Cardio Flashcards
Normal axis
-30 - +90 degrees
PR interval
From atrial depolarisation to ventricular depolarisation *120-200ms
Prolonged = AV block
Shortened = atrial impulse to ventricles quicker i.e. accessory pathway associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White
QRS
Width, height, shape. Normal = 80-120ms.
Narrow = <120ms, impulse down His and Purkinje
Broad = >120ms, abnormal depolarisation, e.g. ectopic
Height: small = <5mm in limb and <10mm in chest, tall = ventricular hypertrophy
Delta = WPW
Pathological Q: >2mm or >40ms
R and S: normally have R wave progression (small in V1 and large in V6) transition S>R to R>S is normally in V3 or V4
ST segment
End of S to start of T: elevation significant if >1mm in 2 or more limb leads or >2mm in 2 or more chest leads, depression significant if >0.5mm in 2 contiguous leads
T wave
Ventricular repolarisation:
tall if >5mm in limb AND >10mm in chest associated hyperacute STEMI and hyperkalaemia
Inverted: *normal in V1 and lead III, associated ischaemia, PE, BBB
U wave
A small deflection after T wave, 0.5mm, best seen in V2 and V3
Seen in electrolyte disturbances, hypothermia, antiarrhythmics e.g. digoxin, more pronounced with slower
Sinus bradycardia Definition Causes Symptoms Treatment
<60bpm where every P wave is followed by a QRS
Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)
Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP
Syncope, fatigue, dizziness, ischaemic chest pain, palpitations depending on cause
Treatment is Rate < 40 or symptomatic - IV atropine -
Temporary pacing wire
Sick sinus syndrome
Dysfunction of SA node with impairment of ability to generate impulse
Normally idiopathic fibrosis of node, also associated with ischaemia and digoxin toxicity (fibrosis may be amyloid or sarcoid)
Causing - Sinus bradycardia, sinoatrial block (Pause length of 2 or more PP intervals), sinoatrial arrest
Treatment - Pacing
Heart block
Causes
Types
Managment
MI/ischaemia (inferior), infection (Lyme disease), immunological (SLE), myocarditis, endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB)
Delay of atrial impulse to ventricles
1st = PR > 0.2s, PR constant, every P followed by QRS
Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS
Mobitz type I (Wenckebach) failure at level of AV node. PR interval progressively lengthens and is then blocked.
Mobitz type II intermittent failure of P wave conduction. Fixed PR interval, dropped QRS waves (2:1 block or 3:1 block)
Unstable - Atropine & Trans cutaneous pacing
Stable - Usually a organic cause & Dual chamber pacing
Sinus tachy
Causes
Ix
Treatment
Every P followed by QRS, rate 100 - 270
Physiological: exertion, anxiety, pain
Pathological: fever, anaemia, hypovolaemia
Endocrine: thyrotoxicosis, phaeo
Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol
Ix - 12 lead ECG, cardiac enzymes, FBC (anaemia), TFT
Treatment
Acute: Hemodynamically stable - Vagal manoeuvres
BB or non-dihydropyridine CCB (diltiazem, verapamil)
Atrial SVT
Causes
ECG findings
Types
Typically from ectopic source in atrial muscle
150-250 bpm (slower than flutter)
Abnormal p-wave morphology
Atrial rate 150-250
Variable ventricular rate but regular
Benign (80-140bpm elderly)
Incessant ectopic (rare)
Multifocal (COPD, varying p-wave morphology)
Atrial tachycardia with block (digoxin toxicity) basically a fast heart block
AVNRT SVT Common? Symptoms ECG Treatment
- Most common cause of paroxysmal narrow complex tachycardia
- Late teens or early 20s
Sudden onset palpitations ± CP, SOB ± syncope
*Neck pulsation
Regular rhythm, narrow QRS, rate 130-250
Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)
Atrial and ventricular depolarisation together - P waves buried in QRS
