Cardiology Flashcards
Sgarbossa criteria - Modified
- Concordant ST elevation ≥ 1 mm in ≥ 1 lead (5points)
- Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3 (3 points)
- Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave (2points)
Yes to any criteria deemed 80% sensitive and 90% specific to identify acute MI
Cardiac Syncope
ECG Patterns to consider
- Ischaemia
- Dysrrhythmias
- AVBs
- WPW
- Long QT or short QT
- Brugada
- HCM
- ARVC
- ASD
Monomorphic VT ECG
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”)
- Very broad complexes > 160ms
- AV dissociation:
- P and QRS complexes at different rates
- P waves are often superimposed on QRS complexes and may be difficult to discern
- Capture beats
- Fusion beats
- +ve or -ve concordance throughout precordial leads
- RSR’ complexes
- Brugada sign = distance from R wave to Nadir of S wave > 100ms in V1-V6
- Josephson’s sign = Notching near nadir of S wave
Heart Murmurs Grades (6)
Grade 1 Very soft, requires an experienced listener
Grade 2 Soft
Grade 3 Moderate and without a thrill
Grade 4 Loud with thrill just palpable
Grade 5 Very loud and thrill easily palpable
Grade 6 Very loud, may be heard without the aid of a stethoscope
Aortic Stenosis Grades
Normal - 3-4cm2 aortic valve SA
2mmHg gradient across valve
Mild - 1-2cm2, <25mmHg,
Moderate - 075-1.0cm2, 25-40mmHg
**Severe **- <0.75cm2, >40mmHg,
Critical - >80mmHg
exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg
Pulsus Paradoxus Differentials
Pericardial Tamponade
Hypovolaemia
Acute asthma
Massive PE
Constrictive pericarditis
HOCM Clinical Exam
If MR present - pansystolic at apex
Systolic murmur heard at lower left sternal edge or apex
INcrease murmur - ↓ preload
- Valsalva, standing after squatting
DEcrease murmur
- ↑ preload - Leg raising or squatting
- ↑ afterload - handgrip
HOCM ECG
● Prominent (typically deep, but narrow) Q waves in the lateral > inferior leads (I, AVL, V5-6). This is a relatively specific sign of HOCM
● High voltages - features of LVH
● Tall R waves in V4-6, I, aVL
● Conduction abnormalities
● Arrhythmias, usually AF or more seriously VT/ VF.
Syncope ECG
- ACS / Arrhythmias / AVBs
- Brugada
- QTc - Short / Long
- Delta Waves WPW
- Epsilon Waves - ARVC
- LVH (HOCM, AS)
- RV Strain
Short PR ECG
< 120ms
Preexcitation syndromes
- WPW + Lown-Ganong-Levine
- Accessory pathway w/ re-entry circuit
AV nodal (junctional rhythm)
- Narrow complex arising from AV node
- P waves absent or abN
- Accelerated => inverted P waves and short PR interval
Long QT Syndrome
Normal QTc 450msec (440 in men, 460 in women)
Short QTc <350msec
QT inversely proprtional to HR
↑QTc represents delayed ventricular repolarisation => ↑ risk of polymorphic VT
Causes
- ↓ K, Mg, Ca
- Clincal Conditions
- MI
- Severe hypothermia
- Raised ICP
- Severe brady-arrhythmias
- Drugs
- Class Ia anti-arrythmics
- Quinidines, procainamide, disopyramide
- Class Ic anti-arrythmics
- Flecaininde
- Class III anti-arrythmics
- Sotalol, amiodarone
- Others
- ABx - macrolides
- Non-sedating antihistamines
- Antipsychotics
- TCAs
- Organophosphates
- Class Ia anti-arrythmics
- Congenital
- Lange Neilson (recessive + deafness)
- Romano-Ward (dominant, no deafness)
RAD Differential
- Normal in kids
- VEBs
- RVH
- LPFB
- Chronic Pulmonary HTN / COPD
- Acute pulm HTN
- Old MI - lateral
- Na channel blockers
- HyperK
- Misplaced leads
- Situs inversus
Wide QRS Differential
- Ventricular -VT
- Paced
- BBB
- WPW
- Metabolic (hyperK, severe acidosis)
- Na Channel blockers
- NS IVCD
Hx
Age>35yrs
Smoking
IHD
Previous VT
Active angina
Mx
Unstable - DCCV
Stable
- Amiodarone 150mg over10mins and rpt x 1
- Lignocaine 1-1.5mg/kg slow IV push
- Sotalol 1mg/kg IV
- Procainamide 100mg q5mins (up to 20mg/kg) - NOT in OZ!
Elevated troponin
Cardiac Causes
(8)
- Cardiac contusion
- Cardiac procedures - DCCV, ablation, PCI, CABG
- CCF - Ac or Chr
- Aortic dissection
- Aortic valve disease
- Arrhythmias
- Cardiomyopathy - HOCM, pregnancy-induced, Takotsubo, Severe CVA, Phaechromocytoma
- Myopericarditis
Elevated troponin
Non-cardiac
(10)
- Resp - Large PE, PHTN, Resp failure
- Neurological - SAH, CVA
- Infective - Sepsis
- Tox - Sympathomimetics
- MSK - Rhabdomyolysis, strenuous exercise
- Infiltrative - sarcoid, amyloid, haemochromatosis, scleroderma
- Trauma - Burns
- Renal - CRF
- GIH
- Autoimmune - TTP
HACEK - significance
Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
- Rare <5-10%
- Gram -ve bacilli
- Native valves
- Hard to culture can take > 5days, culture negative IE
- Rx - ceftriaxone
IE - Organisms
○ Staphylococcus aureus (32%)
○ Strep. Viridans - 18%
○ Enterococci - 10%
○ Coag-negative staph. - 10%
○ Strep. Bovis - 7%
○ Other strep.
