CARDIOLOGY Chapter 11 - Guyton Flashcards by Alasdair Botting

P wave

< 2.5 mm tall and < 0.12 sec long, immediately precedes atrial contraction (wider would signify longer duration for atria to depolarize)

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PR interval

0.12 - 0.20 sec long (normal value of 0.16 sec), this time is needed for the ventricles to fill with blood!

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QRS complex

up to 0.10 sec, immediately precedes ventricular contraction

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T wave

positive when QRS positive, ventricles recover from depolarization (.25-.35 seconds after depolarization), ventricular repolarization

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Why can atrial repolarization not be seen on the ECG?

masked by the QRS complex

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QT interval

0.37 sec for men and 0.40 for women, this represents the time of ventricular contraction, heart rate can be determined with the reciprocal of the time interval between each heartbeat

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How can you calculate HR with the ECG?

HR = 60 sec / R-R interval = BPM, usually take average from 3 cycles

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Explain the flow of electrical current in the heart?

ventricular depolarization starts at the ventricular septum and the endocardial surfaces of the heart, average current flows positively from the base of the heart to the apex, at the end of depolarization the current reverses from 1/100 of a second and flows toward the outer walls of the ventricles near the base (S wave)

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Lead I of Bipolar Limb Leads

negative terminal of the ECG is connected to the right arm and the positive terminal is connected to the left arm

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Lead II of the Bipolar Limb Lead

negative terminal of the ECG is connected to the right arm and the positive terminal is connected to the left leg

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Lead III of the Bipolar Limb Lead

negative terminal of the ECG is connected to the left arm and the positive terminal is connected to the left leg

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Q wave

when initial inflection is negative

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R wave

first positive deflection

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S wave

negative deflection following the R wave

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all negative

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R prime

second positive inflection that occurs after the S wave, only in abnormal ECGs

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Use of lower case in ECG?

to notate an inflection that is not as strong

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Einthoven’s Law

electrical potential of any limb equals the sum of the other two (I + III = II)

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Chest (Precordial) Leads

V1 - V6, very sensitive to electrical potential changes underneath the skin

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Augmented Unipolar Limb Leads

aVR (+ electrode right arm, - electrode left arm), aVL (+ electrode left arm), aVF (+ electrode left leg)

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P pulmonale

Right atrial enlargement/abnormality - we would expect a large P wave > or = 2.5mm tall (no change in duration) in II, III, AVF, V1

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P mitrale

Left Atrial Enlargement, wide P wave > 0.12 sec, amplitude normal or increased

Right Ventricular Hypertrophy

R wave > S wave in right Chest Leads (V1 or V2), Right Axis Deviation, Right Ventricular Strain Pattern, T wave inversions, Main characteristic: too much voltage to the right hand side

T wave inversions

T waves usually tend to go in same direction as QRS complex, If not, it is considered a strain pattern (or T wave inversion)

Left Ventricular Hypertrophy

Horizontal or Left Axis Deviation; This criteria tends not to be universally used; Person who can run a sub 5 min mile may present with this type of EKG

Right Bundle Branch Block (RBBB)

Wide QRS Complex, RSR’ in V1 and V2 often with ST-T changes

Left Bundle Branch Block (LBBB)

Wide QRS complex with broad or notched R wave in V5, V6, I, Loss of normal septal R wave in V1, Loss of normal septal Q wave in V6

Left Anterior Hemiblock (LAHB)

QRS complex < 0.12 sec + QRS axis > -45 degrees

Left Posterior Hemiblock (LPHB)

QRS complex < 0.12 sec + QRS axis > +120 degrees

Transmural MI

Q wave MIs, depolarization is completely blocked, damaged cardiac muscle remains partly or completely depolarized the entire time, injured muscles emit negative charges throughout each heartbeat, causes of current of injury: local ischemia, mechanical trauma, infection

Subendocardial MI

Non Q wave MIs, subendocardial layer is vulnerable to ischemia associated with: angina pectoris, subendocardial infarction

Common ECG changes.

ST segment depression in the anterior or inferior leads, T-wave inversion, down-sloping into the T-wave is abnormal (“J-point”), up-sloping is normal changes can be localized in the inferior leads

Acute Phase MI

S-T elevation; tall, positive (hyperacute) waves | huge

Evolving Phase MI: next day

Deep T wave inversions in leads showing S-T elevation, Development of significant Q-waves

Resolving Phase (Old MI)

significant Q waves appear, Partial or complete regression of ST-T changes

Sinus Bradycardia

HR < 60bpm, often seen in trained people, SA node is beating slow

Sinus Tachycardia

HR > 100 bpm

Atrial arrhythmias

PACman (premature atrial conduction), premature beat due to refractory period in SA node, occurs either with or without conduction, usually P wave present, compensatory pause

Premature Junctional Beat (PJC)

beat from AV junction, Premature beat usually without P wave, Depolarized by the atria before it reaches its critical threshold

Junctional Escape Beat

Beat from AV junction when normal pacemaker (SA node) fails, usually NO P wave, different from PJC in the R-R interval (much longer)

PVCs

premature before the next normal beat is expected QRS wide; T wave and QRS are in opposite directions, compensatory pause, R on T phenomenon, couplets, Bigeminy (PVC-normal cycle-PVC-normal cycle), Trigeminy

SVT

3 or more consecutive PACs, no P-wave present

Atrial flutter

atrial stimulation rate ~ 300 bpm, flutter waves present, represented by ratio of atrial beats: vent. beats, forces AV junction to become pacemaker for ventricles

Atrial fibrillation

stimulated at very rapid rate, up to 600 bpm, presence of f waves or fib. waves, forces AV junction to becomes pacemaker for ventricles

Junctional Escape Rhythm

starts with junctional escape beat and continues to be paced by AV junction, 40-60 bpm, QRS and T-wave are normal

Accelerated Junctional Rhythm

Accelerated junctional rhythm has 60-100 bpm; Junctional tachycardia has 101-180 bpm

Ventricular Tachycardia

3 or more PVCs in a row

Ventricular Fibrillation

presence of f waves, fine or coarse fibrillation

Asystole

ya dead bro

1st Degree AV Heart Block

PR interval is prolonged (>0.2 sec)

2nd Degree AV Heart Block

mobitz 1 (Wenkebach): progressive lengthening of the PR interval until a beat is dropped; mobitz 2: nonconducted sinus P wave without progressive prolongation of PR interval

3rd Degree AV Heart Block

P waves are present; atrial rate faster than the ventricular rate; P waves bear NO relation to QRS; PR intervals variable

Wolff-Parkinson-White Syndrome

QRS complex widened; PR interval shorted; Appearance of delta wave; Often surgically repaired and relatively common