Download Cardiovascular Expert Questions

Cardiovascular expert questions
Approach to a patient with chest pain
About 5% of ED visits are due to chest pain, but accurate diagnosis of the cause remains a challenge.
Acute chest pain refers to
1. recent onset, typically less than 24 h, that causes the patient to seek prompt medical attention,
2. location described on the anterior thorax, and
3. A noxious uncomfortable sensation distressing to the patient.
In most cases, history, examination, investigation and management of chest pain may occur simultaneously
depending on the severity of the suspected cause and the patient’s clinical status.
History taking in patient with chest pain:
 Onset – acute, subacute, acute on chronic, chronic, recurrent.
 Duration – hours, days, months or years.
 Progress – crescendo, decrescendo, intermittent, recurrent.
 Site/ location – right or left, superior or inferior, substernal or any other.
 Description – burning, pressure, stabbing, crushing, dull, throbbing, sharp or constricting.
 Radiation – shoulders, neck, jaw, face, abdomen, arms or back.
 Aggravating or relieving factors – exertion, movement, respiration, coughing, lying or standing,
bending forwards.
 Associated symptoms – shortness of breath, palpitations, nausea, syncope, headache, vomiting,
coughing, fever or leg pains.
 Assessment of risk factors –
o Coronary artery disease – cigarette smoking, diabetes, hypertension, hypercholesterolemia and
family history.
o Aortic dissection – middle aged, male gender, hypertension and Marfan’s syndrome
o Pulmonary embolism – hypercoagulable states, malignancy, recent travel, immobilization or
surgery, OCP use, past DVT.
 AMPLE history – Allergy, Medications, Past medical history, Last meal, and Event
Descriptions of chest pain – classification
 Chest wall pain – somatic pain, sharp in quality, can be precisely localized by a fingertip and
reproducible by direct palpation and/or chest wall movement during stretching or twisting.
 Pleuritic chest pain – somatic pain, sharp in quality, distinctly worsened by breathing or coughing
 Visceral pain – poorly localized, described as aching or heaviness or discomfort
Physical examination
 General appearance of the patient is noted – pale, diaphoretic, anxious, discomfort and cyanosis
 Vital signs and weight are measured and body mass index calculated
 Pulses measured in all extremities and BP measured in both arms
 Neck –
o venous distension and hepatojugular reflux
o palpate carotid pulses, lymphadenopathy or thyroid
o carotid auscultated for bruit
o JVP wave forms observed for abnormalities
 Lungs – checked for symmetry of breath sounds, signs of congestion, consolidation, rubs and effusion
 Cardiac examination
o Apex beat location, other pulsations and heaves
o Auscultation for heart sounds and murmurs
 Chest examined for skin lesions s/o trauma, rashes e.g. herpes zoster and palpated for crepitus and
tenderness
 Abdomen – palpated for tenderness, organomegaly, masses or tenderness
 Legs – examined for pulses, adequacy of perfusion, edema, varicose veins and signs of DVT
 Skin and mucous membranes – examined for Jaundice, pallor, rashes and lesions, IV track marks etc.
Investigations
Bedside

ECG –
o
o
o
o
o
single and serial
look for rate, rhythm disturbances
PR, QRS, QT interval disturbances
PR segment elevations of depressions
ST-T segment changes and T-wave abnormalities
Useful in diagnosis but not exclusion of myocardial ischemia, pulmonary embolism,
pericarditis, myocarditis etc
 BSL – in diabetics as an ancillary investigation as cause/effect
 Arterial blood gases – to assess severity of hemodyanimc and metabolic compromise, rarely diagnostic
 2D-ECHO examination by emergency personnel – pericardial effusion, tamponade, right ventricular
load, wall motion abnormalities, aortic dissection(rarely), cardiac filling and assessment of cardiac
function if feasible
Laboratory
 FBC – anemia, leucocytosis
 EUC – electrolyte disturbance as cause/ effect
 Cardiac markers – CK, troponin I/T
 Serum amylase/lipase
 LFT
 Thyroid function tests
 Inflammatory markers – CRP, ESR – myositis, myocarditis etc
 D-dimer –in patients with low and medium probability of PE
Radiological
 Chest x-ray – departmental /formal or mobile bedside – depending on clinical status of patient – to
determine cause (pneumothorax, rib fractures) or effect (heart failure)
 CTPA and V/Q scan – to rule out PE in d-dimer positive patients with low/medium probability or high
clinical suspicion/ probability
 Formal 2D-ECHO
 Cardiac catheterization and angiography
 Chest CT with contrast – for aortic or major vessel abnormalities
 Ultrasound abdomen – liver causes
 Doppler ultrasound of lower limbs to rule out DVT
Ischemic heart disease and Myocardial Infarction
Ischemic heart disease is a leading cause of death among adults in Australia. Atherosclerotic disease of the
coronary arteries accounts for vast majority of patients with ischemic heart disease.