○ non-HACEK gram negative bacteria
○ Fungi (candida, aspergillus)
○ HACEK
○ Polymicrobial
○ Culture negative - 8%
Duke Criteria for Infective Endocarditis
**Bacterial Endocarditis TIMER **
Major
- Blood Culture +ve - typical organisms
-
Echo +ve
- Echo - Valvular vegetation / abscess / dehiscence
- New valular regurgitation
Minor
- Temperature> 38.0
-
Immunological phenomena
- Osler’s nodes, Roth spots, RhF +ve
-
Micro
- single positive culture but no major criteria
-
Embolic Phemonena
- Arterial emboli, septic emboli (pulmonary), mycotic aneurysm, ICH, conjuntival haemorrhage, Jane way lesions (painless erythematous lesions palms/soles)
- Echo +ve but no major criteria
-
Risk Factors
- CVD
- IVDU
DEFINITE
* 2 MAJOR
* 1 MAJOR + 3 MINOR
* 5 MINOR
Immunologic phenomena
- Glomerulonephritis
- Osler’s nodes - tender nodules on finger/toe tips
- Roth spots - white-centred retinal haemorrhages
- Positive RhF
IE - Surgical Intervention
IE with acute HF
Fungal / Mycotic aneurysm
Recurrent large emboli
Large vegetations >10mm
Persistent bacteraemia
Unstable prosthesis
IE - Complications
- Left sided
- HF / valvular damage
- Emboli - CNS (CVA), systemic
- Right sided
- Emboli - Pulmonary Embolus => infection + infarction
Rheumatic Fever - Jones Criteria
MAJOR
* Joint pain - polyarthritis
* O - Carditis
* N- SC nodules
* Erythema marginatum
* Sydenham’s chorea
MINOR
* Arthralgias
* Fever
* Raised CRP or ESR
* Prolonged PR interval
DIAGNOSIS
Antecedant Strep infection +
- > 2 major
- 1 major + 2 minor
- +ve ASOT (+ve for 4-6 weeks)
- Raised CRP
- Prolonged PR interval
Rx
* Strep infection - PenV stat dose, then Benpen
* Arthritis - Analgesia
* Chorea - valporate/carbamazepine
* Ac HF - ACEi and diuretics
Primary Heart Block DDx
- Normal variant
- Increased vagal tone e.g. athletes
- Electrolyte Distrubance - K+, Mg2+
- Drugs - all antiarrhythmics
- MI
- Myocarditis esp Rh Fever
- Valvular lesions
- Cardiomyopathy
Emergency Pacing Indications
- Bradycardia unresponsive to drug therapy
- 3rd degree heart block
- Mobitz type II second-degree heart block when haemodynamically unstable or operation planned
- Overdrive pacing - TorasdeS or recurrent VT/SVT
- Asystolic pauses (>3s) with sick sinus syndrome + syncope
Transcutaneous
1. Sinus pauses > 3 seconds
2. Bradycardia with severe hypotension
3. RV infarct, inability to pace with TV pacing
Transvenous
* Asymptomatic Mobitz type II
* MI +
* New bifascicular block
* Alternating LBBB and RBBB
* Ant MI as Inf MI lfuid and atropine responsive
* Overdrive pacing of tacharrhythmias
DCCV Contraindications
- Sinus tachycardia
- MAT
- Digoxin-related tachycardia
- Non-schockable rhythms
- AF >48hrs + no anticoagulation
Bradycardia - Secondary Causes
Critical
- Hyperkalaemia
- Ischaemia
- Drugs - Brady bunch
- CNS - raised ICP - deep TW inversions
Emergent
- Hypothermia
- Myxodema coma
- Infection - myocarditis, endocarditis. lyme’s, travel - dengue, malaria, typhoid, legionnaries
- OSA
Special
- Post cardiac / valve surgery
- Ruptured viscus / ectopic - paradoxical bradycardia with vagal response
LAFB - ECG criteria
- Slightly prolonged QRS (may not be >120ms)
- rS complexes in leads II, III, aVF (Dep going away)
- qR complexes in leads I, aVL (Dep going towards)
- Left Axis Deviation (LAD)
LPFB - ECG Criteria
- Slightly prolonged QRS
- rS complexes in leads I and aVL (Dep going away)
- qR complexes in leads II, III and aVF (dep going towards)
- Right Axis Deviation (RAD)
- Absence of RVH or prior lateral MI
BRASH syndrome
- Bradycardia
- Renal failure
- AV block
- Shock
- Hyperkalaemia
Treatment aims
1. Calcium
2. Fluid resus - consider normal bicarb
3. K+ Mx - usual methods +/- frusemide or dialysis if anuric
4. Adrenaline - cardiogenic shock
PPM Indications
- 3d and 2d AV block +
- Symptomatic bradycardia / arrhythmia
- Symptomatic bradycardia secondary to drugs for dysrrhythmia Mx
- AF with pauses >5s
- Catheter ablation of AV node
- Post-op AV block not expected to resolve
- NMD (dystrophies)
- Symptomatic bradycaradia + 20 AV block
- Persistent 30 AV block
- Chronic tri or bi-fascicular block with intermittent type II 20 block or 30 block
