P&P 2 2808NRS EOS Revision
Module 1: CVS
Ischaemic heart disease
1. Common risk factors
Non-Modifiable:
- Age, 45 in males, 55 in females
- Sex, Males more prone as oestrogen is protective, sex irrelevant after 70
- Genetics, predisposed leading to atherosclerosis such as: HTN, DM, high lipids, high amino acids
(homocystine)
Modifiable:
- Hyperlipidaemia which can be genetic, low HDLs (high alcohol, smoking obesity), high LDLs
(smoking, meat and egg fats)
- HTN, causes sheer stress -> causing endothelial damage
- Smoking, causes endothelial damage, oxidises LDLs, reduces HDLs
- Homocystine, causes inflammation, correlation with low folic acid and vitamin B6
- Diabetes, sugar converts to fatty acids (high LDLs), can also cause direct endothelial damage
- Obesity, leads to more vessels -> more pressure -> HTN. Also linked to diabetes
- Sedentary lifestyle
- Stress
2. Categories of IHD
- Angina (stable and unstable) and myocardial infarction
Aetiology of IHD
Insufficient Supply:
- Factors affecting coronary arteries
Ø Atherosclerosis
Ø Arteriosclerosis
Ø Vasospasms
- Myocardial hypertrophy (heart outgrown blood supply)
- Severe anaemias
- Respiratory disease
Increased Demand:
- Tachycardia (e.g. hyperthyroidism)
- Hypertension
- Increased demand due to exercise, mood changes (anger), infection with fever, etc.
Angina Pathophysiology
- Blood supply most often diminished due to either atherosclerotic plaques or coronary vasospasm
- Results in reduced oxygen and nutrient supply to myocardium
- In most cases no permanent damage to myocardium
- Manifests as recurrent, intermittent brief episodes of substernal chest pain, possibly radiating to neck
and left arm
- Often accompanied by pallor (pale), diaphoresis (excessive sweating), and nausea
Stable (exertional)
- Result of an atherosclerotic plaque and/or inappropriate vasoconstriction
, - Blood flow is adequate at rest but compromised upon exertion
- Pain lasts 5-15 minutes, relieved by rest
Unstable
- Marked by an atherosclerotic plaque, an associated thrombus and a greater degree of
vasoconstriction
- Blood flow is compromised at rest, pain without exertion
- Person may also experience nausea, shortness of breath, sweating and possibly vomiting.
Diagnostic tests:
- Stress test
- ECG
- FBC (Hb if anaemia causing oxygen insufficient supply)
- Lipid profile
Treatments
Reduce risk factors of further ischaemic heart disease
- Exercise
- Cessation of smoking
- Change in diet
- Stress reduction
- Drugs to reduce cholesterol levels (statins)
Reduce symptoms
- Drugs to decrease oxygen demand in the heart
Ø Beta blockers
Ø Calcium channel blockers
- Drugs to increase myocardial oxygen supply (peripheral vasodilators)
Ø Organic nitrates
Nitrates
- Peripheral vasodilators acting on both arterial and venous vasculature to reduce workload of the heart
- Dilation of arteries = reduced afterload (resistance that ventricles must overcome to eject blood into
circulation)
- Dilation of veins = decreased venous return and therefore reduced ventricular filling (reduced preload)
overall less work required to eject lower ventricular volume
- E.g. glyceryl trinitrate (nitroglycerine), isosorbide dinitrate and isosorbide mononitrate
Mechanism of action
1. Taken up by endothelial cells of blood vessel wall
2. Converted to nitric oxide (NO) in vascular smooth muscle
3. Nitric oxide increases the intracellular levels of a second messenger and ultimately decreases
intracellular calcium levels
4. Leads to relaxation of vascular smooth muscle and dilation of blood vessels
Adverse effects
Result from excessive vasodilation
- reflex tachycardia
- hypotension
- facial flushing
- syncope
- migraine-like headache (cerebral vasodilation)
Emergency Treatment for angina attack
,1. For a patient known to have angina, a second dose of nitroglycerin be given if pain persists more than 5 minutes. After three doses
within a 10-minute period and no pain relief, the pain should be treated as a heart attack. Call for assistance and emergency
medical intervention.
2. For a patient without a history of angina, emergency medical aid should be sought after 2 minutes without pain relief.
