Physio B Lab Midterm 2

cardiac axis

the general (mean vector) direction of electric impulses as they travel through the heart

normal axis

upper right to lower left

Leads 1, 2, & 3: positive, 3 is sometimes biphasic

right axis deviation causes

hypertrophy in right ventricle, axis shifts to the right of the heart; NORMAL in children and tall thin adults because the left mass of the heart is heavier, swaying the heart to the right

right axis deviation can tell us..

scoliosis, pulmonary hypertension, enlarged heart

right axis deviation

electric vector towards right side of the body; lead 1: negative; leads 2 & 3: positive

left axis deviation causes

hypertrophy of left ventricle; NORMAL in short and stocky individuals (because diaphragm can push up on the heart, causing it to sway to the left) & asymptomatic athletes

left axis deviation can tell us ..

emphysema, hyperkalemia, tricuspid atresia, systemic hypertension

left axis deviation

electric vector toward left side of body;

Lead 1: positive, Leads 2, 3, AVF: negative

right axis deviation

left axis deviation

how fast does EKG paper move?

25 mm/sec

tiny box on EKG paper

1 mm = 0.04 sec

big box on EKG paper

5 mm = 0.2 sec

heart rate

distance between 2 R waves;

HR (bpm) = 1500 / (# of tiny boxes)

PR Interval definition

time from the beginning of the P wave (arial depolarization) to beginning of QRS complex (ventricular depolarization) through AV junction

normal PR interval

0.12 sec - 0.2 sec

3 mm - 5 mm

PR interval > 0.2 sec

heart block

PR interval < 0.12 sec

less blood flow to ventricles, lower cardiac output

PR interval calculation

# of tiny boxes from beginning of P wave to beginning of QRS complex * 0.04 sec

causes of heart block

age, scar tissue from previous heart surgery, side effect of medications, electrolyte imbalance

heart blocks that CAN be asymptomatic

1st or 2nd degree

SA block/junctional rhythm

SA node not leading the rhythm, AV node becomes the pacemaker → P and QRS happen at the SAME time (b/c QRS is larger, can’t see P wave); ABSENT P WAVE IN ALL LEADS

First Degree AV Block

delay in transmission of impulse from the atria to the ventricles; prolonged PR interval consistently in all leads (> .20 sec)

2nd degree AV Block, Type I

increasing PR intervals until a QRS complex is dropped, cycle is resumed with no set pattern; p wave is seen but the impulse does not initiate a ventricular response

2nd degree AV Block, Type II

'“fixed rate” → multiple p waves before the QRS complex; can be a 2:1, 3:1, etc. but will be consistent

Third Degree AV Block/ Complete Heart Block

no association between atria and ventricles; p wave is there but impulse not conducted to ventricles, so a second pacemaker below the block must be active and generate QRS complexes → “escape pacemaker” could be in the Bundle of His or ventricle; P is faster than QRS, could have a double peak T wave

SA block

2nd degree AV Block, type 1

1st degree AV block

2nd degree AV block, type 2 (2:1)

2nd degree AV block, type 2 (3:1)

complete heart block

bundle branches

there is a right bundle branch that transmits the stimulus to the right ventricle, and there is a left bundle branch that transmits the stimulus to the left ventricle

if bundle branch is blocked…

stimulus can still reach the ventricular portion that it was supposed to stimulate; pathway to stimulate the ventricular mass that has the blocked bundle branch is through tissue (cell to cell) outside the normal conduction pathway → conduction slower, causing delay in ability to stimulate ventricular side that has blocked bundle branch

causes of bundle branch blocks

cardiomyopathy, myocardial infarction, hypertension

right bundle branch block (RBBB) can result from…

COPD, pulmonary hypertension

normal deflection of chest leads

V1 & V2: negative; V3 & V4: biphasic; V5 & V6: positive

right bundle branch block (RBBB)

2 upward deflections (R waves) in V1 and/or V2; R’ bigger than R

RBBB why are there 2 R waves?

delay in stimulation of right ventricle, second R wave represents stimulation of the right ventricle; 2 waves: rR’

RBBB

left bundle branch block (LBBB)

2 R waves in V5 & V6; R waves similar in height

LBBB why are there 2 R waves?

delay in stimulation of left ventricle, second R wave represents stimulation of the left ventricle; 2 waves: RR’; 2 R waves can ‘slur’ into each other and be seen as a wide QRS complex

LBBB

right av valve

tricuspid valve

left av valve

bicuspid valve

av valves:

valves between atria and ventricles; also called parachute valves

semilunar valves:

between ventricles and arteries exiting the heart; also called hip-pocket valves (aortic semilunar valve & pulmonary semilunar valve)

hypertrophy

an increase in mass attributable to increases in cell size (not number); term used for elevated mass in ventricles (LVH & RVH)

enlargement

same as hypertrophy but this term is used for elevations in atrial mass (RAE & LAE)

Frank-Starling Law

as larger volume of blood flows into the chambers of the heart, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction → hypertrophy or enlargement of that heart chamber

EKG paper vertical axis

magnitude of electrical activity (mV) 1mm = 0.1 mV

normal atrial size

2.5 boxes wide (0.1 sec) and 2.5 boxes high (0.25 mV)

right atrial enlargement (RAE)

tall p wave (>2.5 mm) in 2/3 of the inferior leads (Lead II, Lead III, and aVF)

causes of RAE

tricuspid stenosis (narrow) or tricuspid prolapse (leaky)

