Cardiovascular Flashcards
Give three cardinal signs of anaphylaxis
Skin rash
Wheeze and inspiratory stridor
Hypotension
List the ABC signs of anaphylaxis
Airway:
* Voice hoarseness
* Stridor
Breathing:
* Rapid breathing
* Wheeze
* Fatigue
* Cyanosis
Circulation:
* Pale clammy
* Hypotension
* Faintness
* Confusion
* Reduced consciousness
Give the pathophysiology of anaphylaxis
IgE-mediated reaction
On first exposure, IgE antibodies are formed specific to the antigen presented.
IgE antibodies attach to high-affinity Fc receptors on basophils and mast cells.
On subsequent exposure, binding of antigen to the IgE antibodies leads to bridging and triggers the degranulation of mast cells.
Cause release of:
Histamine
Prostaglandin D2
Leukotrienes
Platelet-activating factor
Tryptase
Nitric oxide
Eosinophil and neutrophil chemotactic factors
Give the effects of adrenaline on alpha-1, beta-1, and beta-2 receptors
Alpha-1 receptors - peripheral vasoconstriction, which reduces hypotension and mucosal oedema.
Beta-1 receptors - increase the rate and force of cardiac contractions and reduce hypotension.
Beta-2 receptors - reducing inflammatory mediator release from mast cells and basophils and causing bronchodilation.
Define the four types of hypersensitivity
Type 1 IgE-mediated hypersensitivity
* IgE is bound to mast cells via Fc portion. When an allergen binds to these antibodies, cross linking of IgE induces degranulation
Type 2 IgG-mediated cytotoxic hypersensitivity
* Cells are destroyed by bound antibody, either by activation of complement or by Tc cell with Fc receptor for the antibody
Type 3 Immune complex-mediated hypersensitivity
* Antigen-antibody complexes are deposited in tissues, causing activation of complement, which attracts neurtrophils to the site
Type 4 Cell-mediated hypersensitivity
* Th1 cells release cytokines, which activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site
List the variables in QRISK
Demographic information
Age
Gender
Ethnicity
Postcode
Clinical information (13)
Angina or heart attack in 1st degree relative < 60 years age
Smoking status
Diabetic status
Rheumatoid arthritis
Systemic lupus erythematosus
Chronic kidney disease (stage 3, 4, 5)
Atrial fibrillation
Migraine
Erectile dysfunction
Severe mental illness
Under treatment for hypertension
Atypical antipsychotic medication
Regular steroid tablets
Others
Cholesterol/HDL ratio
Systolic blood pressure
BMI = Weight / Height squared
Give the management plan for a QRISK < 10%
Lifestyle modifications
Advise smokers to stop and non-smokers to avoid passive smoking.
Advise weight loss if the person is overweight or obese.
Advise the person to adopt a diet that helps to reduce CVD risk, including:
* Eating unsalted nuts, seeds, legumes, fish, fruit, vegetables and fibre
* Reducing sugars, saturated fats, and salt
* Increase mono-unsaturated fats
Advise the person to keep alcohol consumption within the recommended limits - no more than 14 units per week spread over 3 days or more
Advise the person to be physically active and to avoid prolonged sedentary behaviour, including:
* At least 75 minutes per week of vigorous intensity aerobic activity
* At least 150 minutes per week of moderate intensity aerobic activity
Review relevant co-morbidities
Advice that a further risk assessment should be considered in 5 years.
Give the management plan for a QRISK > 10%
Lifestyle modifications
If lifestyle modification is ineffective or inappropriate, offer Atorvastatin 20 mg daily
List the risk factors for CVD
Non-modifiable
Age
Male sex
Family history
Ethnicity (increased risk in South Asian or sub-Saharan African, reduced risk in South American or Chinese)
Modifiable
Smoking.
Low HDL cholesterol and high non-HDL cholesterol.
Sedentary lifestyle.
Unhealthy diet.
Alcohol intake above recommended levels.
Overweight and obesity.
Comorbidities
Hypertension.
Diabetes mellitus (and pre-diabetes/metabolic syndrome).
Chronic kidney disease.
Dyslipidemia (familial and non-familial).
Atrial fibrillation.
Rheumatoid arthritis, systemic lupus erythematosus, and other systemic inflammatory disorders.
Influenza.
Serious mental health problems (schizophrenia, post-traumatic stress disorder).
Periodontitis.
Define typical, atypical, and non-anginal chest pain
Typical angina - 3 out of 3 following features of chest pain
Atypical angina - 2 out of 3 following features of chest pain
Non-anginal chest pain - 1 out of 3 following features of chest pain
Features of chest pain:
Heavy, tight, gripping central or retrosternal pain that may spread to jaw and arms
Pain occurs with exercise/ emotional stress
Pain eases rapidly with rest/GTN
List the severity classification criteria of stable angina
Class I = Angina with strenuous activity. No angina during ordinary activity
Class II = Angina during ordinary activity
Class III = Angina during low level activity
Class IV = Angina at rest/ any level of exercise
Define unstable angina
Acute coronary syndrome
Angina of recent onset <24 hrs
Define Prinzmetal’s angina
Angina at rest due to coronary vessel spasms
More frequent in women
Define Microvascular angina
Exercise induced angina
Coronary artery normal during angiography
Give the pathophysiology of atherosclerosis
- Endothelial dysfunction triggered by smoking, hypertension or hyperglycaemia.
- Pro-inflammatory, pro-oxidant, proliferative changes in the endothelium.
- Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL).
- Macrophages phagocytose oxidised low-density lipoprotein.
- Smooth muscle proliferation and migration from the tunica media into the intima.
List the acute and chronic presentations of atherosclerosis
Acute:
Stroke
TIA
Thoracic aortic rupture
Thoracic aortic dissection
Abdominal aortic occlusion (rare)
Renal artery occlusion (rare)
Acute mesenteric ischaemia
Acute coronary syndrome
Acute peripheral arterial occlusion
Chronic:
Recurrent TIAs
Vascular dementia
Worsening renal function
Renovascular hypertension
Chronic mesenteric ischaemia
Abdominal angina
Stable angina
Abdominal Aortic Aneurysm
Chronic limb ischaemia
Intermittent claudication
List the differential diagnosis for chest pain
Cardiac causes:
Acute coronary syndrome
Stable angina
Thoracic aorta dissection
- Sudden tearing chest pain radiating to the back
Pericarditis / cardiac tamponade
- Sharp constant sternal pain, relieved by sitting forward
Acute congestive heart failure
Arrhythmias
- Chest pain with palpitations
Pulmonary causes:
Pulmonary embolism
- Acute onset breathlessness, pleuritic chest pain, cough, haemoptysis, syncope
Pneumothorax / tension pneumothorax
- Sudden onset chest pain, breathlessness, tachycardia, pallor
Community acquired pneumonia
- Cough, sputum, wheeze, dyspnoea, pleuritic chest pain
Asthma
- Wheeze, breathlessness, cough
Lung / lobar collapse
- Localised chest pain, breathlessness, cough
Lung cancer
- Chest / shoulder pain, haemoptysis, dyspnoea, weight loss, anorexia, hoarseness, cough
Pleural effusion
- Localised chest pain, progressive breathlessness
List the risk factors for angina
Hyperlipidaemia
Diabetes mellitus
Smoking
Age
Family Hx.
Obesity
Hypertension
Environmental factors for angina
Heavy meals
Cold weather
Emotional stress
Exercise
Name the first line investigations for angina
12-lead resting ECG
Haemoglobin
Lipid profile
Fasting blood glucose / HbA1c
List the ECG changes that may indicate ischaemia or previous myocardial infarction
ST depression (ischemia)
Pathological Q waves (prior infarction)
Left bundle branch block
T-wave abnormalities (T-wave flattening / elevation / inversion)
List the management options for stable angina
Symptom relief:
Sublingual glyceryl trinitrate (GTN)
Regular medications
1. beta-blockers or calcium channel blockers
2. if intolerance/contraindicated:
- long acting nitrates (isosorbide mononitrate)
- ivabradine
- ranolazine
- nicorandil
if symptomatic switch or both
3. plus 2 other anti-anginals
4. revascularisation by PCI or CABG
Drug treatment for secondary prevention
Low dose aspirin 75mg
If stroke / peripheral arterial disease: continue clopidogrel
ACEi for people with stable angina and diabetes mellitus.
When should nitrates not be used in
Acute MI with low filling pressure, acute circulatory failure (shock, vascular collapse), or very low blood pressure.
Hypertrophic obstructive cardiomyopathy, constrictive pericarditis, cardiac tamponade, low cardiac filling pressures, or aortic/mitral valve stenosis.
Diseases associated with a raised intracranial pressure (for example following a head trauma, including cerebral haemorrhage).