Haemodynamically unstable - DC cardioversion
First line: Vagal maneuvers may stop as transiently block AV node
Second line: *Adenosine
Prophylaxis - Drugs affecting AV node: digoxin, diltiazem, verapamil, fleicanide or a B blocker
Curative: radiofrequency ablation
AF Risk factors Causes Precipitants Symptoms
Age, HTN, heart failure, CAD, valvular disease, DM, CKD
CAD, HTN, valvular disease, hyperthyroidism, alcohol
Alcohol, caffeine
SOB, palp, syncope, chest discomfort, stroke/TIA
Chronic AF Management
Rate control
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)
Rhythm control
Cardiovesion with flecanide (Treat with amiodarone for 4w preceding CV)
B Blocker/ AV node ablation
Acute AF treatment
If hemodynamically unstable:
DC cardioversion is preferred + continue thrombophylaxis for 4 weeks
If pharmacological cardioversion - Amiodarone IV
Offer heparin immediately then introduce warfarin
CHADsVasc
HAS BLED
Targert INR
CHF (1), HTN >140/90 (1), >75 (2), DM (1), prior stroke/TIA (2), vasc dis: MI, PVD (1), 65-75 (1), female (1)
Consider male > 1 or anyone > 2, warfarin or NOAC
HASBLED - HTN (>160), abnormal liver or renal 1/2, stroke, bleeding Hx or predisp e.g. anaemia, labile INR, elderly >65, drugs (alcohol, NSAIDs, antipt) 1/2
INR 2-3 (non valvular) (n.b. Prosthetic valves, post MI = 2.5-3.5)
Atrial flutter managment
Rhythm control: cardioversion or medications
DC cardioversion (if >48hours ensure adequate anticoag)
Or IV amiodarone, sotalol, fleicanide
Recurrence: *radiofrequency catheter ablation (90-95% success)
Broad Complex tachycardia types
Ventricular tachycardia
Regular: Monomorphic ventricular tachycardia, right ventricular outflow tract tachycardia, fascicular tachycardia
Irregular: Torsades de Points, polymorphic ventricular tachycardia
Supraventricular with aberrant conduction or ventricular-pre excitation
Aberrant conduction - usually manifests as LBBB or RBBB (Suspect if has prev BBB)
WPW
AF with atrioventricular re-entrance
Nb always treat as VT are more likely and more dangerous
VT ecg changes
ECG normally monomorphic QRS complex (unless disturbed by capture or fusion beats)
Needs 3 in a row
Bizarre QRS morphology as impulse does not follow normal intraventricular conduction
If starts in left vent gives RBBB, if starts in right vent gives LBBB
Ventricular rate 120-300
VT management
Unstable
Stable
Support ABC, O2 and venous access
Monitor ECG, BP, sats
Identify and treat reversible cause e.g. electrolyte abnormalities potassium
Unstable (chest pain, reduced consciousness, heart failure) *reduced CO
Synchronised DC shock (up to 3 attempts)
Amiodarone 300mg IV over 10-20 minutes and repeat shock then 900mg over 24 hours if refractory
If regular/stable (VT) - Amiodarone as above.
VT is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB) or consider ICD implantable cardioversion defibrillator
Nb If stable but irregular = TdP
Torsades de points
Risk
Treatment
Causes
Type of polymorphic ventricular tachycardia in which cardiac axis rotates over a sequence of 5-20 points. QRS amplitude varies similarly giving twisting appearance.
In sinus may be seen as prolonged QTc.
May deteriorate to Ventricular fibrillation
IV magnesium sulphate (2g magnesium for other broad irregular i.e. polymorphic)
Drugs: anti-arrhythmics class III (amiodarone), antibacterials (erythromycin, trimethoprim), TCAs *Electrolyte: hypokalaemia/hypomagnaesaemia
VF
Causes
ECG changes
Treatment
Antiarrhythmic drugs, AF, hypoxia, ischaemia, fast VT, previous heart disease
*Shockable: VF and pulseless VT
Non-shockable: asystole and PEA (pulseless electrical activity)
Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500
Amplitude decreases with duration: coarse to fine.
