Cardiology 1 Flashcards
Automaticity
Cells depolarize without impulse from outside source
Conductivity
Cells propagate the electrical impulse from cell to cell
Contractility
Specialized ability of cardiac muscle to contract
Excitability
Cells respond to electrical stimulus
Types of cardiac muscle cells
Pacemaker
Contractile
Groups of cardiac muscle
Atrial
Ventricular
Excitatory/conductive
Sodium
Major extracellular cation, role in depolarization
Potassium
Major intracellular cation, role in repolarization
Calcium
Intracellular cation, depolarization and myocardial contraction
Chloride
Extracellular anion
Magnesium
Intracellular cation
Resting Potential
Approximately -90mv
More intracellular negative anions than extracellular
Membrane Potential
Separation of charges across the membrane
Depolarization
Sodium enters cell change stop positive intracellular charge
Reversal of charges at the cell membrane
Slow influx of calcium
Repolarization
Returning to resting potential state
Sodium influx stops and potassium leaves cell
Sodium pumped to outside cell
Absolute refractory period
Cell will not respond to repeated action potential regardless of how strong
Relative refractory period
Cell responds to second action potential but must be stronger than usual
Myocardial Cell
Specialized cells of conduction system able to generate action potentials spontaneously
Cardiac Myocytes
Involuntary
Striated
Branched
Tissue arranged in interlacing bundles of fibres
Phase 4
Resting potential phase
Inside of cell negative to outside
Na/K pump maintains concentration gradient through Na/K pump
Phase 0
Rapid Depolarization
Membrane reaches threshold potential and voltage gated fast Na channels open
Na exceeds permeability to K, membrane reaches Na equilibrium
Inside of cell becomes positively charged
Sodium Influx
Phase 1
Partial Repolarization
Chloride ions enter cell cause inactivation of Na channels
K still lost from cell
Slight drop in membrane potential
Phase 2
Plateau
Voltage gated calcium channels open
Contraction of muscle
K leaves cell slowly
Prolonged state of depolarization allowing for muscle contraction
Phase 3
End of rapid repolarization
Ca channels close
K gates open, membrane depolarization
Na/K pump restores membrane potential
SA + AV Node AP Morphology
Phase 4
Phase 0
Phase 3
Progressive depolarization in 4 until threshold
Late Diastole
Both chambers relaxed
Ventricular filling
Atrial systole
Atrial contraction forces small amount of blood to ventricles
End diastolic Volume
Maximum amount of blood in ventricles at end of ventricular relaxation
135mL
Isovolumic ventricular contraction
Pushes AV valve closed, not enough pressure to open semilunar valves
Ventricular Ejection
Ventricular pressure rises and exceeds pressure in arteries
Semilunar valves open and blood ejected
End Systolic Volume
Minimum amount of blood in ventricles
65mL
Iosvolumetric Ventricular Relaxation
Ventricles relax, pressure in ventricles drop
Blood flows back into cups of semilunar valve and snaps them closed
P Wave
First upward deflection
Atrial depolarization
0.1s or less
Followed by QRS
Inverted P waves
When pacing or if initial impulse originates at or below AV node
P wave axis shift
Inverted P waves in II, III, aCF
Left atrial enlargement
PR Interval
Time for impulse to move through atria and AV node
Beginning of P wave to next deflection on baseline
0.12 - 0.2s
Causes of short PRI
Retrograde junctional P waves
WPW pattern
Lown-Ganong-Levine Syndrome
QRS complex
Ventricular depolarization
<0.12s
Q wave
First negative deflection after P wave
Depolarization of septum
Can be normal or pathological
R wave
First positive deflection following P or Q
S wave
Negative deflection following R wave
QRS Interval
Time impulse takes to depolarize ventricles
Beginning of Q to ST segment
<0.12s
What to look for in QRS
Height/Amplitude
Width/duration
Morphology
Presence of Q waves in infarct pattern
Axis along frontal plane
R wave progression
Tall QRS Complexes
Increased hypertrophy of ventricles
Increased abnormal pacer
Increased aberrantly conducted beat
Criteria of Small Complex
Voltage in all limb leads <5 mm
Waves <10mm high in precordial leads
Causes of Small QRS complexes
Obesity
COPD
Pericardial effusion
Severe hypothyroidism
Subcutaneous emphysema