Ischemic heart disease represents a spectrum from chronic stable angina to acute myocardial
infarction (AMI).
Canadian Cardiovascular Society Classification of Angina
Class I Angina occurs only with strenuous, rapid, or prolonged exertion. Ordinary physical
activity does not cause angina.
Class
II
Slight limitation of ordinary activity. Angina occurs with climbing stairs rapidly,
walking uphill, walking after meals, in cold, in wind, or under emotional stress.
Class
III
Marked limitations of ordinary physical activity. Angina occurs on walking 1–2 level
blocks or climbing one flight of stairs at usual pace.
Class
IV
Inability to carry on physical activity without discomfort. Anginal symptoms may be
present at rest.
Principal Presentations of Unstable Angina
Rest angina
Angina occurring at rest and usually prolonged >20 min occurring within a
week of presentation
New-onset
angina
Angina of at least CCSC III severity with onset within 2 mo of presentation
Increasing
angina
Previously diagnosed angina that is distinctly more frequent, longer in
duration, or lower in threshold (increased by at least one CCSC class to at least
CCSC III severity).
Short-Term Risk of Death or Nonfatal Myocardial Infarction by Risk Stratification in Patients
with Unstable Angina
High Risk
Intermediate Risk
At least one of the following features must be No high-risk feature but must have one of the
present
following
Prolonged ongoing (>20 min) rest pain
Prolonged (>20 min) rest angina, now
resolved, with moderate or high likelihood of
CAD
Pulmonary edema, most likely related to
Rest angina (>20 min) not promptly
ischemia
relieved with rest or sublingual nitroglycerine
Angina at rest with dynamic ST changes ≥1
Nocturnal angina
mm
Angina with new or worsening MR murmur
Angina with dynamic T-wave changes
Angina with S3 or new or worsening rales
New-onset CCSC III or IV angina in the
past 2 wk with moderate or high likelihood
of CAD
Angina with hypotension
Pathologic Q waves or resting ST
depression ≤1 mm in multiple-lead groups
(anterior, inferior, and lateral)
Age >65 y
Acute Coronary Syndrome (ACS) is a term used to describe patients who present with acute
chest pain and other symptoms of myocardial ischemia, often with diagnostic or suggestive
electrocardiographic changes of myocardial ischemia. ACS is a useful concept because the triage,
assessment, and initial management of UA and AMI are similar.
Anatomy of the Coronary arterial system
 Left coronary artery (LCA)– arises from the ascending aorta in the left sinus of the aortic
valve →courses through atrioventricular sulcus on the left side → divides into left
circumflex and left anterior descending branch
o Left anterior descending branch(LAD) → courses anterior aspect of heart around
inferior margin → main blood supply to anterior and septal regions of heart →
anastomoses with posterior diagonal branch of RCA
o Left circumflex branch (LCX) → continues around AV sulcus → supplies blood to
some part of the anterior wall and large part of the lateral wall →anastomoses
with RCA
 Right coronary artery (RCA) – arises from the right sinus of the aortic valve → runs in the
AV sulcus between RA and RV → gives off marginal branch and terminates as right
posterior descending artery → supplies right side of the heart and some parts of inferior
aspect of left ventricle.
 AV conduction system receives blood supply from the AV branch of RCA and the septal
perforating branch of the LAD
 Right bunde branch and left posterior division obtain dual blood flow from LAD and RCA
Clinical features
History
 Chest pain – severity, location, radiation, duration and quality
 Associated symptoms – nausea, vomiting, diaphoresis, dyspnea, lightheadedness, syncope
and palpitation
 AMPLE history to be taken
 Cardiac risk factors are modestly predictive of CAD in asymptomatic patients. In ED patients
with CP, cardiac risk factors are poor predictors fro MI or other ACS.
 Traditional risk factors such as HT, DM, tobacco use, DM, family h/o CAD at young age and
hypercholesterolemia are not applicable to female patients. In male patient only DM and
family history are weakly predictive
Physical examination
 Highly variable from normal examination to overt features of heart failure may be present
 S1S2 may be diminished due to poor contractility. S3 present in 15-20% of patients with
AMI.
