Cardiology_Medicine Flashcards
IHD - Types? Definition? Dx? Mx?
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)
Angiography & PCI
- Access usually gained through radial artery (or femoral) –> guide wire passed up through axillary artery –> subclavian artery –> relevant coronary artery
- Guidewire passed via X-ray guidance into the affected coronary artery
- IV unfractionated heparin during the procedure
- PCI - 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
Heart failure def? Pathophysiology? Categories & Causes? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
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:
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:
How does heart failure look on CXR?
Pulmonary oedema (fluffy alveolar shadowing = bilateral perihilar consolidation = batwings distribution) ±:
- Kurly B-lines (peripheral septal lines)
- Cardiomegaly (thoracic ratio >0.5)
- Upper lobe venous diversions (tubes going up towards apex instead of lines)
- Pleural effusion (costo-phrenic blunting)
Atrial fibrillation (AF)
- Def? Causes? Ix? Mx?
Def: rapid, chaotic, and ineffective atrial electrical conduction
- ECG def: irregularly irregular narrow complex tachycardia with no p waves
Causes: idiopathic, cardio (IHD, valvular disease, cardiomyopathy), resp (PE, pneumonia), hyperthyroidism, alcohol
Ix: ECG (absence of p-waves, irregularly irreg rhythm)
Mx:
- Haemodynamically unstable (≤90 BP, chest pain, acute HF) –> DC Cardioversion
OR
- Rate control –> B-blocker (bisoprolol) OR rate-limiting CCB (verapamil - asthma)
OR
- Rhythm control - ONLY if clear reversible cause
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
- NOTE: IV heparin started prior to cardioversion
- Sx onset >48hrs –> anticoagulate for 3wks –> elective cardioversion (also anticoag for 4wks after)
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
AND
- Stroke risk - CHADS-Vasc Vs Orbit/HAS-BLED score –> DOAC (Apixaban)
- If metallic heart valve –> warfarin INR 3-3.5
- Otherwise DOAC
- NOTE: if incidental non-symptomatic AF - normal rate, no other RFs, CHA2DS2-VASc 0 –> anticoagulation not recommended
-
CHF, HTN, Age ≥75rs (2), DM, Stroke (2), Vascular disease, Age 65-74, Sex - female
- Score 1 - consider; ≥2 - DOAC/Warfarin needed
- Lifetime risk = annual risk x estimated years of life left (up to 80 yrs e.g. if 60 then x annual risk by 20)
Types of anticoagulant
Heparins
- LMWH (SC) - VTE prophylaxis BUT bad for renal function
- UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring
DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)
Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions
Virchow’s triad to determine anticoag vs antiplatelets
1) Stasis - coag factor activation–> venous clot (AF, DVT/PE)
* Anticoags (DOAC/Hep/Warfarin) are most effective as coag factors cause clot
2) Vessel wall injury - plaque rupture - thrombogenic material release –> platelets activated –> arterial thrombosis (MI, stroke)
* Antiplatelets (Aspirin/Clopidogrel) most effective as platelets cause clots
3) Hypercoagulability - does not change acutely
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?
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: IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- 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)
MI location based on ECG
- Inferior – right coronary artery (2,3, aVF foot)
- Anterior – left anterior descending artery (V1-2)
- Lateral – circumflex artery (1 ,aVL, V5/6)
- Posterior - ST depression in V2-4, abnormal R wave in V2
Infective endocarditis - RFs? Ix? Dx criteria? Mx?
Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?
Def: infection of heart valves (typically mitral/aortic or tricuspid in IVDU)
RFs: bacteraemia (long-term lines, IVDU, dental work), abn valves (prosthetic, RHD), prev endocarditis, VSD, piercings
Presentation: low-grade fevers, night sweats
- Exam:
- Splenomegaly
- Splinter haemorrhages, osler’s nodes, Janeway lesions, petechiae, Roth spots (eyes)
- Chronic = clubbing (rare, mostly acute now)
Ix:
- Urine dip - haematuria
- Serial BCs (x3 but start empirical abx), ESR
- Transoesophageal Echo (TOE - vegetations)
Dx: DUKE’S CRITERIA (2 major OR 1 major + 3 minor OR 5 minor):
- Major: +ve BC (typical organism), new regurg murmur/veg on echo
- Minor: RF, fever (>38), embolic (vascular) phenomena, immune phenomena, +ve BC (another organism)
- Mx: IV abx for 6wks – fluclox/vanc/gent
Acute in structurally normal heart – In IV drug user the first valve met is tricuspid valve, commonly S. aureus (also most common cause in prosthetic valve endocarditis)
Subacute in structurally abn heart – mitral & aortic valves more commonly affected as high pressure system, more likely damaged valves, commonly Strep Viridans (overall most common cause of endocarditis)
ECG Important Considerations
- Make sure to compare to a previous ECG = dynamic changes (acute)
- Coronary infarcts commonly present as T-wave inversion/RBBB/LBBB, not always with ST-elevation/depression
NSTEMI Mx? Scoring? Ix?