Defibrillation
BB and ICD (implantable cardioverter defibrillators)
Brugada syndrome
Brugada sign
Autosomal dominant gentic condition affecting sodium channels causing sudden death <45yrs
Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T (Brugada sign)
+ Documented VF or PVT
ICD implantable cardioverter defibrillator
PE ECG changes
*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
Assoc RBBB
R heart strain = T wave inversion in V1-V4
Amiodarone Indications Pharmacology Side effects CIs
For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work
Blockade Na/K/Ca channels, antagonist alpha and beta adrenergic receptors which reduces automaticity.
Hypotension during IV infusion.
Chronic use lungs (pneumonitis), prolonged QT (AV block), liver (hepatitis), skin (grey discolouration), hypothyroid (Iodine rich)
Severe hypotension, heart block, thyroid disease
Adenosine
Indications
Pharmacology
Side effects
First line diagnostic and therapeutic in SVT (inc junc)
Adenosine receptor agonist on cell surface.
Very short duration - half life 10s
Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD
CCB Indiactions Pharmacology Side effects CIs
Verapamil (most cardio-selective) + diltiazem (non-dihydropyridine) + amlodipine (dihydropyridine)
Rate control in SVT inc AF +AFl
Decrease Ca entry to vascular and cardiac cells induces relaxation + vasodilation in arterial smooth muscle + myocardial contraction in heart. Reducing rate, contractility and afterload decreases oxygen.
Ankle swelling, flushing, headache - dihydropyridine e.g. amlodipine
Verapamil - constipation, bradycardia, heart block
Diltiazem (mixed)
Don’t prescribe with BB - both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole
B Blockers Indications Pharmacology Side effects CIs
First line in IHD reduce angina CHF improve prognosis AF reduce rate and maintain sinus rhythm SVT to restore sinus rhythm
B1 in heart, B2 in smooth muscle blood vessels and airways
Via B1 reduce force and speed of conduction in heart - reduces cardiac work and oxygen demand and increase myocardial perfusion via prolonging AV refractory.
Lower BP by reducing renin secretion
Fatigue, cold extremities, headache, impotence
Asthma - B2 blockade causes bronchospasm, usually safe in COPD
Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)
Preload
Volume of blood in the ventricles at the end of diastole
Afterload
Resistance LV must overcome to circulate blood
AS Causes Symptoms Signs Imaging
Three thin cusps (bicuspid valve predisposes)
Most frequent valvular heart disease (10% >80) due to senile calcification
CAD - see CAD RF, bicuspid valve (common cause in young), rheumatic fever
Classic triad: chest pain (predisposes to chest pain), heart failure (obstruction -> LV hypertrophy -> LV failure), syncope (insufficient blood)
SOBOE
Slow rising pulse
Narrow pulse pressure (diff between syst and dia)
LV hypertrophy -> apex heave
Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids
ECG: LVH (*S wave V1 depth + R wave height V5/V6 > 35mm) or strain (ST depression and T wave inversion in lateral leads)
CXR: calcification of aortic ring, cardiac enlargement, post stenotic dilatation
*Echo (transthoracic): confirms presence + degree, + left ventricular function + thickness
AS
Management
Complications
If symptomatic - prompt valve replacement - first line
If not fit for surgery
Antibiotic prophylaxis
Second line - balloon valvuloplasty - risk of re-stenosis
TAVI - transcatheter aortic valve replacement
Predisposition to infective endocarditis
Small emboli
Decompensation - increased pressure in pulmonary - CHF
Anticoagulate mechanical heart valves
Target INR 2.5-3.5 for aortic
Target 2-3 for others if no other risk factors (AF, previous stroke then 2.5-3.5)
AR
Causes
Symptoms
Signs
Bicuspid aortic valve (congenital), rheumatic fever (@developing), infective endocarditis, collagen vascular disease, degenerative (@developed)
40-60 - from degenerative
SLE, Marfan’s, Ehler-danlos, Turner’s, aortic dilatation with anky spon, acute AR in IE or aortic dissection (severe chest/back pain)