- 30 and 20 AV block with exercise
PPM Malfunctions
Usually within 6-8 weeks
Usually a lead issue or programming issue
Consider PPM lead infection + endocarditis if pt has fever
LBBB normal, RBBB abnormal - consider lead displacement
Magnet does not turn off PPM - turns of sensing or inhibition function
Causes of malfunction:
-
Failure to capture - No pacing spikes or spike not followed by an atrial/ventricular complex
- Lead fracture / displacement or insulation break
- Exit block
- Battery depletion
-
Inappropriate sensing - Spikes occur prematurely or not at all
- Undersensing - - fails to register deoplarisation (flushing toilet)
- Lead fracture / displacement or insulation break
- Inadequate endocardial contact
- Low voltage P waves and QRS complexes
- Oversensing - detecting signals other than that for the chamber => witholding pacing
- Extra-cardiac signals - artefact, myopotentials
- TW or PW sensing
- Undersensing - - fails to register deoplarisation (flushing toilet)
-
Inappropriate pacemaker rate
- Battery depletion
- Ventriculo-atrial conduction + pace-maker mediated tachycardia
- 1:1 response to atrial dysrhythmias
Other Implantable cardiac devices
LVAD
TAH
Bridge to transplant or destination therapy
All anticoagulated and can presnet with GIH or ICH
Can dvp acquired Von Willebrand’s PLT dysfunction
Dysrrhythmias frequent so pts have AICD
LVAD
- Some - No palpable pulse or BP
- MAP with art line with BP cuff - constant flow indicates MAP
- Assess other vital for perfuson status
- Shock may be RVF - deviced does not support RV - consider dobutamine, dopamine
- Compressions NOT HELPFUL - confirm absence of pump function and fix malfunction
- Some have backup hand pump
TAH
- ECG asytole as no native cardiac activity
- Defib / pacing and chest compressions NOT HELPFUL
PPM - Nomenclature
5 letter code
First 3 anti-bradycardia function
Last 2 additional functions
- Chamber paced - A/V/D/O
- Chamber sensed - A/V/D/O
- Response - Trigger/Inhibit/Dual/O
- Programability - P/M/R/C/O
- Anti-tachcardia functions
Pacing, shock, dual, rate modulation
Common Pacing codes
1. VVI - TV pacing mode
Paces and senses ventricle
No electrical impulse sensed = pace @ a pre-programmed rate
Electrical impulse sensed = pacing inhibited
Asynchronous pacing
- VVIR
As above but rate adaptive mechanism to meet patients physiological needs - DDD
Ventricular pacing and sensing
If SA and AV node functioning then pacemaker will just sense
if not then PPM will tkae over - DDDR
Same as above except has a rate-adaptive mechanism - VOO
Licence to kill - PPM not sensing
Mode for surgery (asynchronous pacing)
Ventricle paced at a pre-programmed rate
Sensing not interfered with by diathermy etc
Need to monitor for R on T with diathermy -> torsades de pointes
PPM Insertion Complications
- Infection
- Usually S. aureas
- Haematoma
- PTx
- Pericarditis
- Thrombophlebitis
- 30-50%
- NB SVC obstruction
- Skin erosion
- Replace unit and ABx
- Pacemaker syndrome
AICDs
Functions - cardioversion, defibrillation, pacing
Indications
- VF/VT with no transient or reversible event
- Spontaneous sustained VT
- Syncope of undetermined origin + induced and sustained VF/VT (EP study)
- Non- sustained VT + CVD + refractory to class I antiarrhythmic
Causes of shock delivery to patient
- Increase VF / VT (ischemia / electrolyte disturbance / drug effect)
- Displaced or break in ventricular lead
- Recurrent non-sustained VT
- Sensing and Shock of SVT
- Oversensing T-waves
- Sensing non-cardiac signals
Causes of syncope
- Recurrent VT with slow shock strength (lead problem / change in defib threshold)
- Hemodynamically significant SVT
- Inadequate backup pacing for bradyarrythmias
Admit patient
- Haemodynamically unstable
- > 2 shocks in one week
- Correctable cause
- Infection
- Disruption of mechanics
Raised ICP ECG
Most commonly seen with SAH, Haemorrhagic CVA
- Deep symmetrical (Giant) TWI throughout
- QT prolongation
- Bradycardia
Others
- Flat T waves
- ST elevation or depression
- ↑ U wave amplitude
- Rhythm disturbances - ST, Junctional, PVCs, AF
ST Elevation on ECG DDx
Vessel Occlusion + ECG patterns