 New onset systolic murmur may signify papillary muscle dysfunction, a flail leaflet of mitral
valve with resultanat MR or a VSD
 Presence of rales, with or without S3 gallop s/o LV dysfunction and left sided HF
 Jugular venous distension, hepatojugular reflux and peripheral edema s/o right sided CCF.
Investigations
Electrocardiography
Published consensus guidelines establish a goal that the initial 12-lead ECG be obtained and
integrated within 10 min of presentation for patients with acute chest pain or other symptoms
suggestive of myocardial ischemia.
Although the ECG is the best immediately available test in the ED, it has relatively low sensitivity for
detection of AMI. The ST segment is elevated on the initial ECG in approximately 50 percent of
patients; i.e., half of the patients who present to the ED with AMI will not have diagnostic STsegment changes on the initial ECG. Most other AMI patients without diagnostic ST-segment
elevation will have ST-segment depression and/or T-wave inversions, and only 1 to 5 percent of
patients with AMI have an entirely normal initial ECG.
Electrocardiographic Criteria for Acute Myocardial Infarction
ST-segment elevations in the distributions shown suggest acute transmural injury. ST-segment
depressions in these distributions suggest subendocardial ischemia.
Location
Anteroseptal
Anterior
Anterolateral
Lateral
Inferior
Inferolateral
True posterior
Right
ventricular
Electrocardiographic findings
QS deflections in V1, V2, V3, and possibly V4
rS deflection in V1 with Q waves in V2–V4 or decrease in amplitude of
initial R waves in V1–V4
Q waves in V4–V6, I, and aVL
Q waves in I and aVL
Q waves in II, III, and aVF
Q waves in II, III, aVF, and V5 and V6
Initial R waves in V1 and V2 >0.04 s and R/S ratio ≥1
Q waves in II, III, and aVF and ST elevation in right-side V4
In case of patient with underlying left bundle branch block , the following three ST-segment patterns
are indicative of AMI (Sgarbossa criteria):
1. ST-elevation 1mm or greater and concordant with the QRS complex
2. ST – depression 1mm or more in leads V1, V2 or V3 and
3. ST-segment elevation ≥ 5mm and discordant with the QRS complex
Serum markers of myocardial injury
ST elevation in the absence of myocardial infarction
See answer in Investigation Expert questions
I Ex
pg 7
Management of hypertensive emergencies
Dis EX
A hypertensive emergency is a condition in which elevated blood pressure results in target organ
damage. Accelerated hypertension is defined as a recent significant increase over baseline blood
pressure that is associated with target organ damage. Hypertensive urgency is defined as severely
elevated blood pressure (sys>220, dias>120 mmhg) with no evidence of target organ damage.
Indications for urgent control of hypertension
 Hypertensive encephalopathy
 Malignant hypertension
 Pre-eclampsia
 Stimulant toxicity
 Acute pulmonary edema
 Ischemic chest pain
 Aortic dissection
Hypertensive encephalopathy and Malignant hypertension
HTE is an uncommon hypertensive emergency resulting from abrupt, sustained rise of BP that
exceeds the limits of cerebral autoregulation.
 MAP over 160mmhg may not be controlled by autoregulation
 Vasospasm with ischemia and increased vascular permeability occurs
 Cerebral edema and hemorrhages eventuate
Assessment
History
 Severe headache common
 Vomiting, drowsiness and confusion
 Seizures and blindness may follow
Examination
 Severe hypertension
 Confusion and altered level of consciousness
 Papilledema and hypertensive retinopathy
 Focal neurological deficit may be present
Differential diagnoses
 Acute renal failure
 Aortic coarctation
 Aortic dissection
 Hyperthyroidism
 Pheochromocytoma
 Intracranial hemmorhage
 Renal artery stenosis
Investigations
Bedside
 BSL
 ECG – to assess extent of hypertensive strain or ischemia, infarction, electrolyte
abnormalities and drug toxicity
 CXR-mobile – features of overt CCF may be present

Urine examination – dipstick examination may reveal significant proteinuria, microscopic
hematuria and red cell or hyaline casts.