Massive myocardial damage/infarction
Infiltrative/restrictive disease such as amyloid cardiomyopathy
QRS Width
Anything >0.12 is abnormal
Causes of Wide QRS
Hyperkalemia
V-tach
Idioventricular rhythms
Drug effects and overdoses
WPW
BBB and inter ventricular conduction delay
Ventricular premature contractions
Aberrantly conducted complexes
5 Steps to ECG interpretation
Rate
Rhythm
P waves
PR interval/relationship
QRS duration
T wave
Repolarization of ventricles
End of ventricular systole
Bi Polar Leads
I/II/III
Unipolar leads
Vector point midpoint of the axis
Augmented limb leads and precordial leads
Augmented limb leads
aVR/aVL/aVF
Augmented chest leads
V1-V6
Vectors from precordial leads
Limb leads: frontal plane
Precordial leads: horizontal plane
R wave progression
Increasingly large R wave in V3-V6
Male QT(c)
<450ms
QT(c) women
<470
QT(c) > 500
Risk of torsades
QT(c)
Estimates QT interval as a standard HR of 60
Prolonged QT(C) men
> 440
Prolonged QT(c) women
> 460
Abnormally short QT(c)
<350ms
Causes of QT prolongation
Drugs: Type IA + III anti arrhythmic, TCAs/phenothiazines
Lytes: Hypokalemia, hypomagnesemia, hypocalcemia
CNS: stroke, seizure bleed
Normal Axis
-30 to 90 degrees
Importance of Axis
Provides insight into chamber enlargement, abnormalities of conduction system, MI and origin of arrhythmias
Electrical Axis
Average direction of depolarization during ventricular contraction of the heart
Causes of Non-Pathological Axis Deviation
Age
Body type
Age axis deviation
Moves leftward with age
Body type Axis deviation
Vertical: tall + thin
Leftward: short and obese
Normal Axis
QRS positive in I and aVF
LAD
Positive QRS lead I, negative aVF
RAD
Negative Lead I, positive aVF
Extreme RAD
Negative I and aVF
Pathological Left axis deviation
Lead I positive, aVF negative
II more negative than positive
Causes of Extreme RAD
V tach
Ventricular pacing
Causes of RAD
Right ventricular hypertrophy
Chronic pulmonary disease
PE
Left posterior fascicular block
Sodium channel blocker
Hyperkalemia
Causes of LAD
Left ventricular hypertrophy
LBBB
Ventricular pacemaker
Left anterior fascicular block
V tach
Inferior MI
Anterior MI
WPW
Ascites
Obesity
Pregnancy
NSR
60-100
Regular
PR constant
QRS normal
Normal heart function
Sinus bradycardia
<60
Regular
PR constant
Normal QRS
Causes of Sinus bradycardia
Normal, beta blocker OD, digoxin, AMI/ischemia, increased ICP
Significance of Bradycardia
Profound bradycardia could decrease CO
Sinus tachycardia
> 100 <200
Regular
PR constant
QRS normal
Causes of sinus tachy
Exercise, anxiety/stress, drugs
Significance of Sinus tach
Usually benign, treat cause
Sinus Arrhythmia
60-100
Irregular
P waves and PR constant
QRS normal
Sinus Node Dysfunction
Abnormalities in SA impulse formation and conduction including sinus brad, sinus pause/arrest, sinoatrial exit block, tachy/brady syndrome
Sinus Pause/Arrest
Failure of impulse formation in sinus node
Rate varies with arrest
Irregular
Normal P waves
Normal QRS
Short Sinus Pause
<2.5s
Long Sinus Pause
> 2.5s
S/sx of Sinus arrest
Lightheaded, syncope, death if escape rhythm does not kick in
Causes of Sinus Arrest
Heart disease, AMI, sinus node dysfunction
Sinus Exit Block
Failure of conduction of SA node impulse
Variying rate
Irregular rhythm, pause same as distance between 2 other P-P intervals
Causes of Sinus exit block
Increased vagal tone
Sinus node dysfunction
Inferior AMI
Digitalis, Ca beta blockers, amiodarone
Tachy-brady syndrome
Rate alternates between too fast and slow
Long pause between heartbeats especially after tachycardia
Atrial Fibrillation
Atrial Rate: 350-650
Ventricular rate: variable
Regularly irregular
No consistent P waves
No PR interval
Clinical significance of A fib
Atrial kick lost
Thrombus from pooled blood common cause of CVA
Atrial Flutter
Atrial rate: 300/min
Regular but not always
Saw toothed pattern of flutter waves, varying ratios
QRS narrow, no true marriage
Origin of A flutter
Single ectopic focus in atria with re-entry mechanism
Ectopic Atrial Dysrhythmias
Site outside of sinus node but in atria creating AP faster than sinus node
Wandering Atrial Pacemaker
Variable rate depending on site of pacemaker, usually 45-100
Irregular
Variable PR
Normal QRS
Variable impulses from atria
Multi-Focal Atria Tachycardia
Wandering Atrial Pacemaker with rates >100