Post MI Complications - Early
- Bradydysrrhythmias
- Tachydysrrhythmias
- Cardiogenic shock
- LV free wall rupture
- Septal rupture
- Papillary muscle rupture → MR
- Pericarditis
- Embolic or Haemorrhagic stroke
- Hyperglycaemia
- Iatrogenic
- AntiPLT, Anticoag, antifibrinolytis complications
- Pseudoaneurysm from arterial cath
STEMI Equivalents ECG Patterns
Long QT
Depends on
HR + gender (M - 440ms, F - 460ms)
Short if <350ms
Congenital
* Lange-Nielson - recessive + deaf
* Romano-Ward - dominant + no deafness
Acquired
* Idiopathic
* Electrolytes - low K, Mg, Ca
* Clinical conditions
* AMI
* Hypothermia
* Raised ICP
* Severe Bradydysrrhytmias i.e. CHB with escape rhythm
* Drugs - by the anti-drugs
* Biotics
* Dysrrhytmics
* Emetics
* Fungals
* Neoplastics
* Psychotics
Significance = dvpt of…
Polymorphic VT
Monomorphic VT
VF
Treatment of Electrical Storm - refractory VT
Definition
- 3 or more episodes of sustained VT (>30s) within 24 hrs
Arrest - Defibrillate
Conscious + unstable = DCCV
Conscious + unstable
- Rx underlying cause
- Consider
- Intubation
- Deep sedation - propofol
- Arterial line - labile haemodynamics
- Anti-arrhythmics (loading + infusion)
- 1st line - Amiodarone up to 900mg loading in 24 hrs
- 2nd line - BB - propanolol 0.15mg/kg over 10mins or esmolol 0.3-0.5mg/kg IV
- 3rd line - lignocaine 1-1.5mg/kg bolus
- MGSO4 + electrolyte replacement
- Double defibrillation (if > 5 shocks not reverted)
- Stellate ganglion block
- ECMO
Treatment of Torsades
Arrest - defibrillate
Conscious - DC cardiovert
MGSO4 - 10mmol over 10-15 minutes
Treat underlying bradyarrhythmia by shortening QT interval
* Atropine
* Isoprenaline
* Overdrive pacing 90-120bpm
Avoid class Ia, Ic and III anti-dysrrhythmics
Treat underlying cause
- Correct electrolytes
- Warming hypothermic pt
Elevated Troponin
The ACSss
- Acute Coronary Ischemia
- ACS
- Variant Angina
- Cocaine
- Coronary Embolism/Vasculitis
- Comorbidities
- Renal, failure, sepsis, ARDS< Stroke, SAH
- Systemic shock states
- Distributive (sepsis, CO, burns)
- Cardiogenic (myocarditis, mycocardial contusion, cardiomyopathy
Thromboylysis CI
Absolute
- Previous ICH or Haemorrhagic CVA
- Ischaemic CVA in last 3/12
- Intracranial neoplasm
- Internal bleeding
- Suspicion of aortic dissection or pericarditis
Relative
- Ischaemic CVA > 3/12 ago
- Severe uncontrolled HTN > 180/110
- Recent trauma last 2/52
- Prolonged CPR > 10 mins
- Major surgery last 3/52
- Oral anticoagulant use
- Known bleeding diathesis or hepatic dysfunction
- Recent internal bleeding in last 4 /52
- Neoplasm with inc bleedin risk
- Recent organ biopsy or vascular puncture
TIMI score
Predictor of adverse outcomes at 14 days and or severe ischaemia requiring urgent PCI
- Age > 65 years
- At least 3 coronary risk factors
- Prior angio show > 50% stenosis
- ST segement deviation
- >2 episodes of angina in last 24 hours
- Aspirin use in last 7 days
- Inc cardiac biomarkers
Point for each parameter
Limitations:
- Score of 0-1 has cardiac event rate of up to 2%
- Score 7 cardiac event rate of up to 41%
- No weights of factors in score
- Angio result may be unknown
- Most predeictive power is biomarker elevation
Echo Tamponande Findings
- Hypoechoic fluid in peri-cardial sac - > 2cm = large > 500ml +
- RV (early)diastolic collapse
- RA (late)systolic collapse
- IVC dilation w/ no variation in respiration
- Sonographic alternans (swinging)
Hypercalcaemia
Serum levels >3mmol/l symptomatic
Calc:
Sx: Stones, Bones, Moans, Groans
Signs: ECG - short QT interval
Mx
Excretion
- IVF
- LOOP diuretic (thiazide makes worse)
- Dialyse
Osteoclast inhibition (dec Ca release)
- Bisphosphonate - Pamidronate 90mg IV
- Calcitonin - PRN for cardiac dysrhythmias - takes 24-48 hrs to work
Brugada Syndrome
Brugada pattern - Type 1 + Clinical signs
Brugada Pattern
Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
Clinical signs
- Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
- Family history of sudden cardiac death at <45 years old .
- Coved-type ECGs in family members.
- Inducibility of VT with programmed electrical stimulation .
- Syncope.
- Nocturnal agonal respiration.
