Ischaemic Heart Disease Flashcards
What are the clinical classifications for unstable angina?
Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina – angina out of the blue – somethings happened to the coronary artery
What is a diagnosis of angina based on?
history
ECG
troponin (no significant rise in unstable angina)
When can an ST elevated MI be diagnosed? (STEMI)
can usually be diagnosed on ECG at presentation
What is a non- ST- elevation MI?
retrospective diagnosis made after troponin results and sometimes other investigation results are available
Where is the ST segment?
ST segment between QRS complex and T wave is elevevated
How can a Q-wave MI or non-Q wave MI be defined?
basis of whether new pathological Q waves develop on the ECG as a result of MI
What are ST elevation MI and MI assosciated with LBBB related to?
larger infarcts
unless effectively treated more likely to lead to pathological Q wave formation, heart failure or death
R wave and MI
R wave generated by electrically viable myocardium under ECG lead – if we replace this with scar tissue lose R wave and you get pathological R wave
NON-Q wave MI?
Poor R wave progression - not much R wave, generate small amount
ST elevation - residual
Biphasic T wave
Q wave MI?
Complete loss of R wave
Cardiac chest pain in MI?
unremitting
usually severe but may be mild or absent
occurs at rest
associated with sweating, breathlessness, nausea and/or vomiting
one third occur in bed at night
Caused by occlusion of arteries
What does MI do?
Usually causes permanent heart muscle damage although this may not be detectable in small MIs
Risk factors for MI?
higher age
diabetes
renal failure
left ventricular systolic dysfunction
elevated NT
proBNP level
Elevated Troponin
What is the initial management for acute coronary syndrome?
Get in to hospital quickly – 999 call
Need defibrillator
Paramedics – if ST elevation, contact primary PCI centre for transfer
Take aspirin 300mg immediately
Pain relief
What is the hospital management for MI?
Make diagnosis
Bed rest
Oxygen therapy if hypoxic
Pain relief – opiates/ nitrates
Aspirin +/- platelet P2Y12 inhibitor
Consider beta-blocker
Consider other antianginal therapy
Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy
Main cause of acute coronary syndrome?
Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases
Some uncommon causes of acute coronary syndrome?
Stress-induced cardiomyopathy
coronary vasospasm without plaque rupture
drug abuse (amphetamines, cocaine)
dissection of the coronary artery related to defects of the vessel connective tissue
thoracic aortic dissection
What is troponin?
Troponin C Troponin I and Troponin T
Protein complex regulates actin:myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for acute coronary syndrome
May not represent permanent muscle damage
Positive troponin is found in?
gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs
Elevated troponin indicates what in patients suspected with ACS?
Higher risk
What are the agonists for platelet activation?
Thrombin > Coagulation
Thromboxane A2
Collagen
5HT
ADP
ATP
Fibrinogen > Fibrin
What is the effect of aspirin?
Irreversible inactivation of cyclo-oxygenase 1
Stops conversion of collagen to Thromboxane A2
What does Thrombin do?
activates platelets – final factor in coagulation cascade as it cleaves fibrin from fibrinogen
What is the fibrinolytic system?
Endothelium releases tissue plasminogen activator (TPA)
TPA > Plasminogen > plasmin > Fibrin to fibrin degradation products
What is P2Y12?
important amplification process in platelet activation
Makes response of platelets much more aggressive
What are some P2Y12 antagonists/ inhibitors?
Clopidogrel
Prasugrel
Ticagrelor
What do P2Y12 inhibtors do?
Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’
Increase risk of bleeding so need to exclude serious bleeding prior to administration
What are some GPIIb/IIIa antagonists?
Abciximab
Tirofiban Eptifibatide
What do GPIIb/IIIa antagonists do?
Only intravenous drugs available
Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS
Increase risk of major bleeding so used selectively
What do anticoagulants do?
Used in addition to antiplatelet drugs
Target formation and activity of thrombin
Inhibit both fibrin formation and platelet activation
What does fondaparinux (anticoagulant) do?
used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used
When do you use full dose anticoagulation?
used during PCI: options are
heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin)
direct thrombin inhibitor bivalirudin (expensive, not used in Sheffield)
When is high dose heparin used?
cardiopulmonary bypass for CABG surgery
When is a coronary angiography usually performed?
for patients with troponin elevation or unstable angina after medical therapy
What is the most used revascularisation procedure?
PCI
What are the factors affecting response to clopidogrel?
Dose
Age
Weight
Disease states such as diabetes mellitus
Drug-drug interactions e.g. omeprazole and strong CYP3A inhibitors
Genetic variants: CYP2C19 loss-of-function alleles
What are adverse effects of P2Y12?
Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance
What are the adverse effects of ticagrelor?
Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel (which are not associated with the same adverse effect but do not have the same evidence for longterm mortality reduction)
Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment
Risk factors for CHD?
Clinical risk factors (hypertension, lipids, diabetes)
Lifestyle risk factors (smoking, diet, physical inactivity)
Environmental risk factors (air pollution, chemicals)
Demographic risk factors (age, sex, ethnicity, genetic)
Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)
What are the coronary arteries?
LCA - LAD, circumflex, diagnonal branch, left marginal of circumflex
RCA- Right marginal artery, posterior descending artery
What is angina?
The onset of chest pain
Mismatch of oxygen demand and supply
What is stable angina?
From exertion and physical activity
Usually relieved by GTN spray
Also calcium channel blockers and beta blockers for long term
Dont use beta blockers for severe asthma
For someone who has heart failure before use non rate limiting CCBs and beta blockers
Non - rate limiting CCB - amlodopine
First line for angina
GTN spray
Second line angina
CCB or Beta blockers
3rd line (contraindications)
CCB and Beta blockers and anti anginal eg ivabradine
Also long lasting nitrate effects
What is the commonest reason for angina?
