CAM201 Lecture 6: Pharmacology- Angina Notes

44 views6 pages

taupefly760

12 Jun 2018

School

University of Tasmania

Department

CAM

Course

CAM201

Professor

Bonnie Bereznicki

For unlimited access to Class Notes, a Class+ subscription is required.

Angina

• Chest pain due to myocardial ischaemia (ischaemic heart disease)- insufficient

oxygen supply to myocardium- oxygen demands of the myocardium is not met

• Can be caused by coronary atherosclerosis (narrowing of vessel lumen) or

vascular spasm of the coronary vessels.

• The pain has a characteristic distribution in the chest, arm and neck.

• Pain may occur at rest, or may be brought on by exertion, cold or excitement.

Factors Affecting Coronary Blood Flow

• The window for coronary blood flow is when aortic pressure is greater than coronary

blood flow.

• The window is during diastole

• The ‘window’ for coronary blood flow may be reduced by:

1. A shortened diastole (when the heart rate increases)- during exercise

2. Increased ventricular end-diastolic pressure- happens with stenosis of the aortic

valve, because more of the blood remains in the ventricles instead of being ejected

into the aorta through the valve

3. Reduced diastolic aortic pressure- also happens with stenosis of the aortic valve.

Types of Angina

Stable angina

• Predictable pain on exertion.

• Caused by a fixed narrowing of the coronary vessels, usually due to atherosclerosis.

find more resources at oneclass.com

Unlock document

This preview shows pages 1-2 of the document.
Unlock all 6 pages and 3 million more documents.

Already have an account? Log in

Unstable angina

• A progressive form of angina – pain occurs more and more frequently and become

more severe over time.

• Pain starts off occurring with exertion only, but over time occurs during rest as well.

• Caused by thrombus associated with a ruptured atheromatous plaque (pathology similar

to myocardial infarction)

• Pharmacological management needs to be is aimed treating the underlying

atheromatous disease (e.g. high blood lipid levels) and not just improving perfusion.

• Risk of AMI is substantial, which can be reduced by aspirin

Classification of Coronary Ischaemia

• Non ST-elevation acute coronary syndrome (NSTEACS)

• Anti-platelet therapy is required to treat cute coronary syndrome to reduce the risk of

clotting- similar pathology of vessel damage → atherosclerotic plaque formation→

thrombosis formation → narrowing of vessel lumen

Coronary Artery Occlusion

• Atherosclerotic plaque can develop due to lipid accumulation in the vessel wall

• Plate aggregation can occur if the plaque becomes damaged due to high pressure, which

results in the formation of a thrombus

• Stable angina is due to a fixed obstruction (no platelet aggregation)

Pharmacological Management of Angina

• Drug therapy for angina is aimed at:

− Relaxing coronary artery smooth muscle (improving perfusion).

− Reducing the oxygen demand of the heart (decreasing cardiac workload).

• Short-acting organic nitrates are used for acute treatment

• Patients who suffer from frequent angina attacks can be prescribed drugs that can be

taken on a daily basis to reduce the frequency:

− Beta1 receptor agonists (cardio-selective beta blockers)- 1st line

− Calcium-channel blockers

Coronary

Ischaemic

Syndromes

Stable Angina

Acute

Coronary

Syndrome

STEMI NSTEACS

NSTEMI Unstable

Angina

find more resources at oneclass.com

Unlock document

This preview shows pages 1-2 of the document.
Unlock all 6 pages and 3 million more documents.

Already have an account? Log in

Document Summary

Stable angina: predictable pain on exertion, caused by a fixed narrowing of the coronary vessels, usually due to atherosclerosis. Angina: non st-elevation acute coronary syndrome (nsteacs, anti-platelet therapy is required to treat cute coronary syndrome to reduce the risk of clotting- similar pathology of vessel damage atherosclerotic plaque formation thrombosis formation narrowing of vessel lumen. Pharmacological management of angina: drug therapy for angina is aimed at: Relaxing coronary artery smooth muscle (improving perfusion). Beta1 receptor agonists (cardio-selective beta blockers)- 1st line. Decreasing the opening of ca2+ channels- reduced contractility, less work. Activation of myosin light chain phosphatase (enzyme responsible for myosin light chain phosphorylation). Myosin light chain dephosphorylated- can no longer bind with actin, reduces heart contraction. Systemic effects: which vascular muscle the drug is targetting depends on dosage, therapeutic and adverse effects are dose related: At low doses, on cause venorelaxation with little effect on arterial resistance.