Myocardial Infarction Pathophysiology
- Occurs when a coronary artery is completely or partially occluded
- Leads to prolonged ischemia (>20 min) and cell death (infarction) of myocardium
- Most common cause of obstruction is atherosclerosis, usually with thrombus attached
- Most commonly affects the left ventricle
- Two main types (based on changes to ECG):
Ø Non-ST-elevation myocardial infarction (NSTEMI)
Ø ST elevation myocardial infarction (STEMI)
Obstruction caused by three main mechanisms:
1. Thrombus formation (on ruptured plaque)
2. Prolonged vasospasm occurs at location of atheroma
3. Lodging of embolus in smaller branch of vessel
- At point of obstruction (and distal) heart tissue becomes necrotic
- Area of injury, inflammation and ischaemia develops around necrotic zone
- Necrotic myocardium releases specific enzymes (used for diagnostic purposes)
- Necrotic myocardium doesn’t regenerate and is gradually replaced with fibrous (nonfunctional)
tissue
- Size and location of the infarct determine the severity of the damage
STEMI vs NSTEMI
Non-ST-elevated myocardial infarction (NSTEMI)
- Partial/intermittent occlusion (thrombus may break down)
- Damage is limited to inner third (partial wall) of myocardium (subendocardial infarct)
- Characterized by ST-depression or T-wave inversion on ECG
ST-elevated myocardial infarction (STEMI)
- Complete occlusion (3 – 6 hours)
- Damage extends to entire wall thickness (transmural infarct)
- Characterized by ST-elevation on ECG
Manifestations
, - Pain: Sudden substernal chest pain that radiates to the left arm, shoulder, jaw, or neck
- Pallor and diaphoresis, nausea, dizziness and weakness, and dyspnea
- Marked anxiety and fear
- Hypotension: the pulse is rapid and weak as cardiac output decreases and shock develops
- Low-grade fever
Diagnostic Tests
1. Typical changes occur in the ECG during the course of a MI, which confirm the diagnosis and assist
in monitoring progress
T wave inversion, ST depression or elevation.
2. Serum enzymes and isoenzymes released from necrotic cells also follow a typical pattern, with
elevations of lactic dehydrogenase (LDH), and creatine phosphokinase with M and B subunits (CK-
MB).
3. Serum levels of myosin and cardiac troponin are elevated a few hours after MI, providing for an
earlier confirmation. A rise in cardiac troponin levels is considered most specific for myocardial
tissue damage.
4. Serum electrolyte levels, particularly potassium and sodium, may be abnormal.
5. Leukocytosis and an elevated CRP and erythrocyte sedimentation rate are common, signifying
inflammation.
6. Arterial blood gas measurements will be altered particularly if shock is pronounced.
7. Pulmonary artery pressure measurements are also helpful in determining ventricular function.
Treatment
Medications
- Anticoagulants and antiplatlets – to reduce clot formation
◦ Antiplatelets – e.g. aspirin and clopidogrel
◦ Anticoagulants – e.g. heparin and warfarin
- Thrombolytics – to breakdown blood clots
◦ “ase” drugs – e.g. streptokinase, reteplase, and tenecteplase
◦ Absolute contraindications – prior intracranial haemorrhage, ischaemic stroke, active bleeding,
known malignant intracranial lesion
- Beta-blocker – to reduce workload
◦ “olol” drugs – e.g. atenolol and metoprolol
- ACE inhibitors – to reduce oxygen demand from heart
◦ “pril” drugs – e.g. enalapril and perindopril
- Analgesics – to reduce pain and sympathetic response
◦ E.g. – morphine
- Statins – to stabilize plaques and lower lipids
◦ “statin” drugs – e.g. atorvastatin and rosuvastatin
- Nitrates – to reduce myocardial oxygen demand and lessen ischaemia (refer to earlier slide)
◦ E.g. – glyceryl trinitrate
Surgery
- Percutaneous coronary intervention (PCI) – to re-establish blood flow
◦ Access coronary artery via radial or femoral artery
◦ Perform emergent coronary angioplasty – inflation of balloon to force expansion of blood vessel
◦ Stent may be used to maintain blood flow
- Coronary artery bypass graft – to re-establish blood flow
◦ Uses segment of saphenous vein or left internal mammary artery
◦ Harvested vessel is connected to coronary artery just distal to blockage
◦ Re-established blood flow to tissue beyond blockage