Laboratory investigations
 FBC – to rule out other concomitant diagnoses
 EUC – to rule out significant electrolyte abnormalities and monitor development of renal
failure
 Cardiac enzymes – to rule out myocardial damage from severe strain
 Coagulation profile
 Other investigations – as indicated e.g. TSH, 24hr urine collection for VMA and
catecholamines
Radiological investigations
 CT brain – in c/o severe headache and focal neurological deficit to rule out significant ICH or
Sol as cause for HT or effect of uncontrolled HT
 Renal ultrasound- if secondary cause for HT sought or later to assess HT damage
 2D-echocardiography – to detect wall thickness, hypertrophy, motion abnormalities and
overall systolic function
Management
Supportive care and monitoring
 Attention to ABC as indicated
 Manage in resuscitation bay with facilities for invasive monitoring of arterial BP, central
venous pressures and access for medications
Definitive management
Goals of therapy
 Rapid reduction of BP to more physiologic levels for patient (not normotensive)
 Maintenance of vital organ perfusion and damage reduction
 Initial goal to reduce BP by approximately 25% in first 24-48hrs
 Volume repletion – depletion may be significant and sodium and volume expansion with NS
must be considered
Medications
No trials exist comparing the efficacy of various agents in treatment of hypertensive emergencies.
Drugs are chosen based on their rapidity of action, ease of use, special situations and convention.
Drugs used in management of HTE may be divided into
 Vasodilators – nitroprusside, hydralazine(indicated in pregnancy)
 Calcium channel blockers – verapamil or diltiazem –rarely used in Australia
 Beta-adrenergic blockers – labetalol, esmolol, metoprolol
 Alpha-adrenergic blockers – phentolamine (indicated in pheochromocytoma)
Vasodilators
Nitroprusside
 Acts by interacting with nitric oxide synthase causing vascular smooth muscle relaxation →
vasodilation and inotropy
 Nearly immediate onset of action and short ½ life –minutes
 Administration requires IV infusion pump, reflective covering on giving set and arterial line
for close monitoring of arterial BP
 Dosing – 0.25 – 10 µg/kg/min
 Contraindicated in hypersensitivity, subaortic stenosis, HOCM, atrial flutter and fibrillation,
CNS trauma
 Risk of cyanide toxicity →
o venous hypoxemia, acidosis, mental status changes and death especially if renal and
liver impairment
o thiocyanate levels >60 mg/l → neurotoxic life threatening when reaches >200mg/L
 methemogobulinemia, headache, nausea and vomiting possible
 cease use if MAP falls below 70mmhg
Hydralazine
 decreases systemic resistance through direct vasodilation of arterioles
 good profile for use in pregnancy, since it improves uterine blood flow
 increases ICP
 dosing - 10 -40 mg IV repeat q15-30mins, infuse at 1-1.5 µg/kg/min
 MAOIs and b-blockers may increase toxicity
 Contraindications – hypersensitivity, mitral valve disease
 Caution in suspected CAH and cerebrovascular disease
Beta-adrenergic blockers
Labetalol
 Blocks β1, β2 and α1 adrenergic sites → ↓ BP
 Close monitoring necessary as hypotension and heart block can occur
 Start PO therapy ASAP with initial IV therapy
 Dosing – 20mg IV over 2min, followed by 40-80mg q10mins <300mg dose/day
 Good profile when used with nitroglycerin, since it abolishes the tachycardia induced by GTN
 Contraindications – cardiogenic shock, bradycardia, AV block, uncompensated CCF,
pulmonary edema and airway limitation or disease
Esmolol
 Excellent for use in those with CAL, LV dysfunction and/or peripheral vascular disease
 Short ½ life of 8mins allows for titration
 Dosing - 500µg/kg/min loading dose for 1min followed by 50-300µg/kg/min IV infusion
 Multiple interactions
 Uncompensated congestive heart failure, bradycardia, cardiogenic shock, AV conduction
abnormalities
 Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical
signs of hyperthyroidism;
 symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is
abruptly withdrawn
 needs large amounts of fluid to run infusion which may not be feasible
 do not use solely or before alpha-blockade in c/o suspicion of pheochromocytoma
Alpha-adrenergic blockers
Phentolamine
 Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and
norepinephrine action, reducing hypertension that results from catecholamine effects on
the alpha-receptors.
 Drug of choice in pheochromocytoma crisis
 Useful in MAOI associated HT crisis, but less titrable as compared to nitroprusside
 Ethanol increases risk for toxicity
 Cerebrovascular and coronary occlusions may occur during therapy
Follow up and disposition
 Patients with hypertensive emergencies should be admitted to the hospital for close
hemodynamic monitoring and administration of IV antihypertensive medications.
 Secondary causes of hypertension should be investigated.
 Oral medications should be initiated as soon as possible in order to ease transition to an
outpatient setting.