Junctional Rhythm
Default rate at 40-60
Regular
Normal if P waves present
Normal QRS
Causes of junctional rhythm
ACS
Drugs: beta blocker, CCB, amiodarone, digoxin
Sinus node dysfunction
Accelerated Junctional
60-100
Junctional Tachycardia
> 100
4 Features of classic SVT
Fast between 140 and 250
Regular
Narrow QRS
NO P waves
AVNRT Pathways
Alpha path: slower, fast refractory
Beta: faster, slower refractory
AVRT
Caused by abnormal anatomical conduction pathway between atria and ventricles
Bypasses AV node, bundle of HIS or both
Early depolarization of ventricle
WPW
Impulse normally in SA passes thru AV nod and accessory pathway
PAC reaches pathway when refractory but AV is not
Re-entry circuity
Delta wave
Slurred upstroke in QRS
Adenosine and WPW
Contraindicated and lethal
V-Tach
120-250 (typical 170)
Regular
Absent p wave
Wide QRS
Origin of Vtach
Ectopic focus in ventricle, possibly accessory pathway
Causes of Vtach
AMI, hypoxia, acidosis, hypokalemia, R on T
ECG Criteria Favouring VT
AV dissociation
Negative or positive concordance in precordial leads
Very broad complexes
Extreme RAD (positive QRS aVR)
Captur beats or fusion beats
Rsr’ in V1
Distance from onset of QRS to S wave is >100ms
Notched S wave (Josephson’s sign)
1st Degree Block
Normal rate
Regular
P wave present
PR interval >0.20s
Normal QRS
Causes of 1st degree block
Age, heart disease slowing conduction through AV node
2nd degree Type I
Normal to brady
Irregular rhythm
Normal P wave
PR increases until QRS dropped
Origin of 2nd degree Type I
SA node with block at or below AV node
Causes of 2nd degree Type I
Ischemia, digoxin toxicity, acute inferior AMI
2nd Degree Type 2
Usually brady
Irregular
P wave Present
PR interval constant until QRS randomly dropped
Uniform ratio 2:1, 3:1, 4:1
Origin 2nd degree Type 2
SA node with block at or below AV
3rd degree Block
Atrial rate: normal
Ventricular rate: 20-50
Regular R-R interval
P wave present
QRS present
No relationship between P and QRS
Origin of 3rd Degree Block
SA node with complete block at AV
Ventricles AV node signal, bundle or ventricles
RBBB
QRS >0.12
Right side of heart last to depolarize, last vector of complex moves towards V1
Upright rsr’ in V1
Negative deflection in V6 as large S wave
LBBB
Left side of heart last to depolarize, terminal vector moves away from V1
Negative deflection in V1
Smith-Modified Sgarbossa Criteria
ST Elevations >1mm in >1 lead
ST depression >1mm in >1 lead of V1-V3
Excessive discordant STE in >1 lead anywhere with >1mm STE, >25% depth of preceding S wave
Atrial Enlargement
Left atrial enlargement commonly caused by mitral valve disease
Right atrial enlargement caused by lung disease
Ventricular Hypertrophy
Sustained HTN forces left ventricle to work too hard
Right VH far less common
right atrial enlargement
Height of P wave >2.5mm in lead II or >1.5mm in V1
Increased amplitude of first portion of P wave
Left atrial Enlargement
Duration of P wave >0.12s in II
P wave notched in II
Pwave inverted or biphasic in V1
Right Ventricular Hypertrophy
RAD
Right atrial enlargement
Tall R wave in V1 >7mm
R wave greater than S in V1
Rsr’ in V1 > 10mm
LVH
Deepest S wave in V1 or V2 and tallest R wave in V5 or V6 >/= 35mm
R in aVL > 12mm
S wave in V1 or V2 >20-25
R wave in V5 >20 or V6 >25
Hypertrophic Cardiomyopathy
Septal hypertrophy positive R wave in V1, LVH and septal Q waves in v5 and v6
RCA
Right ventricle
SA and AV node
Posterior wall
Posterior descending artery to inferior wall
LCA
LAD + Circumflex
Left anterior descending artery
Septum
Left + right BB
Anterior wall
Lateral wall
Circumflex Artery
Lateral and posterior wall
Inferior wall 10%
Ischemia and NSTEMI ECG
Hyperacute T wave
Inverted T wave
ST depression
necrosis ECG
Pathological Q waves
>1mm wide >1/3 R wave
Wellens Syndrom
LAD coronary T wave syndrome
Biphasic/deeply inverted T waves in V2 and V3 persisting after resolved ischemic chest pain
Significance of Wellens Syndrome
Acute Mi in 6-8.5 days post admission
Acute Mi 21.4 days from symptoms
De winter’s T waves
Anterior STEMI equivalent without obvious ST elevation
Tall peaked T waves in precordial leads starting below isoelectric line
RV failure
Preload dependent
Morphology of ST depression
Upsloping non-specific for myocardial ischemia
Horizontal or downsloping = ischemia
