Cardiology 2 Flashcards
1
Q
Define constrictive pericarditis
A
Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.
2
Q
Explain the aetiology/risk factors of constrictive pericarditis
A
- NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure
- Can occur after any pericardial disease process
- More common causes of pericarditis:
o Idiopathic
o Virus
o TB
o Mediastinal irradiation
o Post-surgical
o Connective tissue disease
3
Q
Summarise the epidemiology of constrictive pericarditis
A
- RARE
- Documented in all ages
- 9% of patients with acute pericarditis will develop constrictive pericarditis
- TB has the HIGHEST TOTAL INCIDENCE out of all causes
- More common in MALES
4
Q
Recognise the presenting symptoms and signs of constrictive pericarditis
A
- Gradual-onset of symptoms
- EARLY - symptoms and signs may be very subtle
- ADVANCED - jaundice, cachexia, muscle wasting
- Right Heart Failure Signs
o Dyspnoea
o Peripheral oedema
o Raised JVP
o Kussmaul’s sign (paradoxical rise in JVP on inspiration)
o Pulsatile hepatomegaly
5
Q
Identify appropriate investigations for constrictive pericarditis
A
- CXR - may show calcification of the pericardium
- Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy
- MRI - allows assessment of thickness of pericardium
- CT - same role as MRI
- Pericardial biopsy - may be indicated (especially if suspected infective cause)
6
Q
Define Deep Vein Thrombosis
A
Formation of a thrombus within the deep veins (most commonly in the calf or thigh)
7
Q
Explain the aetiology/risk factors of DVT
A
- Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (look up Virchow’s triad)
- Risk Factors
o COCP
o Post-surgery
o Prolonged immobility
o Obesity
o Pregnancy
o Dehydration
o Smoking
o Polycythaemia
o Thrombophilia (e.g. protein C deficiency)
o Malignancy
8
Q
Summarise the epidemiology of DVT
A
- VERY COMMON
* Especially in hospitalised patients
9
Q
Recognise the presenting symptoms of DVT
A
- Swollen limb
* May be painless
10
Q
Recognise the signs of DVT on physical examination
A
- Examination of the Leg
o Local erythema, warmth and swelling
o Measure the leg circumference
o Varicosities (swollen/tortuous vessels)
o Skin colour changes
o NOTE: Homan’s Sign - forced passive dorsiflexion of the ankle causes deep calf pain
- Risk is stratified using the WELLS CRITERIA (NOTE: this is
different from the PE Wells criteria)
o Score 2 or more = high risk
- Examine for PE
o Check respiratory rate, pulse oximetry and pulse rate
11
Q
Identify appropriate investigations for DVT
A
- Doppler Ultrasound - GOLD STANDARD
- Impedance Plethysmography - changes in blood volume results in changes of electrical resistance
- Bloods
o D-dimer: can be used as a negative predictor
o Thrombophilia screen if indicated
- If PE suspected
o ECG
o CXR
o ABG
12
Q
Generate a management plan for DVT
A
- ANTICOAGULATION
o Heparin whilst waiting for warfarin to increase INR to the target range of 2-3
o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months
o DVTs extending beyond the knee require anticoagulation for 6 months
o Recurrent DVTs require long-term warfarin
- IVC Filter
o May be used if anticoagulation is contraindicated and there is a risk of embolisation
- Prevention
o Graduated compression stockings
o Mobilisation
o Prophylactic heparin (if high risk e.g. hospitalised patients)
13
Q
Identify possible complications of DVT
A
- PE
- Venous infarction (phlegmasia cerulea dolens)
- Thrombophlebitis (results from recurrent DVT)
- Chronic venous insufficienc
14
Q
Summarise the prognosis for patients with DVT
A
- Depends on extent of DVT
- Below-knee DVTs have a GOOD prognosis
- Proximal DVTs have a greater risk of embolisation
15
Q
Define gangrene and necrotising fasciitis
A
- Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
- Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes
16
Q
Explain the aetiology/risk factors of necrotising fasciitis
A
- Gangrene
o Tissue ischaemia and infarction
o Physical trauma
o Thermal injury
o Gas gangrene is caused by Clostridia perfringens
- Necrotising Fasciitis
o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms
- Risk Factors
o Diabetes