Severe anaemia.
Closed-angle glaucoma.
Severe hypotension, or hypovolaemia
List the anti-anginal medications
Vasodilators
* Isosorbide mononitrate
* Glyceryl trinitrate
Beta-blockers
* Bisoprolol
Calcium-channel blockers
* Verapamil, diltiazem, amlodipine
Ivabradine
Nicorandil
Ranolazine
Aspirin
When should bisoprolol be used cautiously
COPD
AV conduction block
Acute heart failure
List the side effects of bisoprolol
Fatigue
Peripheral vasoconstriction (cold peripheries)
Erectile dysfunction
Bronchospasm
When are verapamil and diltiazem contraindicated
Severe bradycardia
LV failure with pulmonary congestion
2/3 degree AV block
List the side effects of Verapamil, Diltiazem, Amlodipine
Verapamil: constipation
Diltiazem: ankle oedema
Amlodipine: ankle oedema, reflex tachycardia
List the side effects of Ivabradine
Bradycardia
Phosphenes
When is Ivabradine contraindicated
Sick sinus syndrome
AV block
List the side effects of Nicorandil
Headaches
Flushing
Oral ulceration
List the side effects of Ranolazine
Constipation
Dizziness
Lengthened QT
When should acute coronary syndrome be suspected
Any patient with acute chest pain which includes pain in arms, back, jaw that
* Lasts longer than 15 minutes
* Is associated with nausea and vomiting, marked sweating, breathlessness
* Is either new in onset or occurs as sudden worsening of known stable angina
List the causes of acute coronary syndrome
atherosclerosis
stress-induced (Tako-Tsubo) cardiomyopathy
coronary vasospasm without plaque rupture
coronary dissection due to connective tissue defects
drug induced (amphetamine, cocaine)
thoracic aorta dissection
List the 6 types of MI
1 - MI spontaneous with ischaemia. due to primary coronary event
2 - MI secondary to ischaemia, due to increased demand and reduced supply
3 - MI in sudden cardiac death
4a - MI in PCI
4b - MI in stent thrombosis
5 - MI in CABG
Give the early management of STEMI
300 mg loading dose aspirin as soon as possible and continue indefinitely unless contraindicated
Immediately assess eligibility for reperfusion therapy. Otherwise medical management.
Reperfusion therapy:
Angiography with follow-on primary PCI
* Offer if presenting in 12 hours of symptoms and PCI can be delivered in 120 mins
* Consider if presenting more 12 hours after symptoms and continuing myocardial ischaemia or cardiogenic shock
* Consider radial in preference to femoral access
Drug therapy for primary PCI:
* Offer prasugrel with aspirin if not already taking oral anticoagulant
* Offer clopidogrel with aspirin if taking an oral anticoagulant
* Offer unfractionated heparin with bailout GPI for radial access
* Consider bivalirudin with bailout GPI if femoral access needed
Fibrinolysis
* Offer if presenting in 12 hours of symptoms and PCI not possible in 120 mins
Drug therapy for fibrinolysis:
* Give an antithrombin (heparin) at the same time
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk
Medical management
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk
Give the early management of NSTEMI/Unstable Angina
Initial antiplatelet therapy - 300 mg loading dose aspirin as soon as possible and continue indefinitely unless contraindicated
Initial antithrombin therapy - fondaparinux unless high bleeding risk or immediate angiography
Use GRACE to predict 6-month mortality and risk of cardiovascular events:
Low risk (predicted 6-month mortality ≤ 3%)
* Consider conservative management without angiography
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk
Intermediate or higher risk (predicted 6-month mortality > 3%)
* Offer immediate angiography if clinical conditions are unstable.
* Otherwise, consider angiography (with follow-on PCI if indicated) within 72 hours if no contraindications such as comorbidity or active bleeding
* Offer prasugrel with aspirin if not already taking oral anticoagulant
* Offer clopidogrel with aspirin if taking an oral anticoagulant
* Offer systemic unfractionated heparin in catheter laboratory if having PCI
List the variables involved in GRACE risk score
Age
Heart rate/pulse
Systolic BP
Creatinine
Cardiac arrest at admission YES/NO
ST segment deviation on ECG YES/NO
Abnormal cardiac enzymes
Killip class (signs/symptoms)
* I - No congestive heart failure
* II - Presence of S3 gallop or bibasilar rales or both
* III - Pulmonary oedema
* IV - Cardiogenic shock
List the complications of MI
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler’s syndrome
Embolism
Recurrence, regurgitation
List the causes of pericarditis
Idiopathic (most common)
Viral
Coxsackie virus
HIV
EBV
CMV
Mumps
Herpes
Bacterial
TB
meningococcal
staphylococcal
streptococcal
pneumococcal
mycoplasmosis
borreliosis
chlamydia
h.influenzae
Fungal
candidiasis
histoplasmosis
coccidioidomycosis
Post myocardial injury syndrome
myocardial infarction (Post-MI early, Dressler’s syndrome late)
surgery
radiation
Myxoedematous pericarditis
Chylopericardium
Uraemic pericarditis
Malignancy
primary malignancy of heart
mesothelioma
metastatic pericarditis
Breast / lung carcinoma
Lymphoma
Leukaemia
Melanoma
Autoimmune
rheumatic fever
SLE
RA
scleroderma
Drug induced
procainamide
hydralazine
doxorubicin
isoniazid
cyclophosphamide
Familial idiopathic pericarditis
List the presentations of Dressler’s syndrome
Fever
Pleuritic pain
Pericardial effusion
Raised ESR
Give the management of Dressler’s syndrome
NSAIDs
Describe the pathophysiology of Dressler’s syndrome
autoimmune reaction against antigenic proteins formed as the myocardium recovers
When does Dressler’s syndrome occur
Tends to occur around 2-6 weeks following a MI.
List three complications of pericarditis
Chronic recurrent pericarditis
Cardiac tamponade
Constrictive pericarditis
Give the natural history of acute pericarditis
<4-6 weeks
List the presentations of acute pericarditis
Pleuritic chest pain that is exacerbated by movement, relieved by sitting forward
Pericardial friction rub
Pericardial effusion
List the ECG features in acute pericarditis
Saddle shaped ST elevation
PR depression
Define Recurrent pericarditis
Recurrence after an initial episode of acute pericarditis with an intervening symptom-free interval of ≥4 to 6 weeks.
Define Incessant pericarditis
Signs and symptoms lasting >4 to 6 weeks but <3 months without remission.
Define Chronic pericarditis
Signs and symptoms persisting for >3 months.
What can constrictive pericarditis be caused by
TB
hemopericardium
rheumatic heart disease
bacterial infection
List the investigations considered in pericarditis
ECG
* upwards concave ST-segment elevation globally with PR depressions in most leads
* J-point depression and PR elevation in leads aVR and V1
Serum troponin - Elevation reflects myocardial involvement
Pericardiocentesis - Urgent in cardiac tamponade
CRP - Elevated
Serum urea and electrolytes - Elevated levels of urea suggest a uraemic cause
FBC - Leukocytosis in acute or infectious aetiology
LFT - Liver congestion may be present if the patient is developing cardiac tamponade.
CXR - Normal / Increased cardiothoracic ratio if large pericardial effusion is present (> 300mL)
Transthoracic echocardiography
* pericardial effusion
* absence of left ventricular wall motion abnormalities
* thickened and/or bright appearance of pericardium if actively inflamed
* evidence of respiratory variation in ventricular filling
Give the management for acute pericarditis
70~90% self limiting
NSAIDS (aspirin / ibuprofen) + PPI + Colchicine
Exercise restriction
List the high risk groups that may require inpatient management of pericarditis
Fever > 38C
Subacute onset
Large effusion
Cardiac tamponade
Unresponsive to therapy
List the clinical features of pericardial effusion
Soft distant heart sound
Obscured apex beat
Pericardial friction rub due to pericarditis early on, then quieter as fluid accumulates - best heard over the left sternal border with the patient leaning forwards at end-expiration
Pulsus paradoxus - decrease in systolic blood pressure of >12 mmHg during inspiration
Ewart’s sign - dull percussion below L scapula angle
List the ECG changes in pericardial effusion
Sinus tachycardia.
Low QRS voltage.
Electrical alternans.
Name the first line investigation for pericardial effusion
Transthoracic echocardiography
Give the CXR feature of pericardial effusion
water-bottle-shaped cardiac silhouette with distinct pericardial fat stripe
List the clinical features of cardiac tamponade
Tachycardia
Tachypnoea
Hypotension
Elevated jugular venous pressure
Distended neck veins
Kussmaul’s sign (a rise in venous pressure with inspiration)
Pulsus paradoxus
Give the Beck’s triad of cardiac tamponade
Hypotension
Distant heart sounds
Elevated jugular venous pressure
List ECG changes in cardiac tamponade
low QRS voltages
electrical alternans
List the management approaches in cardiac tamponade
Pericardiocentesis under echocardiographic guidance
Surgery drainage
What population groups do infective endocarditis most commonly affect?
