Cardiology Flashcards
Two AF characteristics on the ECG
RR intervals are irregularly irregular
No distinct p waves
How can you classify AF?
Paroxysmal: at least one episode >30s, resolves within 7 days
Persistant: lasts more than 7 days or requires termination with medication or cardioversion
Permanent: does not resolve on cardioversion, sinus rhythm cannot be achieved and AF deemed the final rhythm
Risk factors for AF
Cardiac: Cardiomyopathy IHD/heart failure Valvular disease HTN
Resp: COPD, pneumonia, PE, pleural effusion, lung cancer
Endocrine: diabetes, thyrotoxicosis
Infection
Electrolyte disturbances
Drugs: bronchodilators, thyroxine (+alcohol/caffeine)
Signs and symptoms of AF
Symptoms: Dizziness/confusion Palpitations Chest pain Breathlessness Dyspnoea
Signs: Raised JVP Tachycardia Murmurs Irregular pulse Hypotension
AF investigations
Bedside: blood pressure, ECG
Bloods: FBC, U&Es, TFTs, magnesium, calcium, cholesterol
Imaging: CXR, CT/MRI if emboli, transthoracic echo
CHADSVASC score
Congestive heart failure Hypertension 140/90 Age >75 (2) Diabetes Stroke/TIA/thromboembolism (2) Vascular disease Age (65-74) Sex (female)
CHADSVASC score interpretation
> 2 anti-coagulate
1 consider anti-coagulation
HAS-BLED score
Hypertension Abnormal liver/renal function Stroke Bleeding Liable INRs Elderly (>65) Drugs/alcohol
3 methods of AF treatment
Rate control (>65, IHD)
Rhythm control (<65, first presentation, symptomatic, CHF)
Anti-coagulation
Catheter and surgical ablation
Rate control medication for AF
Beta blockers (metopralol, bisoprolol) CCBs (verapamil cardia selective) Digoxin (in sedentary patients)
What is the complication of BB and CCBs being co-prescribed?
AV heart block
Rhythm control in AF
First rate control with beta blockers
Electrical cardioversion
Drugs: amiodarone, sotalol, flecainide (pill in the pocket for paroxysmal AF)
This should be followed by 4 weeks of anticoagulation
Cardioversion considerations in AF
Identifiable reversible cause
Heart failure
Onset <48 hours: immediate cardioversion due to bleeding risk
Onset >48 hours: 3 weeks of anticoagulation before cardioversion due to risk of thromboembolism
When would you choose to rhythm control in an AF patient?
Rate control unsuccessful or symptoms persisting
Younger patient (to prevent permanent AF)
Recurrent symptomatic episodes
First onset AF (DC cardioversion if unstable)
Reversible cause
Co-existent HF
Anticoagulation options in AF
Warfarin (vitamin K antagonist) - regular INR monitoring
NOACs - rivaroxaban/apixaban (dirext Xa inhibitor)
Mechanism of low-molecular weight heparin?
Inhibition of antithrombin III leading to factor Xa inhibition
Mechanism of aspirin?
COC inhibitor
Causes of irregularly irregular heart beat
AF
Atrial/ventricular ectopics
Atrial flutter with variable block
What cardiac change does Wolff-Parkinson-White cause?
Supraventricular tachycardia
what causes a sawtooth ECG pattern, and what treatment is there?
Atrial flutter (ventricular rate is dependent on degree of AV block - atrial rhythm usually 300/min) Same treatment as AF, although more sensitive to cardioversion
What investigations would you use to identify the cause of a TIA
Large vessel occlusions:
Carotid duplex ultrasound
MRA
CTA
Cardiac analysis:
Transthoracic Echo
ECG
Holter monitoring
Treatment of permanent AF?
Rate control and anti-coagulation
Adverse effects of amiodarone
Thyroid disease
Interstitial lung disease
Hepatotoxicity
What is the mechanism of digoxin toxicity?
Triggered activity in which there are afterdepolarisation oscillations in membrane activity
What are the three mechanisms of arrhythmogenesis?
Automaticity Re-entry (most common) Triggered activity (digoxin toxicity)
What is the mechanism of Class I anti-arrhythmics?
Slow depolarisation (depress phase 0). Inhibits fast sodium channels and so reduce sodium entry.
Class I anti-arrhythmics examples
IB: phenytoin (also decreases length of action potential)
IC: flecainide (just depresses phase 0)
Class I anti-arrhythmics side-effects
Nause and vomiting SLE-like syndrome (flecainide) Negative inotropic (weaken muscle contractions) Proarrhythmic CNS toxicity
Class II anti-arrhythmics mechanism?
Catecholamine antagonist at the beta-adrenoreceptors
Negative inotrope and chronotrope (reduce HR and contraction strength)
Reduce conduction at AV node
Reduce rate of spontaneous depolarisaiton at SA node (reduces slope of phase 4)
Class II anti-arrhythmics examples and side effects?
Bisoprolol
Propanalol
Bradycardia Postural hypotension Insomnia Bronchoconstriction Erectile dysfunction Hypoglycaemia AV nodal heart block
Class III anti-arrhythmics mechanism?
Prolong action potential by blocking potassium channels (prolongs phase 2)
Class III anti-arrhythmics examples and side effects
Amiodarone
Nausa, thyroid dysfunction, peripheral neuropathy, photosensitivity, proarrhythmic, hepatitis, potentiates warfarin and digoxin
Sotalol (same as Class II)
What are the two different kinds of CCBs?
Dihydropyridines (anti-hypertensive e.g. amlodipine and nifedipine)
Non-dihydropyridines (anti-arrhythmics e.g. verapamil and diltiazem)
Class IV anti-arrhythmics mechanism
Block L-type calcium channels in autorhythmic cells (reduce rate of spontaneous depolarisation)
Negative inoptrope and chronotrope
Digoxin mechanism
Inhibits Na/K ATPase pump in cardiomyocytes
Increases intracellular calcium
More forceful contractions (positive inotrope)
What needs monitoring when a patient is on digoxin?