Adjunct
Oxygen therapy– to increase oxygen supply
Module 1: CVS
Ischaemic heart disease
1. Common risk factors
Non-Modifiable:
- Age, 45 in males, 55 in females
- Sex, Males more prone as oestrogen is protective, sex irrelevant after 70
- Genetics, predisposed leading to atherosclerosis such as: HTN, DM, high lipids, high amino acids
(homocystine)
Modifiable:
- Hyperlipidaemia which can be genetic, low HDLs (high alcohol, smoking obesity), high LDLs
(smoking, meat and egg fats)
- HTN, causes sheer stress -> causing endothelial damage
- Smoking, causes endothelial damage, oxidises LDLs, reduces HDLs
- Homocystine, causes inflammation, correlation with low folic acid and vitamin B6
- Diabetes, sugar converts to fatty acids (high LDLs), can also cause direct endothelial damage
- Obesity, leads to more vessels -> more pressure -> HTN. Also linked to diabetes
- Sedentary lifestyle
- Stress
2. Categories of IHD
- Angina (stable and unstable) and myocardial infarction
Aetiology of IHD
Insufficient Supply:
- Factors affecting coronary arteries
Ø Atherosclerosis
Ø Arteriosclerosis
Ø Vasospasms
- Myocardial hypertrophy (heart outgrown blood supply)
- Severe anaemias
- Respiratory disease
Increased Demand:
- Tachycardia (e.g. hyperthyroidism)
- Hypertension
- Increased demand due to exercise, mood changes (anger), infection with fever, etc.
Angina Pathophysiology
- Blood supply most often diminished due to either atherosclerotic plaques or coronary vasospasm
- Results in reduced oxygen and nutrient supply to myocardium
- In most cases no permanent damage to myocardium
- Manifests as recurrent, intermittent brief episodes of substernal chest pain, possibly radiating to neck
and left arm
- Often accompanied by pallor (pale), diaphoresis (excessive sweating), and nausea
Stable (exertional)
- Result of an atherosclerotic plaque and/or inappropriate vasoconstriction
, - Blood flow is adequate at rest but compromised upon exertion
- Pain lasts 5-15 minutes, relieved by rest
Unstable
- Marked by an atherosclerotic plaque, an associated thrombus and a greater degree of
vasoconstriction
- Blood flow is compromised at rest, pain without exertion
- Person may also experience nausea, shortness of breath, sweating and possibly vomiting.
Diagnostic tests:
- Stress test
- ECG
- FBC (Hb if anaemia causing oxygen insufficient supply)
- Lipid profile
Treatments
Reduce risk factors of further ischaemic heart disease
- Exercise
- Cessation of smoking
- Change in diet
- Stress reduction
- Drugs to reduce cholesterol levels (statins)
Reduce symptoms
- Drugs to decrease oxygen demand in the heart
Ø Beta blockers
Ø Calcium channel blockers
- Drugs to increase myocardial oxygen supply (peripheral vasodilators)
Ø Organic nitrates
Nitrates
- Peripheral vasodilators acting on both arterial and venous vasculature to reduce workload of the heart
- Dilation of arteries = reduced afterload (resistance that ventricles must overcome to eject blood into
circulation)
- Dilation of veins = decreased venous return and therefore reduced ventricular filling (reduced preload)
overall less work required to eject lower ventricular volume
- E.g. glyceryl trinitrate (nitroglycerine), isosorbide dinitrate and isosorbide mononitrate
Mechanism of action
1. Taken up by endothelial cells of blood vessel wall
2. Converted to nitric oxide (NO) in vascular smooth muscle
3. Nitric oxide increases the intracellular levels of a second messenger and ultimately decreases
intracellular calcium levels
4. Leads to relaxation of vascular smooth muscle and dilation of blood vessels
Adverse effects
Result from excessive vasodilation
- reflex tachycardia
- hypotension
- facial flushing
- syncope
- migraine-like headache (cerebral vasodilation)
Emergency Treatment for angina attack
,1. For a patient known to have angina, a second dose of nitroglycerin be given if pain persists more than 5 minutes. After three doses
within a 10-minute period and no pain relief, the pain should be treated as a heart attack. Call for assistance and emergency
medical intervention.
2. For a patient without a history of angina, emergency medical aid should be sought after 2 minutes without pain relief.
