Cardiology Flashcards
How do you approach reading an EKG?
- Rate
- Rhythm
- Axis
- Interval
- Waveform
- Summary
What are the key waveforms on the EKG?
What type of rhythm?
Sinus tachycardia with hidden p waves (camel hump)
What type of rhythm?
Sinus tachycardia, 150 bmp
Common causes of sinus tachycardia? (non-pharm and pharm)
Non-pharmacological
- Exercise
- Pain, anxiety
- Hypoxia, hypercarbia
- Acidaemia
- Sepsis, pyrexia
- Pulmonary embolism
- Hyperthyroidism
Pharmacological
- Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine
- Sympathomimetics: amphetamines, cocaine, methylphenidate
- Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine
- Others: caffeine, theophylline, marijuana
What rhythm?
Atrial Flutter with 2:1 Block
There are inverted flutter waves in II, III + aVF at a rate of 300 bpm (one per big square)
There are upright flutter waves in V1 simulating P waves
There is a 2:1 AV block resulting in a ventricular rate of 150 bpm
Note the occasional irregularity, with a 3:1 cycle seen in V1-3
This is the classic appearance of anticlockwise flutter.
What rhythm?
Atrial Flutter with Variable Block
Inverted flutter waves in II, III + aVF with atrial rate ~ 300 bpm
Positive flutter waves in V1 resembling P waves
The degree of AV block varies from 2:1 to 4:1
The diagnosis of flutter with variable block could be inferred here from the R-R intervals alone (e.g. if flutter waves were indistinct) — note how the R-R intervals during periods of 4:1 block are approximately double the R-R intervals during 2:1 block.
What rhythm?
Atrial flutter with 4:1 block
There are inverted flutter waves in II, III + aVF at a rate of 260 bpm.
There are upright flutter waves in V1-2 (= anticlockwise circuit).
There is 4:1 block, resulting in a ventricular rate of 65 bpm.
The relatively slow ventricular response suggests treatment with an AV nodal blocking agent.
What rhythm?
Atrial Flutter with Variable Block
The block varies between 2:1 and 4:1
The presence of positive flutter waves in lead II suggests a clockwise re-entry circuit (= uncommon variant).
What rhythm?
Atrial Flutter with 2:1 Block
There is a narrow complex tachycardia at 150 bpm.
There are no visible P waves.
There is a sawtooth baseline in V1 with flutter waves visible at 300 bpm.
Elsewhere, flutter waves are concealed in the T waves and QRS complexes.
The heart rate of 150 bpm makes this flutter with a 2:1 block.
NB. Flutter waves are often very difficult to see when 2:1 block is present.
Remember
Suspect atrial flutter with 2:1 block whenever there is a regular narrow-complex tachycardia at 150 bpm — particularly when the rate is extremely consistent.
In contrast, the rate in sinus tachycardia typically varies slightly from beat to beat, while in AVNRT/AVRT the rate is usually faster (170-250 bpm).
To tell the difference between these rhythms, try some vagal manoeuvres or give a test dose of adenosine — AVNRT/AVRT will often revert to sinus rhythm, whereas slowing of the ventricular rate will unmask the underlying atrial rhythm in sinus tachycardia or atrial flutter.
What are some characteristics of Atrial Fibrillation?
Atrial Fibrillation (AF) is the most common sustained arrhythmia.
The incidence and prevalence of AF is increasing.
Lifetime risk over the age of 40 years is ~25%.
Complications of AF include haemodynamic instability, cardiomyopathy, cardiac failure, and embolic events such as stroke.
Characterised by disorganised atrial electrical activity and contraction.
Causes of atrial fibrillation?
- Ischaemic heart disease
- Hypertension
- Valvular heart disease (esp. mitral stenosis / regurgitation)
- Acute infections
- Electrolyte disturbance (hypokalaemia, hypomagnesaemia)
- Thyrotoxicosis
- Drugs (e.g. sympathomimetics)
- Pulmonary embolus
- Pericardial disease
- Acid-base disturbance
- Pre-excitation syndromes
- Cardiomyopathies: dilated, hypertrophic.
- Phaeochromocytoma
What rhythm? General characteristics?
Atrial Fibrillation
Irregularly irregular rhythm.
No P waves.
Absence of an isoelectric baseline.
Variable ventricular rate.
QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
Fibrillatory waves may mimic P waves leading to misdiagnosis.
What rhythm?
Atrial Fibrillation
Irregular ventricular response .
Coarse fibrillatory waves are visible in V1.
“Sagging” ST segment depression is visible in V6, II, III and aVF, suggestive of digoxin effect.
What rhythm?
Atrial fibrillation:
Irregular ventricular response.
Coarse fibrillatory waves are visible in V1.