Acute - cardiovascular collapse
SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea)
Early diastolic murmur as R2IS sitting forward in expiration not well transmitted to carotids
Collapsing water hammer pulse
Wide pulse pressure
Austin Flint soft rumbling low pitched late diastolic murmur heard at apex
ECG - LVH (RV1 + SV5/6 >35mm)
MS
Causes
Symptoms
Signs
Congenital, rheumatic fever (most common), degenerative calcification (elderly) (SLE, RA, IE, amyloid)
Asymptomatic for years then deteriorate
Progressive breathlessness (SOBOE, orth, PND), palpitations due to AF, systemic emboli
Symptoms due to enlarged LA - hoarseness, dysphagia
Malar flush (CO2 retention), raised JVP, RVH - laterally displaced apex/RV heave (4th intercostal tricusp), signs of RHF (hepatomegaly, ascites, peripheral oedema) Mid-late diastolic murmur best heard in left lateral
ECG: AF, large LA P-mitrale (bifid), RVH (dominant R wave in V1 >7mm tall, dominant S wave in V5/V6 >7mm deep)
CXR: LA enlargement, interstitial oedema (Kerley A/B lines), prominent pulmonary vessels
MR
Causes
Symptoms
Signs
Second most common, assoc females, low BMI, advanced age
Now less rheumatic fever so most common cause is degenerative
MI, CAD, IE, post mitral valve surgery, Ehler-Danlos, SLE, rheumatic fever,
Chronic MR eventually causes heart failure and breathlessness
Pansystolic blowing murmur at apex radiating to axilla
Laterally displaced apex beat
S3 gallop
ECG: enlarged LA: P-mitrale, AF
CXR: enlarged left atrium and left ventricle
Echo: confirm Dx and severity (based on jet into atrium)
Jones Peace criteria
What for?
Stand for?
Rheumatic fever - Strep pyogenes
Joints - large joint arthritis - NSAID (red, hot, swollen)
O (heart 40%) - carditis - pancarditis pericardium, myocardium, endocardium (valv) Tachycardia, murmur, pericardial rub
Nodules (10%) painless and subcutaneous on extensors
Erythema marginatum (5%) - pale red macules/papules 1-3cm
Sydenham’s chorea (20%) jerking of upper limbs - purposeless
PR interval prolongation (not if carditis major)
ESR very raised
Arthralgia (not if arthritis)
CRP very raised
Elevated temp (>90% are over 39 degrees)
Infective endocarditis
Organisms
Risk factors
Which valve commonest?
Fever + new murmur = endocarditis until proven otherwise
Staphylococci (aureus) invasive procedures/drug users, streptococcus viridans (subacute) (dental procedures), enterococcus or strep pyogenes
Valve disease/ replacement Congenital structural heart Previous IE Hypertrophic cardiomyopathy IVDU
Mitral
IE
Diagnosis
Treatment
Duke’s classification BE|BEFVIP 2 major, 1 major + 3 minor, 5 minor
Blood culture: 2 separate +ve blood cultures
Echo: evidence of endocardial involvement: vegetation/abscess
Blood culture 1 +ve blood culture
Fever >38
Vascular phenomena: major arterial emboli, janeway lesions, IC haem
Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, RF
Predisposition - e.g. IVDU, heart condition
Start ABX empirical (IV)
General: amoxicillin + gentamicin for native valve
Severe sepsis: vancomycin + gentamicin
Confirm staph: 4W IV flucloxacillin (or vancomycin if MRSA)
Confirm strep 4W IV benzylpenicillin
Nb. Blood cultures (subacute or chronic = 3 sets from peripheral sites with 6hrs between them, acute = start
Cardiomyopathy
Myocardial disorder in which heart muscle is structurally and functionally abnormal without CAD, valvular disease, HTN, congenital
Dilated - *most common, left or both ventricles dilated with impaired contraction
Ischaemic, alcoholic, thiamine def (Beri-beri), coxsackie, chagas, SLE. + 3rd/4th heart sound + cardiomegaly (displaced apex)
Hypertrophic - 2nd common, left/right ventricular hypertrophy, usually familial (AD) - beta myosin. Strong association with Mitral regurg. Forceful apex beat, &
Harsh ejection systolic murmur
Restrictive - rare, reduced diastolic filling with near normal systolic function e.g. amyloid, fibrosis, sarcoidosis, radiation, haemochromatosis, Loefflers
Myocarditis
What?