Myocardial Infarction Pathophysiology
- Occurs when a coronary artery is completely or partially occluded
- Leads to prolonged ischemia (>20 min) and cell death (infarction) of myocardium
- Most common cause of obstruction is atherosclerosis, usually with thrombus attached
- Most commonly affects the left ventricle
- Two main types (based on changes to ECG):
Ø Non-ST-elevation myocardial infarction (NSTEMI)
Ø ST elevation myocardial infarction (STEMI)
Obstruction caused by three main mechanisms:
1. Thrombus formation (on ruptured plaque)
2. Prolonged vasospasm occurs at location of atheroma
3. Lodging of embolus in smaller branch of vessel
- At point of obstruction (and distal) heart tissue becomes necrotic
- Area of injury, inflammation and ischaemia develops around necrotic zone
- Necrotic myocardium releases specific enzymes (used for diagnostic purposes)
- Necrotic myocardium doesn’t regenerate and is gradually replaced with fibrous (nonfunctional)
tissue
- Size and location of the infarct determine the severity of the damage
STEMI vs NSTEMI
Non-ST-elevated myocardial infarction (NSTEMI)
- Partial/intermittent occlusion (thrombus may break down)
- Damage is limited to inner third (partial wall) of myocardium (subendocardial infarct)
- Characterized by ST-depression or T-wave inversion on ECG
ST-elevated myocardial infarction (STEMI)
- Complete occlusion (3 – 6 hours)
- Damage extends to entire wall thickness (transmural infarct)
- Characterized by ST-elevation on ECG
Manifestations
, - Pain: Sudden substernal chest pain that radiates to the left arm, shoulder, jaw, or neck
- Pallor and diaphoresis, nausea, dizziness and weakness, and dyspnea
- Marked anxiety and fear
- Hypotension: the pulse is rapid and weak as cardiac output decreases and shock develops
- Low-grade fever
Diagnostic Tests
1. Typical changes occur in the ECG during the course of a MI, which confirm the diagnosis and assist
in monitoring progress
T wave inversion, ST depression or elevation.
2. Serum enzymes and isoenzymes released from necrotic cells also follow a typical pattern, with
elevations of lactic dehydrogenase (LDH), and creatine phosphokinase with M and B subunits (CK-
MB).
3. Serum levels of myosin and cardiac troponin are elevated a few hours after MI, providing for an
earlier confirmation. A rise in cardiac troponin levels is considered most specific for myocardial
tissue damage.
4. Serum electrolyte levels, particularly potassium and sodium, may be abnormal.
5. Leukocytosis and an elevated CRP and erythrocyte sedimentation rate are common, signifying
inflammation.
6. Arterial blood gas measurements will be altered particularly if shock is pronounced.
7. Pulmonary artery pressure measurements are also helpful in determining ventricular function.
Treatment
Medications
- Anticoagulants and antiplatlets – to reduce clot formation
◦ Antiplatelets – e.g. aspirin and clopidogrel
◦ Anticoagulants – e.g. heparin and warfarin
- Thrombolytics – to breakdown blood clots
◦ “ase” drugs – e.g. streptokinase, reteplase, and tenecteplase
◦ Absolute contraindications – prior intracranial haemorrhage, ischaemic stroke, active bleeding,
known malignant intracranial lesion
- Beta-blocker – to reduce workload
◦ “olol” drugs – e.g. atenolol and metoprolol
- ACE inhibitors – to reduce oxygen demand from heart
◦ “pril” drugs – e.g. enalapril and perindopril
- Analgesics – to reduce pain and sympathetic response
◦ E.g. – morphine
- Statins – to stabilize plaques and lower lipids
◦ “statin” drugs – e.g. atorvastatin and rosuvastatin
- Nitrates – to reduce myocardial oxygen demand and lessen ischaemia (refer to earlier slide)
◦ E.g. – glyceryl trinitrate
Surgery
- Percutaneous coronary intervention (PCI) – to re-establish blood flow
◦ Access coronary artery via radial or femoral artery
◦ Perform emergent coronary angioplasty – inflation of balloon to force expansion of blood vessel
◦ Stent may be used to maintain blood flow
- Coronary artery bypass graft – to re-establish blood flow
◦ Uses segment of saphenous vein or left internal mammary artery
◦ Harvested vessel is connected to coronary artery just distal to blockage
◦ Re-established blood flow to tissue beyond blockage
Adjunct
Oxygen therapy– to increase oxygen supply