Kidney function ECG changes (ST depression, T wave changes, PR prolongation)
Digoxin side effects
Nausea and vomiting
Visual disturbances (yellow rings, change to colour perception)
Proarrhythmic
Insomnia
Adenosine mechanism and what is it treatment for?
Slows heart rate
Treats supraventricular tachycardia
Atropine mechanism and what is it treatment for?
Increases heart rate
Treats sinus bradycardia and AV block
What is magnesium sulfate used to treat?
Polymorphic ventricular tachycardia (torsades des pointes)
Digoxin toxicity
Tests and monitoring of amiodarone?
LFTs and TFTs
Every 6 months on starting
Which patients should you not start flecainide on?
Coronary heart disease
Treatment for regular ventricular tachycardia?
Amiodarone (IV 300mg)
Which anti-arrhythmic can prolong QT interval?
Sotalol
Must have regular ECG monitoring
Three stages of hypertension
- 140/90 (135/85 ABPM) (plus end-organ damage, CVS, renal disease, diabetes, >20% CVS risk on Framingham calculator)
- 160/100 (150/95 ABPM)
- 180/110
Causes of secondary hypertension
Renal: renovascular disease, internal disease (CKD, AKI, glomerulonephritis)
Endocrine: Cushing’s, Acromegaly, Conn’s, phaeochromocytoma
Drugs: SSRIs, oral contraceptives, glucocorticoids, NSAIDs, EPO
Coarctation of the aorta
What symptoms and signs might you see with hypertension (either reflecting end-organ failure or secondary cause)
Symptoms: blurred vision, palpitations, chest pain, dyspnoea, headaches, new onset neuropathy
Signs: retinopathy, cardiomegaly, arrhythmias, proteinuria, uraemia
KWB retinopathy grades
- generalised arteriolar narrowing (silver wiring)
- focal narrowing and arteriovenous nipping
- retinal haemorrhages and cotton wool spots (retinal nerve fibre layer micro-infarcts leading to exudation of axoplasmic materials)
- papilloedema
Investigations for a patient with newly diagnosed hypertension?
Bedside: BP, urinalysis, fundoscopy, ECG
Bloods: FBC, U&Es, HbA1c/fasting glucose, cholesterol
Special tests: ambulatory BP, renal US, endocrine tests (aldosterone:renin ratio)
What are the BP targets in <80s and >80s?
<80s: 140/90
>80s: 150/90
(130/80 if renal disease and proteinuria or diabetes)
What is malignant hypertension?
180/110 with papilloedema and/or retinal haemorrhage
Signs: Uncontrollable epistaxis Haematuria Epistaxis Raised ICP - headaches and nausea
Treatment of malignant hypertension/hypertensive emergency?
IV nitroprusside (nitric oxide releasing) or labetalol Phentolamine (alpha adrenergic antagonist)
Over 24-48 hours so as to avoid hypoperfusion
Causes of aortic regurgitation?
Aortic leaflets:
rheumatic heart disease (commonest in developing countries)
congenital (bicuspid/quadcuspid)
degenerative (calcification) - commonest in developed
infective endocarditis
Aortic root: aortitis, aortic dissection (Stanford A), connective tissue disorders (Marfan’s)
Syphilis
Organisms causing infective endocarditis and rheumatic heart disease?
Infective endocarditis: strep viridans, staph aureus, enterococci
Rheumatic heart disease: post-strep Group A (pyogenes) auto-immune condition
What connective tissue disorders can cause aortic and mitral regurgitation?
Marfan’s: defective FBN1 gene
Ehlers-Danlos: collagen defects
What other chronic inflammatory diseases is aortitis associated with
Rheumatic arthritis
Anylosing spondilitis
Takayasu arteritis
Complicates giant cell arteritis
What are the complications of acute aortic regurgitation?
Reduced coronary flow leading to angina or MI
Increased end-diastolic pressure leads to pulmonary oedema and dyspnoea and eventually cardiogenic shock
What cardiac changes might you see in a patient with chronic aortic regurgitation?
Increased preload, leading to left ventricular dilatation and hypertrophy
Greater contractility
Eventual heart failure
Acute aortic regurgitation clinical features
Bilateral basal crackles
Raised JVP
Dyspnoea
Chest pain (consider angina or MI)
Chronic aortic regurgitation clinical features
Palpitations Angina Dyspnoea Water hammer pulse (collapsing) Wide pulse pressure
Chest signs: displaced apex, early diastolic decrescendo murmur (left sternal edge, high pitched and blowing), soft s1 and s2
Eponymous signs associated with aortic regurgitation
de Musset’s: head bobbing with each heart beat
Quincke’s: pulsation of nail beds
Muller’s: vibrating uvula
Investigations for aortic regurgitation
Bedside: BP, ECG (LVH)
Bloods: FBC, U&Es, clotting, cholesterol
Imaging: echo (origin of regurgitant jet, its size, aortic valve pathology and hypertrophy), CXR (cardiomegaly, aortic dilatation, calcification)
Special: cardiac MRI, cardiac catheterisation, ECG exercise stress testing
Aortic regurgitation management
Surgery if acute or severe (determined by LVH, pressure gradient and valve area)
Transcatheter aortic valve replacement (TAVR)
Mechanical valve: for younger patients, need anti-coagulation, longer lifespan
Bioprosthetic: older patients, don’t need anti-coagulation, 10 year lifespan
What is the order of valves affected by rheumatic heart disease?
- Mitral
- Aortic
- Tricuspid
- Pulmonary
What are the classic stigmata of infective endocarditis?
FEVER AND NEW MURMUR
(FROM JANE)
Fever
Roth spots: retinal haemorrhages
Osler nodes: painful, red lesions on fingers
Murmur
Janeway lesions: painless plaques on palms or soles due to septic emboli
Anaemia
Nails (splinter haemorrhages)
Emboli
+ pallor, weight loss, glomerulonephritis
How is infective endocarditis diagnosed?