What rhythm? General characteristics?
Monomorphic Ventricular tachycardia
Ventricular Tachycardia (VT) is a broad complex tachycardia originating in the ventricles.
There are several different varieties of VT — the most being Monomorphic VT.
What is the clinical significance of ventricular tachycardia?
Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”).
The presence of pre-existing poor ventricular function is strongly associated with cardiovascular compromise.
Decreased cardiac output may result in decreased myocardial perfusion with degeneration to VF.
Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in all cases of VT.
Features suggesstive of ventricular tachycardia (compared to broad complex tachcycardia)?
Very broad complexes (>160ms).
Absence of typical RBBB or LBBB morphology.
Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF.
AV dissociation (P and QRS complexes at different rates).
Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.
Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.
Josephson’s sign – Notching near the nadir of the S-wave.
RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.
Some causes of monomorphic ventricular tachycardia?
Ischaemic Heart Disease
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Chaga’s Disease
What rhythm?
Monomorphic VT:
Classic monomorphic VT with uniform QRS complexes.
Indeterminate axis.
Very broad QRS (~200 ms).
Notching near the nadir of the S wave in lead III = Josephson’s sign.
What rhythm?
Monomorphic VT:
Very broad complexes (~ 200 ms in V5-6).
Northwest axis (-120 degrees).
Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.
Joesphson’s sign – Notching near the nadir of the S wave is seen in leads II, III, aVF.
Possibly some superimposed P waves in aVF.
What rhythm?
Monomorphic VT alternates withventricularbigeminy. The ventricular complexes have the following features:
Very broad QRS duration (> 160 bpm).
Positive concordance in the precordial leads (dominant R waves in V1-6).
Brugada’s sign – time from onset of QRS to nadir of S wave > 100 ms; best seen in leads aVR and aVL.
The presence of normal sinus beats (capture beats) in the second half of the ECG further supports the diagnosis of VT.
Approach to syncope?
Sudden or gradual?
Sudden - cardiac/neuro. Regains consciousness suddenly, think cardiac. Get an echo for HOCM AS MS. Get EKG CKMB/Trop telemetry for ischemia and arrhythmia. Regains gradual, think neurological seizure. Get head ct and EEG
gradual - toxic/metabolic. Think glucose, oximetry, Utox, CBC.
Risk factors for CAD
DM, tobacco, HTN, HLD, fhx premature CAD, age >45 men, >55 women. Patients with DM have highest rates of CAD.
most common side effect of ACEi and ARBs?
7% cough
Major side effects of statins and which tests NEED to order?
transaminitis (1%) therefore AST/ALT
Myositis (0.1%, CPK is not indicated)
How is angioplasty superior to thrombolytics?
survival and mortality benefit
fewer hemorrhagic complications
liklihood of MI (less arrhythmia, less CHF, fewer septal ruptures, tamponade, valve rupture)
Must be done within 90min
Complications include coronary artery rupture, restenosis, hematoma at femoral artery entry site
contraindications to thrombolytics?
melena
cns bleeds
recent surgery (within 2 weeks)
HTN 180/110
nonhemorrhangic stroke within last 6 mo
Done within 12 hours, ideally within 30 min
Best for STEMI
Most likely diagnosis for dyspnea:
Sudden onset, clear lungs
pulmonary embolus
Most likely diagnosis for dyspnea:
sudden onset, wheezing, increasing expiratory phase
asthma
Most likely diagnosis for dyspnea:
slower, fever, sputum, unilateral rales/rhonchi
pneumonia
Most likely diagnosis for dyspnea:
decreased breath sounds unilaterally, tracheal deviation
pneumonthorax
Most likely diagnosis for dyspnea:
circumoral numbness, caffeine use, hx of anxiety
panic attack
Most likely diagnosis for dyspnea:
pallor, gradual onset overa days to weeks
anemia
Most likely diagnosis for dyspnea:
pulsus paradoxus, decreased heart sounds, JVD
tamponade
Most likely diagnosis for dyspnea:
palpitations, syncope
think arrhythmia
Most likely diagnosis for dyspnea:
dullness to percussion at bases
pulmonary effusion
Most likely diagnosis for dyspnea:
long hx of smoking, barrel chest
COPD
Most likely diagnosis for dyspnea:
recent anesthetic use, brown blood, not impoved with O2, clear lungs to ascultation, cyanosis
methemoglobinemia
Most likely diagnosis for dyspnea:
burning building or car, wood burning stove inside in winter, suicide attempt
carbon monoxide poisoning
Most likely diagnosis for dyspnea:
orthopnea, peripheral edema, rales on lung exam, JVD, paroxysmal nocturnal dyspnea (worsening at night during sleep), S3 gallop
CHF, clinical diagnosis