Cardiac arrhythmias
Mechanisms of arrhythmias
Two basic mechanisms:
 Increased or decreased automaticity
 Altered conduction
Re-entrant arrhythmias
 Due to reduced conduction of electrical impulses in the cardiac system
 Results in an impulse being able to repeatedly pass retrogradely up and then down the
normal conduction system or through an alternative pathway
Cause of arrhythmias
Ischemic heart disease
 Most common cause of serious arrhythmias presenting to ED
Congenital heart disease
 Valvular and myocardial defects
 Hypertrophic cardiomyopathy
 Hypertensive heart disease
Structural heart disease
 Cardiomyopathies
 Acquired valvular defects
 HT cardiomyopathy
Electrolyte disturbance
 Hyper- / hypo – kalemia
 Hypomagnesemia
Metabolic
 Hypoxia
 Hypercarbia
 Hypothermia
 Hyperthyroidism
Drugs
 Antiarrhythmic agents
 Cocaine
 Amphetamines
 TCA
 Phenothiazines
 Na-channel blocking agents
 K-channel blocking agents
Trauma
 Commotion cordis – VF precipitated by direct blunt chest trauma
Classification
Tachycardias
Broad complex
Narrow complex
Regular
 SVT
 Sinus tachycardia
 Atrial flutter
Irregular
 Atrial fibrillation
 Sinus rhythm with
multiple ectopic
beats
Regular
 VT
 Sinus tachycardia
with conduction
defect
 SVT with aberrant
conduction
Irregular
 A fib with aberrant
conduction
 WPW and A Fib
 VF
Management options in Arrhythmias
No management required
 Where resuscitation is inappropriate
 Preferred option in minor transient arrhythmias
o Sinus arrhythmia
o Atrial ectopic beats
o Ventricular ectopics with no R on T phenomenon
o Accelerated idioventricular rhythm
o Arrhythmias associated with hypothermia
o Mobitz I second degree heart block
o Transient arrhythmia during vomiting
Non-pharmacological measures
Supraventricular arrhythmias
 Intention to increase vagal tone
o Valsalva manoeuvre
o Carotid sinus massage – use with caution in elderly, check for bruit.
o Diving reflex – effective in children
o Ocular massage – generally avoided
Ventricular arrhythmias
 Precordial thump – indicated in monitored pulseless VT or unconscious patient at scene
Pharmacological measures
Pharmacological measures are usually used for all hemodynamically stable arrhythmias requiring
treatment.
Electrical
Cardioversion
 Usually used for
o Hemodynamically unstable tachyarrhythmias
o Drug resistant tachyarrhythmias in stable patients
o AF with rapid ventricular response onset <72hrs or after anticoagulation
 Types
o R wave synchronised or
o Unsynchronised
Electrical pacing
 Types
o Transcutaneous
o Transvenous
o Overdrive
 Usually reserved for drug resistant bradycardias and tachycardias or temporizing measure
until definitive therapy
Supraventricular tachycardia
SVT is a common arrhythmia in patients with or without structural or ischemic heart disease. It is not
usually associated with major hemodynamic instability.
Causes of SVT
 AV-nodal re-entry
o 60% of cases
o Slow and fast pathways
o Localised to nodal or peri-nodal pathways
 Accessory pathways
o 30% of cases
 SA/Atrial
o 10% of cases
Assessment
History
 Symptoms
o Palpitations
o Chest tightness
o Symptoms of associated causes or complications – e.g. hyperthyroidism, syncope
 Chest tightness
o Common
o Dose not usually indicate myocardial ischemia
o Unless onset prior to palpitations, recurs after reversion or if associated with ST
segment and T wave changes
Causes
 Idiopathic
 Structural heart disease
 Thyrotoxicosis
 Occurs in 2% of patients with AMI
Precipitants
 Alcohol
 Caffeine
 Stimulants
 Ischemia
 Hypokalemia
 Pregnancy
 Cannabis
Complications
 Syncope
 Heart failure
Examination
 Look for signs of precipitants
 Careful re-examination of heart after reversion to look for structural abnormalities – e.g.
murmurs
Investigations
Bedside
 ECG
o Pre- and post-reversion
o Narrow complex regular tachycardia
o Rarely broad complex if underlying conduction disturbance present
o Rate usually 150 – 180 bpm, >220bpm s/o accessory pathway
o
St-depression poor predictor of ischemia and should be investigated with EST post
reversion if indicated
o ST-T changes may persist after reversion
 Other investigations – if indicated
o No other investigation required in young patient with uncomplicated recurrent
idiopathic SVT
o CXR
o EUC
o FBE
o TFT
o Cardiac markers
o BSL
Management
Non-pharmacological
 Vagal manoeuvres should be tried first
o Valsalva manoeuvre
o Carotid sinus massage
o Dive reflex
Pharmacological
 Adenosine –
o incremental doses of 3mg, 6mg, 12mg IV tried through a large bore cannula as
proximal as possible, usually cubital fossa.