Immediate:
- Aspirin PO stat AND Ticagrelor OR Clopidogrel PO stat
- Fondaparinux SC
On discharge (give all despite BP/HR):
- Aspirin for life
- Ticagrelor OR Clopidogrel for 1 year (2 needed for 1 year as stent impregnated with Tacrolimus
- Ramipril (ACEi) - titrate up to 10mg
- Atorvastatin
- Bisoprolol (B-blocker) - titrate up to 10mg
Scoring Risk: GRACE score
Ix if high risk: cathlab for angiogram (will be started on IV unfractionated heparin instead of fondaparinux as procedure is very thrombogenic) –> PCI (stent)
Heart failure key consequences x2
1) Reduced CO (SV*HR) –> shock, tachycardia, AKI
2) Congestion –> pulmonary oedema + peripheral oedema
Acute HF vs ACS
Irregularly irregular heart rhythm - Dx? Ix? Mx?
AF - narrow complex tachycardia with no p-waves
Ix:
- ECG, Echo (valve check)
- Bloods - U&E, Mg (QT interval), Troponin (ischaemic), TFTs
Mx:
- Haemodynamically unstable –> DC cardioversion
- Rate control - Bisoprolol 2.5mg OD (max 10mg, can use rate-lim CCB)
- Rhythm control - if clear reversible cause: <48hrs = DC/chemical cardioversion (flecanide/amiodarone); >48hrs = anticoag 3-4wks (clot may have formed)
- Stroke risk Mx - CHADS-Vasc Vs HAS-BLED/ORBIT - Apixabab 5mg BD (DOAC, can use Warfarin)
How do you calculate ejection fraction? What are the different types of HF based on ejection fraction?
Ejection fraction = SV/End Diastolic Volume
HF w/ preserved EF: >50% - inadequate filling of stiff ventricles
- Causes: volume overload (valve regurg), pressure overload (HTN), decreased distensibility (constrictive pericarditis)
- No drugs w/ prognostic benefit, Mx Sx w/ diuretics
HF w/ reduced EF: <40% - inadequate emptying of ventricles from outflow obstruction or impaired contractility
- Causes: MI, cardiomyopathy, arrhythmia
Types of anticoagulant
- Heparins
- LMWH (SC) - VTE prophylaxis BUT bad for renal function
- UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring
- DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)
- Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions
Virchow’s triad + anticoagulants vs antiplatelets
1) Stasis - coag factor activation–> venous clot (AF, DVT)
* Anticoags are most effective as coag factors cause clot
2) Vessel wall injury - plaque rupture - thrombogenic material release –> platelets activated –> arterial thrombosis (MI, stroke)
* Antiplatelets most effective as platelets cause clots
3) Hypercoagulability - does not change acutely
Bibasal crackles indicates what? Ix? Mx?
Fluid overloaded with pulmonary oedema = acute heart failure
HF = pumping of blood by heart isn’t meeting body demands
Ix:
- Bedside - ECG
- Bloods - ABG, troponin, BNP
- Imaging - CXR, Echo (further down the line)
Acute HF Initial Mx:
- Immediate: sit patient up, O2 15L/min NRM
- Medical: IV furosemide (higher dose if on LT Tx), GTN, Morphine IV
- If no improvement: repeat furosemide (after 15mins) –> consider CPAP
Long-term HF Mx:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart
- ACEi - reduce strain on heart
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
ECG changes in IHD
ST-elevation
Ischaemic changes
- Dynamic T-wave inversion
- ST depression
What heart condition is malar flush associated with?
Mitral stenosis
Key features of mitral stenosis
- Malar flush
- Middle-aged female
- AF
- Tapping apex beat (palpable/loud first heart sound)
- Quiet blowing mid-diastolic murmur –> accentuate leaning to left and listening over mitral area while holding breath exhaled –> if can’t be heard then would get the patient to do exercise
Complications of MI
FAP (failure, arrhythmias, pericarditis)
Arrythmias (incl. VF)
Heart failure
Pericarditis
- Early - positional chest pain day after MI –> give NSAIDs
- Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)
3rd & 4th heart sounds - sounds & cause?