Modified Duke’s criteria (requires blood cultures and echo)
MAJOR: 2 separate positive blood cultures, endocardial involvement
MINOR: (FIVE)
Fever >38
IV drug user or predisposing heart condition
Vascular phenomena (myocotic aneurysm or Janeway)
Echo findings
Immunological findings (Rheumatoid factor, Osler nodes, glomerulonephritis)
Innocent murmurs characteristics (7s)
Soft Systolic Short Symptomless Sounds (normal s1 and s2) Standing/sitting (vary with position) Special tests normal (echo/ECG)
What is the effect of inhibiting ACE?
Reduction of angiotensin II leading to: Reduced ADH (lowering H2O) Reduced aldosterone (lower Na, Ca, H2O; raised K) Reduced vasoconstriction Reduced sympathetic activity
What are some adverse effects of ACE-i?
Persistent dry cough (build-up of bradykinin in lungs)
Headache
Postural hypotension
Rashes
Angioedema
TERATOGENIC (inhibit foetal urine production leading to oligohydramnios)
Who should you not give ACE-i to?
Pregnant women
Renal failure
Severe illness (can result in AKI, especially if also on NSAIDs)
Action of dihydropyridine CCBs and examples?
Block voltage-gated L-type calcium channels
Reduces vasoconstriction
Amlodipine, nifedipine
Adverse effects of CCBs?
Headache Flushing Peripheral oedema Reduced cardiac contractility Dizziness Constipation
Action of thiazide diurectics?
Block Na/Cl channels in distal convoluted tubules of kidney, preventing Na/Cl/H2O entering tubule cells
Long-term anti-hypertensive effects mainly due to vasodilation
Examples of thiazide diuretics and their adverse effects
Bendroflumethiazide
Indapamide
Electrolytes: LOW magnesium, sodium, potassium, HIGH calcium
Metabolites: HIGH glucose, uric acid (gout)
GI: disturbances
Severe: pancreatitis, cholestasis, agranulocytosis
Impotence
Frequency
TERATOGENIC
Alpha-1 blockers action and examples
Block alpha-1 adrenoreceptors in vascular smooth muscle
Reduced arteriolar tone
Venous dilation
Doxazosin
Adverse effects of alpha-1 blockers
Headaches Postural hypotension Dizziness Nausea Rhinitis Frequency
Beta blockers mechanism of action
Reduced renin production
Negative inotropic and chronotropic effects
Vasodilation
Beta blockers adverse effects
Cold peripheries Erectile dysfunction Bronchoconstriction/asthma exacerbation Postural hypotension Headache AV nodal heart block Hypoglycaemia Insomnia
Contraindications for beta blockers
Pheochromocytoma (unless given with alpha blocker - phenoxybenzamine)
Asthma
Severe peripheral arterial disease
Bradycardia (especially if with verapamil)
Starling equation
Net pressure = hydryostatic pressure - oncotic pressure (pull of proteins in blood)
Ohm’s law
Flow = change in pressure/resistance
Poiseulle’s law
Resistance (R) ∝ η x L / r4
(inversely proportional to radius^4)
OR
Flow (F) ∝ 𝚫p x r4 / η x L
Cardiac output =
stroke volume x heart rate (average of 5L)
What effect does the vagus nerve have on the heart?
Acts on SAN and AVN and contractile cells to reduce HR
SAN: Increases K+ permeability and action potential length
AVN: increases k+ permeability and AVN delay
contractile cells: reduces strength of contractions
What relationship does the Frank-Starling Law describe?
between preload (LVEDP) and stroke volume
Signs and symptoms of acute coronary syndrome?
Can be silent in MI if elderly or diabetic
Symptoms: chest pain >15 mins, SOB, sweating, nausea and vomiting
Signs: pale, clammy, hypotension, pulmonary oedema, tachycardia
ACS investigations
Bedside: obs, BP, glucose, ECG
Bloods: FBC, U&Es, TFTs, LFTs, cholesterol, Mg
Cardiac enzymes: troponin T/I, CK-MB, myoglobin
Imaging: CXR, transthoracic echo
Special: coronary angiogram
What changes would you see on an ECG following an MI (how do STEMI, NSTEMI and unstable angina differ)?
STEMI: minutes-hours: hyperacute T waves 0-12 hours: STEMI 1-12 hours: Q wave development Days: T wave inversion Weeks: T wave normalisation and persistent Q waves
NSTEMI and UA: may have signs of MI, T wave inversion or no changes
When can you measure troponins after MI? And when else might you see them raised?
6-12 hours (usually 8 hours rise)
New tests can be done 3 hours after event
Prognostic value
CKD,PE
Immediate management of ACS
MONA
IV morphine (2.5-5mg) + anti-emetic (10mg metoclopramide)
Oxygen (if <94%) - 15l/min via high flow non-rebreather mask
GTN
Aspirin 300mg
(+ metoclopramide)
Hospital management of STEMI
Aspirin + second antiplatelet (clopidogrel, prasugrel or ticagrelor) –> PCI within 120 mins –> LMWH
Fibrinolysis (alteplase) –> PCI 6-24 hours
Lifelong aspirin, 12 months of second antiplatelet
IV glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) if 6-month mortality >3%
How should UA or NSTEMI be managed according to GRACE scoring?
High risk (>3%):
- Angiography within 72 hours (fondaparinux if not possible);
- dual antiplatelet (lifelong aspirin and 12 months clopidogrel)
- if chest pain continues - glycoprotein inhibitor (IV eptifibatide, or tirofiban)
- PCI if chest pain continues
Medium risk (1.5-3%): dual antiplatelet
Low risk (<1.5%): lifelong aspirin only
What are the 8 factors considered in GRACE scoring and what does it estimate?