Elderly
Young IVDU
Young congenital heart disease
List the aetiology for infective endocarditis
Dental procedures/disease - viridian groups streptococcus (s. mutans, s. milleri, s. oralis, s. sanguis)
Native prosthetic valve endocarditis
* early theatre/ICU acquired (staph. aureus, staph. epidermidis)
* late community acquired (staph. aureus, viridian group strep)
IVDU
Prolonged IV catheter dwelling
Prolonged hospital stay (enterococcus faecalis)
Underlying GU disease
Diabetes
List the common causative micro-organisms for infective endocarditis
Viridans group streptococci (s. mutans, s. milleri, s. oralis, s. sanguis)
Staphylococcus aureus
Enterococci
List the diagnostic criteria for infective endocarditis
Modified Duke Criteria
Major
Consistent positive culture for typical microorganisms of IE
Echocardiography
* wall motion abnormalities
* abscess
New prosthetic valve dehiscence / valvular regurgitation
Minor
Predisposition
* IVDU
* predisposing heart disease
Vascular phenomena
* Janeway lesions
* intracranial haemorrhage
* conjunctival haemorrhage
* arterial emboli
* septic pulmonary infarction
* mycotic aneurysm
Immunological phenomena
* Osler’s nodes
* Roth spots
* Glomerulonephritis
* Rheumatic fever
Microbiological evidence
Fever > 38
Definite IE =
2 major
1 major + 3 minor
0 major + 5 minor
List the clinical features of infective endocarditis
General
* Malaise
* Clubbing
Skin
* Janeway lesions
* Osler nodes
* Splinter haemorrhage
* Petechiae
Neurological
* Mycotic abscess
* Cerebral emboli
Eyes
* Roth spot
* Conjunctival haemorrhage
Splenomegaly
Renal - Haematuria
Cardiac
* Murmur
* Cardiac failure
Give the first line investigation for infective endocarditis
TTE Echocardiography:
* abscess
* vegetation
* valvular dysfunction
* Assess ventricular function
What may be seen on ECG in aortic root abscess
PR prolongation / heart block
What may been seen on CXR in infective endocarditis
pulmonary oedema in L side disease
pulmonary emboli/abscess in R side disease
What may been seen on FBC in infective endocarditis
Reduced Hgb
Elevated CRP, ESR, WCC
List the management for infective endocarditis
Suspected staph. IE (IVDU / Recent IV device / cardiac surgery)
* Vancomycin + gentamicin
Staph. IE
* Vancomycin / benzylpenicillin / flucloxacillin + gentamicin
Clinical IE not suspected Staph.
* Penicillin + gentamicin
Strep. IE
* IV benzylpenicillin + gentamicin
Enterococcal IE
* IV amoxicillin + gentamicin
Give two types of bradycardia
Sinus bradycardia
AV block
List the intrinsic and extrinsic causes for sinus bradycardia
Extrinsic causes
Hypothermia
Hypothyroidism
Cholestatic jaundice
Increased ICP
Drugs
* Beta-blockers
* Digitalis
Neurally mediated syndromes (syncope / presyncope)
* POTS
* Vasovagal attack
* Carotid sinus syndrome
Intrinsic causes
Post-MI ischaemia / infarction of the sinus node
Sick sinus syndrome
* Idiopathic
* IHD
* Myocarditis
* Cardiomyopathy
Define types of heart blocks
1st degree AV block
Prolonged PR interval longer than 0.2 seconds
Every atrial depolarisation followed by ventricular depolarisation
2nd degree AV block
* Mobitz I: progressive PR prolongation until a P wave fails to conduct - Blockage in AVN
* Mobitz II: regular PR, intermittently failed to conduct - Blockage in infra-nodal level eg. His-Purkinje
* Fixed ratio: every 2/3 P waves conduct
3rd degree AV block
All atrial activity failed to conduct to ventricles
Life maintained by spontaneous escape rhythm
List causes of 3rd degree AV block
Congenital
* Structural heart disease eg. transposition of great vessels
* Autoimmune
Idiopathic fibrosis
* Lev’s disease (progressive distal His-purkinje fibrosis)
* Lengrene’s disease (proximal His-purkinje fibrosis)
Ischaemic heart disease
Non-ischaemic heart disease
* idiopathic cardiomyopathy
* calcific aortic stenosis
* infiltrations (amyloidosis, sarcoidosis, neoplasm)
Cardiac surgery
* aortic valve replacement
* CABG
* VSD repair
Iatrogenic eg. radio frequency AV ablation
Drug induced
* b-blockers
* amiodarone
* digoxin
* non-dihydropyridine CCB
Infections
* endocarditis
* Chaga’s disease (Trypanosoma cruzi)
* Lyme disease
Autoimmune eg. SLE, RA
NMD eg. DMD
When does escape rhythms occur?
when supraventricular impulse arriving at AVN/ventricles less than intrinsic rate of ectopic pacemaker
List the causes for broad complex escape rhythm
Lev’s
Lengrene’s
IHD
Myocarditis
Cardiomyopathy
Give the ECG characteristics of right bundle branch block
MARROW
Tall late R in V1
Deep S in I, V6
Give the ECG characteristics of left bundle branch block
WILLIAM
Tall late R in I, V6
Deep S in V1
List the causes for right bundle branch block
Pulmonary embolism
Pulmonary stenosis
Pulmonary HTN
MI
Fallot’s tetralogy
Congenital cardiac disorders
Conductive tissue fibrosis
Chaga’s disease (Trypanosoma cruzi)
Isolated congenital anomaly - 5% healthy population
List the causes for left bundle branch block
(Extensive LV disease)
Aortic stenosis
MI
HTN
Severe coronary disease
List the four classes of anti-arrhythmics
Class I Na+ channel blockers
Ia (moderate) - procainamide, quinidine
Ib (weak) - phenytoin, lidocaine
Ic (strong) - propafenone, flecainide
Class II beta-blockers
Propanolol
Metoprolol
Class III K+ blockers
Amiodarone
Sotalol
Class IV Ca+ blockers
Verapamil
Diltiazem
List three characteristics of POTS
Exaggerated heart rate: increase >30 bpm, or an absolute increase to 120 bpm within 10 minutes of standing or head-up tilt
Symptoms of cerebral hypoperfusion: light-headedness, blurred vision, cognitive difficulties, generalised weakness in response to postural change
In the absence of orthostatic hypotension and cardiac causes of sinus tachycardia
Explain the pathophysiology of AV nodal reentrant tachycardia
There are two pathways within the AV node:
The slow pathway: a slowly-conducting pathway with a short refractory period.
The fast pathway: a rapidly-conducting pathway with a long refractory period.
Mechanism of re-entry in “slow-fast” AVNRT:
1. A premature atrial contraction (PAC) arrives while the fast pathway is still refractory, and is directed down the slow pathway
2. The ERP in the fast pathway ends, and the PAC impulse travels retrogradely up the fast pathway
3. The impulse continually cycles around the two pathways
List the ECG features in AVNRT
Regular tachycardia ~140-280 bpm
Narrow QRS complexes (<120ms)
P waves invisible or immediately before / after QRS (due to spontaneous A and V activation)
List the ECG features in AVRT
Pre-excitation
* Short PR interval
Orthodromic AVRT
* Normal QRS duration
* Retrograde P wave after QRS
Antidromic AVRT
* Wide QRS with delta wave
* P wave rarely seen
* If P wave visible, it is retrograde and occurs just before QRS
List the ECG features in Wolff-Parkinson-White syndrome
Shortened PR interval < 0.12 s
Delta wave
QRS prolongation > 0.12 s
Discordant ST and T changes
Give the acute and chronic management for AVNRT and AVRT
Acute
Hemodynamically unstable (hypotension / pulmonary oedema) - cardioversion
Hemodynamically stable
* vagal manoeuvres eg. carotid massage
* valsava manoeuvres
* facial immersion in cold water
If physical unsuccessful - IV adenosine
Long term:
Radio-frequency ablation of accessory pathway
Class Ic antiarrhythmic - flecainide, propafenone
Beta-blockers
Class III antiarrhythmic - sotalol, dofetilide, azimilide
Verapamil, diltiazem
Multichannel blocker - amiodarone
List the side effects of IV adenosine
bronchospasm
flushing
chest pain
sense of impending doom
heaviness of limbs
List the side effects of amiodarone
Long QT syndrome
Polymorphic ventricular tachycardia
Interstitial pneumonitis
Hyper / hypothyroidism
Abnormal liver biochemistry
Sun sensitivity
Slate grey discoloration
Corneal deposition
Optic neuropathy
List three most common causes for atrial fibrillation
Hypertension
Coronary artery disease
Myocardial infarction
Define paroxysmal, persistent, and permanent AF
Paroxysmal AF - episodes > 30 seconds but < 7 days (often < 48 hours) that are self-terminating and recurrent.
