Cardiovascular Flashcards
A patient has malar flush and rumbling mid-diastolic murmur (loudest on exp on left side). What is the Dx?
Mitral stenosis
Pan systolic murmur following MI with features of heart failure - what is the murmur?
Mitral regurgitation - due to ischaemic to papillary muscles
Most common heart defect in Down’s?
AVSD (others - VSD, ASD, PDA, ToF)
How does a thrombolytic/fibrinolytic agent work? What different types exist?
Plasminogen activators - dissolve IV clots to Tx acute MI, DVT/PE, acute ischaemic stroke, occlusion of indwelling catheter etc.
During thrombosis platelets activate prothrombin to form thrombin. This converts fibrinogen to fibrin forming a matrix.
This is counterbalanced by plasmin derived from plasminogen. tPA is a natural fibrinolytic in epithelial cells. All thrombolytic agents are proteases cleaving plasminogen to plasmin.
Agent types:
1. Fibrin-specifc agents - need fibrin present for conversion and work best for STEMI/PE/acute ischaemic stroke. E.g. alteplase
2. Non-fibrin-specific agents - act systemically as don’t require fibrin present e.g. streptokinase (less efficacy but reduced risk of IC haemorrhage, increased risk of allergy, no repeat use for 6 months), urokinase (used for indwelling catheters/PV thrombosis)
TXA can be used to reverse action of these agents.
ECG findings based on electrolyte abn?
K:
* Hyperkalaemia - ECG tall tented T-waves, wide QRS, prolonged PR - causes cardiac toxicity/muscle weakness - caused by drugs (k-sparing diuretics, ACEi/ARB, digoxin), Addison’s.
* Hypokalaemia - ECG U-waves (V2/3), T-waves wide/flat, ST depression - causes muscle weakness/resp failure - caused by diarrhoea/vom, malnutrition, aldosteronism, drugs (insulin, corticosteroids)
Ca:
* Hypercalcaemia - ECG short ST, wide T-wave - causes thrones, stones, bones, grones, and psychic moans - caused by primary hyperparathryoidism, malignancy
* Hypocalcaemia - long ST, long QT - causes neuro Sx - caused by pancreatitis, rhabdomyolysis etc
Na - no effect on ECG:
* Hypernatremia - causes thirst/neuro Sx - caused by dehydration, diabetes insipidus, hyperaldosteronism
* Hyponatremia - causes neuro Sx - caused by diuretics, SIADH, heart/liver/renal disease, diarrhoea
Summarise ACS guidelines
- For all ACS (STEMI/NSTEMI/UA) - give aspirin life-long
- STEMI within 12hrs Sx-onset & can do PCI within 120 mins - corronary angio + PCI, if not:
- If within 12hrs - fibrinolysis
- If not within 12hrs but myocardial ischaemia/cardio shock - angio
- Otherwise add Ticagrelor (Clopidogrel if high bleed risk)
- After angio add prasugrel (if no previous anticoag, otherwise clopi), if done via radial route give unfr heparin, femoral give bivalirudin (either with bailout GPI) - NSTEMI/UA - give fondaparinux (if low bleed risk, CR >265 consider unfr heparin) –> do GRACE/HEART score:
- If low risk add Ticagrelor
- If high risk/young for angio - Secondary prevention - ACEi, DAPT (12m), B-blocker (12m or forever if rLVEF, if CI for diltiazem/verapamil), Statin
- IF heart failure with rLVEF start aldosterone antag e.g. spironolactone (3-14d post-MI, after ACEi)
Give an overview of pericarditis
- Inflam of pericardium
- Acute form - new onset inflam lasting under 6-weeks
- Triad - chest pain, pericardial friction rub on auscultation, ECG widespread ST elevation (other Ix - bloods inflam, echo - pericardial effusion)
- Tx - NSAIDs + Colchicine
- Complications - recurrence, tamponade, constrictive pericarditis
Give an overview of aortic dissection
- Seperation in aortic wall intima –> blood flow into false channel (inner & outer layers of media)
- > 50yrs, sudden tearing substernal/intrascapular pain (+/- syncope, heart/renal failure, mesenteric/limb ischaemia)
- Ix with CT/MRI/ECHO
- If ascending aorta/arch - URGENT repair, otherwise b-blocker (or surgery if complicated), needs lifelong surveillance
After how long do trop levels peak after MI? Other causes of raised trop?