o Peripheral vascular disease
o Leg ulcers
o Malignancy
o Immunosuppression
o Steroid use
o Puncture/surgical wounds
17
Q
Summarise the epidemiology of gangrene and necrotising fasciitis
A
- Gangrene - relatively COMMON
* Necrotising fasciitis and gas gangrene - RARE
18
Q
Recognise the presenting symptoms of gangrene and necrotising fasciitis
A
- Gangrene
o Pain
o Discolouration of affected area
o Often affects extremities or areas subject to high pressure
- Necrotising Fasciitis
o Pain
- Often seems SEVERE and out of proportion to the apparent physical signs
o Predisposing event (e.g. trauma, ulcer, surgery)
19
Q
Recognise the signs of gangrene and necrotising fasciitis on examination
A
- Gangrene
o Painful area = erythematous region around gangrenous tissue
o Gangrenous tissue = BLACK because of haemoglobin break down products
o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
- Necrotising Fasciitis
o Area of erythema and oedema
o Haemorrhagic blisters may be present
o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)
20
Q
Identify appropriate investigations for gangrene and necrotising fasciitis
A
- Bloods - FBC, U&Es, glucose, CRP and blood culture
- Wound Swab, Pus/Fluid Aspirate - MC&S
- X-ray of affected area - may show gas produced in gas gangrene
21
Q
Define heart block
A
- 1st Degree AV Block: prolonged conduction through the AV node
- 2nd Degree AV Block:
o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle ten begins again.
o Mobitz Type II: intermittent or regular failure of conduction through the AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)
- 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle
22
Q
Summarise the epidemiology of heart block
A
250,000 pacemakers are implanted every year and they are mostly for heart block
23
Q
Explain the aetiology/risk factors of heart block
A
- MI or ischaemic heart disease (MOST COMMON)
- Infection (e.g. rheumatic fever, infective endocarditis)
- Drugs (e.g. digoxin)
- Metabolic (e.g. hyperkalaemia)
- Infiltration of conducting system (e.g. sarcoidosis)
- Degeneration of the conducting system
24
Q
Recognise the presenting symptoms of heart block
A
- 1st Degree - asymptomatic
- 2nd Degree - usually asymptomatic
- Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole)
o May also cause dizziness, palpitations, chest pain and heart failure
25
Recognise the signs of heart block on physical examination
* Often NORMAL
* Check for signs of a potential cause of heart block
* Complete Heart Block
o Slow large volume pulse
o JVP may show cannon a waves
* Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously
* Mobitz Type II and 3rd Degree Heart Block
o Signs of reduced cardiac output (e.g. hypotension, heart failure)
26
Identify appropriate investigations for heart block
* ECG - GOLD STANDARD
o First Degree - fixed prolonged PR interval (> 0.2 s)
o Mobitz Type I (Wenckebach) - progressively prolonged PR interval, culminating in a P wave that is NOT followed by a QRS complex. The pattern then begins again. 'Going, going, gone'.
o Mobitz Type II - intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
o Complete Heart Block - no relationship between P waves and QRS complexes. If QRS is initiated in the:
* Bundle of His - narrow complex
* More distally - wide complex and slow rate (~ 30 bpm)
* CXR
o Cardiac enlargement
o Pulmonary oedema
* Bloods
o TFTs
o Digoxin level
o Cardiac enzymes
o Troponin
* Echocardiogram
o Wall motion abnormalities
o Aortic valve disease
o Vegetations
27
Generate a management plan for heart block
* Chronic Block
o Permanent pacemaker is recommended in:
* Complete heart block
* Advanced Mobitz Type II
* Symptomatic Mobitz Type I
* Acute Block
o If associated with clinical deterioration use IV atropine
o Consider temporary (external) pacemaker
28
Identify the possible complications of heart block
* Asystole
* Cardiac arrest
* Heart failure
* Complications of any pacemaker inserted
29
Summarise the prognosis for patients with heart block
Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease
30
Define hypertension
* Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions.
