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
Strategies to Manage Heart Failure
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 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
3 or more P wave morphologies
Rate > 100 bpm
N QRS
Irregular
Isoelectric baseline between P waves
COPD - RVH
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 Complications
Consider Aortic dissection with
CP + CVA
CP + paralysis
CP + hoarseness (recurrent laryngeal nerve)
CP + limb ischemia
VT vs SVT
Valvular HD Table
Valvular Disease Examination Signs