Age Heart rate CHF Renal function Elevated biomarkers ST segment deviation Cardiac arrest Systolic BP
6 month mortality risk in patients with NSTEMI or UA
Long-term management of ACS
Beta blocker and ACE-i (if not contraindicated) - bisoprolol and ramipril up to 10mg
Dual antiplatelet therapy (aspirin and clopidogrel 75mg OD)
Artorvastatin 80mg OD
Cardiac complications of MI
Pericarditis (autoimmune - Dressler’s syndrome 2-10 weeks after)
Mitral regurgitation (secondary to ischaemia and rupture of papillary muscles) - systolic murmur
Complete heart block (AV node ischaemia from right coronary artery occlusion)
Ventricular tachycardia
HF
Recurrent MI
Thromboembolism
Ventricular aneurysm
What effect does COX enzyme have?
Production of prostaglandins and thromboxane A2 –> platelet aggregation
Acute pericarditis vs STEMI ECG changes?
Pericarditis:
widespread ST changes
PR depression
saddle-shaped ST elevation
STEMI
ST elevation greater in III than II
Convex or horizontal ST elevation
ST depression in leads other than aVR or V1
Most common cause of acute pericarditis? Treatment?
Viral secondary to coxsackie B infection
NSAIDs and colchicine
Which artery are most inferior MIs supplied by, and what leads will be affected? What other artery may be occluded in other patients?
Right Coronary Artery
II, III, aVF
Circumflex will sometimes supply posterior descending artery
Three stages of atherosclerosis
- Endothelial damage: LDL deposits under epothelium which are oxidised and cause more damage. Monocyte recruitment to tunica intima
- Plaque formation: monocytes become macrophages (lipid-laden = foam cells), multiple foam cells - fatty streak. Muscle cells from tunica media migrate and cover to form lipid rich atheroma with plaque on top
- Plaque rupture: leads to platelet aggregation and vessel occlusion
Artery occluded in posterior MI and ECG changes?
Left circumflex artery or RCA
ST DEPRESSION V1-V3
Tall R waves V1 and V2; upright T waves
Anterior MI artery
Left coronary artery
Anteroseptal MI artery and leads affected
LAD
V1-V3
Lateral MI - which artery and leads are affected?
left circumflex
Leads I, aVL and V4-V6
When does CK peak following MI, and what is it useful to assess?
24 hour peak
Recognition of re-infarction
Contraindications of fibrinolysis
Absolute: Active bleeding Bleeding disorder Previous haemorrhagic stroke Ischaemic stroke last 6 months Recent major surgery or head trauma Suspected aortic dissection CNS neoplasm
Relative: anticoagulation peptic ulcer pregnancy or less than 1 week postpartum TIA in preceding 6 months Recent trauma/surgery last 2 months infective endocarditis
Dressler’s syndrome features and treatment
1-4 weeks post MI Low grade fever Sharp chest pain Raised ESR Pericardial rub and pericardial effusion
Tx: NSAIDs or steroids
Signs and symptoms of left ventricular heart failure
Symptoms: Dyspnoea Wheeze Cough Paroxysmal nocturnal dyspnoea Orthopnoea Nocturnal cough (pink froth) Haemoptysis Fatigue and lethargy Exercise intolerance
Signs: Tachypnoea and cardia Cyanosis Pulsus alternans S3 (gallop rhythm) Inspiratory basal crackles Pleural effusion Cardiomegaly
Signs and symptoms of right ventricular heart failure
Symptoms: abdominal discomfort fatigue nausea peripheral oedema
Signs: tachycardia hepatomegaly ascites cachaxia cardiomegaly raised JVP pitting oedema right ventricular heave
Signs and symptoms of aortic stenosis
SAD (syncope, angina, dyspnoea)
Epistaxis (acquired von Willebrand’s)
Signs: Ejection systolic murmur (low-pitched in second right intercostal space) Sustained apex, thrill Slow rising pulse Narrow pulse pressure Soft S2 if severe S4 sign of LVH Reversed splitting
Causes of aortic stenosis
Calcification - >65s, most common cause
Bicuspid valve - congenital, <65s, turbulent flow leads to stenosis and calcification
Rheumatic heart disease - post-Strep A autoimmune condition leading to inflammation
What compensatory changes do you see in the heart in aortic stenosis?
Increased left ventricular hypertrophy
Increased pressure gradient across the valve
Left ventricular heart failure (bibasal crackles and dyspnoea)
Exertional syncope
Angina due to increased O2 demands from the heart and reduced coronary flow
Investigations for suspected aortic stenosis
Bedside:
BP
ECG: LVH (deep S-waves in V1 and V2, tall R-waves V5 and V6)
Bloods: FBC, U&Es, cholesterol, clotting
Imaging:
CXR - typically small heart, but cardiomegaly if HF occurs; dilated ascending aorta - can be normal!avl
Transthoracic Echo - ejection fraction, valve area, ventricular hypertrophy
Special:
Cardiac catheterisation
Cardiac MRI
ECG exercise stress testing
How is the severity of aortic stenosis assessed?
Transaortic pressure
Aortic valve area
Management of aortic stenosis
Surgery in severe or symptomatic cases
Valvotomy - percutaneous ballon or open (forces valve leaflets apart)
Valvular replacement:
Mechanical - for younger patients, long lifespan, lifelong anti-coagulation
Bioprosthetic - older, no anti-coagulation needed, 10 year lifespan
TRANSCATHETER AORTIC VALVE REPLACEMENT (TAVR) if open surgery not indicated
Complications of aortic stenosis
Sudden death
Infective endocarditis
Arrhythmias
Cardiac failure
How might you distinguish aortic stenosis from sclerosis?
Sclerosis: normal pulse, normal heart sounds, quiet and soft murmur
Most common effected areas in infective endocarditis
Left sided native or prosthetic valves
Right sided native valves
Devices e.g. pacemaker or defibrillator
Angiotensin II receptor blockers - side effects
Hypotension
Hyperkalaemia
What is first degree heart block?
PR interval >0.2s
Commonly asymptomatic and no need for intervention
What is second degree heart block?
Mobitz i: progressive prolongation of PR interval until a dropped beat (no QRS) [Wenckebach]
Mobitz ii: normal PR interval, but P-wave often not followed by QRS complex
What is third degree heart block?