* Malignant Hypertension: BP > 200/130 mm Hg
31
Summarise the epidemiology of hypertension
* VERY COMMON
| * 10-20% of adults in the Western world
32
Explain the aetiology/risk factors of hypertension
* Primary
o Essential or idiopathic hypertension
o Responsible for > 90% of cases
* Secondary
o Renal
* Renal artery stenosis
* Chronic glomerulonephritis
* Chronic pyelonephritis
* Polycystic kidney disease
* Chronic renal failure
o Endocrine
* Diabetes mellitus
* Hyperthyroidism
* Cushing's syndrome
* Conn's syndrome
* Hyperparathyroidism
* Phaeochromocytoma
* Congenital adrenal hyperplasia
* Acromegaly
o Cardiovascular
* Coarctation of the aorta
* Increased intravascular volume
o Drugs
* Sympathomimetics
* Corticosteroids
* COCP
o Pregnancy
* Pre-eclampsia
33
Recognise the presenting symptoms of hypertension
* Often ASYMPTOMATIC
* Symptoms of complications
* Symptoms of the cause
* Accelerated or Malignant Hypertension
o Scotomas (visual field loss)
o Blurred vision
o Headache
o Seizures
o Nausea and vomiting
o Acute heart failure
34
Recognise the signs of hypertension on physical examination
* Blood pressure should be measured on 2-3 different occasions before diagnosing hypertension
* The lowest reading should be recorded
* Examination may reveal information about causes:
o Radiofemoral delay = coarctation of the aorta distal to the left subclavian artery
o Renal artery bruit = renal artery stenosis
o Fundoscopy to detect hypertensive retinopathy
Keith-Wagner Classification of Hypertensive Retinopathy
i. Silver wiring
ii. As above + arteriovenous nipping
iii. As above + flame haemorrhages + cotton wood exudates
iv. As above + papilloedema
35
Identify appropriate investigations for hypertension
* Bloods:
o U&Es
o Glucose
o Lipids
* Urine Dipstick
o Blood and protein (e.g. if glomerulonephritis)
* ECG
o May show signs of left ventricular hypertrophy or ischaemia
* Ambulatory blood pressure monitoring
o Excludes white coat hypertension
* Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram)
36
Generate a management plan for hypertension
* Conservative
o Stop smoking
o Lose weight
o Reduce alcohol intake
o Reduce dietary sodium
* Investigate for secondary causes (mainly in young patients)
* Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage. Multiple drug therapies often needed.
o ACE Inhibitors or Angiotensin Receptor Blockers - first line if:
* < 55 yrs
* Diabetic
* Heart failure
* Left ventricular dysfunction
o CCBs - first line if:
* > 55 yrs
* Black
* NOTE: thiazide diuretics can be used if CCBs are not tolerated
o Beta-Blockers
* Not preferred initial therapy
* May be considered in younger patients
* CAUTION: combining with thiazide diuretic may increase risk of developing diabetes
* May increase risk of heart failure
o Alpha-Blockers
* 4th line
* May be used in patients with prostate disease
* Target BP
o Non-Diabetic: < 140/90 mm Hg
o Diabetes without proteinuria: < 130/80 mm Hg
o Diabetes WITH proteinuria: < 125/75 mm Hg
* Severe Hypertension Management (Diastolic > 140 mm Hg)
o Atenolol
o Nifedipine
* Acute Malignant Hypertension Management:
o IV beta-blocker (e.g. esmolol)
o Labetolol
o Hydralazine sodium nitroprusside
o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction
* This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high
* Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted
* A rapid drop in blood pressure with constricted vessels will cause an infarction
37
Identify the possible complications of hypertension
* Heart failure
* Coronary artery disease
* Cerebrovascular accidents
* Peripheral vascular disease
* Emboli
* Hypertensive retinopathy
* Renal failure
* Hypertensive encephalopathy
* Posterior reversible encephalopathy syndrome (PRES)
* Malignant hypertension
38
Summarise the prognosis for patients with hypertension
* Good prognosis if well controlled
* Uncontrolled hypertension is associated with increased mortality
* Treatment reduces incidence of renal damage, stroke and heart failure
39
Define infective endocarditis
Infection of intracardiac endocardial structures (mainly heart valves)
40
Explain the aetiology/risk factors of infective endocarditis
* Most common organisms causing infective endocarditis:
o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis
o Staphylococci (35%) - S. aureus and S. epidermidis
o Enterococci (20%) - usually E. faecalis
o Other organisms:
* Haemophilus
* Actinobacillus
* Cardiobacterium
* Coxiella burnetii
* Histoplasma (fungal)
* Pathophysiology
o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia
o The vegetations are made up of platelets, fibrin and infective organisms
o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities
o Activation of the immune system can lead to the formation of immune complexes --> vasculitis, glomerulonephritis, arthritis
* Risk Factors
o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)
o Prosthetic heart valves
o Turbulent blood flow (e.g. patent ductus arteriosus)
o Recent dental work/poor dental hygiene (source of S. viridans)
41
Summarise the epidemiology of infective endocarditis
* UK Incidence: 16-22/1 million per year
42
Recognise the presenting symptoms of infective endocarditis
* Fever with sweats/chills/rigors
o NOTE: this might be relapsing and remitting
* Malaise
* Arthralgia
* Myalgia
* Confusion
* Skin lesions
* Ask about recent dental surgery or IV drug use
43
Recognise the signs of infective endocarditis on physical examination
* Pyrexia
* Tachycardia
* Signs of anaemia
* Clubbing
* New regurgitant murmur or muffled heart sounds
* Frequency of heart murmurs:
o Mitral > Aortic > Tricuspid > Pulmonary
* Splenomegaly
* Vasculitic Lesions
o Roth spots on retina
o Petechiae on pharyngeal and conjunctival mucosa
o Janeway lesions (painless macules on the palms which blanch on pressure)
o Osler's nodes (tender nodules on finger/toe pads)
o Splinter haemorrhages
44
Identify appropriate investigations for infective endocarditis
* Bloods
o FBC - high neutrophils, normocytic anaemia
o High ESR/CRP
o U&Es
o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive
* Urinalysis
o Microscopic haematuria
o Proteinuria
* Blood Culture
o Do microscopy and sensitivities as well
* Echocardiography
o Transthoracic or transoesophageal (produces better image)
* Duke's Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs
45
Generate a management plan for infective endocarditis
* Antibiotics for 4-6 weeks
* On clinical suspicion = EMPIRICAL TREATMENT
o Benzylpenicillin
o Gentamicin
* Streptococci - continue the same as above
* Staphylococci
o Flucloxacillin/vancomycin
o Gentamicin
* Enterococci
o Ampicillin
o Gentamicin
* Culture Negative
o Vancomycin
o Gentamicin
* SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics
46
Identify the possible complications of infective endocarditis
* Valve incompetence
* Intracardiac fistulae or abscesses
* Aneurysm
* Heart failure
* Renal failure
* Glomerulonephritis
* Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
47
Summarise the prognosis for patients with infective endocarditis
* FATAL if untreated
| * 15-30% mortality even WITH treatment
48
Define ischaemic heart disease
* Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome.
* ACS can be further subdivided into:
o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
o NSTEMI
o STEMI - ST elevation with transmural infarction
o NOTE: MI = cardiac muscle necrosis resulting from ischaemia
(Laz page 75 has a good picture)
49
Summarise the epidemiology of ischaemic heart disease
* COMMON
* Prevalence: > 2 %
* More common in males
* Annual incidence of MI in the UK ~ 5/1000
50
Explain the aetiology/risk factors of ischaemic heart disease
* Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
* This is usually due to atherosclerosis
* Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli
* Atherosclerosis pathophysiology
o Endothelial injury leads to migration of monocytes into the subendothelial space
o These monocytes differentiate into macrophages
o Macrophages accumulate LDL lipids and become foam cells
o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans
o This leads to the formation of an atherosclerotic plaque
* Risk Factors
o Male
o Diabetes mellitus
o Family history
o Hypertension
o Hyperlipidaemia
o Smoking
51
Recognise the presenting symptoms of ischaemic heart disease
* ACS
o Acute-onset chest pain
o Central, heavy, tight, crushing pain
o Radiates to the arms, neck, jaw or epigastrium
o Occurs at rest
o More severe and frequent pain that previously occurring stable angina
o Associated symptoms:
* Breathlessness
