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BIOL122 Lecture Notes - Lecture 5: Troponin, Calcium Channel Blocker, Transdermal Patch

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ACU
Department
Biological Sciences
Course
BIOL122
Professor
Eileen

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Coronary Artery Disease (CAD)
Myocardial requirements:
• Adequate blood flow: oxygen and nutrients
• Balance between oxygen supply and demand: oxygen demand increases if
HR speeds up or force of contraction becomes stronger.
Coronary artery disease:
• Narrowing/ blockage of coronary arteries: atherosclerosis
• Inadequate blood flow to myocardium: less oxygen and nutrients, damage
and death of cells
Risk factors of CAD:
- Aging
- Smoking
- Family history
- Hypertension
- Obesity
- Diabetes
- Lack of exercise
- Hyperlipidaemia
Pathogenesis of CAD: severe chronic atherosclerosis that causes narrowing of
the lumen of one or more coronary arteries
Angina pectoris:
• Chest pain caused by insufficient blood flow and oxygen to heart muscle:
imbalance between hearts oxygen demand and supply
• Blood flow is restored, pain recedes and heart is not permanently
damaged
Forms of Angina Pectoris:
- Stable angina: chest pain associated with exertion
- Unstable angina: chest pain with less exertion
- Variant angina: pain occurs at rest
Pathogenesis (angina)
• Atherosclerosis develops in coronary artery
• Plaques protrude into lumen
• Partial obstruction to blood flow
• Less oxygen available to myocardium
• Increased cardiac demand (exercise)
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• Anaerobic respiration
• Increased adenosine phosphate in ECF
• Chest pain
Consequences of Ischemia:
• Heart attack
- Part of the heart muscle is destroyed, causing serious and in
some cases fatal heart damage
• Irregular heart rhythm (arrhythmia)
- Electrical impulses in heart may malfunction, causing your
heart to beat too fast, too slow or irregularly
• Heart failure
- Damage to heart muscle can reduce its ability to effectively
pump blood. Over time this can lead to heart failure
ECG changes (myocardial ischemia)
Abnormalities in ST segment:
Myocardial infraction:
• Reduced blood flow through coronary arteries
• Myocardial cells die from lack of oxygen
• Collagen scar forms
Pathogenesis:
• Disruption of atherosclerotic plaque: rupture
• Clotting cascade (thrombus)
• Coronary artery occlusion
• Myocardial cell death
• Scar tissue formation
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Clinical manifestations (MI)
• Severe crushing chest pain
• Angina pectoris before MI in some people
• Shortness of breath due to pulmonary congestion and oedema
• Cardiogenic shock
• Dysrhythmia
Diagnosis: (MI)
• ECG:
+ to detect ischemia or acute coronary injury
+ STEMI, NSTEMI
• Cardiac markers:
+ creatine kinase, troponin
+ leak out of injured myocardial cells into blood
+ levels rise over time
Treatment:
• Glyceryl trinitrate: vasodilator
• Coronary stenting: pushes back plaque and restores blood flow
• Coronary artery bypass graft: healthy blood vessel is connected to coronary
artery slightly past site of blockage
Stroke:
Brain blood supply:
• Receives 20% of cardiac output: top priority for blood, nerve cells will die
without oxygen
• Cerebral arteries: middle, anterior and posterior
• Circle of Willis: back up routes for blood flow
• Cerebral blood flow stable:
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Document Summary

Myocardial requirements: adequate blood flow: oxygen and nutrients, balance between oxygen supply and demand: oxygen demand increases if. Hr speeds up or force of contraction becomes stronger. Coronary artery disease: narrowing/ blockage of coronary arteries: atherosclerosis. Inadequate blood flow to myocardium: less oxygen and nutrients, damage and death of cells. Pathogenesis of cad: severe chronic atherosclerosis that causes narrowing of the lumen of one or more coronary arteries. Angina pectoris: chest pain caused by insufficient blood flow and oxygen to heart muscle: imbalance between hearts oxygen demand and supply, blood flow is restored, pain recedes and heart is not permanently damaged. Stable angina: chest pain associated with exertion. Unstable angina: chest pain with less exertion. Pathogenesis (angina: atherosclerosis develops in coronary artery, plaques protrude into lumen, partial obstruction to blood flow, less oxygen available to myocardium. Increased adenosine phosphate in ecf: chest pain. Part of the heart muscle is destroyed, causing serious and in some cases fatal heart damage.

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Related Questions

Medical History:
A 31 yr old man, a two pack per day smoker, presented to the emergency department complaining of sudden-onset, 10/10 crushing substernal chest pain associated with shortness of breath and diaphoresis that began 30 min prior to arrival. He had no previous history of cardiovascular disease.
Physical exam: Height 192 cm, weight 153.8 kg, BMI 41.6 kg · m–2 (class III obesity); blood pressure 178/101 mmHg, pulse 75 beats · min–1, respiratory rate 20 breaths · min–1, temperature 36.7 ∞C; normal heart sounds, lungs clear to auscultation, normal peripheral pulses
Electrocardiogram: Normal sinus rhythm, rate 72 beats · min–1; ST-segment elevation V1-V4
Chest radiograph: Normal Blood work: Elevated cTn and CK-MB; glucose normal; blood lipids: total cholesterol 200 mg · dl–1, HDL-C 45 mg · dl–1, LDL-C 134 mg · dl–1, triglycerides 104 mg · dl–1
Chest CT: No evidence of aortic dissection Echocardiogram: Left ventricular ejection fraction 45%, hypokinesis of the anteroseptal wall, borderline left ventricular enlargement, normal diastolic function, normal cardiac valves

Diagnosis:
Acute anterior wall STEMI.