Persistent AF - episodes > 7 days (spontaneous termination unlikely after this time) or < 7 days but requiring pharmacological or electrical cardioversion.
Permanent AF - AF that:
* Fails to terminate using cardioversion
* Is terminated but relapses within 24 hours
* Longstanding AF (usually > 1 year) in which cardioversion has not been indicated or attempted (accepted permanent AF).
List the causes of AF
Cardiac causes
Congestive heart failure.
Rheumatic valvular disease.
Atrial / ventricular hypertrophy.
Wolff–Parkinson–White syndrome.
Sick sinus syndrome.
Congenital heart disease.
Inflammatory / infiltrative disease (pericarditis, amyloidosis, myocarditis).
Non-cardiac causes
Pulmonary embolism
Thyrotoxicosis
Diabetes mellitus
Acute infection
Autonomic neural dysfunction
Electrolyte depletion
Hypokalemia
Hyponatremia
Cancer
Primary lung cancer involving the pleura and pericardium
Breast cancer and malignant melanoma metastasising to the pericardium
Dietary and lifestyle factors
Excessive caffeine intake.
Alcohol abuse
Obesity
Smoking
Medication exposure
Thyroxine
Bronchodilators
List the complications of AF
Stroke and thromboembolism
Heart failure
Uncontrolled AF
* Tachycardia-induced cardiomyopathy
* Critical cardiac ischaemia
List the clinical features of AF
Breathlessness.
Palpitations.
Chest discomfort.
Syncope or dizziness.
Reduced exercise tolerance, malaise/listlessness, decrease in mentation, polyuria.
List the differential diagnoses of an irregular pulse
Atrial flutter
Atrial extrasystoles
Ventricular ectopic beats
Sinus tachycardia
Supraventricular tachycardias
* atrial tachycardia
* atrioventricular nodal re-entry tachycardia
* Wolff-Parkinson-White syndrome
Multifocal atrial tachycardia (severe pulmonary disease)
Sinus rhythm with premature atrial or ventricular contractions
List the ECG features of AF
Irregularly irregular rhythm
No P wave
Fine oscillations at baseline - f wave
Ventricular rate 160-180
Rapid irregular QRS rhythm
List the acute management of AF
Treat provocation factor eg. chest infection, thyrotoxicosis, alcohol intoxication
Cardioversion
* direct DC shock
* flecainide, propafenone
* IV antiarrhythmic
Give the first line rate control treatment in AF
beta blockers OR rate-limiting CCB (diltiazem / verapamil)
When should an anticoagulation be offered in AF?
CHA2DS2VASc score of 2 or above
List the anticoagulation offered in AF.
Factor Xa inhibitor:
* Apixaban
* Edoxaban
* Rivaroxaban
Factor IIa (Thrombin) inhibitor:
* Dabigatran
List the variables in CHA2DS2VASc score
Congestive heart failure (1)
Hypertension (1)
Age > 75 (2)
Diabetes Mellitus
Stroke/TIA (2)
Vascular disease (1)
* prior myocardial infarction
* peripheral arterial disease
* aortic plaque
Age 65~74 (1)
Sex = female (1)
List the complications of sustained ventricular tachycardia
Syncope / presyncope
Hypotension
Cardiac arrest
Give the ECG feature in ventricular tachycardia
Rapid broad ventricular rhythm > 0.14 s
Give the management of ventricular tachycardia
Hemodynamically unstable - DC cardioversion
Hemodynamically stable
* IV beta-blocker
* Class I / amiodarone
Define torsades de pointes
A form of polymorphic ventricular tachycardia occurring the context of QT prolongation
List the causes of long QT syndrome
Congenital
Electrolyte abnormalities:
* Hypokalaemia
* Hypomagnesaemia
* Hypocalcaemia
Drug causes
Antiarrhythmic
* Class Ia: quinidine, disopyramide
* Class Ic: propafenone, flecainide
* Class III: sotalol, amiodarone
Tricyclic antidepressant
Phenothiazine
Antipsychotics
* Chlorpromazine
* Haloperidol
* Droperidol
* Quetiapine
* Olanzapine
* Amisulpride
* Thioridazine
Quinolones
Macrolides
* Erythromycin
* Clarithromycin
Chloroquine
Hydroxychloroquine
Quinine
Methadone
Poisons - inorganic phosphate insecticides
Other causes
Bradycardia
Acute MI
Mitral valve prolapse
Diabetes
Prolonged fasting
CNS disorders
List the clinical features of long QT syndrome
Syncope
Palpitations
Ventricular fibrillation
Sudden death
Polymorphic ventricular tachycardia - Torsades de Pointes
List the managements in long QT syndrome
Correct electrolyte disturbances
Stop causative drugs
Maintain HR with AV pacing
IV isoprenaline
Magnesium sulphate given over 10-15 mins for acquired long QT
Give the ECG feature in ventricular fibrillation
shapeless rapid oscillations
List presentations in ventricular fibrillation
pulseless
unconscious
respiration cessation
List the chest auscultation areas
Aortic area - R sternum, 2nd ICS
Pulmonary area - L sternum, 2nd ICS
Erb’s point - L sternum, 3rd ICS
Tricuspid area - L sternum, 4th ICS
Mitral area - L midclavicular line, 5th ICS
When may the S4 heart sound be present?
(Blood forced into a stiff / hypertrophic ventricle)
Aortic stenosis
Hypertrophic cardiomyopathy
Heart failure
Give the normal and symptomatic mitral valve area
Normal mitral valve area: 4~6 cm2
Symptomatic when area <2 cm2
List the causes of mitral stenosis
Rheumatic heart disease (most common) -following group A beta-haemolytic strep (S. pyogenes) infection
Congenital mitral stenosis
Lutembarcher’s syndrome (Combination of acquired mitral stenosis, ASD)
Mitral annular calcification
Metastasis
Give the pathophysiology in mitral stenosis
LA pressure increases in order to maintain CO, leads to LA hypertrophy
Increased pressure in pulmonary vein, artery and RH
Increased pulmonary capillary pressure causes pulmonary oedema
Pulmonary HTN causes
* RH hypertrophy, dilation, failure
* Eventually tricuspid regurgitation
List the clinical symptoms in mitral stenosis
Dyspnoea (increased pLA, vascular congestion, P oedema) / Orthopnoea / Paroxysmal nocturnal dyspnoea
Peripheral oedema (P HTN, RH failure)
Haemoptysis
Large LA predisposes to:
* Atrial fibrillation (palpitations)
* Systemic emboli
List the signs in mitral stenosis
Mitral facies
Small volume regular pulse in early stenosis
Atrial fibrillation
Jugular venous distention - RH failure
Tapping impulse parasternally on L side
List the auscultatory findings in mitral stenosis
Mid-diastolic rumbling murmur
Opening snap
Load S1 if valve is pliable (doesn’t occur in calcific M stenosis)
Tapping apex beat
Pulmonary HTN
* Right parasternal heave
* Loud pulmonary component of S2
Give the gold standard investigation in mitral stenosis
TTE
List the management options for mitral stenosis
Diuretics - Reduce LA pressure, relieve mild symptoms
* Furosemide
* Bumtanide
Balloon valvotomy
List the causes of mitral regurgitation
Common
Rheumatic Heart Disease
Infective endocarditis
Ischaemic heart disease
Myxomatous disease
Diseases of myocardium - DCM, HCM
Rheumatic autoimmune disease eg. SLE
Collagen diseases - Marfan’s, EDS
Drugs
* DPA agonists
* Centrally acting appetite suppressants
Give the pathophysiology of mitral regurgitation
LV hypertrophy (50%)
LA dilation
List the clinical features in mitral regurgitation
Dyspnea and orthopnea
Fatigue and lethargy (reduced CO)
Congestive cardiac failure (late RH failure)
Cardiac cachexia
Subacute IE, thromboembolism
List the auscultation findings in mitral regurgitation
Pansystolic murmur (regurgitation during systole)
Mid-systolic click
Laterally displaced apex beat (apex radiates to axilla)
Systolic thrill
Soft S1 (incomplete apposition of M valve)
Prominent S3 (blood rush to LV during early diastole)
Give the normal and symptomatic aortic valve area
Normal aortic valve area = 3~4 cm2
Symptomatic when ¼ normal area
List the causes for aortic stenosis
Calcific aortic valvular disease (most common)
Bicuspid aortic valve
Rheumatic fever
Chronic Kidney Disease
Paget’s disease of the bone
Radiation
SLE
What is bicuspid aortic valve associated with?