IHD
Risk factors for IHD?
Age
Cigarette smoking
Family history
Diabetes mellitus
Hyperlipidemia
Hypertension
Kidney disease
Obesity
Physical inactivity
Stress
Male
What are the exacerbating factors for angina? (Supply)
Anemia - not enough blood to carry oxygen - causes angina
Hypoxemia
Rarer -
Polycythemia
Hypothermia
Hypovolaemia
Hypervolaemia
What are the exacerbating factors for angina? (Demand)
Hypertension
Tachyarrhythmia
Valvular heart disease
Hyperthyroidism
Hypertrophic cardiomyopathy – muscle of heart has excessive growth
What are the environmental causes of angina?
Exercise
cold weather
heavy meals
emotional stress
What is the physiology of myocardial ischemia?
Myocardial ischemia occurs when there is an imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:
- Impairment of blood flow by proximal arterial stenosis, narrowed coronary artery
- Increased distal resistance eg left ventricular hypertrophy
- Reduced oxygen-carrying capacity of blood eg anemia
What are some types of angina?
Crescendo angina
Unstable angina
(both due to CHD)
Prinzmetal’s angina (coronary spasm) – very rare – vessesles become narrow with coronary spasm
Microvascular angina (Syndrome X) ‘ANOCA’
Epidemiology of angina
More prevalent in men than women
What is the history we need to check for IHD?
Personal details (demographics, identifiers)
Presenting complaint
History of PC + risk factors
Past medical history
Drug history, allergies
Family history
Social history
Systematic enquiry
What are the cardiac symptoms of IHD?
Chest pain (tightness/ discomfort)
Breathlessness
No fluid retention (unlike heart failure)
Palpitation (not usually)
Syncope or pre-syncope (very rare)
What are the factors pointing towards ischaemic cardiac pain?
Character
Location
Provoking factors
Relieving factors
Associated symptoms
Associated risk factors
What are the differential diagnoses of chest pains?
Myocardial ischemia
Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Gastro-oesophageal (reflux, spasm, ulceration)
What are the treatment options for IHD?
Reassure
smoking
Weight
Exercise
diet
Advice for emergency
Medication
Revascularisation
Why is the CT coronary angiogram used and what is it used for?
Good ‘rule-out’ test and at spotting severe disease
Not so good at moderate disease
Anatomical, not functional
Do it on a single breath hold
What is excercise testing used for?
Good functional test
But relies upon patient’s ability
To walk on a treadmill
(useless for elderly, obese,
arthritic etc)
What are myoview scans used for?
Uses pharmacological stressor (regadenoson) to
Increase HR and CO
Fuzzy pictures: imperfect sensitivity and specificity
What are stress echos used for?
Pharmacological stressor
Highly skilled operative required
Seeks regional wall abnormality
Not often used
What is the best of the non invasive tests?
Perfusion MRI
What are the effects of beta blockers on the heart?
decreased HR (-ve chronotropic )
decreased Left ventricle contractility (-ve inotropic)
Both of these lead to:
decreased cardiac output > decreased O2 demand
Beta blocker side effects
Tiredness
Nightmares
Erectile dysfunction
Bradycardia
Cold hands and feet
What are contrainidicators of beta blockers?
Never give beta blockers to someone with asthma – blocks beta blockers – bronchoconstrictor
What are the effects of nitrates (venodilators)
Ischaemia occurs
arterioles dilate
Decreased BP
Decreased afterload
Decreased venous return
Decreased preload
coronary arteries dilate
Main effect is on venous return – expands venous capacity – reduces pre load on heart – small affect on arterioles
Dilates coronary arteries
What do Calcium channel blockers do?
Decrease HR >
Decreased LV contraction and decreased work >
Arteries dilate >
Decreased BP >
Decreased Afterload >
Decreased O2 demand >
Coronary arteries dilate
What are the side effects of calcium channel blockers?
Flushing
Postural hypotension
Swollen ankles
Aspirin
Cyclo-oxygenase inhibitor
↓ prostaglandin synthesis, incl. thromboxane
↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic
Gastric ulceration
Statins
HMG CoA Reductase inhibitors
Reduce manafucture of LDL cholesterol
Used in CVD
RAAS System
Angiotensinogen from liver (Renin from JG apparatus)>
Angiotensin 1 (ACE from lung)> Angiotensin 2 Causes vasoconstriction
Angiotensin 2 > Alodsterone from adrenal cortex > Na+ pump activated (distal renal tubule) > Na+ +H20 retention (kidney) ascending renal tubule
Example of ACE inhibitors
Ramipril
Example of ARBs
LOSARTAN
Who are ACE inhibitors given to?
Given to patients
With IHD and
HBP or DM
Treatment summary for angina
Immediately GTN Spray
Long term calcium channel blockers and beta blockers
Secondary prevention aspirin, ACE inhibtor, beta blockers clopidogrel
What is PCI?
Percutaneous coronary intervention
Coronary angioplasty/ stenting
What is a CABG?
cORONARY ANGIOgram bypass graft
Pros of PCI
Less invasive
Convenient
Repeatable
Acceptable
Cons of PCI
Risk stent thrombosis
Risk restenosis
Can’t deal with complex disease
Dual antiplatelet therapy
Pros of CABG
Prognosis
Deals with complex disease
Cons of CABG
Invasive
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay
Time for recovery
