
Milk thistle – Silymarin - > HDL levels
Fiber - < Cholesterol
Phytosterols - < Cholesterol
Soy - < Cholesterol absorption from GI tract
CoEnzyme Q10 – HMG CoA reductase inhibitors –
natural statins
Coronary Thrombogenesis
During an Acute Coronary Syndrome
Angina
Clinical Manifestations
Angina – Chest Pain
Stable Angina Pectoris – intermittent, same pattern of onset, duration,
intensity of symptoms - 3-5 mins.
Silent Ischemia – 80% of patients with ischemia are asymptomatic
Prinzmetal’s Angina – variant – not precipitated by physical activity – may
be due to spasm
Nocturnal Angina – occurs at night but not necessarily during sleep or in
recumbent position
Angina Decubitis – recumbent position – relieved by standing
Unstable Angina – Unpredictable or may evolve from stable angina –
increasing frequency, duration, intensity
CAD
Clinical Manifestation – Diagnostics
History & Physical Examination
EKG / Echocardiogram / Stress Echocardiogram
Thallium Stress Test (perfusion scanning) cold spots where tissue is
inadequately perfused
CAT scan- calcium score/CT coronary angiogram
MUGA (Multiple gated radioisotope scan) – left ventricular function
MRI of the heart
PET (Positron emission computed tomography) – evaluate coronary artery
patency