Transcript PPT

Adult Medical-Surgical Nursing
 Atherosclerosis and Coronary Heart Disease
Reduced Blood Flow to Cardiac Muscle:
 Conditions reducing blood flow to cardiac muscle
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are:
Atherosclerosis of coronary arteries
Acute vasospasm (vasoconstriction)
Hypotension
Acute blood loss
Severe anaemia = ↓ O2 supply
Congenital anomaly (ASD; VSD)
↑ O2 demand:Thyrotoxicosis, cocaine abuse, exercise
 Atherosclerosis
Atherosclerosis: Description
 An abnormal accumulation of lipid (fatty) deposits
and fibrous tissue within the arterial blood vessel
walls
 May affect all arteries of the body
 Narrows the lumen
 Leads to reduced blood flow (↓ O2 and nutrients to
the tissues): ischaemia
 May cause infarction of affected area (tissue death)
Atherosclerosis: Aetiology
 Non-modifiable risk factors:
 ↑ risk with age (especially after 65 years)
 Males and post-menopausal women more at risk
(oestrogen protects)
 Family history = genetic tendency
Atherosclerosis: Aetiology
 Modifiable risk factors:
 Cholesterol abnormality (↑ blood lipids) related to:
 Diet: ↑ animal fats (LDL) and ↓ vegetable and fish
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oils (HDL)
Salt intake (BP)
Obesity, lack of exercise
Smoking
Hypertension/ Diabetes Mellitus
Atherosclerosis: Pathophysiology
 Lipids are deposited on the intima of the arterial wall
 Inflammatory response: phagocytosis by killer T-
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lymphocytes and macrophages
Smooth muscle cells form a fibrous cap over the dead
fatty lesion = plaque/ atheroma
Plaque protrudes, narrowing the arterial lumen
Increases pressure in the lumen
Obstructs oxygenated blood flow
→ ischaemia of tissue supplied
Prolonged ischaemia → infarction
Thrombus Formation:
 The arterial blood flow under pressure ruptures the
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fibrous cap (of the plaque) if thin →
Haemorrhage
→ clot/ thrombus (platelet aggregation on the
damaged wall)
May completely obstruct artery
→ ischaemia and infarction
Atherosclerosis: Prevention
 Diet: ↑ intake of HDL (vegetable and fish oils) and ↓
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LDL (animal fats)
Restrict salt intake
Exercise and weight control
Stop smoking
Antilipid medication
Vasodilators
Anti-platelet aggregate
 Coronary Atherosclerosis
Coronary Atherosclerosis: Description
 Atherosclerosis of the coronary arteries which supply
oxygenated blood to the myocardium
 Coronary arteries are more at risk of atherosclerosis
and narrowing because they twist and turn
 A progressive narrowing of the lumen reduces blood
flow → ischaemia will eventually lead to:
 Myocardial Infarction
Coronary Atherosclerosis: Diagnosis
 ECG
 Stress ECG
 Cardiac catheterisation
 Chest Xray
 Echo cardiogram
 Blood chemistry, lipids, ABG, LFT, KFT, glucose,
coagulation, CBC
 Cardiac enzymes (to exclude infarct)
Coronary Atherosclerosis
 Coronary atherosclerosis is characterised by:
 Angina
 Coronary Thrombosis and Myocardial Infarction
 Angina:
Angina
 Chest pain: (Angina Pectoris) is a condition
describing the pain experienced from myocardial
ischaemia
 Acute and severe gripping sub-sternal or retro-
sternal pain radiating to the axillae, neck or jaw
Angina: Classification
 Stable Angina:
 Chest pain on exertion
 Usually lasts 5 - 15 minutes
 Relieved by rest or medication
 Unstable Angina:
 Chest pain at rest
 Occurs frequently/ lasts longer
 Only relieved by medication
 Often precedes Myocardial Infarction*
 Myocardial Infarction (MI):
 (An acute emergency situation)
Myocardial Infarction: Description
 Myocardial Infarction: death of cardiac muscle tissue
resulting from ischaemia (most often related to
coronary thrombosis; other causes slide 2)
 Infarcted myocardial cells release enzymes and
proteins through the destroyed cell wall: ↑ cardiac
enzymes in the blood circulation
 Infarction interferes with normal myocardial
function causing weakness and maybe irregularity
Myocardial Infarction: Outcomes
 Myocardial scarring and weakness
 Poor conduction of electrical impulses →
dysrhythmias and weak cardiac output (can lead to
cardiogenic shock)
 Unaffected heart muscle has excess work to achieve
adequate cardiac output →
 Cardiomegaly
 Cardiac failure
Myocardial Infarction: Clinical Manifestations
 Chest pain (Angina):
 Acute, sub-sternal, radiating to shoulders and
possibly hands
 Prolonged, unresponsive to vasodilators (medication
for angina)
 Nausea, vomiting, pallor, sweating (cold, clammy
skin), hypotension, rapid, “thready” weak pulse:
shock
 Dyspnoea, dizziness, restlessness, anxiety
Myocardial Infarction: Diagnosis
 History and clinical picture
 12-lead ECG reveals site and degree of ischaemia/
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infarction
Continuous monitoring
Cardiac enzymes (↑ if infarction) (see slide 22)
Blood chemistry, lipids, ABG, LFT, KFT, glucose,
coagulation, CBC
Cardiac catheterisation
Cardiac Enzymes
 Creatinine-kinase (CKMB specific)
 Lactic Dehydrogenase (LDH 1)
 Troponin 1
 Myoglobin (myo-haemoglobin)
 (raised when infarction has occurred)
Myocardial Infarction: Acute Management
 Analgesia: IV Morphine
 ECG/ continuous monitoring
 Humidified O2 with high flow rate
 Anti-platelet aggregate
 Vasodilator: Nitroglycerin
 Anticoagulant: Heparin
 Thrombolytic agent (within 30 mins)
 Cardiac catheterisation: Urgent Coronary
Angioplasty (PTCA) and Stent* to maintain patency
(treatment of choice).
Surgery for Coronary Atherosclerosis
 Angioplasty (PTCA): Removal of plaque and
insertion of stent(s) to maintain patency
 Anti-platelet aggregate prescribed for several months
post-stent
 Patient with severe atherosclerosis may require
Coronary Artery Bypass Graft (CBG) using graft
from:
 The deep saphenous vein
 The internal mammary arteries
Nursing Considerations
 Patient education about condition, diet and weight
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control, exercise, smoking
Ensure medications understood including
precautions and monitoring for anticoagulant/ antiplatelet therapy
Emergency care in ICU if admitted with chest pain
Awareness and competence in administering
medications
Psychological/ emotional support