o Given rapidly as bolus followed by 20mls of NS
o Adverse effects in 30% of patients – dyspnea, chest pain, anxiety, bronchospasm,
bradycardia, ventricular ectopy, non-sustained monomorphic VT
o Effects usually last only few seconds
o Reverts 90% of patients, 15% recur after first dose
 Verapamil –
o May be tried if no significant hypotension and narrow QRS
o Contraindicated in children <1yr
o 80% reversion with 5mg IV, 90% with 10mg IV
o Pre-treatment with 5ml calcium gluconate 10% decreases hypotensive effects
 Flecainide
 Beta-blockers – if thyrotoxicosis present
Prophylaxis
 Flecainide
 Digoxin and verapamil in combination as verapamil needs large doses
 Radio frequency ablation if accessory pathway present
 Ablation may be tried for nodal re-entry SVT with 1-2% risk of CHB
Wolf Parkinson White syndrome (WPW)
About 1% of population have accessory pathways, only 50% of those ever develop symptoms. Men
are more commonly symptomatic then women.
Features
 Supraventricular tachyarrhythmias
 ECG
o PR <0.12s
o Delta waves on ECG – early depolarisation of free ventricular wall from accessory
pathway
o May have pseudo-infarction pattern
Accessory pathway location
 Left lateral (type C) – 60% of cases (+ve V1V2)
 Left posteroseptal, right posteroseptal or anteroseptal – 30% of cases
 Right lateral (type B) – 10% of case (-ve V1V2)
Direction of electrical conduction
 Orthodromic –
o Through normal conduction pathway down the ventricles and return conduction to
atria via accessory pathway
o Present in 95% patients with SVT with accessory pathway
 Antidromic –
o Downward conduction via accessory pathway and return conduction to atria via AV
node
o Present in 5% of patients with accessory pathways
o Causes AF and irregular widened complexes
Management
SVT and WPW –
 Verapamil contraindicated if antidromic conduction present due to risk of precipitating VF
 Procainamide or flecainide usually effective
AF and WPW
 Verapamil/ digoxin enhance conduction through accessory pathway
 Adenosine – unlikely benfit and may increase ventricular response
 Flecainide
o Drug of choice
o Slows conduction in accessory pathways
o Dose: 150mg IV over 30mins (2mg/kg)
Ventricular arrhythmias
Ventricular tachycardia
Pathophysiology
 Usually re-entrant
o Most common in first 30mins following AMI
o May occur up to 3days after AMI
 Increased automaticity
o >12hrs post-MI
o Damage to epicardium produces denervation and increased sensitivity of distal
myocardium to catecholamines
o Endocardial lesions interrupt vagal fibres causing unopposed sympathetic activity
Types
Monomorphic
 QRS morphology same for all complexes
 More common in structural/ ischemic heart disease
 Right ventricular outflow tachycardia
o LBBB pattern
o RAD
o Responsive to beta blockers and CCB
Polymorphic
 Beat to beat variations in QRS morphology
 Torsades des pointes is a subclass based on QT interval prolongation
 Mostly associated with toxicities
Assessment
Examination
 Hypotension commonly present but not universal, so not useful in diagnosis
 Canon A waves in JVP – due to AV dissociation
 Variable intensity first heart sound, unchanged 2nd heart sound
ECG criteria
 Aim: to differentiate VT(common) from SVT with aberrant conduction
o Absent RS complex in any precordial lead approximately 100% specific for VT
o RS interval – b/w onset of R and deepest part of S if >100ms <95% specific for VT
o QRS width – usually >140ms in 95% cases, <110ms in 5% cases
o AV dissociation – notching of QRS complex at different positions, 40% cases, >75%
specific
o
o
Fusion beats – both impulse reach AV node at same time causing fusion of narrow
QRS complex with wide ventricular complex – indicates AV dissociation
Capture beats – normal QRS complex amongst broad complexes – indicates AV
dissociation
o
Concordanace of QRS vectors in precordial leads i.e. all positive or all negative – 20%
sensitivity and 90%specificity
o VT axis usually -90 to and ±180 degrees i.e. LAD or RAD make VT more likely
Historical criteria
 2 or more of following factors indicate 95% probability of VT
o Age >35y
o Active angina
o Previous AMI
Management
Regular broad complex
tachycardia