Aortic Stenosis
Valve is too small, narrow or stiff
Most common isolated valve lesion
M>F 4:1
Disease of age
RF
* Congenital biscupid valve 50%
* Calcific AS 25%
* RhF - rare 15%
* Coarctation of aorta
Symptoms
* Angina
* Increased O2 demand - LVH
* Reduced O2 suppley to coronary arteries - LVH
* Postural dizziness
* Syncope
* due to fixed stroke volume
* SOB
Signs
* Pulse - slow rising, sustained and small volume
* BP - Reduced SBP and pulse pressure
* Palpation
* Apex - hyperdynamic, displaced
* Thrill - base of heart, aortic region is severe
* HS
* S4
* Split S2
* Soft or absent S2
* Occasionally early ejection click - indicated mobile valve
* Murmur
* Harsh ESM, 2nd RICS with radiation to carotids
* Accentuated by leaning forward and breath held in expiration
Complications
- Exertional syncope
- Angina
- IE
- LVF - late
- Sudden death
- Heyde’s syndrome = AS + GI angiodysplasia, vWF syndrome (shear stress)
Mx
* CVS RF modification
* CCF Mx - AVOID B Blockers but cautious use of
* Digoxin, ACEi, Diuretics
* Surgery
* AVR 25% 1 yr mortality w/out surgery
* TAVI
* Aortic balloon valvotomy - temporising measure in unstable pt
Slow and tight
Acute Aortic Stenosis
Symptomatic AS (potential to be sick)
- IV Fluids: overall, AS is preload dependent, and these patients may require IVF resuscitation to maintain cardiac output
- Inpatient admission for echo + evaluation for surgery for AVR
Patients with severe AS and failing LV (currently really sick AS), consider the following:
- Nitroprusside may dec afterload, improve systolic and diastolic function and dec myocardial ischaemia
- Inotropes - dobutamine
- Early consultation w/ cardiology for balloon dilatation for temporising measure
- Ultimately need AVR
Aortic Stenosis Take home points
Preload dependent
- Higher preload for normal systolic function
- Avoid diuretics and BB or CCB and GTN
Rate
- Aim HR 50-60
- Slower rate allows hypertrophic LV to relax in diastole
Rhythm
- Maintain SR
- Do not cope with AF => loss of diastolic filling time
Contractility
- Increased contractility mechanism to adjust to valve narrowing
- Avoid BB or CCB
Afterload
- Afterload fixed - stenosis in AV not peripheral ciculation
- Avoid hypertension
- More important to avoid hypotension - if DBP falls to low then coronaries will not have enough filling pressure - keep DBP high
Aortic regurgitation
Retrograde flow of blood from AV to LV during diastole
Causes
- Primary Valve
- Bicuspid, IE, RhF, vasc dx, degen aortic valve dx
- Aortic root disruption
- Marfan’s, HTN, congential
- Aortitis - syphilis, RA, Ank spond, GCA, Takayasu
- Acute
- Bacterial endocarditis
- Type A dissection
- Thoracic trauma
Complications
- IE
- LHF
- Angina
Symptoms
- Initially nil
- Exertional SOB, angina, palpitations
Signs
- Pulse
- Collapsing /Waterhammer
- Corrigans - prominent carotid pulsation
- Quincke’s - visible pulsation of nail bed with light compression
- de Musset’s - head bob with each heart beat
- Muller - systolic uvula pulsation
- BP
- SBP mildly increased
- DBP reduced
- PP increased
- Palpation
- Apex - Hyperkinetic, displaced
- Thrill - Occ left sternal edge
- HS - soft 2nd HS
- Murmur
- Early decrescendo diastolic murmur
- Valve lesion - left sternal edge
- Root lesion - right sternal edge
- Accentuated sitting up and expiration
- Austin Flint murmur - mid diastolic murmur at apex sitting forward and expiration
- Femoral artery murmurs
- Traube’s - pistol shot femoral pulses
- Duroziez’s - sys and dias murmur over partially occluded distal femoral
Mx
- Acute
- Inotropes + vasodilators titrated to BP
- Chronic
- Vasodilators
- Ace inhibitor
- BB
- Surgery
Aortic Regurgitation take home
Preload
- Highly preload dependent => forward flow
- Avoid GTN
Rate
- Keep HR higher - 90bpm
- Regurgitant flow occurs in diastole = keep diastolic time shorter
Rhythm
- Cope with AF
Contractility
- Needs to be high to maintain CO
- Avoid BB, CCB
- Dobutamine
Afterload
- Higher the afterload = > more regurgitation into LV
- CCB if not decompensated CCF
- Sodium nitroprusside - only for decompensated as decreases preload and afterload
Wellen’s ECG Criteria
- Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
- ECG pattern present in pain-free state
- Isoelectric or minimally-elevated ST segment (< 1mm)
- No precordial Q waves
- Preserved precordial R wave progression
- Recent history of angina
- Normal or slightly elevated serum cardiac markers
Wellen’s Significance
Clinical significance
- Critical LAD stenosis
- High risk for anterior wall MI within the subsequent days to weeks
- Require invasive therapy
- Poor prognosis with medical Mx and may suffer MI or cardiac arrest if inappropriately stress tested
LVH ECG criteria
- R in V5/V6 + Sin V1 > 35mm
- R in aVL > 11mm
- Max R + max S in precordial leads > 45mm
- Lots of others
LVH w/ Repolarisation abnormality or “strain”
Repolarisation abnormality increases specificity
- ST depression in I + aVL or V4-6
- Asymmetrical inverted T waves in leads above
- STE V1-3 +/- aVR
- QRS widening (non-specific IVCD)
LVH vs Ischaemia
No great methods but consider…
- Symmetrical TWI in I/aVL/V4-6
- Horizontal ST depression
- Excessive discordant STE in V1-3
Endocarditis Prophylaxis
High-risk individuals to whom antibiotic prophylaxis should be provided are as follows [4,5]:
- Prosthetic valves
- PMHx IE
- Cyanotic CHD
- 6/12 months post cardiac surgery + prosthetic material
- Aortic regurgitation
Procedures indicated
- Dental
- Implanted cardiac devices
- Procedure in infected/colonised tissue
Antibiotic Regime
- Amoxycillin 2g PO 60 mins before procedure
- Clindamycin 600mg PO if penicillin allergic
Fast and Loose
Acute Aortic Regurgitation
Acute - Type Aortic dissection or endocarditis or blunt chest trauma
AR → dec stroke volume → compensatory tachycardia to maintain CO
Stiff LV → inc LV pressure → prevents forward flow from LA → pulmonary congestion
Severe AR → progressive hypotension, peripheral vasoconstriction, and cardiogenic shock.