aortic root dilation
aortic coarctation
aortic dissection
Give the pathophysiology of aortic stenosis
- obstructed LV emptying
- increased pLV, LV hypertrophy
- relative ischaemia, angina
- arrhythmia
- LV failure
List the symptoms of aortic stenosis
Triad of: (SAD - Syncope, Angina, Dyspnoea)
Fatigue
List the signs in aortic stenosis
Carotid pulse - pulsus tardus et parvus (slow and weak pulse)
Narrow pulse pressure
Apical heave
Thrills in aortic region
Reduced or absent S2 over aortic area
Radiation of murmur to carotid artery
List the auscultatory findings in aortic stenosis
Crescendo decrescendo systolic ejection murmur
Soft S2 (immobile aortic valve)
Systolic ejection click (valve immobile and calcified)
Prominent S4
List the causes in aortic regurgitation
Bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis
Give the pathophysiology in aortic regurgitation
- blood reflux from aorta to LV during diastole
- increased volume of blood pumped in aorta to maintain CO,
- LV dilation and hypertrophy, increased O2 demand
- decreased coronary perfusion due to diastolic runoff during diastole
- eventually cardiac ischaemia
List the presentations in aortic regurgitation
Aangina pectoris
Dyspnoea (exertional)
Displaced apex beat
List the auscultation findings in aortic regurgitation
Diastolic blowing murmur at L sternal border (Austin Flint murmur)
Large volume pulse
Collapsing pulse
Wide pulse pressure
Prominent carotid pulsations (Corrigan’s sign)
Displaced apex beat
Give the classification of heart failure
HF with reduced ejection fraction (HFrEF): LVEF ≤40%
HF with mildly reduced EF (HFmrEF): LVEF 41% ~ 49%
HF with preserved EF (HFpEF): LVEF ≥50%
List the four most common causes of heart failure
Coronary artery disease
Hypertension
Valvular heart disease
Myocarditis
List the causes for chronic heart failure
Myocardial disease
Coronary artery disease (most common).
Hypertension.
Cardiomyopathies:
* Familial.
* Infective.
* Autoimmune
* Toxins
* Pregnancy.
* Infiltrative (sarcoidosis, amyloidosis, haemochromatosis, connective tissue disease).
Valvular heart diseases
Pericardial disease:
Constrictive pericarditis.
Pericardial effusion
Congenital heart disease.
Arrhythmias
High output states
Anaemia.
Thyrotoxicosis.
Phaeochromocytoma.
Septicaemia.
Liver failure.
Arteriovenous shunts.
Paget’s disease.
Thiamine (vitamin B1) deficiency.
Volume overload
End-stage chronic kidney disease.
Nephrotic syndrome.
Obesity.
Drugs including:
Alcohol.
Cocaine.
NSAIDs, beta-blockers, and CCBs (may worsen pre-existing heart failure).
List the complications of chronic heart disease
Arrhythmias
* Atrial fibrillation
* Ventricular arrhythmias
Depression
Cachexia
Anaemia
Chronic kidney disease
Acute kidney injury
Sexual dysfunction
Sudden cardiac death
List the typical symptoms in chronic heart disease
Breathlessness
Peripheral oedema
Fatigue, decreased exercise tolerance
Lightheadedness, history of syncope
List the risk factors in chronic heart disease
Coronary artery disease
Hypertension
Atrial fibrillation
Diabetes mellitus
Drugs, alcohol
Family history of:
* heart failure
* sudden cardiac death under the age of 40 years
List the signs in chronic heart failure
Tachycardia
Elevated JVP
Cardiomegaly
Laterally displaced apex beat, S3, S4
Tachypnoea, pleural effusion, basal crepitations
Peripheral oedema, ascites
Tender hepatomegaly
Give the first line investigation in chronic heart failure
NT-pro-BNP / BNP levels - Elevated
List CXR findings in chronic heart failure
Cardiomegaly (increased cardiothoracic ratio)
Pulmonary congestion
Pulmonary vascular congestion (vascular redistribution, Kerley B lines)
List the treatment algorithm in chronic heart failure
Symptomatic treatment: loop diuretics
1. First line: ACEi + beta-blockers
2. If ACEi intolerant: ARB
3. If ACEi and ARB intolerant: hydralazine + nitrate
4. Consider:
Digoxin
Ivabradine
List the drugs that should be avoided in HFrEF
Non-dihydropyridine calcium-channel blockers - Diltiazem, Verapamil
Class Ic antiarrhythmics - Propafenone, Flecainide
Thiazolidinediones - Pioglitazone
Dipeptidyl peptidase-4 (DPP-4) inhibitors - alogliptin, linagliptin, saxagliptin, sitagliptin
NSAIDs
List the causes of secondary hypertension
Vascular:
Renal artery stenosis
Coarctation of aorta
Pre-eclampsia
Renal:
Chronic kidney disease
Chronic pyelonephritis
Diabetic nephropathy
Glomerulonephritis
Nephrotic syndrome
Polycystic kidney disease
Obstructive uropathy
Renal cell carcinoma
Endocrine:
Pheochromocytoma
Primary hyperaldosteronism
Cushing’s syndrome
Acromegaly
Hyperthyroidism
Hypothyroidism
Hyperparathyroidism
Drugs:
Alcohol
Ciclosporin.
Cocaine, amphetamine, and other substances of abuse.
Combined oral contraceptive.
Corticosteroids.
Erythropoietin.
Leflunomide.
Liquorice — present in some herbal medicines.
NSAIDs
Oestrogens (hormone replacement therapy)
ADHD stimulants
* methylphenidate, atomoxetine, dexamfetamine, lisdexamfetamine.
Sympathomimetics
Venlafaxine
Others
Pregnancy
Connective tissue disorders
* Scleroderma
* Systemic lupus erythematosus
* Polyarteritis nodosa
Retroperitoneal fibrosis
Obstructive sleep apnoea
List the hypertension staging system
Stage 1
Clinical 140/90-159/99
ABPM 135/85-149/94
Stage 2
Clinical 160/100-180/120
ABPM 150/95
Stage 3
Clinical 180/120 mmHg or higher
Define malignant hypertension
Severe increase in blood pressure to 180/120 mmHg or higher with signs of retinal haemorrhage and/or papilloedema
List the risk factors for hypertension
Increasing age
Gender
* Women <65 years tend to have a lower blood pressure than men.
* Between 65–74 years women tend to have a higher blood pressure
Ethnicity - black African / Caribbean more likely
Genetics
Social deprivation
Co-existing diabetes / kidney disease
Lifestyle
* Smoking
* Excessive alcohol consumption
* Excess dietary salt
* Unhealthy diet
* Obesity
* Lack of physical activity
Anxiety and emotional stress
List the complications for hypertension
Heart failure.
Coronary artery disease.
Stroke.
Chronic kidney disease.
Peripheral arterial disease.
Vascular dementia.
List the fundoscopy findings in hypertensive retinopathy
Arteriolar narrowing
Arteriolar venous nipping (constriction of veins at crossing points)
‘Cotton wool spots’ on the retina (due to ischaemic changes)
Flame haemorrhages or papilloedema
When should secondary hypertension be suspected
Young (<40 years)
Rapid onset
Sudden change in blood pressure when previously well controlled on a particular therapy
Resistant hypertension
When should same-day specialist referral be made in hypertension?
A clinic blood pressure of 180/120 mmHg and higher with
* Signs of retinal haemorrhage and/or papilloedema (accelerated hypertension)
* Life-threatening symptoms (new onset confusion, chest pain, signs of heart failure, acute kidney injury)
Suspected pheochromocytoma
* labile or postural hypotension, headache, palpitations, pallor, abdominal pain, diaphoresis
List the medical treatment for hypertension
Step 1 treatment
ACEi / ARB first line in
* Age < 55 and not of black African or Caribbean origin.