Causes?
Ix?
Acute or chronic inflammation of myocardium
Similar to myocardial infarction with fever
*Viral infection fever, malaise, lethargy, fatigue
Coxsackie virus
Immune mediated: SLE, sarcoidosis, scleroderma
Toxic: alcohol, heavy metals
Electric shock
FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT
+ve Viral serology
*Gold standard - endomyocardial biopsy
ECG: ST elev/dep + T wave inversion
RHF vs LHF symptoms 4x each
RHF: peripheral oedema, abdo distension (ascites), facial engorgement, pulsing in neck and face (tricuspid regurg)
LHF: dyspnoea, fatigue, cold peripheries, muscle wasting, orthopnoea, PND, nocturnal cough - pink frothy sputum
Signs of HF (5)
Tachypnoea, tachycardia, cool peripheries, cyanosis, displaced apex (LV dilatation), RV heave (pulmonary HTN), raised JVP
Cardiac asthma: bilateral basal end-inspiratory crackles ± wheeze
Peripheral oedema, tender hepatomegaly (pulsatile at TR)
Gallop rhythm due to S3 or murmur of mitral or aortic valve disease
Ix for HF
If previous MI -> 2 week wait for specialist and doppler echo (LV func, diastolic func, LV thickness, valvular disease)
No previous MI -> BNP measurement (B-type natriuretic hormone) - released into blood when myocardium stretched. >400 pg/ml - 2 week wait for specialist and doppler. 100-400 - 6 week. <100 - heart failure unlikely
12 lead ECG for aetiology, and treatment: rate control in AF, pacing for bradycardia
FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes
CXR: for other causes of breathlessness. HF ABCDE (alveolar - bat wing, kerley B - interstitial, cardiomegaly >50% cardiothoracic ratio, dilated upper lobe, effusion)
Acute HF treatment
Oxygen + IV diuretics (furosemide) ± NIV (only if severe dyspnoea + acidaemia) or IV (if resp failure or reduced conc)
When stable: BB (bisoprolol or metoprolol) + ACEI (or ARB) + aldosterone antagonist (spironolactone) *monitor renal function, electrolytes, HR and BP for diuretics and BB
Follow up in 2 weeks
Chronic HF treatment
Lifestyle (ex, smoking, alc, diet), patient education, depression
Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic
Inform DVLA, air travel likely ok
Medical for LV systolic dysfunction
1st: ACEI + BB - monitor with U+E, Cr, eGFR for ACEI (start low and increase dose)
2nd: Aldosterone antagonist (spironolactone), ARB or hydralazine with nitrate - monitor K+
3rd: digoxin or ivabradine or cardiac resynchronisation
4th: Implantable cardioverter defibrillator if previous ventricular arrhythmia
Statins
When?
Side effects?