- rise 2-4hrs, peak 18-24hrs, last several days
- PE, other heart issue, renal failure, sepsis, rhabdomyolysis
Driving rules for MI
- Cease for 1wk if - successful angioplasty (incl in STEMI)/PPM-insertion
- Cease 4wk if - CABG/MI
- Cease completely if unstable angina uncontrolled
- Notify DVLA if AAA ≥6cm (disqualified if ≥6.5cm) or arrythmia (incapacitated)
Other to note - no sex for 1/12, return to work after 2/12 (stop if pilot/air traffic control)
ECG changes depending on STEMI location? How long for ECG changes to resolve?
Lateral leads - left circumflex/LAD
Inferior leads (or posterior) - RCA/LCx
Anterior/septal - LAD
ST-T changes resolve in days-weeks (longer if ischaemia causes infarction)
QRS including pathological Q-wave - PERMANENT
What are the complications of MI by time period after the event?
- Arrythmias - VF/VT (20%), AF (15%)
- Ischaemia (high CK) - re-occlusion, postinfarct angina –> angio + corronary revasc
- Mechanical:
- LVSD/HF - Killip’s classification (severity of HF post-MI)
- 24h-7d: 1) Ventricular septal - angina/pul oedema, new pansystolic murmur LLSB -> surgery. 2) free wall rupture - bleeding into pericardium (-> tamponade) -> needs pericardiocentesis/surgery
NOTE: pseudoaneurysm = contained left ventricular free walk rupture - Acute MR (normally inf/posterior infarct from isch/necrosis/papillary muscle rupture) = pansystolic murmur
- L. vent aneurysm, R vent failure, L vent outflow obstruction
- Inflammatory - Dressler’s syndrome (pericarditis) - 2-4wks post-MI - self-limiting fever + pericardial/pleural pain –> Tx with NSAIDS/steroids/drainage
- Systemic - PE/DVT, mural thrombosis & systemic embolism
- Depression - suicide
Give an overview of chronic heart failure
Classification:
- LVEF (<40 low, 41-49 mild, 50 preserved)
- NYHC (1 - no limit on physical activity, 2 - slight, 3 - marked, 4 - Sx at rest)
NT-proBNP > 2000 - 2wk referral/echo, 400-2000 - 6wk referral/echo
Acute heart failure findings on CXR? Ix? Mx?
- Bat wing opacities 2. Kerley B lines 3. Cardiomegaly 4. Dilated upper lobe vessels 5. Pleural effusion
Sit upright and 15L NRM, consider IV dia/morphine, Furosemide IV (x2 oral dose), GTN IV 0.5mg/hr (only if BP >90), consider CPAP/NIV if acidotic
If BNP > 100 or NT-proBNP > 300 transthoracic echo
Acute severe MR - surgical replacement
Critical AS - surgical replacement/TAVI
LVSD - ACEi, Aldosterone antag, B-blocker (d/c after stable for 48hrs)
Hypertension Management
BP in clinic >140/90 —> repeat (both arms should be measured if >15 repeat then use measurement in higher arm)
BP 140/90-180/120 - AMBM (ambulatory - 2 measurements/hr requiring 14 measurements)/HBPM (Home - x2 measurements daily for 4-7d, discard 1st day) to confirm Dx
>180/120 with retinal haemorrhage/papilloedema/Sx - same day specialist R/V
Classification:
1 >140/90 with AMBM 135/85
2 >160/100 with AMBM 150/95
3 >180/120
Accelerated/malignant = signs of retinal haemorrhage/papilloedema
?secondary cause of HTN if: <40yrs, Low Na/High K, eGFR <60, Pro/Blood in urine
Most common secondary cause: Renal
Signs of cardiac tamponade? Possible ECG findings? Tx?
- Beck’s triad - JVP, low BP, reduced HS
- Pulsus paradoxus - >12mmHg/9% normal insp decrease in SBP (also caused by const pericarditis, restrictive CMO, severe obs pul disease, PE)
- Kussmaul sign - increased venous pressure/distension on inspiration
- Ewart/Pins sign - if large pericardial effusion, dullness/bronchial breath sounds/bronchophony below angle L scapula
ECG - sinus tachy, low voltage QRS, electrical alternans, PR segment depression
Pericardiocentesis
Mx of stable angina?
