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