Need to monitor
QRISK2 > 10% (10 year risk) - primary prevention (20mg) if <84 History of CVD Familial hypercholesterolaemia Anyone over 85 80mg for secondary prevention
Myalgia, stiffness, weakness, cramping (usually at around 6 months)
Liver function test
Secondary causes of hypertension
Renal disease: intrinsic (75%) i.e. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, or renovascular renal artery stenosis -> increased renin by decreased perfusion
Endocrine: cushings, conns, thyroid, phaeo (liable and postural hypotension), acromegaly, hyperparathyroid
Coarctation aorta
Pre-eclampsia and pregnancy
Drugs - decongestants, COCP, steroids
Malignant hypertension
Malignant/accelerated hypertension (syst>200 or dia>130) + evidence of end-organ damage: *same-day assessment and immediate treatment (dec BP in hours) Hypertensive urgency (syst>180, dia>120) without end-organ damage, may dec BP over days
End organ damage
Brain - Encephalopathy: seizure, vomiting, nausea
Dissection - delayed/weak femoral pulses
Pulmonary oedema - heart failure
Nephropathy - proteinuria ± loin bruit
Eclampsia
Papilledema
Retinopathy (hypertensive)
Grade 1: tortuous retinal arteries + silver wiring
Grade 2: AV nipping
Grade 3: flame haemorrhages and cotton wool spots
Grade 4: papilloedema
TLD used in HTN
Indapamamide
Lead areas & vessels on ECG
V3, V4 - Anterior - LAD
I, V5, V6 - Lateral - circumflex
II, III, aVF - Inferior - RCA
V1, V2 - Septal - LAD
Symptoms of angina (3)
1 - constricting discomfort in front of check, neck, shoulders, jaw, arms
2 - precipitated by physical exertion
3 - relieved by rest or GTN in *5 minutes
*typical if all, atypical if 2/3, non-anginal = 1 or 0
Angina Ix
12 lead ECG: ischaemic changes @exercise stress test
ST/T wave flattening or inversion
FBC (anaemia), FBG (diabetes), FBChol/triglycerides, LFT (baseline before statin) U+E (renal func), TFT (increased work, hypo assoc cholesterol)
Refer all with suspected angina to Rapid Access Chest Pain Clinic for confirmation of Dx and severity assessment- Urgently - within 2 weeks
Angina management
Stop activity: use GTN (spray/tablets), if pain doesn’t ease 2nd dose @ 5 minutes, 3rd dose @ 5 minutes, wait 5 minutes then 999 (i.e. after 15 mins total)
Short acting nitrate: GTN (with explanation as above) to prevent
First line anti-anginal: BB (atenolol, lower HR and BP, bradycardia, cold hands/feet, fatigue) or CCB (diltiazem/verpamil/amlodipine - ankle swelling, flushing)
Second line: combination - (must be Amlodipine) CCB + BB
If intolerant or CI: consider long acting nitrate or nicorandil or ivabradine
Reduce cardiac RF
Aspirin 75mg or clopidogrel- antiplatelet (establish bleeding tisk), statin if indicated, ACE-I for HTN/diabetes
Review at 2-4 weeks
ACS
Types
In young
In old/diabetic
STEMI (ST elevation and acute CP > 20 mins)
NSTE-ACS - acute CP + transient/persistent ST depression or T wave inversion/flattening
-NSTEMI - with a rise in troponin levels
-Unstable angina - without
Consider non-atherosclerotic -> coronary emboli (infected valve), vasculitis, coronary artery spasm, cocaine, increased O2 requirement (hyperthyroidism), decreases O2 delivery (anaemia)
Elderly or DM may not have CP
ACS ix
12 lead ECG
ST elevation - transient = angina, fixed = acute infarction
ST depression or T wave inversion = unstable angina or NSTEMI
Pre-existing CAD = LVH, Q waves
Cardiac enzymes: troponin T, troponin I, CK-MB (creatinine kinase)
Within 6 hours - troponins most sensitive (3-6 hours post infarct - max at 12-24 hours) *test troponins at 6 and 12 hours
If unstable angina minor elevations in trop may suggest future risk
CK is cardiac specific, troponins are a marker for cardiac necrosis but also marker for skeletal muscle injury
Bloods: FBC (anaemia and baseline for anticoagulants), blood glucose (hyperglycaemia is common = poor prog), renal function, electrolytes, lipids, TFT
Imaging:
CXR (complications of ischaemia i.e. pulmonary oedema etc. , or PE, pneumothorax, TAA),
TTE wall motion abnormalities
ACS immediate management
Resuscitation: ABCDE (IV fluids)
Pain: GTN + intravenous opioid with antiemetic (morphine + metoclopramide)