* Sweating
* Nausea and vomiting
* SILENT INFARCTS occur in the elderly and diabetics
* Stable Angina
o Chest pain brought on by exertion and relieved by rest
52
Recognise the signs of ischaemic heart disease on physical examination
* Stable Angina
o Check for signs of risk factors
* ACS
o There may be NO CLINICAL SIGNS
o Pale
o Sweating
o Restless
o Low-grade pyrexia
o Check both radial pulses to rule out aortic dissection
o Arrhythmias
o Disturbances of BP
o New heart murmurs
o Signs of complications (e.g. acute heart failure, cardiogenic shock)
53
Identify appropriate investigations for ischaemic heart disease
* Bloods
o FBC
o U&Es
o CRP
o Glucose
o Lipid profile
o Cardiac enzymes (troponins and CK-MB)
o Amylase (pancreatitis could mimic MI)
o TFTs
o AST and LDH (raised 24 and 48 hours post-MI, respectively)
* ECG
o Unstable Angina or NSTEMI:
* May show ST depression or T wave inversion
o STEMI:
* Hyperacute T waves
* ST elevation (> 1 mm in limb leads, > 2 mm in chest leads)
* New-onset LBBB
* Later changes:
* T wave inversion
* Pathological Q waves
o Relationship between ECG leads and the side of the heart
* Inferior: II, III, aVF
* Anterior: V1-V5/6
* Lateral: I, aVL, V5/6
* Posterior: Tall R wave and ST depression in V1-3
* CXR
o Check for signs of heart failure
* Exercise ECG
o Indications
* Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
* Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
* NOTE: digoxin is associated with giving a false-positive result
o Results:
* Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
* Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
* NOTE: beta-blockers reduce heart rate and so should be stopped before the test
* Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
* Radionuclide Myocardial Perfusion Imaging (rMPI)
o Uses Technetium-99m sestamibi or tetrofosmin
o Can be performed under stress or at rest
o Stress testing shows low uptake in ischaemic myocardium
* Echocardiogram
o Measures left ventricular ejection fraction
o Exercise or dobutamine stress echo may detect regional wall motion abnormalities
* Pharmacological Stress Testing
o This is used in patients who are unable to exercise
o Pharmacological agents can be used to induce a tachycardia, such as:
* Dipyridamole
* Adenosine
* Dobutamine
o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
* Cardiac Catheterisation/Angiography
o Performed if ACS with positive troponin or if high risk on stress testing
* Coronary Calcium Scoring
o Uses specialised CT scan
o May be useful in outpatients with atypical chest pain or in acute chest pain that isn't clearly due to ischaemia
54
Generate a management plan for ischaemic heart disease
* Stable Angina
o Check for signs of risk factors
* ACS
o There may be NO CLINICAL SIGNS
o Pale
o Sweating
o Restless
o Low-grade pyrexia
o Check both radial pulses to rule out aortic dissection
o Arrhythmias
o Disturbances of BP
o New heart murmurs
o Signs of complications (e.g. acute heart failure, cardiogenic shock)
Identify appropriate investigations for ischaemic heart disease
* Bloods
o FBC
o U&Es
o CRP
o Glucose
o Lipid profile
o Cardiac enzymes (troponins and CK-MB)
o Amylase (pancreatitis could mimic MI)
o TFTs
o AST and LDH (raised 24 and 48 hours post-MI, respectively)
* ECG
o Unstable Angina or NSTEMI:
* May show ST depression or T wave inversion
o STEMI:
* Hyperacute T waves
* ST elevation (> 1 mm in limb leads, > 2 mm in chest leads)
* New-onset LBBB
* Later changes:
* T wave inversion
* Pathological Q waves
o Relationship between ECG leads and the side of the heart
* Inferior: II, III, aVF
* Anterior: V1-V5/6
* Lateral: I, aVL, V5/6
* Posterior: Tall R wave and ST depression in V1-3
* CXR
o Check for signs of heart failure
* Exercise ECG
o Indications
* Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
* Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
* NOTE: digoxin is associated with giving a false-positive result
o Results:
* Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
* Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
* NOTE: beta-blockers reduce heart rate and so should be stopped before the test
* Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
* Radionuclide Myocardial Perfusion Imaging (rMPI)
o Uses Technetium-99m sestamibi or tetrofosmin
