Cardiology_Medicine Flashcards

1
Q

IHD - RFs? Types? Definition? Dx? Mx? Complications?

A

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)
  • 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)
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2
Q

Heart failure def? Causes? Pathophysiology? Categories & Causes? Classification? Ix? Mx?

A

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)
  • 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

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)

Complications:

  • Reduced CO (SV*HR) –> shock, tachycardia, AKI
  • Congestion –> pulmonary oedema + peripheral oedema
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3
Q

Atrial fibrillation (AF)

  • Def? Causes? Ix? Mx?
A

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)

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)
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4
Q

SVT - Def? Types? Presentation - case example? Mx?

A

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
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5
Q

Key heart murmurs?

Accentuation manoeuvres?

Causes?

Left vs right heart valve abn epidemiology?

Mx?

Complications of prosthetic heart valves?

A

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
  • 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
  • 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
  • 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
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6
Q

MI location based on ECG

A
  • 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
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7
Q

Infective endocarditis - RFs? Ix? Dx criteria? Mx?

Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?

A

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)

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11
Q

3rd & 4th heart sounds - sounds & cause?

A

3rd = rapid ventricular filling = volume overload e.g. HF (reduced EF/systolic)

  • KEN…TU.CKY (deee. de.de)

4th = atrial contraction against stiff ventricles = pressure overload e.g. longstanding AS & other causes of left ventricular hypertrophy (HTN heart disease, HOCM, HF with preserved EF/diastolic)

  • TE.NE..SSEE (de.de.deee)
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12
Q

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?

A
  1. HF so severe pressure insufficient to perfuse brain & heart alone –> 100% death if untreated
  2. Treat with inotrope - dobutamine/dopamine –> increase perfusion of coronary arteries (saves 1/10)
  3. Temporary external pacing –> permanent pacemaker

Q: cold peripheries & low UO

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13
Q

Apex beat displacement vs left ventricular hypertrophy?

A
  • 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
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14
Q

Indications for CABG? Vessels used for graft? Meds post-CABG?

A

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)
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15
Q

2 days of chest pain following 4 days of generalised muscle aches

  • Worse on inspiration & lying flat
  • Low-grade fever
  • Exam: pericardial rub

Causes? Dx? Ix? Mx?

A

Pericarditis

Causes:

  • Viral (most common)
  • MI (can be Dressler’s syndrome)
  • TB (constrictive)
  • Uraemia (CKD where urea high –> pericarditis) = indication for haemodialysis (HUMP)
  • Hydralazine (AI pericarditis)
    • NOTE: also causes drug-induced lupus
  • SLE, RF, radiation

Presentation:

  • Pleuritic chest pain, worse lying flat
  • Exam: pericardial rub - “creaking/scratching”
    • Tip - put on all-fours, put stethoscope on sternal edge, hold inspiration

Ix:

  • ECG: ST elevation widespread
  • Only slightly raised/normal troponin

Mx: colchicine (3 months) + NSAIDs (ibuprofen, max 2wks)

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16
Q

Causes of raised JVP (>4cm)?

A

JVP + hepatojugular pressure (RUQ), rockstar hand

PQRST:

  • Pul HTN/PE/Pericarditis/Pericardial effusion/PS
  • Quantity of fluid (fluid overloaded)
  • RHF
  • SVC obstruction
  • Tamponade/TR
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17
Q

SVC obstruction - presentation? Tx?

A

Presentation: swollen face and neck and distended veins on her chest in background of cancer

Mx: dexamethasone to reduce tumour swelling

  • Insert EV stent if stridor (after intubation and steroids)
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18
Q

Bradycardia arrhythmia with a palpable pulse (peri-arrest) - Mx?

A

Innitial: A-E

  • If unstable - 500mcg IV atropine (/5mins up to 3mg)
    • Also considered unstable if:
      • Recent asystole >3s/Mobitz T2 AV block/3rd degree heart block
    • Caution in acute MI, C/I if heart transplant
  • If persistent –> transcutaneous pacing + analgesia/sedation (very painful)
    • If can’t be achieved properly –> IV isoprenaline/adrenaline (specialist help)
  • Arrange transvenous pacing (temporary if recent asystole >3s/Mobitz T2 AV block/3rd degree heart block)
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19
Q

Heart block causes? types? Ix? Mx? Complications?

A

Causes:

  • MI/IHD (MOST COMMON)
  • Inf (RHD, IE)
  • Drugs (digoxin)
  • Metabolic (hyperkalaemia)
  • Infiltration of conducting system (e.g. sarcoidosis)
  • Degeneration of conducting system

Types:

  • First Degree AV block - fixed prolonged PR interval (> 0.2 s) - ASYMPTOMATIC
  • Second degree AV block:
    • Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
      • Normally asymptomatic
    • Mobitz Type II - intermittently P wave NOT followed by a QRS
      • May be regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
      • Can cause:
        • Stokes-Adams Attacks (syncope caused by ventricular asystole)
        • Dizziness, palps, chest pain, HF
  • Complete AV heart block - no relationship between P waves and QRS complexes
    • Presentation as in Mobitz T2

Ix: ECG

  • Bloods: TFTs, Digoxin, cardiac enzymes (troponin, CK, BNP)
  • CXR (cardiac enlargement, pulmonary oedema)
  • Echo (wall motion abn, aortic valve disease, vegitations)

Mx:

  • Acute block - if clinical deterioration:
    • IV atropine
    • Consider temporary transcutaneous pacing
  • Chronic block:
    • 1st degree monitored
    • Permanent pacemaker in:
      • Symptomatic Mobitz T1
      • Advanced Mobitz T2
      • Complete heart block

Complications: asystole, cardiac arrest, HF, surgical complications of pacemaker insertion

20
Q

Types of pacemaker? When to use each type? Complications?