* T2DM
CCB first line in
* Age > 55, no T2DM
* Of black African or Caribbean origin, no T2DM
* If CCB untolerated - offer indapamide (thiazide-like diuretic)
If there is evidence of heart failure - indapamide (thiazide-like diuretic)
Step 2 treatment
If not controlled with ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)
If not controlled with CCB
* ACEi/ARB
* Indapamide (thiazide-like diuretic)
Step 3 treatment
Combination of
* ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)
Step 4 treatment
If blood potassium level 4.5 mmol/L or less - low-dose spironolactone
If blood potassium level > 4.5 mmol/L - alpha-blocker / beta-blocker
List the contraindications for ACEi
Angio-oedema
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women
List the adverse effects for ACEi
Reduced ACE:
Hyperkalaemia
Renal impairment
Hypotension
Increased Kinin (ACE inactivates bradykinin)
Cough
Angio-oedema
Anaphylactoid reaction
List the contraindications for ARB
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women
List the adverse effects for ARB
Renal impairment
Hyperkalaemia
Angio-oedema
Dizziness
List the risk factors for peripheral arterial disease
Smoking
Diabetes mellitus
Advanced age
Hypertension
Hypercholesterolaemia
Atherosclerotic disease
Chronic kidney disease
High serum homocysteine
List the Fontaine stages of peripheral arterial disease
Stage I: asymptomatic
Stage IIa: mild claudication
Stage IIb: moderate to severe claudication
Stage III: ischemic rest pain
Stage IV: ulceration or gangrene
Give the first line investigation and findings in peripheral arterial disease
Ankle-brachial index
* < 0.5 severe arterial disease
* 0.5 ~ 0.8 presence of arterial / mixed / venous disease
* 0.8 ~ 1.3 no evidence of significant arterial disease
* > 1.3 maybe arterial calcification
List the 6Ps of acute limb ischaemia
Pain
Paralysis
Paraesthesias
Pulselessness
Pallor
Perishingly cold
List the causes of acute limb ischaemia
Thrombotic
* Chronic atherosclerotic stenosis
* Hypercoagulation
* Prosthetic / venous grafts de novo
Emboli
* Cardiac thrombus
* Cardiac arrhythmias
List the interventions for acute limb ischaemia
Endovascular
* Percutaneous catheter-directed thrombolytic therapy.
* Percutaneous mechanical thrombus extraction.
Surgical interventions
* Surgical thromboembolectomy.
* Endarterectomy.
* Bypass surgery.
* Amputation if the limb is unsalvageable.
List the complications form acute limb ischaemia
Compartment syndrome - reperfusion of ischaemic muscles can cause oedema and increased compartmental pressure
Reperfusion injury - products of cell death are released when blood flow to the ischaemic limb is restored.
* Rhabdomyolysis
* Cardiac dysrhythmia
* Acute kidney injury
* Multiorgan failure
* Disseminated intravascular coagulation
List the risk factors for chronic limb ischemia
Smoking
Diabetes
Hypercholesterolaemia
HTN
List the signs in chronic limb ischaemia
Cold dry skin, lack of hair
Diminished / absent pulses
Ulceration associated with dark discolouration / gangrene
List the management in chronic limb ischaemia
Risk factor management
Naftidrofuryl oxalate (5 HT antagonist, vasodilator, reduce lactic acid build up)
Surgery when severe, disabling:
* angioplasty
* bypass
List the clinical presentation for varicose veins
Lower extremity pain
Fatigue
Itching and/or heaviness
Worsen with prolonged standing
Associated with dilated tortuous veins
List the complications for varicose veins
Chronic venous skin changes
Superficial venous thrombosis
Venous ulceration
Bleeding
List the pathophysiology of varicose veins
Incompetent valves
Blood pass from deep to superficial venous system
Venous hypertension, dilation of superficial veins
List the risk factors for varicose veins
Increasing age
Family history
Female sex
Pregnancy
Contraceptive pills
Obesity
Prolonged standing or sitting
History of deep vein thrombosis
Give the first line investigation and findings for varicose veins
Duplex ultrasound
* Reflux
* Valve closure >0.5 second in the superficial system and >1.0 second in the deep system
List the intrinsic and temporary risk factors for deep vein thrombosis
Intrinsic risk factors
Age > 60 years.
Male sex.
A history of DVT.
Overweight / obese.
Cancer.
Heart failure.
Acquired / familial thrombophilia.
Inflammatory disorders (eg. vasculitis, inflammatory bowel disease).
Temporary risk factors
Significant immobility.
Significant trauma or direct trauma to a vein (eg. intravenous catheter).
Hormone treatment (eg. hormone replacement therapy).
Pregnancy and the postpartum period.
Dehydration.
What is the most serious complication for deep vein thrombosis
pulmonary embolism
List the presentations in deep vein thrombosis
Asymmetrical leg swelling
Unilateral leg pain
Superficial vein dilation
Calf warmth / tenderness / swelling / erythema
List the variables in Wells score
Active cancer (Treatment or palliation within 6 months)
Bedridden recently >3 days or major surgery within 12 weeks
Calf swelling >3 cm compared to the other leg (Measured 10 cm below tibial tuberosity)
Collateral (non varicose) superficial veins present
Entire leg swollen
Localised tenderness along the deep venous system
Pitting edema, confined to symptomatic leg
Paralysis, paresis, or recent plaster immobilisation of the lower extremity
Previously documented DVT
Alternative diagnosis to DVT as likely or more likely
List the investigations and findings for deep vein thrombosis
Wells score ≥2: DVT likely - Venous ultrasound
* Abnormal B-mode image: inability to fully compress lumen of vein using ultrasound transducer
* Abnormal Doppler: reduced or absent spontaneous flow
Wells score <2: DVT unlikely
1. D-dimer level (results available within 4 hours)
2. If elevated: Venous ultrasound
List the investigations required before starting anticoagulation
Full blood count
Urea and creatinine
Liver function tests
Clotting screen (prothrombin time (PT) and activated partial thromboplastin time (aPTT))
List the management approach for deep vein thrombosis
Suspected DVT - Apixaban (interim therapeutic anticoagulation)
Confirmed proximal DVT - Receive anticoagulation for at least 3 months
First line: Apixaban / rivaroxaban
Alternatives
* LMWH for at least 5 days followed by dabigatran / edoxaban
* LMWH concurrently with a vitamin K antagonist for at least 5 days
List the management approaches in phlegmasia cerulea dolens
Anticoagulation with low molecular weight heparin or unfractionated heparin
Vascular surgery
Elevated affected leg
List the risk factors for pulmonary embolism
Personal / family history of DVT.
Recent surgery.
Significant immobility.
Active cancer.
Antiphospholipid antibody syndrome.
Lower limb trauma.
Recent myocardial infarction.
Increasing age.
Pregnancy
Oral contraception
Hormone replacement therapy
Cigarette smoking
Long-duration travel
Obesity
List the symptoms for pulmonary embolism
Dyspnoea
Tachypnoea
Pleuritic chest pain (normally localised to one side)
Features of DVT
Cough and haemoptysis
Retrosternal chest pain (RV ischaemia)
Syncope / presyncope (RV failure)
List the ECG features in pulmonary embolism
Sinus tachycardia
S1Q3T3
* Deep S wave in lead I
* Q wave in III
* Inverted T wave in III
T wave inversion V1~3
RBBB
Right axis deviation
P pulmonale
List the variables in Two-level PE Wells score
Clinical features of deep vein thrombosis (leg swelling, pain, palpation of the deep veins) +3
Heart rate > 100 bpm +1.5
Immobilisation +1.5
Previous DVT or PE +1.5
Haemoptysis +1
Cancer +1
An alternative diagnosis is less likely than PE — plus 3 points.
Give the interim therapeutic anticoagulation in pulmonary embolism
apixaban
List the investigation approaches for pulmonary embolism
Two-level PE Wells score > 4: PE likely
* 1st line: CT pulmonary angiogram
Two-level PE Wells score < 4: PE unlikely
* D-dimer within 4 hrs
* If positive, arrange CTPA
Give the pathophysiology of superficial vein thrombophlebitis
Thrombus formation in a superficial vein, and inflammation in the tissue surrounding the vein.
List the aetiologies for superficial vein thrombophlebitis
Vessel wall damage
Catheterisation
IV drugs
Sclerotherapy
Inflammatory vascular diseases
Stasis
Varicose veins
Immobilisation
Hypercoagulability
Oral contraceptive medicines
Inherited or acquired thrombophilia
List the clinical signs in superficial vein thrombophlebitis
Pain
Tenderness
Induration
Warmth
Erythema
Palpable cord along the course of a superficial vein
Give the first line investigation and finding in superficial vein thrombophlebitis
Duplex ultrasonography
* Lack of compressibility or intraluminal thrombus in the superficial veins
Where does aortic aneurysms most commonly affect?
Abdominal
Iliac
Popliteal
Femoral
Thoracic
Give the definition of aortic aneurysm
Permanent pathological dilation of the abdominal aorta with a diameter over 1.5 times the expected anteroposterior diameter of that segment given the person’s sex and body size.
List the risk factors for aortic aneurysms
Increasing age
Male sex
Smoking
Hypertension
Positive family history
Diabetes mellitus
Chronic obstructive pulmonary disease
What may aortic aneurysms be secondary to?
Atherosclerosis
Trauma
Infection (syphilis, E. coli, salmonella, mycotic aneurysm)
Genetic (MFS, EDS)
When is AAA screening offered?
all men the year they become 65 years old.