o Can be performed under stress or at rest
o Stress testing shows low uptake in ischaemic myocardium
* Echocardiogram
o Measures left ventricular ejection fraction
o Exercise or dobutamine stress echo may detect regional wall motion abnormalities
* Pharmacological Stress Testing
o This is used in patients who are unable to exercise
o Pharmacological agents can be used to induce a tachycardia, such as:
* Dipyridamole
* Adenosine
* Dobutamine
o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
* Cardiac Catheterisation/Angiography
o Performed if ACS with positive troponin or if high risk on stress testing
* Coronary Calcium Scoring
o Uses specialised CT scan
o May be useful in outpatients with atypical chest pain or in acute chest pain that isn't clearly due to ischaemia
55
Identify the possible complications of ischaemic heart disease
* STABLE ANGINA
o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
* All patients should receive aspirin 75 mg/day unless contraindicated
o Immediate symptom relief (e.g. GTN spray)
o Long-term management
* Beta-blockers
* Contraindicated in:
* Acute heart failure
* Cardiogenic shock
* Bradycardia
* Heart block
* Asthma
* Calcium channel blockers
* Nitrates
o Percutaneous coronary intervention (PCI)
* Performed in patients with stable angina despite maximal tolerable medical therapy
o Coronary artery bypass graft (CABG)
* Occurs in more severe cases (e.g. three-vessel disease)
* UNSTABLE ANGINA/NSTEMI
o Admit to coronary care unit
o Oxygen, IV access, monitor vital signs and serial ECG
o GTN
o Morphine
o Metoclopramide (to counteract the nausea caused by morphine)
o Aspirin (300 mg initially, followed by 75 mg indefinitely)
o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
o LMWH (e.g. enoxaparin)
o Beta-blocker (e.g. metoprolol)
o Glucose-insulin infusion if blood glucose > 11 mmol/L
o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
* Undergoing PCI
* At high risk of further cardiac events
o If little improvement, consider urgent angiography with/without revascularisation
o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH
* Morphine
* Oxygen
* Nitrates
* Anticoagulants (aspirin + clopidogrel)
* Beta-blockers
* ACE inhibitors
* Statins
* Heparin
* STEMI
o Same as UAP/NSTEMI management except:
* Clopidogrel
* 600 mg if patient is going to PCI
* 300 mg if undergoing thrombolysis and < 75 yrs
* 75 mg if undergoing thrombolysis and > 75 yrs
* MAINTENANCE: 75 mg daily for at least 1 year
* If undergoing primary PCI:
* IV heparin (plus GlpIIb/IIIa inhibitor)
* Bivalirudin (antithrombin)
o Primary PCI
* Goal < 90 min if available
o Thrombolysis
* Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase)
* Only considered if within 12 hours of chest pain with ECG changes and not contraindicated
* Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis
o Secondary Prevention
* Dual antiplatelet therapy (aspirin + clopidogrel)
* Beta-blockers
* ACE inhibitors
* Statins
* Control risk factors
o Advice
* No driving for 1 month following MI
o CABG
* Considered in patients with left main stem or three-vessel disease
Identify the possible complications of ischaemic heart disease
* Increased risk of MI and other vascular disease (e.g. stroke, PVD)
* Cardiac injury from an MI can lead to heart failure and arrhythmias
* Early Complications (within 24-72 hrs)
o Death
o Cardiogenic shock
o Heart failure
o Ventricular arrythmias
o Heart block
o Pericarditis
o Myocardial rupture
o Thromboembolism
* Late Complications
o Ventricular wall rupture
o Valvular regurgitation
o Ventricular aneurysms
o Tamponade
o Dressler's syndrome
o Thromboembolism
* MNEMONIC for Complications of MI
o Death
o Arrhythmias
o Rupture
o Tamponade
o Heart failure
o Valve di
o Aneurysm
o Dressler's syndrome
o Embolism
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Summarise the prognosis for patients with ischaemic heart disease
* TIMI score (0-7) can be used for risk stratification
o NOTE: TIMI = thrombolysis in myocardial infarction
o High scores are associated with high risk of cardiac events within 30 days of MI
* Killip Classification of acute MI can also be used:
o Class I: no evidence of heart failure
o Class II: mild to moderate heart failure
o Class III: over pulmonary oedema
o Class IV: cardiogenic shock