SVT with aberrancy
Try Adenosine
Ventricular tachycardia
Unstable/ symptomatic
Synchronised cardioversion


Stable
Amiodarone recommended
150mg IV over 10m q10mins
up to 2.2g IV/24h
Pulseless VT should be treated as VF – unsynchronised cardiversion if synchronised does not
work
If diagnosis in doubt, consider and treat as VT especially if unstable – if stable adenosine may
be tried but unlikely to cause any effect
Electrical cardioversion
 Emergent if
o Hypotensive
o Severe chest pain/discomfort
o Florid APO
 Elective in other cases
 Successful in 90% cases
 Biphasic 50J or monophasic 90J doubling each time
Overdrive pacing
Pharmacological
 Lignocaine
o More effective in ischemic VT
o 100mg bolus (20% effective), +50mg bolus (+10%)
o Non-effective in non-ischemic VT and thus avoided
 Procainamide
o Most effective agent but negative inotrope which limits its use
o Effective in 75% of case
o 100mg bolus, followed by 50mg/min until 500mg or reversal
 Sotalol
o 1.5mg/kg over 5min
o 65% effective and only used if hemodynamically stable and QTc normal
 Amiodarone
o Least cardiac depressive, promoted by ACC/AHA
o Dosing as above, 30% effective with bolus
Special circumstances
 Digitalis toxicity – phenytoin used to be suggested but digoxin FAB
 Chloral hydrate toxicity – beta-blockers
 Na channel blockers – bicarbonate
 Hypothermia – rapid rewarming, bretylium and magnesium
 Stimulants – alpha and beta-blockers
 Correct electrolyte abnormalities – Hypokalemia/ hypomagnesemia
Prophylaxis
 Poor LV function – Amiodarone
 Good LV function – sotalol
 Radiofrequency ablation
 Automatic implantable defibrillator
Torsades De Pointes and prolonged QT interval
ECG features
 Cyclical multiform ventricular ectopic complexes that vary about an isoelectric axis due to 2
ventricular ectopic foci – twisting of the point
 Usual rate 150-300/min, QT>0.6s or QTc>0.4s
 Other features
o Ectopy
o Bradycardia
o High grade AV block
o Long initiation sequence
 Late PVC
 Prolonged coupling interval
 R on T phenomenon
Risk factors
 Prolonged QTc
 Female gender
 Bradycardia
 Recent reversion of AF with QT
prolonging drug
 CCF
 Digitalis therapy
 Rapid administration of QT
 Severe hypomagnesemia
prolonging drug e.g. sotalol
Causes of prolonged QT
Electrolyte abnormalities
Heart disease
 Hypomagnesemia
 Cardiomyopathy
 Hypocalcemia
 Severe CCF
 Hypokalemia
 Myocardial ischemia
 CHB
 Hypertension
Poisoning
Congenital
 Type I and III arrhythmics
 Lange Jervil Nielsen syndrome
o Associated deafness
 Phenothiazines – haloperidol,
o Autosomal recessive
thioridazine
 Romano Ward syndrome
 TVA
o No deafness
 Carbamazepine
o Autosomal dominant
 Lithium
Other
 Organophospahates
 Hypothyroidsm
 Cisapride
 SAH
 Terfenadine when used with
erythromycin
 Quinolones
Management
Avoid class I antiarrhythmics if any doubt about type of VT – especially torsades – catastrophic
 K replacement to 4.5 – 5.5 mmol/L
 Magnesium sulphate 2g bolus
 Isoprenaline – drug overdrive pacing
 Atropine if OPC poisoning is the cause
 Calcium
 Beta blockers/ sedation/ sympathectomy for congenital causes
 Alkalinisation with bicarbonate if Na-channel blocker cause
Bradycardia
See heart block question in cardiovascular past questions
Antiarrhythmic drugs
Vaughan – Williams classification of antiarrhythmic drugs
Class
I
IA
IB
IC
II
Mechanism
Na channel blockers
Prolong action potential
Shorten action potential
No effect on action potential
Beta-blockers
III
IV
V
K channel blockers
Ca channel blockers
Other mechanisms
Drugs
Quinidine, procainamide
Lidocaine, phenytoin
Flecainide
Metoprolol, esmolol,
propranolol
Amiodarone, Sotalol
Verapamil, diltiazem
Digoxin, Adenosine
Class I drugs:
Class 1a: atrial fibrillation, flutter, SVT and VT
Drug
Quinidine
Comment
Moderate anticholinergic
Procainamide
Weakly anticholinergic,
Side effects
Conchonism (blurred vision,
tinnitus, headache, psychosis),
cramping and nausea, enhances
digoxin toxicity
Lupus like syndrome in 25-30%
Class 1b: VT
Lidocaine
relatively short ½ life
of patients
IV only: VT and PVCs
Good efficacy in ischemic
myocardium, nil otherwise
Debatable
Digoxin-induced arrhythmias
Phenytoin