3rd = rapid ventricular filling = HF (reduced EF/systolic)
- KEN…TU.CKY (deee. de.de)
4th = atrial contraction against stiff ventricles = longstanding AS & other causes of left ventricular hypertrophy (HTN heart disease, HOCM, HF with preserved EF/diastolic)
- TE.NE..SSEE (de.de.deee)
In the context of HF what is cardiogenic shock? How do you treat? How do you treat rate-dependent cardiogenic shock (complete heart block)?
How will they describe cardiogenic shock in question?
- HF so severe pressure insufficient to perfuse brain & heart alone –> 100% death if untreated
- Treat with inotrope - dobutamine/dopamine –> increase perfusion of coronary arteries (saves 1/10)
- Temporary external pacing –> permanent pacemaker
Q: cold peripheries & low UO
Apex beat displacement vs left ventricular hypertrophy?
- Apex beat displaced by dilation = exam finding – caused by fluid overload
- LVH = ECG Dx (peaked R-waves, ST depression and T-wave inversion in lateral leads) – caused by pressure overload e.g. HTN
What is widespread ST elevation?
Acute pericarditis
RFs for IHD?
HTN, DM, Smoking, FHx IHD, Hypercholesterolaemia
What drug should be held for 48hrs before and after an angiogram?
Metformin
What drug caused this ECG in AF patient
Flecainide can convert AF to 1-1 atrial flutter (normally given with bisoprolol to compensate) >200bpm
Complications of prosthetic heart valves
FIBAT
- Failure
- Infection
- Bleeding - MAHA
- Anaemia
- Thromboembolic phenomena
AS vs aortic sclerosis signs?
AS:
- Radiates to carotids
- Slow-rising pulse
- Narrow pulse pressure
- Heaving apex beat
- Severe = absent 2nd heart sound
Aortic sclerosis (calcification) = just murmur
AS - causes? Sx? Signs? Indications for surgery?
Causes:
- Calcific degeneration
- Bicuspid valve e.g. Turner’s syndrome (XO female) - develop 10yrs earlier
Sx: ASH (in this order)
- A - angina
- S - syncope
- H - HF
Signs:
- Key:
- Radiates to carotids
- Slow-rising pulse
- Narrow pulse pressure
- Severe = absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat, longer murmur is worse
Indications for surgery: symptomatic (syncope) OR CCF
Mx: TAVI (transcatheter aortic valve implantation) or surgical replacement
- inf endocarditis abx prophylaxis
- long-term Warfarin (not DOAC)
- Medical Mx: anti-HTN + anti-lipids + statin
What arrhythmia is common in AS and metallic aortic valve?
AF
What should I look for if they have a midline sternotomy scar (cardio)?
Long saphenous vein harvesting in the leg = CABG
Indications for CABG? Vessels used for graft? Meds post-CABG?
Indications:
- Left main-stem disease
- 2+ vessel disease
- Failure of medical Mx
- Concomitant (aortic) valvular replacement
Grafts:
- Great saphenous vein
- Internal thoracic (mammary) artery - NOW the most commonly used
Meds post-CABG:
- DAPT - aspirin + ticagrelor (for 12 months then just aspirin) ± specialist opinion
- Cardio-selective beta-blocker (bisoprolol)
- ACEi (or ARB)
- *
Mitral regurgitation - causes? presentation?
Causes:
- Chr:
- Myxomatous degeneration
- Functional (w/ LV dilatation)
- Acute:
- IE
- Papillary muscle rupture (supplied by posterior intraventricular artery, after inferior/posterior MI)
Presentation:
- Pan-systolic murmur
- Radiates to axilla
- Severe: displaced/thrusting apex beat, LVF, 3rd HS
Causes of HF?
Distinguishing between observations during cardio PACES station
- Murmur - AS, aortic sclerosis, MR
- Sternotomy w/ Warfarin - Metalic valve, CABG + AF
- Sternotomy no Warfarin - Tissue valve, CABG
- Oedema (& none of above) - CCF
HTN Mx?
Prolonged QT, twisting of QRS complexes - Dx? Causes of long QT?
How to Tx?
Torsades de pointes (form of VT)
Causes:
- Low Ca/Mg/K –> Prolongs QT
- Drugs - Clari, Ciprofloxacin, Haloperidol
- Inherited - Romano- Ward (AD no deafness), Jervell-Lange-Nielsen (AR sensorineural deafness)
Tx: IV Mg SO4 (also used for refractory VF, all other VTs treated with Amiodarone)
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:
- Prepare for DC cardioversion
- IV amiodarone, b-blocker