RAE

left atrial enlargement (LAE)

wide P wave (> 0.1 sec in duration) in 2/3 of the inferior leads (Lead II, Lead III, and aVF); b/c takes longer to reach to and depolarize left atria enlarged mass OR wide P wave in Lead 1 AND 2 waves (one up and one down) in V1

causes of LAE

bicuspid stenosis (narrow) or bicuspid prolapse (leaky)

LAE

RVH

electrical vector directed toward right side; positive V1 or V2, biphasic or negative V5 or V5

cause of RVH

pulmonary valve stenosis or prolapse

RVH

LVH

deflection pattern normal but because of the larger mass → magnitude of deflection pattern greater than normal; add amplitude of S wave in V1 or V2 + amplitude of R wave in V5 or V6, if greater than or equal to 35 mm

cause of LVH

normal adaptation to exercise, aortic valve stenosis or prolapse

LVH

ectopic focus/pacemaker

an excitable group of cells that causes a premature heartbeat outside the normally functioning SA node of the heart

cause/factors that aggravate ectopic focus:

cause: unknown

factors that aggravate: alcohol, smoking, caffeine

PVC (premature ventricular contraction/complex)

when stimulation of ventricles (‘ectopic focus’) occur in one or more areas within the ventricle before the normal stimulation from the SA node arrives; longer QRS with weird morphology b/c ectopic firing of a focus disrupts normal sequence of cardiac activation → 2 signals because ectopic foci fires independent of normal firing

criteria to diagnose PVC

1. no p wave

2. wide QRS complex (greater than 0.1 sec)

   1. T wave usually points in the direction opposite to the QRS wave

normal QRS interval

0.04-0.1 sec

unifocal PVC

PVC originates in one focal point within the ventricle; looks the same in any lead

multifocal PVC

PVC originates in more than one focal point within the ventricle; looks different in any given lead; can have 2 different morphologies in the same lead

continuous PVCs

PVC with a pattern; if every other beat is a PVC → bigeminy; if every third beat is a PVC → trigeminy; if every fourth beat is a PVC → quadrigeminy

unifocal ventricular trigeminy

V Tach (ventricular tachycardia)

3+ PVCs in a row, looks like the blade of a saw

v tach

R on T PVC

R wave of the PVC (or S wave) occurs on the T wave of the preceding beat; when this occurs, individual goes into V fib (ventricular fibrillation) because cells haven’t fully repolarized

V fib (ventricular fibrillation)

rapid, irregular signals causing the heart’s ventricles to quiver uselessly instead of pumping blood

v fib

sudden cardiac arrest (SCA)

sudden loss of all heart activity due to an irregular heart rhythm; breathing stops, person becomes unconscious; brain cells begin to die within 4-6 minutes; without immediate treatment → death :(

symptoms of SCA

collapse, no pulse, no breathing

causes of SCA

cardiomyopathy (enlarged heart) in young adults and athletes, atrial flutter or atrial fibrillation, coronary artery disease

risk factors of SCA

smoking, hypertension, obesity, diabetes

3 phases of cadiac arrest

1. electrical phase (0-4 minutes after); heart still has supply of oxygen and glucose, conditions favorable for resuscitation; heart can respond to defibrillation

2. circulatory phase (4-10 minutes after); oxygen stores exhausted, myocardial cells switch to anaerobic metabolism; CPR needed to restore O2 and glucose to enhance possibility of successful defibrillation

   1. metabolic phase (10+ minutes after): heart muscle acidic and ischemic, begins to die; chances of resuscitation are unfavorable

cardiac arrest management

call 911, CPR, AED, act QUICKLY

defibrillation is advised for…

v tach and v fib

defibrillation is NOT advised for…

asystole (absence of electrical activity - flatline; electrical activity organized but there is no cardiac output); use stimulant then do defibrillation

resuscitation

emergency care provided to restore vital body functions; successful defibrillation depends on effective CPR (interruptions in chest compressions minimized)

CPR instructions

no breathing → do CPR; push hard and fast at 100-120 compressions/minute; check airway, deliver rescue breaths after every 30 compressions IF YOU HAVE BEEN TRAINED; if not: continue chest compressions, allow chest to rise completely between chest compressions; AED (automated external defibrillators)

a fib (atrial fibrillation)

crash cart

self-contained, mobile unit that contains lifesaving supplies; defibrillator and heart monitor usually on top of the cart

first drawer of the crash cart

medications, alcohol swabs, NaCl, dopamine, etc.

2nd drawer of the crash cart

intubation materials, endotracheal tubes, laryngoscope

3rd drawer of the crash cart

airway suction materials, intubation materials, suction catheter kit, endotracheal tubes

4th drawer of crash cart

IV starting equipment, disinfectant, tape, etc.

5th drawer of crash cart

IV solutions, NaCl solution, dextrose solution, etc.

6th drawer of crash cart

prepackaged kits for various urgent and emergent procedures, sterile gloves, lumbar puncture kit

layers of the heart wall

epicardium (largest) → myocardium → endocardium; blood supply comes from outside of the heart and goes in

blood supply to the heart wall

left anterior descending artery (aka ‘widow maker’) → if blocked, heart attack is fatal; patients can have multiple heart attacks depending on the location

coronary arteries

vessels that deliver oxygen rich blood to the myocardium

coronary circulation

circulation of blood in the blood vessels of the heart muscle; epicardium to endocardium