Mx
Treatment: Definitive treatment for severe acute AR is immediate surgical intervention
In ED:
- Intubate if necessary
- Nitroprusside → afterload reduction, decreased LV preload, and results in reduced regurgitant volume
- Dobutamine: inotrope → inc contractility and SV
- Add in nitroprusside to increase forward flow and temporize the patient
- ABx for suspected endocarditis
Treatment Pitfalls:
NO Beta blockers - decrease reflex tachycardia, but that tachycardia is currently maintaining their cardiac output. Decreased HR will worsen AR due to more time in diastole
Acute Mitral Regurgitation
Acute: IE, papillary muscle rupture, trauma
Chronic: MV prolapse, Rh HD, Cardiomyopathy, LVF, connective tissue disorders, congenital, DXT
Clinical
- Chest - pan-systolic, blowing, high pitched murmur
- ECG - P mitrale, RAD, LVH strain, AF
- CXR - LVH, LA dilation, APO
Severity - regurg fraction
- Mild <30%
- Mod 30-50%
- Severe >50%
Mx
- Fast (forward flow) and loose (dec afterload)
- Dobutamine
- Sodium nitroprusside
HEART Score
6 week risk of MACE
Score:
- 0-3 = <2%, D/C home
- 4-6 = 12-16.6%, admitted
- >7 = 50-65%, early invasive measures
QTc calculation
Formulae
- Bazett’s
- QTc = QT (msec) / √RR (s)
- Overcorrects for fast HR (>100) and undercorrects for slow HR (<60) - unreliable outside these ranges
- Framingham
- QTc = QT + 0.154(1-RR)
- Hodges
- QTc = QT + 1.75(HR-66)
- Half R-R Rule
- QTc should be < 1/2 R-R rule = unreliable
- QT Nomogram
- Best method in context of drug toxicity
- Median of 6 readings
Strategies to Manage Heart Failure
CXR findings in LVF
Frequency of LVF CXR findings in descending order
- Dilated upper lobe vessels
- Cardiomegaly
- Interstitial oedema
- Enlarged pulmonary artery
- Pleural effusion
- Alveolar oedema
- Prominent SVC
- Kerley B Lines
ARVC ECG
- T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
- Epsilon wave (most specific finding, seen in 50% of patients)
- QRS widening in V1-3 (> 110ms)
- Prolonged S wave upstroke of 55ms in V1-3
- Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours
- Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)
HTN Guidelines
Myocarditis
Myocarditis Causes
WPW
AF w/ RVR, rapidly conducting accessory pathways exist that can carry atrial impulses to the ventricle at rates exceeding 250 bpm. AV nodal blocking agents cause both faster and preferential conduction through these accessory pathways, which can result in extremely rapid ventricular response rates and deterioration to ventricular fibrillation. For these reasons, AV nodal blocking agents are contraindicated in preexcitation AF.
SVT ECG
- Rate 140-180 bpm in adults, > 220 suggest accesory pathyway
- Kids - >220 bpm infants and >180 small children
- Regular NCT
- Occ RBBB w/ abberant conduction
- P waves variable
- Typical (90%) - buried in QRS complex
- Atypical (10%) - retrograde or inverted in INF leads, positive P wave V1r
- Rate related ST depression
- QRS alternans - phasic variation assoc w/ AVNRT and AVRT
- STE aVR 70% sensitive and specific for accessory pathway SVT
SVT Mx
- Synchronsied DC shock if unstable
a. 1-2J/kg in children
STABLE
2. Vagal manoeuvres
a. Neonates, <6mo - facial immersion ice water 5-10s, ice-cold face cloth or ice slurry bag over face 15-30s
b. Older infants - ice slurry
c. Older / Adults - modified valsalva
3. Drugs
a. Adenosine 100mcg/kg
b. Sotalol 0.5-1.5mk/kg or verapamil - NOT for infants
c. Verapamil 5mg over 5mins / flecainide 2mg/kg over 30mins
d. Amiodarone 5mg/kg IV
SVT Mechanism Re-entry
Subtypes of AVNRT
1. Slow-Fast (80-90%)
i. Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction
2. Fast-Slow (10%)
i. Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway fpr retrograde conduction
3. Slow-Slow (1-5%)
i. Slow AV nodal conduction for anterograde conduction and slow left atrial fibres for retrgrade conduction
Summary of AVNRT subtypes
No visible P waves? –> Slow-Fast
P waves visible after the QRS complexes? –> Fast-Slow
P waves visible before the QRS complexes? –> Slow-Slow
Cardiac Axis
MFAT
Supraventricular rhythm - usually benign
3 or more sites of atiral ectopy
Not amenable to DCCV
Causes
1. COPD - hypoxia, hypercapnoea, acidosis
2. CVD - IHD/CCF/HTN
3. Metabolic - hypo K/Mg
4. Drugs - sympathomimetics, digoxin
5. Sepsis
Mx
1. Rx underlying cause
2. Rate control if sustained RVR
3. Ablation V node
MFAT
3 or more P wave morphologies
Rate > 100 bpm
N QRS
Irregular
Isoelectric baseline between P waves
COPD - RVH
Atrial Fibrillation Causes
Cardiac
IHD
Valvular disease
Cardiomyopathy
Pericarditis / Myocarditis
CVD - HTN, Obese,
ASD
Atrial myxoma
Non-Cardiac
Sepsis
Electrolyte disurbance
PE
Drug and alcohol intoxication
Thyrotoxicosis
Lung Cancer