Treatment:
1. Emergent cardiac catheterization (began 46 min after initial presentation to the hospital): total occlusion of the proximal left anterior descending (LAD) coronary artery, mild diffuse narrowing of the circumflex and right coronary arteries. The LAD occlusion was treated with thrombectomy, percutaneous coronary angioplasty, and placement of a drug-eluding stent, with good result.
2. Medical treatment: Aspirin, heparin, intravenous nitroglycerin, clopidogrel, abciximab, atorvastatin, carvedilol, lisinopril, nicotine patch.
3. Nicotine dependence consultation.
4. Referral to outpatient cardiac rehabilitation. Complications: None Hospital dismissal: Occurred approximately 48 h after admission; appointments made to see primary physician and to begin outpatient cardiac rehabilitation program in 5 d; follow-up blood work, ECG, and cardiology appointment in 8 wk Dismissal medications: Carvedilol, aspirin, clopidogrel, lisinopril, nicotine patch, simvastatin

Outpatient Exercise Test Results (Performed 8 D after Hospital Dismissal)
8.0 min duration (treadmill), normal blood pressure and electrocardiographic responses, peak heart rate 164 beats · min–1, V.O2peak = 3.04 L · min−1 (20.8 ml ∑ kg−1 ∑ min−1; 47% of expected), no angina reported
Exercise Prescription:
Outpatient cardiac rehabilitation program: Began 5 d after hospital dismissal; initial evaluations included assessments of neuromuscular function (normal), depression (normal), and potential sleep apnea (abnormalBerlin questionnaire, abnormal overnight oximetry resulted in referral for a sleep consultation); meeting with registered dietitian.
Exercise prescription: Goals included weight loss, increased aerobic and muscular fitness; frequency of three supervised sessions per week in cardiac rehabilitation facility plus three or four independent sessions per week (total frequency of six or seven sessions each week); average intensity using target heart rate 130 to 140 beats · min–1 (60-70% heart rate reserve), RPE 12 to 14; high-intensity intervals (to begin 2 wk after starting cardiac rehabilitation) using RPE 17, heart rate <160 beats · min–1; duration initially set at 10 to 15 min (not including warm-up, cool-down, strength training), gradually increasing to 45 to 60 min per session; types of exercise to include outdoor or treadmill walking, elliptical trainer; resistance training (to begin 2 wk after starting cardiac rehabilitation) using free weights and weight machines, initially one set of 8 to 15 slow repetitions, exercises for the major muscle groups, two or three sessions per week; lifestyle or general physical activity including walking short distances during the day, yard work, physical activity at work (return to work as restaurant equipment installer 4 wk after myocardial infarction).

Outcomes from 11 WK of Cardiac Rehabilitation Program
Medication compliance: Excellent (self-report) Exercise training: Frequency six or seven sessions per week (two or three supervised sessions per week); aerobic exercise duration 50 to 60 min per session; aerobic interval training two or three sessions per week (initially treadmill grade walking for 30 s progressing to slow jogging on treadmill for up to 4 min, three to five high-intensity intervals per session); resistance training two or three sessions per week, two or three sets of 8 to 15 repetitions, major muscle groups. Body weight: Stopped eating fast food and desserts, had more fruit, vegetables, poultry, fish; weight loss = 20.8 kg (BMI still excessive, 33.8 kg · m–2). Repeat cardiopulmonary exercise test: 10.5 min duration (treadmill), normal blood pressure and electrocardiographic responses, peak heart rate 162 beats · min–1, V.O2peak = 4.16 L · min−1 (31.2 ml ∑ kg−1 ∑ min−1; 71% of expected), 37% increase in V.O2peak (L · min−1), no angina reported. Tobacco use: One or two cigarettes daily. Blood pressure: 126/80 mmHg. Blood lipids: Total cholesterol 126 mg · dl–1, HDL-C 33 mg · dl–1, LDL-C 80 mg · dl–1, triglycerides 65 mg · dl–1. Recommendations: Stop smoking; continue medications, exercise program, and heart-healthy eating habits; continue efforts for weight loss; return appointment with cardiac rehabilitation team in 3 mo.

Discussion:
This patient was extremely young and was fortunate to realize the importance of promptly seeking medical attention with the onset of symptoms. His hospital course included standard diagnostic testing for acute myocardial infarction with subsequent timely coronary angiography with PCI of the infarct-related artery. Fortunately he did not develop serious complications and was discharged from the hospital after only 2 d. He enrolled in outpatient cardiac rehabilitation 1 wk after his MI. Of concern, he was markedly obese and may have had obstructive sleep apnea based on his abnormal Berlin questionnaire; he was referred for further evaluation in the Sleep Clinic. His course during rehabilitation was very favorable, and he did not experience post-infarction angina. He was successful in exercise and weight loss and demonstrated a remarkable increase in aerobic capacity. His challenge will be to continue taking his medications, stop smoking completely, eat a healthy diet, maintain his exercise program, and control his other coronary risk factors.

Questions:
1. What were this patient’s coronary risk factors?

2. What clinical tests were used to make the diagnosis of an acute ST-segment elevation anterior wall myocardial infarction?

3. What classes of cardiovascular medications were prescribed for this patient?

4. Compare the two cardiopulmonary exercise tests for this patient. What were the similarities? What were the differences?

5. Review the patient’s exercise prescription and program. Were the established goals achieved? Would you alter the exercise program in any fashion?

6. How effective was the patient in controlling his coronary risk factors by the time he completed 11 wk in the outpatient cardiac rehabilitation program?

7. What is his most important remaining coronary risk factor?

8. What component of the recommendations given to him at the completion of 11 wk of cardiac rehabilitation will potentially help him in sustaining his efforts at secondary prevention?