- B-Blocker and/or CCB (amlodipine/nifedipine)
- Add/switch to long-acting nitrate/nicorandil (risk of ulceration)
- Ivabradine/Ranolazine
Secondary prevention: consider Aspirin, Statins, ACEi
Acute limb ischaemia - Def? Presentation? Ix? Mx?
-
Def: a sudden decrease in limb perfusion that threatens the viability of limb
- AF = major RF for acute limb ischemia
-
Presentation - 6Ps:
- Pale
- Pulseless
- Painful
- Perishingly cold
- NOTE: need immediate vascularisation (<6hrs) if:
- Paralysis
- Paraesthesia (esp worrying)
-
Ix (after initial Mx):
- Bedside: ABPI (PAD), ECG (AF)
- Bloods: FBC, U&E, clotting, HbA1c, lipid profile
- Imaging: duplex USS, CT/MR angiography
-
Mx:
- Initial:
- A-E, IV access, analgesia
- IV heparin infusion - reduces the chance of the clot getting worse
- Limb viability:
- Immediate - tender muscles, loss of power, loss of sensation
- Urgent - pale, pulseless, painful, cold
- Irreversible - fixed, mottled skin, woody, hard muscles
- Refer to vascular surgery:
- Thrombotic - local intra-arterial thrombolysis, angioplasty, bypass
- Embolic - embolectomy/local intra-arterial thrombolysis/bypass
- Initial:
AAA key Sx & ruptured Sx? Ix? Mx?
Sx:
- Central abdo pain
- Radiates to back
- Bloating
- Pulsatile mass on palpation (expansile - moves to sides)
- NOTE: always consider if abdo pain + RFs (male, >65yrs, HTN, smoking etc.)
Ruptured AAA Sx:
- Severe pain radiating to back
- Visible pulsating abdo mass
- Shock (circulatory compromise)
Ix:
- Abdo duplex USS if part of national screening - male age 65yrs
- CT angiography if stable but suspicious of rupture
Mx:
-
<5.5cm –> Conservative: monitor w/ USS + RF modification
- <4.5cm –> yearly USS
- 4.5≤x<5.5com –> 3 monthly USS
- Medical: optimise BP control, statin, aspirin
- Sx/>5.5cm/expanding >1cm/yr –> Surgical: endovascular (catheter into aorta to insert stent)/open repair
Aortic dissection - def? Sx? Ix? Mx?
Def: tear in tunica intima (inner layer of BV) –> blood collection between tunica intima and tunica media –> false lumen (can occlude blood flows through aorta) –> AR, myocardial ischaemia, stroke
Sx: sudden onset, central tearing chest pain –> radiating to between shoulder blades
- Hx of intermittent claudication
- Haemodynamic instability (high HR, low BP)
- Before left subclavian artery - left arm smaller than right arm
- After left subclavian artery - lower body less developed than upper body
Ix:
- BP in both arms - radio-radial delay
- ECG, CXR (widened mediastinum)
- Gold-standard: CT-aortogram w/ contrast
Mx:
- Stanford A (ascending aorta) - more WORRYING (compromise blood to brain, cause aortic regurg):
- BP control - B-blockers & CCB (aim 100-120mmHg)
- Immediate referral for vascular surgery
- Stanford B (descending aorta)
- BP control - B-blockers & CCB (aim 100-120mmHg)
- Urgent referral to vascular surgery (repair likely if complicated)
Comparing different types of vascular ulcers:
- Hx
- Location
- Characteristics - ulcer & surrounding skin
- Tx
Venous:
- Hx: varicose veins, previous DVT, obesity, preg, recurrent phlebitis
- Location: lower calf-medial malleolus
- Characteristics: mild pain
- Ulcer - shallow/flat margins, exudate, sloughing @base, granulation tissue
- Surrounding skin - haemosiderin staining, eczematous, oedematous, thickening skin, (normal CRT)
- Tx: compression bandaging, leg elevation, surgical Mx
Arterial:
- Hx: HTN, DM, smoking, prev vascular disease
- Location: pressure points, toes/feet, lateral malleolus, tibia
- Characteristics: painful
- Ulcer - punched-out/deep, irreg shape, necrosis, no exudate (unless inf)
- Surrounding skin: thin, shiny, reduced hair, 6Ps (pallor, pain, perishingly cold, pulselessness, paraesthesia, paralysis)
- Tx: revascularization (e.g. bypass), anti-platelet, manage RFs
Neuropathic:
- Hx: DM (peripheral neuropathy), trauma, prolonged pressure
- Location: plantar foot, tip of toe, lateral-fifth metatarsal
- Characteristics: no pain
- Ulcer - deep, surrounded by callus, insensate (no feeling)
- Surrounding skin - dry, cracked, callus, insensate
- Tx: off-loading pressure, topical GF
Pressure:
- Hx: limited mobility
- Location: bony prominence, heel
- Characteristics:
- Ulcer - deep, macerated (moist, wrinkly)
- Surrounding skin - atrophic skin, lost muscle mass
- Tx: off-loading pressure, reduced moisture, increased nutrition
IHD - RFs? Types? Definition? Dx? Mx? Complications?