Complete heart block
No association between P-wave and QRS complex
Characteristics of cardiac tamponade
Beck’s triad: muffled heart sounds, hypotension, raised JVP
Dyspnoea
Tachycardia
Absent Y descent on JVP due to limited R ventricular filling
Pulsus paradoxus (abnormal BP drop on inspiration)
ECG: electrical alternans (alternating QRS heights)
Signs and symptoms of acute pericarditis
Chest pain, may be pleuritic - relieved on sitting forward Dyspnoea Tachypnoea Tachycardia Pericardial rub Non-productive cough
Causes of acute pericarditis
Coxsackie (+ varicella, influenza, mumps) Dressler's syndrome (post-MI) Uraemia (fibrinous pericarditis) TB Hypothyroidism Trauma Malignancy Connective tissue disease (RA, SLE)
70-year-old woman is found to have a pan-systolic murmur after presenting with dyspnoea. A soft S1 and split S2 is also noted
Mitral regurgitation
Risk factors for mitral regurgitation?
Female Older Collagen disorders (Marfan's, Ehler-Dalnos) Low BMI Renal dysfunction MI Mitral prolapse or stenosis
Causes of mitral regurgitation?
MI (damage/ischaemia to papillary muscle or chordae tendenae)
Infective endocarditis
Rheumatic heart disease
Mitral valve prolapse
Congenital
Signs and symptoms of mitral regurgitation
Fatigue, SOB, oedema
Soft S1 (incomplete closure of mitral valve) Split S2 if severe Pansystolic murmur (blowing) over apex and radiating to axilla
Mitral regurgitation investigations
BP
ECG: broad P-waves (atrial enlargement)
CXR: cardiomegaly
Transthoracic Echo - assessment of severity
Management of mitral regurgitation
Nitrates, diuretics, positive inotropes, intra-aortic balloon pump (increases cardiac output)
HF: ACE-i, beta blockers, spironolactone
§
Severe - surgery (either repair or valve replacement)
What is aortic dissection?
Tear in the tunic intima of the wall of the aorta
What is aortic dissection associated with?
Hypertension Trauma Syphilis Collagen disorders (Marfen's, Ehlers-Danlos) Bicuspid aortic valve Pregnancy Turner's and Noonan's
Features of aortic dissection
Tearing chest pain radiating to back
Aortic regurgitation
HTN
Absent subclavian pulse
Carotid dissection
Specific arteries (angina from coronary, paraplegia from spinal, limb ischaemia from distal aorta)
Rarely ECG changes (sometimes ST elevation)
Types of aortic dissection
Stanford A: ascending (2/3s)
Stanford B: descending
Which drugs can lead to gout?
Loop diuretics
Thiazides
Pyrazinamide
What ECG changes would you see in a PE?
SINUS TACHYCARDIA
RBBB
Right axis deviation
Inverted T waves
How does the New York Health Association classify heart failure?
Class I-IV based on exercise ability (normal - unable without discomfort); and symptoms (none - at rest)
What is the difference between systolic and diastolic heart failure?
Systolic: reduced LV ejection fraction (pumping out reduced proportion of its blood), ventricular dilatation
Diastolic: HF with preserved ejection fraction, ventricular hypertrophy
Main causes of heart failure
Vascular: previous infarction; hypertension
Electrical: arrhythmias (leading to cardiac compensation)
Muscular: dilated cardiomyopathy, hypertrophic cardiomyopathy, congenital heart disease
Valvular: stenosis or regurgitation
High-output: anaemia, thyrotoxicosis, septicaemia, liver failure - leading to reduced peripheral resistance
What is the Frank-Starling law?
Increased preload (stretching of myocytes) leads to increased contractility (i.e. stroke volume)
This is up to a point. After preload increases to a certain threshold, stroke volume plateaus and then decreases
What are the main determinants of stroke volume?
Preload
Cardiac contractility
Afterload (pressure against which the ventricles must contract)
Signs and symptoms of heart failure
Symptoms:
Resp - SOB, orthopnoea, paroxysmal nocturnal dyspnoea, wheeze
General - fatigue, ankle swelling, abdominal pain, weight loss, cachexia
Signs:
Raised JVP, peripheral oedema, bibasal crackles, hepatomegaly, ascites, displaced apex, S3/S4, pulsus alternans
What urgent investigation would you do in suspected HF, and in which cases would you carry it out?
Echocardiogram <2 weeks
Patients with: previous MI, severe symptoms, BNP >400, evidence of valvular disease or renal dysfunction
General investigations in patients with suspected HF
Bedside: BP, ECG (LVH, infarct), urinalysis (renal dysfunction)
Bloods: FBC (exclude anaemia or infection), U&Es (exclude renal causes of odema), TFTs (exclude thyrotoxicosis), cholesterol and HbA1c (CV risk stratification), LFTs (exclude liver failure), BNP
Imaging: CXR, echo
Special: cardiac catheterisation, cardiac biopsy, 24 hour ECG, lung function tests
What might you see on a CXR in a patient with HF?
Alveolar oedema (perihilar shadowing)
Kerley B (fluid in septae of secondary lobules)
Cardiomegaly
Upper lobe Diversion
Pleural Effusion (blunting of costrophrenic angle)
Lifestyle modifications for a patient with HF
Patient education
Smoking, weight, diet, sexual and travel advice
One-off pneumococcal vaccine and annual flu vaccine
What condition is classically associated with S4?
hypertrophic obstructive cardiomyopathy
What heart condition does alcohol abuse commonly cause?
Dilated cardiomyopathy
Management of HF
ACE-i (ramipril 1.25mg OD - 5mg BD) - check renal function
Beta blockers (bisoprolol 1.25mg OD) - double dose every 4 weeks untel target reached; NOT IN BRADY, ASTHMA, COPD or PULMONARY OEDEMA
+/- spironolactone
If still symptomatic then consider:
Hydralazine + nitrate (esp if Afro)
ARB
If still symptomatic:
- digoxin
- cardiac resynchronisation therapy
Management of heart failure with preserved ejection fraction
Loop diuretics for symptom control
Address co-morbidities and underlying causes
Management of acute pulmonary oedema
FOND
Furosemide 40mg
O2 high-flow
Nitrates
Diamorphine
What is considered a normal ejection fraction?