Dual antiplatelet: loading dose *300mg aspirin + ticagrelor 180mg
Assess O2 sats: give high flow O2 if <94%
Monitor with 12 lead ECG
NSTEMI mamangement
GTN + Morphine + Metaloclopramide
O2
Loading does of Aspirin and Ticagrelor - Both go down long term
Fondaparinux (antithrombotic) if angiography planned > 24 hours, hep if < 24 hours)
Assess future risk with TIMI
Revascularisation (PCI or CABG) if appropriate if medium to high
-discontinue ATP 5 days pre CABG
STEMI mamangement
GTN + Morphine + Metaloclopramide
O2
Loading does of Aspirin and Ticagrelor - Both go down long term
ECG
*Immediately assess suitability for reperfusion: PCI or fibrinolysis
Offer coronary angiography + PCI if can be given within 120mins and within 12 hours of onset)
For PCI must use an injectable anticoagulant unfractionated heparin + ticagrelor
If beyond 12 hours offer coronary angiography + if evidence of continuing ischaemia
Offer fibrinolysis (2nd choice) if PCI cannot be given within 120 mins - alteplase (tissue plasminogen activator), streptokinase
CABG - for multiple artery infarction
Drugs for secondary prevention, cardiac rehabilitation, lifestyle changes
Drugs post MI (5)
ACEI,
Dual antiplatelet (aspirin + clopidogrel)
BB
Statin,
Monitor BP, monitor renal function, assessment of LV function
Acute complications of MI
Acute MI (5-10%), cardiogenic shock, ischaemic mitral regurgitation, arrhythmia
Early pericarditis (10%) - 24-96 hours, generally asymptomatic
Dressler’s syndrome: late pericarditis, inflammatory reaction in response to necrotic tissue, occurs at *2-8 weeks - severe chest pain, worse supine
Cardiac arrest management
ABC call 999
999
A+B (if breathing turn to recovery)
C - CPR 30:2, when airway secured = uninterrupted compressions and ventilate at 10/min
D defibrillator: AED automated external defibrillator
Complete 2 minutes of CPR between debif attempts
After 3rd shock give adrenaline + amiodarone
2 minutes CPR
Adrenaline
2 minutes CPR
Adrenaline
Pericarditis
Symptoms
Causes
Chest pain
Dull, sharp, burning, pressing (up to severe)
Felt substernal or precordial
Radiates to neck or left trapezius
*Aggravated by inspiration, cough, swallow, lying flat
*Relieved by sitting up and lying forward
Viral: *coxsackie, EBV + staphylococcal/haemophilus... Rheum: *SLE, sarcoid + …. Post MI: *Dressler’s 24-72 hours Drugs: hydralazine Other: *uraemia
Pericarditis ECG changes
Stage 1, diffuse concave ST segment elevation (saddle shape) with concordance of T waves, PR depression. Stage 2, return to normal and T wave flatten.
Stage 3, T inversion.
Stage 4 resolution of T wave
Pericarditis managment
Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis)
Admit if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs
*falling blood pressure and shock - suspect cardiac tamponade - immediate peircardiocentesis with echo
Cardiac tamponade What Commonly associated with? Symptoms/Signs? ECG Management
Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise
Pericarditis, malignancy (breast/lung), Dressler’s, infective (HIV, TB), connective tissue (SLE, RA, dermatomyositis, systemic sclerosis), trauma
Anxiety, fatigue, oedema, dyspnoea, tachyc, tachyp
O/E: Beck’s triad if acute (muffled, JVP, hypotension) + distended neck veins, hepatomegaly, tachyc/p, pulsus paradoxus (*exaggeration of normal decrease in BP on inspiration, distinguish CT from pericardial effusion)
Low voltage QRS complex. Electrical alternans. Amplitude increases and decreases beat to beat QRS
O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis
Acute limb ischaemia
- 6 Ps: pale, pulseless, pain, perishingly cold, parasthesia, paralysed
- mottling -> irreversible
Urgent hand-held doppler + urgent angiography:
Requires re-vasc in 4-6 hours with *immediate heparinisation
If embolism = surgical embelectomy (Fogarty balloon emolectomy catheter)
If thrombotic = thrombolysis, angioplasty or bypass
*Find the source of the emboli: ECG, echo, aortic USS
ACE inhib CI in
Bilateral renal artery stenosis
Peripheral vascular disease
Ix
Mangement
ABPI
Clopidogrel
Risk factor management
Assess for stenting/angioplasty
Vasodilator therapy
Aortic dissection
What?