AF - Rhythm Control vs Rate Control
RHYTHM
Lone AF w/ clear onset < 48 hrs
Young < 65yrs
Pt Preference
Significantly symptomatic
Assoc HF
HD unstable
No/few comorbidities
Unlikely to revert spontaneously - i.e. required DCCV before
RATE
Age > 65 yrs
Onset > 48 hrs
90% revert w/ Rx if < 48 hrs duration
50% revert > 48hrs
Presence of CCF
Previous episodes AF
Failed antiarrhythmic therapy
Structural cardiac lesions
Dilated LA
Secondary AF
DCCV for AF
AF - Chemical Reversion Strategies
HTN
3 classifications we care about:
1. Hypertensive emergency = BP > 180/110 +acute target-organ dysfunction (clinical or Ix)
2. Poorly controlled chronic HTN (no end organ dysfunction)
- Some drugs can elevate BP i.e. steroids, NSAIDs, stimunlants, decongestants, appetite suppressants
3. Newly elevated BP - not an ED diagnosis
Pathophysiology
● Macrocirculation
○ High SVR (due to peripheral arteriole back up from SNS and RAAS activation) increase LV mass
○ LVH - Diastolic dysfunction
○ Elevated LA end diastolic pressures
■ Acute SVR rise = Flash pulmonary edema
■ Chronic = LVH - leads to ischemia (outgrowing blood supply) and eventual thinning of myocardium
○ Thus end with big floppy bag of systolic dysfunction
● Microcirculation
○ Critical luminal narrowing - occlusion and ischemia
○ “Silent” ischemic episodes lead to primary cause of chronic end organ damage
○ Lumen thinning - aneurysm and rupture
■ Results in tissue edema, fibrinoid necrosis, and MAHA
Hypertensive emergencies
BP > 180/110 + and organ dysfunction
❏ Abrupt rise in BP overwhelms autoregulation = endothelial injury
❏ Post injury, a major vascular smooth muscle relaxant (NO) is decreased
❏ Further increase of SVR = downward spiral that maintains elevated BP
❏ Left unchecked, this leads to terminal arteriole dilation and rupture
BP >180/110 +
HA / Blurred vision
AMS / Seizures
Focal Neuro Deficits
Chest pain / SOB
Renal failure
Hypertensive Emergency Management Targets and Options
General principles for lowering BP rapidly in the ED:
1. Blood pressure should almost never be rapidly lowered (except in aortic dissection).
2. Lower pressure by no more than 25%, to avoid ischemia in organs auto-regulated to higher BP.
3. Therapies that correct the cause (e.g. phentolamine if the BP is elevated by catecholamines) will be most effective.
4. Monitor the symptoms to determine whether the BP has been adequately lowered.
BP Targets
Ischaemic Stroke <220/120
Ischaemic Stroke w/ thrombolysis >185/110
ICH <180/90
SAH <160/90
Pre-eclampsia < 140/90
Aortic DIssection BP <120/80 and HR 60
IV Antihypertensive Agents
Aortic Dissection Risk Factors
MAJOR
HTN
Congential Heart Disease
Aortic stenosis - bicuspid aortic valve, coarctation aorta
CT disease - Marfan’s, Ehlers-Danlos
OTHER
Iatrogenic - post-cardiac surgery, balloon dilatation for coarctation
Cocaine
Pregnancy
Inflammatory - Vasculitis - GCA, Takayasu
Weight lifting
Aortic Dissection CXR
Widened mediastinum (52-75%)
Dilatation aortic arch (31-47%)
Obliteration aortic knuckle
Double density of aorta (suggesting true and false lumen)
Localised prominence along aortic contour
Distortion L main bronchus
NGT / Tracheal devation to R
Calcium sign (>6mm betw/ intimal calcium and outer aortic wall
Pleural effusion L > R
Cardiomegaly
Changes in configuration oarta subsequent xrays (47%)
Aortic Dissection Complications
Consider Aortic dissection with
CP + CVA
CP + paralysis
CP + hoarseness (recurrent laryngeal nerve)
CP + limb ischemia
Aortic Dissection Classification
Stanford
Type A: 62% involves ascending aorta +/- descending
Surgery usually indicated
Type B: 38% Involves descending aorta (beyond Left subclavian artery only.
Medical Mx w/ BP control.
Older pts, heavy smokers w/ chronic lung disease w/ atherosclerosis and HTN.
DeBakey
1: Entire aorta affected
2: Confined to the ascending aorta
3: Descending aorta affected distal to subclavian artery
3a: thoracic aorta only
3b: abdominal aorta involved
Indications for Surgery Type B Dissection
Leaking or ruptured aorta
End organ ischaemia
Extension despite medical Mx
Refractory pain
Severe uncontrolled HTN
Aneurysm vs Pseudoaneurysm
Pseudoaneurysms, are abnormal outpouchings or dilatation of arteries which are bounded only by the tunica adventitia, the outermost layer of the arterial wall
True aneurysms, which are bounded by all three layers of the arterial wall.
Pseudoaneurysms typically occur when there is a breach in the vessel wall such that blood leaks through the inner wall but is contained by the adventitia or surrounding perivascular soft tissue.
Causes:
Iatrogenic - angiogram,
Trauma
Vasculitides
AMI - LV false aneurysm
Post-op AAA Repair Complications
Complications anytime post-op
● Infection - difficult to diagnose!