RFs: HTN, DM, Smoking, FHx IHD, Hypercholesterolaemia
Stable angina - chest pain on exertion relieved by rest
- Path - mismatch in O2 supply and demand to the myocardium
- Ix: CT-angiogram
- Mx:
- B-blockers - reduces HR req for activity –> reduced likelihood of mismatch in O2 supply & demand
- GTN spray - reduce myocardial preload + reduces strain
- RF modification –> reduced risk of progression
Acute coronary syndrome - Sx caused by sudden reduced BF to the myocardium
- Dx:
- ST-elevation = STEMI
- Troponin raised = NSTEMI (+ dynamic T-wave inversion, ST depression)
- Unstable angina pectoris (pain at rest) = ischemia NOT infarct
- Generic ACS Mx - MONA BASH
- ALL immediate:
- 5-10mg Morphine IV + Nitrates (GTN spray)
- Dual antiplatelet therapy (DAPT) - 300mg Aspirin STAT + 300mg Clopidogrel STAT (or 180mg PO Ticagrelor)
- ALL long-term:
- Continue DAPT
- 1 year: 75mg OD Aspirin + 75mg OD Clopidogrel (or 90mg BD Ticagrelor)
- >1yr - 75mg OD Aspirin
- B-blocker (1.25-10mg Bisoprolol OD)
- ACEi (1.25-10mg Ramipril OD)
- Statin (80mg Atorvastatin OD)
- Continue DAPT
- ALL immediate:
- STEMI Mx: establish coronary reperfusion ASAP
- Sx <12hrs: PCI BUT if no PCI within 2hrs Dx –> thrombolysis (e.g. tPA - tissue plasminogen activator)
- Sx >12hrs: invasive coronary angiography ± PCI if needed
- PCI:
- If having PCI give Prasugrel (instead of Clopi/Ticagrelor)
- PCI accessed via radial (or femoral) artery, guidewire passed via X-ray guidance into the affected coronary artery AND IV unfractionated heparin during the procedure –> stent inserted impregnated with an anti-proliferative agent (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so DAPT needed for 1yr
- If PCI with stents inserted –> DAPT 12 months
- NSTEMI Mx:
- 2.5mg SC Fondaparinux (direct factor 10a inhibitor)
- Risk stratify - GRACE criteria (& others)
- High risk = invasive coronary angiography (within 48-72hrs)
Complications: FAP (failure, arrhythmias, pericarditis)
- Heart failure, arrhythmias (incl. VF)
- Pericarditis
- Early - positional chest pain day after MI –> give NSAIDs
- Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)
Heart failure def? Causes? Pathophysiology? Categories & Causes? Classification? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
Causes:
- RVF:
- Acute: MI, inf endocarditis, PE
- Chr: Cor pulmonale, LVF
- LVF:
- Acute: ischaemic/hypertensive CMO, valvular HD
- Chr: MI, inf endocarditis
Pathophysiology:
- RHF - right side of the heart pumps deoxygenated blood from the body to the lungs to be reperfused - if the RH is not pumping effectively you get the fluid collection in the peripheries = PERIPHERAL OEDEMA
- LHF - left side of the heart pumps oxygenated blood from the lungs to the body - if the LH is not pumping effectively you pooling of blood in the lungs = PULMONARY OEDEMA
- Reduced CO –> shock, tachycardia, AKI
- CO = SV*HR
- Ejection fraction = SV/End-diastolic Volume
Categories:
- HF w/ preserved ejection fraction (left ventricular >50%) = inadequate filling of ventricles during diastole (from ventricular stiffness)