55-70%
What is cor pulmonale and what are its causes?
Abnormal enlargement and dysfunction of right side of the heart due to pulmonary hypertension
PE
COPD
Pulmonary fibrosis
Causes of LBBB
Cardiomyopathy
Aortic stenosis
IHD
HTN
Treatment of severe bradycardia with signs of shock?
IV atropine 500mcg boluses
Transcutaneous pacing if necessary
Causes of S3
Normal if <30 (<50 for women)
Left ventricular failure
Constrictive pericarditis
Mitral regurgitation
Causes of S4
HOCM
Aortic stenosis
HTN
Management if patient on warfarin has INR 5-8 (no bleeding)
Withhold two doses warfarin
Reduce subsequent maintenance dose
Causes of RBBB
Right ventricular hypertrophy PE Increased right ventricular pressure (cor pulmonale) MI Atrial septal defect Myocarditis or cardiomyopathy
Management of a patient on warfarin due to undergo surgery
If can wait 6-8 hours give IV Vit K
If emergency: four-factor prothrombin factor complex
Major and minor criteria of rheumatic heart disease (2 major/1 major and 2 minor)
Major: Erythema marginatum (pink rings on torso or inner limb surfaces) Sydenham's chorea (late) Polyarthritis Carditis and valvulitis Subcutaneous nodules
Minor: Raised ESR/CRP Pyrexia Arthralgia Prolonged PR interval
Treatment of rheumatic heart disease
IM Benzylpenicillin
Admit and bed rest
10 day penicillin (long-term)
Aspirin as needed
Cause of mitral stenosis
RHEUMATIC HEART FEVER
Features of mitral stenosis
Mid-diastolic murmur (low-rumbling) Tapping apex (non-displaced) Malar flush AF Loud S1, opening snap Low volume pulse
Mitral stenosis CXR and ECG features
CXR: left atrial enlargement
ECG: bifid p waves or absent p waves
Most common cause of death following MI? What management would you consider for such patients
Cardiogenic shock (but actually VF)
Inoptropic support
Coronary angiography
Echo
Surgical intervention
Common causes of cardiogenic shock following MI?
Damage to ventricular myocardium leading to reduced ejection fraction
Left ventricular free wall rupture
What initial tests would you perform in someone with suspected pericarditis?
ECG (may be normal in 10%)
Echo (pericardial effusion)
Troponin (exclude MI or show myocardial involvement)
Complications of acute pericarditis
Chronic pericarditis Cardiac tamponade (due to pericardial effusion)
Management of VSD and shock post-MI
Inotropic support Intra-aortic balloon pump Analgesia Consider angiogram Positive pressure ventilation Transfer to cardiothoracic unit Swann-Ganz pulmonary artery catheter
Normal pressures and oxygen sats in heart chambers
RA: 0-4mmHg (70%)
RV: 20/0-4mmHg (70%)
LV: 105/0-5 (95-100%)
Antibiotic management of infective endocarditis (for each organism)
Empirical: benpen, gentamicin
Strep: benpen and amoxicillin
Staph: fluclox and gentamicin
Aspergillus: miconazole
Definition of supraventricular tachycardia?
Narrow complex tachycardia
Acute and long-term management of SVT
Acute:
Vagal manoeuvres (valsalva, carotid sinus massage)
IV adenosine - 6mg, 12mg, 12mg (verapamil if asthmatic)
Electrical cardioversion
Long-term:
Beta-blocker
Radio-frequency ablation
What manoeuvres can patients use to terminate SVT attacks?
Head in icy water
Pressing on eyeballs
Finger down throat
All stimulate vagus nerve, slowing AV node conduction
What kind of tachy is Wolf-Parkinson-White and what are the ECG findings?
Atrioventricular re-entry tachy
Wide QRS with Delta waves (slurred upstroke)
Left axis deviation in most cases
Short PR
Associations of WPW and treatment
HOCM Thyrotoxicosis Mitral valve prolapse Ebstein anomaly ASD
Tx:
Radio-frequency ablation (definitive)
Sotalol (not if AF), flecainide, amiodarone
Anterolateral MI leads and artery?
V2, V3, I and aVL
Investigations for suspected aortic dissection
Bloods
BP both arms (20mmHg difference)
ECG: any ischaemia, right heart strain or AF in PE
CXR: widened mediastinum
CT thoracic aorta: quantify damage and assess for possible repair
Immediate management of aortic dissection
Admit to intensive care
Antihypertensives (reduce BP and HR) - IV sodium nitroprusside, beta blocker
Oxygen and analgesia
Surgery
Definitive treatment of type A and B aortic dissections
A: median sternotomy and cardiopulmonary bypass for aortic root repair/replacement
CONTRAINDICATED - evolving CVA or renal failure
B: BP control (surgery if aortic expansion evidence)
ECG changes in LVH
V1 or V2 S wave >30mm
V5 or V6 R wave >30mm
What might lead to a false LVH diagnosis?
Obesity
Emphysema
Pericardial effusion
Young people with thin chest walls
Marfan’s syndrome features
Tall and long limbed High arched palate Pes planus Pectus excavatum Aortic dilation (aortic aneurysm, dissection, regurgitation, mitral prolapse) Upwards lens dislocation, blue sclera, myopia Arachnodactyly Scoliosis Pneumothoraces
Most common cause of death in HOCM and what is the hereditary pattern?
Arrhythmia
Autosomal dominant
HOCM features
AUTOSOMAL DOMINANT
Exertional dyspnoea and angina
Syncope following exercise
Ejection systolic murmur
Arrhythmia
Sudden death (ventricular arrhythmia, arrhythmia, HF)
Jerky pulse, large a waves, bisferiens (double beat)
Echo and ECG features of HOCM
Echo (MR SAM ASH)
Mitral Regurgitation
Systolic Anterior Motion of the mitral valve leaflet
Asymmetric hypertrophy
ECG
ST and T wave changes, progressive T wave inversion
Deep Q waves
AF
Management of HOCM
Amiodarone Beta blocker Cardiac defibrilator Dual chamber pacemaker Endocarditis prophylaxis
Drugs to avoid in HOCM
ACE-i
Nitrates
Inotropes
How should suspected DVT be investigated if Wells’ score is >/=2 points?