List the possible outcomes and actions after AAA screening
No aneurysm found (less than 3.0 cm) — no further scans are required.
Small AAA (3.0 cm to 4.4 cm) — the person is placed under surveillance and a repeat scan offered in 12 months.
Medium AAA (4.5 cm to 5.4 cm) — the person is placed under surveillance and a repeat scan offered in 3 months.
Large AAA (5.5 cm or larger) — the person is referred to a vascular surgeon.
List the symptoms of rapid expansion or rupture of AAA
Severe epigastric pain radiating to back
Hypotension
Tachycardia
Profound anaemia
Sudden death
Give the definition for aortic dissection
Dissection in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.
List the acute aortic syndromes
Aortic dissection
Intramural haematoma
Penetrating aortic ulcers
List the predisposing factors in aortic dissection
Autoimmune rheumatic disorders
MFS
EDS
List the Stanford classification of aortic dissection
Type A: Dissection proximal to L subclavian artery origin
Type B: Dissection distal to L subclavian artery origin
Type B dissection has a better prognosis
List the DeBakey classification of aortic dissection
Type 1: extends to abdominal aorta (ascending + descending)
Type 2: localised to ascending aorta (ascending)
Type 3: Tear originates distal to the left subclavian artery and extends through the thoracic aorta (3A) or extends beyond the visceral segment (3B) (descending)
List the signs of aortic dissection
Sudden onset of severe central chest pain that radiates to the back and arms
Shock
Neurological symptoms secondary to loss of blood to spinal cord
Aortic regurgitation
Cardiac tamponade
Coronary ischaemia
Absent peripheral pulses
Distal dissection:
* Acute kidney disease
* Visceral ischaemia
* Acute lower limb ischaemia
Give the CXR sign of aortic dissection
widened mediastinum
List the medical treatment for aortic dissection
IV beta-blockers to achieve
* Heart rate <60 beats per minute
* Systolic blood pressure (SBP) 100-120 mmHg
IV opioids
* Pain relief, decrease sympathetic tone and facilitate haemodynamic stability.
If heart rate and SBP not adequately controlled
* Add vasodilator eg. sodium nitroprusside
What is the most common form of cardiomyopathy
Hypertrophic cardiomyopathy
Give the inheritance of hypertrophic cardiomyopathy
Autosomal dominant
* MYH7 (beta-myosin heavy chain)
* MYBPC3 (myosin binding protein C)
Describe the pathology in hypertrophic cardiomyopathy
abnormal, thickened, disorganised collagen matrix
septal thickening from myocyte hypertrophy
Give the complication for hypertrophic cardiomyopathy
HFpEF - diastolic dysfunction
Give the presentation in symptomatic hypertrophic cardiomyopathy
Dyspnoea
Chest pain
Syncope with exertion
Cardiac arrhythmias
Sudden death
List the physical examination findings in hypertrophic cardiomyopathy
Double apical impulse
Brisk carotid upstroke (jerky carotid pulse)
List the auscultation findings in hypertrophic cardiomyopathy
Systolic ejection murmur at lower left edge
* accentuated by exercise and standing
* lessened by lying supine or squatting
S4
List the ECG findings in hypertrophic cardiomyopathy
Prominent Q waves in leads II, III, aVF, V5, V6
List the managements in hypertrophic cardiomyopathy
Symptomatic:
Chest pain, dyspnoea: beta-blockers +/- verapamil
LV outflow tract obstruction: disopyramide
Describe the pathology in arrhythmogenic cardiomyopathy
progressive replacement of myocardium with fibro-fatty material
Describe the Mendelian inheritance of arrhythmogenic cardiomyopathy
Autosomal dominant
List the ECG findings in arrhythmogenic cardiomyopathy
T inversion and broad QRS in V1-3
Epsilon wave - small positive deflection buried in the end of the QRS complex
RBBB
List the Task force criteria for arrhythmogenic cardiomyopathy diagnosis
Structural abnormalities of RV and RV outflow tract
Fibro-fatty replacement of myocytes on tissue biopsy
Repolarisation and conduction abnormalities on ECG
Ventricular tachycardia / extrasystoles on Holter monitoring
Family Hx. of ACM in first / second relative
Premature sudden death < 35 years due to ACM
List the management approaches in arrhythmogenic cardiomyopathy
Non-life threatening arrhythmias - beta blockers
Symptomatic arrhythmias - amiodarone / sotalol
Refractory / life threatening arrhythmias - ICD
Intractable arrhythmia / cardiac failure - cardiac transplantation
List the causes of dilated cardiomyopathy
Familial DCM - Autosomal dominant
Sporadic DCM causes
Myocarditis
* Coxsackievirus
* Adenovirus
* Erythrovirus
* HIV
* Mycobacteria
* Chaga’s disease (Trypanosoma Cruzi)
Toxins
* Alcohol
* Chemotherapy
* Heavy metal
Autoimmune disorders
Endocrine disorders
Neuromuscular disorders
List the clinical features in dilated cardiomyopathy
Heart failure (HF-rEF)
Cardiac arrhythmias
Conduction defects
Thromboembolism
Sudden death
List the ECG findings in dilated cardiomyopathy
AF
Ventricular premature contractions
Ventricular tachycardia
List the four types of shock
Hypovolaemic
Cardiogenic
Distributive
Obstructive
List the causes of shock
Hypovolemic
Haemorrhage
Fluid depletion
Cardiogenic
Myocardial infarction
Atrial fibrillation
Ventricular tachycardia
Bradyarrhythmias
Toxic substances
Excessive rise in blood pressure
Infection
* Pneumonia
* Infective endocarditis
* Sepsis
Acute mechanical cause
* Myocardial rupture
* Chest trauma
* Acute valvular incompetence
Distributive
Sepsis
Anaphylaxis
Brainstem or spinal injury (neurogenic)
Obstructive
Pulmonary embolism
Cardiac tamponade
Tension pneumothorax
List the clinical presentations in shock
Hypotension
SBP < 90 mmHg
MAP < 65 mmHg
Decrease ≥40 mmHg from baseline
Skin changes
Sweating and cyanosis of the skin, lips, or tongue
Cold or clammy peripherally
Oliguria (<0.5 mL/kg/hour)
Mental status changes
Agitation, confusion, and distress
Unresponsiveness
General features
Airway compromise
Dyspnoea
Hypoxaemia
Fever
Hypothermia
Define sepsis
Life-threatening organ dysfunction due to a dysregulated host response to infection.
List the most common causative organisms
Staphylococcus aureus
Pseudomonas species
Escherichia coli
List the risk factors for sepsis
Extremes of age
Frail
Immunocompromised
* Diabetes mellitus
* HIV
* Cirrhosis
* Sickle cell disease
* Asplenia
* Drug treatment eg. anticancer, oral corticosteroids
Trauma, surgery, or other invasive procedures in the past 6 weeks
Any breach of skin integrity (cuts, burns, blisters, skin infections)
IV drug or alcohol misuse
Indwelling lines or catheters
Women who are pregnant, are post-partum, or have had a termination of pregnancy or miscarriage in the past 6 weeks
List the complications for sepsis
Death
Organ dysfunction and failure
* Acute kidney injury
* Cholestasis
* Heart failure
* Acute respiratory distress syndrome
* Acute lung injury
Recurrent and secondary infection
Coagulopathy
* Thromboembolism
* Disseminated intravascular coagulation
Reduced quality of life
Neurological sequelae
* Focal neurological deficits and hearing loss in bacterial meningitis
* Polyneuropathy in sepsis and multi-organ failure
Psychological
List the signs for sepsis
New-onset confusion, disorientation, agitation
Temperature
* Fever
* Hypothermia
Respiratory distress
Hypotension
Capillary refill time and oxygen saturation - poor peripheral perfusion
Skin changes
* Mottled or ashen appearance; pallor or cyanosis of the skin, lips, or tongue; cold hands or feet.
* Non-blanching petechial rash - meningococcal disease
* Breach of skin integrity or infection
A weak high-pitched or continuous cry (in children under 5 years of age).
Dehydration
List the sepsis six
Take
Blood Cultures
Lactate
Urine output
Give
Fluids
Antibiotics
Oxygen
List the four AHA stages of heart failure
Stage A: at risk for heart failure
People who are at risk for heart failure but do not yet have symptoms or structural or functional heart disease
Stage B: pre-heart failure
People without current or previous symptoms of heart failure but with either structural heart disease, increased filling pressures in the heart or other risk factors
Stage C: symptomatic heart failure
People with current or previous symptoms of heart failure
Stage D: advanced heart failure
People with heart failure symptoms that interfere with daily life functions or lead to repeated hospitalizations
List the four AHA classes of heart failure
Class I
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation or shortness of breath.