Class 1c: life threatening SVT and VT
SVT
Flecainide
Can induce serious VT
Class II – beta-blockers
Class III – potassium channel blockers

Prolong QT interval and increase ERP, thus suppressing tachyarrhythmias due to re-entry

Increased risk of Torsades de pointes with QT prolongation
Drug
Amiodarone
Therapeutic uses
SVT and VT
Sotalol
Ventricular
arrhythmias, atrial
flutter and
fibrillation
Comments
Very long ½ life (25-60days), class I,II,III & IV actions
Potentially serious side effects – pulmonary fibrosis, thyroid
abnormalities
Also has class II activity
Hypotension, bradycardia can be severe, CHB may occur
especially AF reverts to sinus rhythm
Class IV drugs – calcium channel blockers
Role for pre-hospital thrombolysis in STEMI
Pre-hospital thrombolysis has proven clinical benefits in the management of acute myocardial infarction (MI).
If the targets for administering thrombolysis, in particular call-to-needle time, are to be met, then it seems
likely that its use will be more widespread. With appropriate training and support, paramedics can
competently perform 12-lead electrocardiograms (ECGs) and administer thrombolysis. Cardiologists should be
prepared to undertake paramedic training and play a central role in the development of protocols and
pathways for the administration of pre-hospital thrombolytic therapy.
Pros
Thrombolytic treatment for acute MI is of greatest
benefit in reducing mortality by 20-50%, if it is
administered within the first hour of symptom onset.
Pre-hospital thrombolysis should be considered
where local 'call-to-hospital' times are likely to
exceed 30 minutes so that a 'call-to-needle' target
time of less than 60 minutes could be achieved.
A recent meta-analysis of randomised, controlled
trials of pre-hospital thrombolysis (delivered by
paramedics, general practitioners or mobile ICUs)
showed that pre-hospital thrombolysis can reduce
the relative risk of short-term, all-cause hospital
mortality by 17% compared with in-hospital
thrombolysis
A prospective controlled study undertaken by
Derbyshire Ambulance Trust in 1997 concluded that
trained paramedics can reliably diagnose MI by 12lead ECG and reduce 'door-to-needle' time by
admitting directly to a coronary care unit. These
findings were reinforced by a 1998 study, which
concluded that 88% of paramedic-delivered patients
with suspected MI subsequently had the diagnosis
confirmed.
It has been demonstrated that general practitioners
can safely carry out pre-hospital thrombolysis.
Cons
Increased need for cardiologist involvement in
paramedic training and clinical governance
arrangements for networks
Logistical issues:
 Special capability ambulances
 Drug stocking in ambulances
 Increased paramedic training and
responsibility
Protocols for paramedics will need to be sufficiently
clear to effectively replace this clinical judgement.
They will need to include a full set of operating
procedures for the recording of ECGs, the
transmission of ECG data via telemetry and the
administration of thrombolytics (with advice on how
to obtain informed consent).
Interest, motivation and availability for this role
appears largely limited to those working in isolated,
rural areas. While there is clearly a place for general
practitioner-led thrombolysis in such areas,
ambulance paramedics have emerged as the best
placed providers of pre-hospital thrombolysis on a
wider basis, since they offer rapidity of response,
access to a defibrillator and communication with the
hospital.
The NICE appraisal points out the practical difficulties
of giving controlled-rate infusions in pre-hospital
settings and, for streptokinase, concerns about
higher rates of allergic reactions and hypotension
which are more difficult to manage away from
hospital. For pre-hospital use, NICE therefore
recommends the use of a bolus thrombolytic –
either reteplase or tenecteplase. There are
differences in administration of these two drugs.
Tenecteplase requires a single bolus but is weight
adjusted – this may cause problems for paramedics.
Reteplase does not require this dosage adjustment
but has to be given as two separate intravenous
injections, 30 minutes apart.