- Causes of ventricular stiffness:
- Volume overload (valve regurg)
- Pressure overload (HTN)
- Decreased distensibility (constrictive pericarditis)
- Causes of ventricular stiffness:
- HF w/ reduced ejection fraction (left ventricular <40%) = inadequate emptying of ventricles during systoles (from outflow obstruction/impaired contractility)
- Causes of outflow obstruction/impaired contractility:
- MI, Cardiomyopathy, Arrythmia
- Causes of outflow obstruction/impaired contractility:
NYHA classification:
- 1 - no limitation on activity
- 2 - comfortable at rest but dyspnoea on ordinary activity
- 3 - marked limitation on ordinary activity
- 4 - dyspnoea at rest
Ix:
- Bedside: ECG - detects if anything precipitating HF (arrhythmia/ischaemic event)
- Bloods: ABG (if resp compromise from pul oedema), troponin (ACS), BNP (HF screening)
- Imaging: CXR (visualise pul oedema, cardiomegaly), ECHO (valvular abn/regional wall mov abn)
Mx: MON BA (out of MONA BASH)
- Immediate:
- Sit the patient up (reduce venous return to heart –> less strain)
- O2 15L/min NRM
- Medical:
- IV furosemide (loop diuretic) - remove excess fluid + venous dilation (reduce preload)
- Nitrates (GTN/Isosobide Mononitrate) AND Morphine - reduce preload on the heart
- Long-term:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart, do not give acutely if severe HF as will kill them
-
ACEi - reduce strain on heart
- After the above if LVEF <35% & Sx –> mineralocorticoid antagonist e.g. spironolactone
- 3rd line - by specialist: Sacubitril/Valsartan (entresto), Ivabradine & CRT
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
- Reduced ejection fraction - prognostic benefit:
Complications:
- Reduced CO (SV*HR) –> shock, tachycardia, AKI
- Congestion –> pulmonary oedema + peripheral oedema
SVT - Def? Types? Presentation - case example? Mx?
Def: regular narrow-complex tachycardia with no p-waves + supraventricular origin
Junctional types:
- AVNRT - local re-entry circuit within AV node
- AVRT - re-entry circuit between atria and ventricles –> after SVT termination = delta wave = WPW syndrome:
- Assoc w/ HOCM
- Avoid digoxin, verapamil, amiodarone (reduce conduction down SAN –> worsen retrograde conduction –> risk of VT)
- Can use B-blocker/flecainide instead
Case example: 23yrs, 1-hr palpitations + SoB, 2 similar episodes prev following alcohol, this time severe chest pain
Mx:
- Unstable tachycardia (<90 BP/chest pain/acute heart failure) –> synchronised DC Cardioversion
-
Vagal manoeuvres (increase parasympathetic stim via vagus nerve to slow conduction via AV node)
- Valsalva manoeuvre (blow out through nose while pinching + shut mouth) - breath through 50ml syringe
-
Adenosine 6mg –> 12 mg –> 12mg
- NOTE: if adenosine CI (e.g. asthma) –> VERAPAMIL (rate-limiting CCB)
- Other:
- IV B-blocker/amiodarone/digoxin
- Synchronised DC Cardioversion
Key heart murmurs?
Accentuation manoeuvres?
Causes?
Left vs right heart valve abn epidemiology?
Mx?
Complications of prosthetic heart valves?