Arrange leg vein ultrasound within 4 hours
If negative, take D-dimer
If US not possible in 4 hours, carry out D-dimer and give LMWH while waiting for US within 24 hours
How should DVT/PE be managed?
Initial LMWH or fondaparinux - continued for 5 days or until INR is >2 for at least 24 hours (6 months if active cancer)
Warfarin (or other vitamin K antagonist) within 24 hours - continued for 3 months and then reassessed (extended if unprovoked DVT and no bleeding risk)
Thrombolysis if massive PE (hypotensive etc)
What investigations would you carry out for a patient with an unprovoked DVT?
Cancer Ix:
Full examination, CXR, bloods (FBC, calcium, LFTs) and consider abdo-pelvic CT/mammogram if >40
Antiphospholipid antibodies (Hughes/APS) Hereditary thrombophilia screening
What is taken into consideration when deciding a dose for LMWH?
Weight of patient
Renal function
How is heparin monitored?
Activated partial thromboplastin time (APTT)
Causes of sinus bradycardia
Athletics Hypothyroidism Hypothermia Legionnaire's, typhoid MI
Investigations for infective endocarditis
ECG Echo Blood cultures (3 sets) - from peripheral vein MC&S US abdomen (possible splenic infarcts)
Complications of infective endocarditis
TIA Complete heart block AKI HF Vertebral osteomyelitis
Risk factors for infective endocarditis
Miscarriage IVDU Prosthetic heart valve Chronic cholecystitis Pneumonia Colonic malignancy
What are the two contraindications for statins
Pregnancy Macrolide antibiotics (risk of rhabdomyolosis)
Causes of cardiac arrest
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypocalcaemia, hypoglycaemia, acidaemia
Hypothermia
Thrombosis
Tension pneumothorax
Tamponade
Toxins
Action of loop diuretics and examples?
Inhibit Na-K-Cl transporter in ascending loop of Henle
Furosemide, bumetanide
Treatment of stable angina?
BETA BLOCKER (or CCB unless HF)
+ Aspirin and simvastatin
Normal QRS range
80-100ms
Features of coarctation of the aorta
HF/HTN
Poor feeding
Lethargy, SOB
Hypoperfusion of lower extremities - weakened femoral pulses
Notching of inferior border of ribs
Systolic murmur loudest at left sternal border
Apical click
Associated with: Turner's Bicuspid aortic valve Neurofibromatosis Berry aneurysms
First-line investigation for PE, and when is it contraindicated>
CT pulmonary angiogram
contraindicated if renal impairment as contrast is nephrotoxic - carry out V/Q (ventilation-perfusion) scan instead
Pulmonary angiography gold standard but significant complications
What is the DRAGON score used for?
3-month outcome in ischaemic stroke patients receiving tissue plasminogen activator
Indications for urgent surgical valve replacement in infective endocarditis?
Severe congestive heart failure
Overwhelming sepsis despite Abx
Pregnancy
Recurrent embolic episodes despite abx
What ECG changes might you see in a patient with a pulmonary embolism?
SINUS TACHYCARDIA
Large S wave lead I Large Q wave lead III Inverted T wave lead III S1Q3T3 RBBB
Causes of raised proBNP
Renal dysfunction Age >70 LVH Ischaemia Hypoxaemia (PE) Sepsis COPD Liver cirrhosis Diabetes
What drugs can cause a prolonged QT interval?
TCAs Sotalol Amiodarone Chloroquine Erythromycin
What conditions can cause a prolonged QT interval?
Hypo - calcaemia, kalaemia, magnesaemia
MI
Myocarditis
SAH
Hypothermia
Management of ventricular tachycardia
If adverse signs (<90 systolic BP, chest pain, HF) - immediate cardioversion
Amiodarone (central line)
Lidocaine (not if severe LV impairment)
Electrical cardioversion if these fail
Implantable cardioverter-defibrillator
Management of coarctation of the aorta in newborn
IV prostaglandins to keep patent ductus arteriosus
Surgical correction
How is angina diagnosed?
- Constrictive pain in chest, neck, shoulders, jaw or arms
- Worsened by physical exertion
- Relieved within 5 mins by GTN
3 = typical angina 2= atypical angina 1 = non-anginal pain
Investigations for typical/atypica angina
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (e.g. stress echo, MRI)
3rd line: invasive coronary angiography
When would you refer a patient with acute chest pain?
Current or within last 12 hours - emergency admission
12-72 hours ago - same-day admission
> 72 hours - ECG and full assessment with troponin before deciding
Adverse effects of statins
Myopathies: rhabdomyolysis, myalgia, myositis
Liver impairment (must check baseline, 3 and 12 month LFTs): only stop statin if transaminise rises and persists at 3 times normal
Avoid if hx of cerebral haemorrhage
What is pulsus paradoxus and in whom would you see it?
Drop of systolic BP by 10mmHg on inspiration
Seen with cardiac tamponade and asthma
Features of Takayasu’s arteritis, and what is its management?
ASIAN FEMALES Systemic arteritis features - headache, malaise Unequal BP in both arms Absent limb pulses Renal artery stenosis associated Carotid bruit Aortic regurgitation Claudication
Mx: steroids
Features of hypokalaemia on an ECG
Prolonged PR
U waves
Small or absent T wave
Long QT
Causes of hypokalaemia with and without HTN
HTN:
Cushings, Conn’s, Liddle’s syndrome
Without:
Diuretics, renal tubular acidosis, GI loss (diarrhoea/vomiting)
Features of hypokalaemia
Muscle weakness, hypotonia
Predisposition to digoxin toxicity - take care if giving digoxin to a patient on diuretics
Hypercalcaemia features on ECG
Short QT
J (osborne) waves
Adverse effects of loop diuretics
LOW sodium, calcium, potassium, magnesium, chloride (alkalosis)
Ototoxicity
Hypotension
Gout
Renal impairment (dehydration and direct toxic effect)
What valvular disease is associated with PCOS?