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 Â· mâ2 (class III obesity); blood pressure 178/101 mmHg, pulse 75 beats Â· minâ1, respiratory rate 20 breaths Â· minâ1, temperature 36.7 âC; normal heart sounds, lungs clear to auscultation, normal peripheral pulses
Electrocardiogram: Normal sinus rhythm, rate 72 beats Â· minâ1; ST-segment elevation V1-V4
Chest radiograph: Normal Blood work: Elevated cTn and CK-MB; glucose normal; blood lipids: total cholesterol 200 mg Â· dlâ1, HDL-C 45 mg Â· dlâ1, LDL-C 134 mg Â· dlâ1, triglycerides 104 mg Â· dlâ1
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 Â· minâ1, V.O2peak = 3.04 L Â· minâ1 (20.8 ml â kgâ1 â minâ1; 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 Â· minâ1 (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 Â· minâ1; 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 Â· mâ2). Repeat cardiopulmonary exercise test: 10.5 min duration (treadmill), normal blood pressure and electrocardiographic responses, peak heart rate 162 beats Â· minâ1, V.O2peak = 4.16 L Â· minâ1 (31.2 ml â kgâ1 â minâ1; 71% of expected), 37% increase in V.O2peak (L Â· minâ1), no angina reported. Tobacco use: One or two cigarettes daily. Blood pressure: 126/80 mmHg. Blood lipids: Total cholesterol 126 mg Â· dlâ1, HDL-C 33 mg Â· dlâ1, LDL-C 80 mg Â· dlâ1, triglycerides 65 mg Â· dlâ1. 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 patientâs 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 patientâs 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?

Case History- An 11-month old Boy who's blue and short of breath

Chief Complaint: An 11-month old boy brought to the pediatric clinic with difficulty breathing.

History: Austin Green, an 11-month old Caucasian boy was brought by his foster parents to the Pediatric clinic with comnplaint of dyspnea (i.e difficulty breathing) and fatigue. These episodes last for several minutes, occur daily, and happen most copmmonly during exertion (i.e exercise). Austin spent the first 9 months of his life with hisbiological parents, but recent social problems have necessitated that he receive foster care.His foster parents have had him for the past month, and they have note that these "breathing spells" have become more frequent and severe over period of time. They also note that Austinb's shortness of breath diminishes somewhat if he lies down. Interestingly, he frequently assumes a squatting position during these episodes, and this seems to reduce hsi symptoms as well. His foster parents report that Austin has had no nausea, vomiting, change in appetie, or change in bowel or bladder habits. He is currently on no medications and no known allergies. There is no medical information available about any othefr member of Austin's biological family.

Lab. test results:

Hematocrit 43% normal (37-47%)

Hemoglobin 14mg/dl (normal 12-16ml/dl)

PH =7.21 (normal range=7.35 to 7.45)

[HCO^-3]=18meq/L (normal range=22 to 26 me=Eq/L)

1. The cardiologist ordered X-ray that showed decreased blood flow to the lungs. A follow-up echocardiogram revealed the following abnormalities in Austin's heart. (A) a narrowing of pulmonic valve, (B) a thickening of right ventriclewall, (C) a ventricular septal hole allowing direct exchange of blood between the right and the left ventricles, (D) an aorta that was shifted in position so that it was over-riding the right venbtricl, allowing it to recieve blood from both the left and the right ventricle.

What is the name of Austin's condition?

2. What is specifically causing the heart murmur?

3. Why did the chest X-ray show freduced pulmonary blood flow?

4. Austin has a thickening right ventriclewall. what type of hypertropy is this?

Why does Austin have this particular type of ventricular hypertrophy? BE SPECIFIC

5. Why di Austin's EGG show a right-shufted ventricular depolarization axis?

6. Which way will blood typically flow through Austin's ventricular septal defect(i.e from the left ventricle to the right ventricle, or vice versa? explain your answer in detail

7. Why is Austin cyanotic? BE SPECIFIC

8. Why does supplemental oxygen therapy did not correct Austin's cyanosis? BE SPECIFIC

9. How might the squatting position help relieve Auatin's dyspnea?

10. Why is Austin's...

(a) arterial pCO2 higher than normal?

(b). arterial [HCO^-3] lower than normal?

(c). arterial PH lower than normal?

11. Describe treatments for Austin's condition?

CAM201 Lecture 6: Pharmacology- Angina Notes

Document Summary

Get access

Related Documents

CAM201 Lecture Notes - Lecture 4: Systolic Geometry, Valvular Heart Disease, Heart Valve

BIOM20002 Lecture Notes - Lecture 56: Hypovolemia, Peptic Ulcer, Hematemesis

PHAR 301 Lecture Notes - Lecture 6: Hmg-Coa Reductase, Coronary Artery Disease, Myocardial Infarction

Related Questions