A

Types:

  • Implantable Cardioverter Defibrillator (ICD, has a thicker end)
  • Single-chamber pacemaker (right ventricle)
    • Used in permanent AF (no organised atrial contraction so atrial lead not required to sense contraction)
    • Rarely can have atrial lead only - if SA disease in young with good AV conduction
  • Dual-chamber pacemaker (right atrium & ventricle)
    • Can have ICD dual-chamber pacemaker
    • Used in paroxysmal AF/all other scenarios (there is sometimes organised atrial contraction - this is sensed by the atrial lead)
  • Cardiac Resynchronisation Therapy/Biventricular pacemaker (right ventricle, left ventricle ± right atrial lead)
    • Can have ICD biventricular pacemaker

When to use each type:

  • Atrial lead only → Sino-atrial disease in young people with good AV node conduction
  • RV lead only → Pacing whilst in permanent atrial fibrillation
  • Dual-lead → All other scenarios (paroxysmal AF, bradycardia)
  • CRT → LV dysfunction + broad QRS –> end-stage HF
  • Indications for ICD:
    • Primary prevention = @risk of serious ventricular arrhythmia
      • Familial cardiac conditions (hypertrophic cardiomyopathy, long QT)
      • Previous surgical repair of congenital HD
      • Previous MI + LVEF <35% + HF Sx
    • Secondary prevention = had previous serious ventricular arrhythmia wo/ treatable cause
      • Cardiac arrest from VT/VT
      • Spontaneous sustained VT AND:
        • Syncope/haemodynamic compromise OR
        • LVEF <35% + sign HF Sx (NYHA 3+)
      • NOTE: VT/VF from STEMI has treatable cause (open occluded vessel)

Complications:

  • Surgical complications - infection, bleeding, damage to underlying structures
  • Displacement (of lead)
  • Pacemaker syndrome (if ventricular lead with no atrial) –> AV node conducts in retrograde direction = mitral/tricuspid regurge + HF Sx
21
Q

Pros/cons of TAVI?

A

Pros: no bypass required, no large scars
Cons: higher risk of stroke compared to open replacement

22
Q

Different pulse forms? Causes?

A

Pulsus paradoxus - greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

  • severe asthma, cardiac tamponade

Slow-rising/plateau

  • AS

Collapsing

  • AR, PDA
  • hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Pulsus alternans - regular alternation of the force of the arterial pulse

  • severe LVF

Bisferiens pulse - ‘double pulse’ - two systolic peaks

  • Mixed aortic valve disease
  • HOCM (also causes ‘Jerky’ pulse)
23
Q

Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?

A

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
24
Q

Cardiac tamponade - key finding on exam? Triad? Mx?

A

Pulsus paradoxus - BP variation between inspiration & expiration (≥10)

Beck’s triad (50%):

  • Raised JVP
  • Muffled heart sounds
  • Hypotension

Mx:

  • IV fluids (RV filling depends on venous pressure & effusion is constricting)
  • Echo –> refer to cardiology for pericardiocentesis
    • Coagulation profile (to prep for pericardiocentesis)
25
Q

Case:

  • 26yrs, BP 180/100, femoral pulses weaker than radial pulse
  • Mid-systolic murmur in infra-scapular area
  • Trying to get pregnant unsuccessfully for 2yrs

What is the Dx? Assoc? What is there a risk of & what advice is given?

A

Young + very high BP –> must be secondary HTN (causes: endo - Conn’s, Phaeo; coarctation of Aorta (CoA), renal artery stenosis, chronic renal failure)

CoA - tissue restricting flow across aortic arch

  • Murmur across the coarctation = left infrascapular area (due to turbulent BF)
  • Lower body underdeveloped vs upper (97% men going to gym)
  • Assoc: Turner’s (+ Marfan’s, Ehlers-Danlos)
    • Short stature, webbed neck, wide-spaced eyes, lack of other secondary sexual characteristics, shield-like chest, short 4th metacarpals/tarsals
  • Advice: avoid extreme isometric exercises e.g. weight-lifting –> risk of aortic dissection
    • ​How do you Dx dissection? CT aortogram w/ contrast
26
Q

How do you know this is the JVP and not the carotid pulse?

A
  • Not palpable
  • Double pulsation
  • Obliterated when pressure applied at base of neck
  • Rises with hepatojugular reflux
  • Height changes with respiration
27
Q

Types of cardiac scar?

A
  • Midline sternotomy + leg scar = CABG
  • Midline sternotomy (no leg scar) = Valve replacement most likely (rarely can be CABG without vein graft)
  • Left subclavicular -> pacemaker, debfibrillator, resynchronisation device
  • L shaped scars under either breast -> L/R Thoracotomy