Key murmurs:
-
AS = ejection systolic + radiates to carotids, slow rising pulse, narrow pulse pressure, heaving apex beat
- Sound: Wooooshhh
- Severe AS - absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat
- A longer murmur is worse (small space for blood to pass through = takes longer)
-
MS = mid-diastolic + LLP, malar flush, AF, loud/palpable S1 “tapping” apex, pul HTN (loud P2 - pul thrill)
- Sound: Wooosh de (loud S1) de (early diastolic snap)
-
AR = early diastolic + sitting forward (LLSE), collapsing pulse, wide pulse pressure, displaced apex
- Sound: de woooshhhh
- Severe AR –> Austin-flint murmur = ‘Rumbling mid-diastolic murmur’
- Best heard at apex, caused by blood flowing back through aortic valve and over mitral valve
- Shorter murmur is worse (quicker to flow back through large hole)
-
MR = pan-_systolic_ + radiates to left axilla, AF, displaced thrusting apex, LVF/pul HTN
- Sound: Woooooshhh (holosystolic)
- NOTE: same pattern for pulmonary & tricuspid (pul stenosis & tricuspid regurgitation = systolic)
- TR - pulsatile liver
- PS - radiates to back, assoc w/ Noonan’s (AD, webbed neck, wide-spaced eyes etc.)
Accentuation manoeuvres:
- R-sided murmurs (tricuspid + pulmonary) –> louder on INspiration = blood goes IN to right-side of heart
- L-sided murmurs (aortic + mitral) –> louder on EXpiration = blood EXits left-side of heart
- AS radiates to the carotids + louder on leaning forward + listen on right sternal edge
- MS louder on turning to the left, MR radiates to axilla
Causes:
- AS (stenosis/sclerosis): senile calcification (aortic valve)
-
MR:
- Acute: - IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- Chronic - myxomatous degeration
-
AR:
- Acute (infective endocarditis, aortic dissection)
- Chronic (CTD, RHD, HTN, congenital)
- MS: rheumatic heart disease (RHD)
Left vs Right valve abn:
- Left = more common as higher pressure system, more likely in damaged valves, commonly Strep Viridans
- Right = more common in IV drug users –> tricuspid valve is first valve reached, commonly S. aureus
Management:
- AS:
- C: 6-monthly ECHO, exercise-stress test if asymptomatic
- M: RF optimisation (statins, HTN, DM), HF Sx (diuretics, ACEi)
- S: Based on severity/comorbid - STS-PROM (surgical risk calc)
- If severe AS:
- Medically fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
- Not fit = Transcatheter aortic valve replacement (TAVR)
- Acutely Sx/cardiogenic shock = Balloon valvuloplasty
- If severe AS:
- MR:
- M:
- ACEi ± B-blockers (as HTN worsens MR)
- Tx AF & anti-coagulate
- Diuretic (if refractory to surgery)
- S: for acute MR (post-MI, chordae tendinae rupture), asymptomatic LVEF <60%, symptomatic LVEF >30%
- Valve _R_epair > _R_eplacement
- M:
- AR:
- M: asym + Reassurance (good prog)
- Unfit for surgery/waiting - ACEi & vasodilators (e.g. hydralazine)
- S: acute/Sx/severe = surgery
- Valve _R_eplacement > _R_epair
- M: asym + Reassurance (good prog)
-
MS:
- C: asymptomatic - Monitor
- M:
- AF Tx, anti-coagulate & diuretics (if Sx/severe)
- S: Sx/severe - can do balloon valvuloplasty/replacement
- Valvuloplasty = lateral thoracotomy scar
- Do not do percutaneously if persistent left atrial thrombus/rigid calcified valve –> need open heart surgery (CABG, concurrent severe MS)
Complications of prosthetic heart valves: FIBAT
- Failure
- Infection
- Bleeding - MAHA
- Anaemia
- Thromboembolic phenomena
Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?
VT or SVT w/ aberrancy
- SVT >200bpm, also often irregular
- VT more likely if LAD
- Acutely treat any broad complex tachy as VT until proven otherwise
Presentation: palpitations, light-headed, chest pain, syncope, seizure
- Tachycardia, LVF
- ACS most common cause
- NEVER IGNORE palpitations & light-headedness
Ix: ECG - regular broad complex tachycardia
- U&E (Mg, Ca, K), TFTs, Troponins
Mx:
- Unstable tachycardia (BP <90, chest pain, acute cardiac failure) = DC cardioversion
- Stable:
- IV amiodarone, b-blocker –> prepare for DC cardioversion