Mitral valve prolapse
How many days before a surgery should warfarin be stopped, and what should INR be less than?
5 days before
<1.5 INR
Management of aortic stenosis patients?
Aortic valve replacement if symptomatic or >40mmHg aortic valve gradient
What are the Levine grades of murmur?
1: faint murmur
2: slight murmur
3: moderate murmur without palpable thrill
4: loud with palpable thrill
5: very loud with extremely palpable thrill and heard with stethoscope edge
6: can hear with stethoscope off the chest
Takotsubo cardiomyopathy features
Crushing central chest pain following severely stressful event
Echo: apical ballooning of myocardium (octopus pot)
What ECG changes are indications for immediate thrombolysis or PCI?
ST elevation of >1mm (one small square) in at least two consecutive inferior leads II, III, avF, avR
LBBB
ST elevation of >2mm in 2 or more consecutive anterior leads
Management of orthostatic hypotension
Lifestyle measures - adequate salt and hydration
Compression stockings
Fludrocortisone (increases sodium reabsorption and plasma volume) or midodrine
Counter-pressure manoeuvres and head-tilt sleeping
What is Eisenmenger’s syndrome?
Reversal of a left to right shunt once the right ventricle is so large it overcomes the pressure in the left leading to cyanosis. Child comes in cyanosed with haemoptysis, RVF, having had pansystolic murmur at birth.
Associated with uncorrected ASD, VSD and patent ductus arteriosus
Managed by lung-heart transplant
What heart condition are alcoholics predisposed to?
Dilated cardiomyopathy (dilated left ventricle, <40% left ventricle ejection fraction)
ECG changes with hypothermia
Prolonged PR, QT and QRS J waves Brady <60bpm Shivering artefacts VT, VF, asystole <16 degrees
Bus or lorry driver post-MI going back to work
Must notify DVLA and stay off work for 6 weeks. DVLA will then determine safety to return
Target INR for a patient who has suffered more than one PE
3.5
Broad complex tachycardia following MI and drop in BP
Ventricular tachycardia
66-year-old woman suddenly develops dyspnoea 10 days after having an anterior myocardial infarction. Her blood pressure is 78/50 mmHg, JVP is elevated and the heart sounds are muffled. There are widespread crackles on her chest and the oxygen saturations are 84% on room air.
Left ventricular free wall rupture
Orthostatic hypotension diagnosis
> 20mmHg drop in systolic or >10mmHg drop in diastolic after 3 mins of standing
Young male smoker with painful hands and feet, cold and pale extremities (Raynaud’s) and ulcers
Buerger’s syndrome
Features of constrictive pericarditis
JVP with X + Y descent
positive Kussmaul’s (rise in JVP on inspiration)
Dyspnoea, RHF signs (oedema, hepatomegaly, ascites)
Pericardial knock (loud S3)
CXR: pericardial calcification
What investigations must you do for a patient starting on a statin?
LFTs baseline, 3 and 12 months
DVLA advice post MI
cannot drive for 4 weeks
First line test for coronary artery disease?
CT angiogram
Immediate management of MI
Dual antiplatelet therapy - Aspirin + clopidogrel/ticagrelor
Morphine + metoclopramide (antiemetic)
Anticoagulation for 24-72 hours: heparin/fondaparinux
Angiography (within 24 hours for STEMI, 72 hours for NSTEMI)
How to treat bradycardia
Pacemaker
Commonest cause of leg pain following bypass surgery?
Reperfusion
What is required prior to giving a CT angiogram?
Beta blocker (lowers heart rate before scan) U&Es - ensure renal function before giving CT contrast
Diagnosis of rheumatic heart disease?
ASO titre
How many small squares on an ECG is 1 second?
25mm
P waves in normal sinus?
Positive in I, II and avF
Negative in avR
Sinus arrhythmia
Increased HR on inspiration, decreases on expiration
Regularly irregular
Still fulfils criteria for sinus rhythm
Characteristics of premature atrial complex on an ECG?
Positive p wave (lead II)
Narrow QRS
Different morphology of p wave
Premature junctional complex characteristics
Absent or inverted p wave (II)
Narrow QRS
Premature ventricular complex characteristics
Wide qrs
No p wave
T wave opposite to r wave
Sinus brady characteristics ecg
narrow qrs
p wave present
HR <60
SVT characteristics ecg
HR >150
Indistinguishable p wave
Narrow qrs
Regular
Atrial flutter ecg characteristics
Sawtooth p waves >250
Narrow qrs
Often 2:1 ratio (can be confused with SVT)
Junctional arrhythmia ecg
40-60 HR
Absent/inverted p wave
Narrow qrs
When would you not treat AF with BB and CCB?
If patient has CHF - treat instead with digoxin and amiodarone
Which patients should you not start on ACE-i for blood pressure?
Non-diabetics over55
Afro-Carribean
Women expecting to get pregnant
Definitive management of WPW syndrome?
Radiofrequency ablation of the accessory pathway
Medical: sotalol, amiodarone, flecainide
Treatment of torsades de pointes
Magnesium sulphate
Cause of J waves U waves Delta waves Q wave
J wave: hypothermia and hypercalcaemia
U wave: hypokalaemia
Delat wave: WPW
Q wave: previous MI
Causes of ejection systolic murmur
Pulmonary stenosis Aortic stenosis HOCM Tetralogy of Fallot Atrial septal defect
When should you prescribe anticoagulation to a patient following a stroke?
2 weeks after the event (as long as haemorrhage excluded)
Most important causes of ventricular tachy
Hypokalaemia
Hypomagnesaemia
Normal PR interval?
3-5 small squares
Normal QRS interval
3 small squares
Next investigation if BNP is high in patient with suspected heart failure?
Transthoracic echo