Where?
Presentation?
Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen
Type A (70%) - aortic arch and ascending aorta proximal to *L subclavian Type B (30%) - descending aorta distal to L subclavian CV RF + aortic disease + cocaine/amfetamines + M/ED + bicuspid valve
Initial phase: Sudden tearing/sharp pain radiating to back, pulse loss
Expansion phase: pressure increase causes rupture to pericardium (tamponade), or pleural space or mediastinum
*Pain maximal at onset, migrates as dissection progresses
Aortic dissection managment
Manage HTN aggressively - aim 100-120SBP
IV beta blockers (labetalol) to reduce ventricular contraction
IV nitroprusside (emergency vasodilator)
Surgical repair
Thoracic aortic aneurysm presentation
Pain: chest, neck, upper back, mid back, epigastrium, acute - rupture imminent? dissection is sudden, tearing
Symptoms due to local compression: hoarseness, cough, stridor, dyspnoea, SVC obstruction, dysphagia
Marfans and Aortic aneurysm
Require lifelong BB, regular imaging of aorta and restriction physical activity
AAA
Pain in back, abdomen, loin or groin *DDx for loin to groin
Pulsatile abdominal swelling
May rupture -> shock
Distal trashing - dusky fingers from dislodged thrombus debris
Rupture of AAA
Presentation
Management
Thoracic: chest pain indistinguishabe from MI + haemoptysis ± cardiac tamponade
Abdominal: classic triad: flank/back pain, hypotension, pulsatile abdominal mass
Pale + sweaty, weak thready pulse, hypotension
FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E
CXR, AXR (75% are calcified)
ECG for MI
Large bore IV access
Group and crossmatch, order 4-6 units blood, FFP, Pt
Immediate theatre
Hypovolaemic shock
Cause
Presentation
Management
Blood loss - haemorrhage, fluid loss - dehydration/burns/pancreatitis
Cold, unwell, anxious, faint, SOB, pain (from bleeding)
Pale, sweaty, tachypnoea, cold peripheries, increased CRT, hypotension, tachycardia
Raise legs
ABCDE
Crossmatch + blood for Ix as previous + catheter + ABG
Airway + high flow O2 + 2 large bore IV cannula
Fluid resus saline or Hartmann’s 500ml over 15 mins *may give 2l total then escalate
If haemorrhagic shock give blood as soon as possible O-ve
Pain relief - pain increases metabolic rate and increases ischaemia IV opiates
*vasopressors cause further tissue ischaemia
Surgery to stem blood loss: e.g. REBOA after resus
Cardiogenic shock
Cause
Presentation & Signs
Management
Most often caused by acute MI (affecting anterior wall) - or pericardial tamponade/severe constrictive pericarditis or obstructive PE or tension pneumothorax
CP, N+V, dyspnoea, sweat, confusion/disorientation, palpitations
O/E: pale, mottled, slow CR, hypotension, tachy/brady, JVP, oedema, 3rd/4th HS, quiet HS
A+B - intubation ± mechanical ventilation, O2
C - gain venous access often require central venous access as peripherally shut down - send bloods (FBC, U&E, BNP, Trop,)
IV fluid if depleted volume 250ml bolus (cardiac dysfunction)
Monitor - cardiac monitoring, BP - art line, venous pressure - CVC, urinary catheter
Pain relief *IV morphine and cardiac inotropes *dopamine or dobutamine
Revascularisation