Class II
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, shortness of breath or chest pain.
Class III
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, shortness of breath or chest pain.
Class IV
Symptoms of heart failure at rest. Any physical activity causes further discomfort.
Give the first line investigation in heart failure and potential actions
Elevated NT-pro-BNP / BNP levels
> 2000 ng/litre - TTE within 2 weeks
400~2000 ng/litre - TTE within 6 weeks
< 400 ng/litre (47 pmol/litre) - heart failure less likely
Compare Janeway lesions vs Osler’s nodes
Janeway lesions: painless, blanching red macules on the thenar/hypothenar eminences
Osler’s nodes: painful raised erythematous lesions, typically on the pads of the fingers
What is the gold standard investigation for heart failure
TTE
List the CXR signs of heart failure
Cardiomegaly (increased cardiothoracic ratio)
Pulmonary congestion
Pulmonary vascular congestion (vascular redistribution, Kerley B lines)
List the ECG signs of heart failure
LV hypertrophy
Atrial enlargement
Conduction abnormalities eg. LBBB
Underlying coronary artery disease
What can serum natriuretic peptides be reduced by
Obesity
African or African–Caribbean family background
Diuretics
ACEi
Beta‑blockers
ARBs
Mineralocorticoid receptor antagonists
List the causes of high levels of serum natriuretic peptides other than heart failure
Age over 70 years
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Pulmonary embolism (hypoxaemia)
Renal dysfunction [eGFR < 60 ml/minute/1.73 m2]
Sepsis
COPD
Diabetes
Cirrhosis
List the treatment algorithms in heart failure
- ACEi + beta-blockers
* Symptomatic treatment: loop diuretics - ARB
- hydralazine + nitrate
- Digoxin / ivabradine
List the drugs that should be avoided in HFrEF
Non-dihydropyridine calcium-channel blockers - Diltiazem, Verapamil
Class Ic antiarrhythmics - Propafenone, Flecainide
Thiazolidinediones - Pioglitazone
Dipeptidyl peptidase-4 (DPP-4) inhibitors - alogliptin, linagliptin, saxagliptin, sitagliptin
NSAIDs
List the causes of acute heart failure
IHD
Valvular heart disease
HTN
Acute / chronic kidney disease
Atrial fibrillation
List the symptoms and signs of acute heart failure
Dyspnoea / Orthopnoea / Paroxysmal nocturnal dyspnoea
Ankle swelling
Reduced exercise tolerance
Fatigue
Elevated jugular venous pressure
S3 (gallop rhythm)
Pulmonary crepitations
List the hypertension severity staging
Stage 1
Clinical 140/90 ~ 159/99
ABPM 135/85 ~ 149/94
Stage 2
Clinical 160/100 ~ 180/120
ABPM 150/95
Stage 3
Clinical 180/120 mmHg or higher
Give the definition of malignant hypertension
Severe increase in blood pressure to 180/120 mmHg or higher with signs of retinal haemorrhage and/or papilloedema
List the secondary cause for hypertension
Vascular
* Renal artery stenosis
* Coarctation of aorta
* Pre-eclampsia
Renal
* Chronic kidney disease
* Chronic pyelonephritis
* Diabetic nephropathy
* Glomerulonephritis
* Nephrotic syndrome
* Polycystic kidney disease
* Obstructive uropathy
* Renal cell carcinoma
Endocrine
* Pheochromocytoma
* Primary hyperaldosteronism
* Cushing’s syndrome
* Acromegaly
* Hyperthyroidism (increased systolic BP)
* Hypothyroidism (increased diastolic BP)
* Hyperparathyroidism
Drugs
* Alcohol
* Ciclosporin.
* Cocaine, amphetamine, sympathomimetics
* ADHD stimulants
* Venlafaxine
* Combined oral contraceptive, oestrogens
* Corticosteroids.
* Erythropoietin.
* Leflunomide.
* NSAIDs
Pregnancy
Connective tissue disorders
* Scleroderma
* Systemic lupus erythematosus
* Polyarteritis nodosa
Retroperitoneal fibrosis
Obstructive sleep apnoea
List the risk factors for primary hypertension
Increasing age
Gender
* Women <65 years tend to have a lower blood pressure than men.
* Women 65–74 years tend to have a higher blood pressure
Ethnicity - black African / Caribbean more likely
Genetics
Social deprivation
Co-existing diabetes / kidney disease
Lifestyle
* Smoking
* Excessive alcohol consumption
* Excess dietary salt
* Unhealthy diet
* Obesity
* Lack of physical activity
Anxiety and emotional stress
List the complications for heart failure
Heart failure.
Coronary artery disease.
Stroke.
Chronic kidney disease.
Peripheral arterial disease.
Vascular dementia.
List the symptoms and signs for hypertension
Usually asymptomatic
May present with
* Headaches
* Nosebleeds
* Visual symptoms
* Neurological symptoms
When should secondary hypertension be suspected
Young (<40 years)
Rapid onset
Sudden change in blood pressure when previously well controlled on a particular therapy
Resistant hypertension
List the fundoscopy findings for hypertensive retinopathy
Arteriolar narrowing
Arteriolar venous nipping (constriction of veins at crossing points)
‘Cotton wool spots’ on the retina (due to ischaemic changes)
Flame haemorrhages or papilloedema
List the treatment algorithms for hypertension
Step 1 treatment
ACEi / ARB first line in
* Age < 55 and not of black African or Caribbean origin.
* T2DM
CCB first line in
* Age > 55, NOT T2DM
* Black African or Caribbean origin, NOT T2DM
* If CCB untolerated - indapamide (thiazide-like diuretic)
If there is evidence of heart failure - indapamide
Step 2 treatment
If not controlled with ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)
If not controlled with CCB
* ACEi / ARB
* Indapamide (thiazide-like diuretic)
Step 3 treatment
Combination of
* ACEi / ARB
* CCB
* Indapamide (thiazide-like diuretic)
Step 4 treatment - resistant hypertension
* K+ 4.5 mmol/L or less - low-dose spironolactone
*K+ > 4.5 mmol/L - alpha-blocker (doxazosin, terazosin) / beta-blocker
List the contraindications for ACEi
Angio-oedema
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women
List the adverse effects for ACEi
Reduced ACE:
* Hyperkalaemia
* Renal impairment
* Hypotension
Increased Kinin (ACE inactivates bradykinin)
* Cough
* Angio-oedema
* Anaphylactoid reaction
List the contraindications for ARB
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women
List the adverse effects for ARB
Renal impairment
Hyperkalaemia
Angio-oedema
Dizziness
List the Thiazide diuretics. What channel do they act on?
Hydrochlorothiazide
Bendroflumethiazide
Na+Cl- co-transporter in DCT
List the Loop diuretics. What channel do they act on?
Furosemide
Bumetanide
NKCC channel on the in thick ascending limb of loop of Henle, cause Na+, K+, Cl- loss in urine
What channel does spironolactone act on
ALD-Na+ channel DCT
What channels does amiloride act on
ENaC, collecting duct
List the contraindications for spironolactone
Addison’s disease.
Acute renal insufficiency, significant renal compromise, anuria.
Hyperkalaemia.
List the causes of ejection systolic murmurs
High cardiac output state
* severe anaemia
* fever
* athletes (bradycardia → large stroke volume)
* pregnancy
* thyrotoxicosis
* liver cirrhosis
* arteriovenous fistula.
Pulmonary flow murmur (increased RV stroke volume)
* atrial septal defect
* pulmonary regurgitation
Aortic flow murmur (increased LV stroke volume)
* aortic regurgitation
Valvular stenosis
* aortic stenosis
* pulmonary stenosis
Other valve abnormalities
* mechanical aortic or pulmonary valve
* aortic sclerosis (turbulent flow without significant pressure gradient)
Subvalvular obstruction
* hypertrophic obstructive cardiomyopathy
* subaortic membrane
List the causes of pan systolic murmurs
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
List the causes for bradycardia in sinus rhythm
Sleep
Athletic training
Hypothyroidism
Medication:
* Beta-blockers
* Digoxin
* Verapamil, diltiazem
List the causes for tachycardia in sinus rhythm
Exercise
Pain
Excitement/anxiety
Fever
Hyperthyroidism
Medication:
* Sympathomimetics, e.g. salbutamol
* Vasodilators
List the causes for elevated JVP
Heart failure
Pulmonary embolism
Pericardial effusion
Pericardial constriction
Superior vena cava obstruction
When may Kussmaul’s sign be seen
(paradoxical rise of JVP on inspiration)
Constrictive pericarditis
Severe right ventricular heart failure
Restrictive cardiomyopathy
List the causes for displaced apex beat
(LV systolic dysfunction)
Heart failure
Aortic regurgitation
Mitral regurgitation