○ Graft contamination
○ Adjacent infectious spread
○ Hematogenous seeding
● Aortoenteric fistula (AEF)
○ Consider with GI bleeding + PMHx AAA surgery
● Pseudoaneurysm (anastomotic aneurysm)
○ Arise from the leaking anastomosis site
Delayed Complications:
1. Infection
2. Ischemic complications
a. Spinal cord ischemia
b. CVA
c. Extremity ischemia
d. Visceral ischemia (Celiac/SMA/Renal)
e. Post implantation syndrome (fever, leukocytosis and reactive inflammation, can get uni/bilateral reactive pleural effusions - SIRS to the max)
3. Aortoenteric fistula
4. Pseudoaneurysm (anastomotic aneurysm)
5. Chylous Ascites / Chylothorax
6. Endo Leak
i) Blood flow outside graft lumen - BUT contained within the aneurysm sac
ii) up tp 20% of patients who have had repair!
iii) Grade I-IV
Acute limb ischaemia
Acute limb threatening ischaemia
Aterial occlusion cause severe symptoms when there is no collateral circulation
Femoral 45% > Iliac 20% > Popliteal 10%
RF
Age > 60, M>F
Embolic - AF, IVDU
Thrombotic - HTN, DM, Hyperlipdaemia, smoking
Iatrogenic - recent arterial cannulation, Bier’s block
Trauma - endothelial injury
Symptoms / Signs
6 P’s - pain, pallor, pareasthesia, paralysis, perishingly cold, Pulseless
Cyanosis
Late signs - pain, tense swelling and tender muscle belly
> 12 hrs of symptoms leads to irreversible limb ischaemia
Ix
ABPI (>1.0 normal, <0.9 aterial Dx, 0.5-0.9 claudication, <0.5 rest pain)
Vascular USS
DSA, CTA, MRA
Mx
Analgesia
Heparin
Correct aggravating factors - dehydration, sepsis, arrhythmias, MI)
Urgent revascularisation
- Thrombus extraction
- Thrombo-aspiration
- Surgical thrombectomy
- +/- bypass grafting
ABPI
Ankle-Brachial Pressure Index
Highest Ankle systolic / Highest Brachial systolic
1.0-1.3 Normal
0.9 Mild Dx
0.5-0.8 Moderate Dx - Claudication
<0.4 Severe Dx - Rest Pain
Absolute contraindications Thrombolysis
Neuro
1. ICH ever
2. SOL
3. CVA, dementia, CNS damage w/in 1 yr
4. HI or brain surgery 6 months
Trauma
1. Major surgery, trauma or bleedin last 6 weeks
2. Traumatic CPR within 3 weeks
Haem
1. Internal bleeding last 6 weeks
2. Known bleeding disorder
Other
1. Suspected aortic dissection or pericarditis
Thrombolysis - Relative contraindications
CVS
1. Uncontrolled HTN 180/110
2. Infective endocarditis
3. Intra-cardiac thrombi
Neuro
1. TIA 6 months
2. Dementia
GI
1. Acute pancreatitis
2. Active PUD
3. Advanced liver disease
Resp
1. Cavitating TB
Vasc
1. Puncture non-compressible vessel 2 weeks
Bleeding risk
1. NOAC / warfarin
2. Previous thrombolysis
VT vs SVT
AICD indictaions
- VF or sudden cardiac death survivors
- VT-associated syncope not caused by MI or other correctable cause
- Risk of SCD - Long QT, HOCM, Brugada
- Cardiomyopathy
- Minimally symptomatic VT with EF <35%
- Dysrhythmia resistant to anti-arhythmics or if anti-arrhythmics contra-indicated
Prosthetic Heart Valves - Complications
Primary Valve Failure
1. Acute - tearing or broken component - sudden death, APO, MI
2. Chronic - calcification or thrombus - HF, unstable angina, haemolytic anaemia
Mx
Major haemodynic instability -> valve replacement
Afterload reduction - GTN
Inotropic support - dobutamine
IABP
Thromboembolism
Caged > single leaflet > bileaflet
15% within 5 yrs implant, greatest risk first 3 months
Mitral > others
Subtherpaeutic anti-coagulation
Metallic Valve thrombosis
Mx
Anti-coagulate
Thrombolytic therapy
Surgical replacement
Endocarditis
Haemolytic Anaemia
MAHA - low grade 70%, severe 5%
Complications of Anti-coagulation
Bleeding
Skin necrosis
Atheromatous Cholesterol embolism
Recurrent thrombosis
Teratogenic effects
Valvular HD Table
Valvular Disease Examination Signs
Infective endocarditis Complications
Risk Factors
Prosthetic valves - 30%
Worldwide is Rh Fever
IVDU
Organisms
Staph no most common cause
Strep species - viridans (dental), bovis
Enterococcus (older esp > 60yrs)
Predisposition
Structural - Rh HD, MV prolapse, Prosthetic valves, CHD, Cardiomyopathy, Previous IE
IDVU - mostly RHS lesions
FB - PPM, CVC
Immunosuppression / DM
Poor dental hygiene
Complications
Destruction of valve + acute severe HF
Conduction Abnormality
Septic emboli
- Unexplained CVA
- Septic arthritis
- Organ abscess - CNS, lung, hepatic, splenic
- Organ infarction
- Generalised sepsis
Immune
- glomerulonepritis
RBBB
QRS >0.12s
Slurred S wave I, aVL, V5, and V6 (Depolarization moving away from these leads)
RSR’ in V1 and V2 with R’ > R (Depolarization moving toward these leads)
Causes
1. IHD
2. RVH
3. PE
4. Cardiomoypathy
5. RHD
6. CHD
7. Myocarditis
8. Lenegre-Lev Disease (degenerative fibrosis)
DDx
Brugada syndrome
