Physiology 11, 12

Front 1

remain contracted until a few milliseconds after the end of the T repolarization wave.

Back 1

The ventricular fibers

Front 2

this approximates the time of ventricular contraction

Back 2

Q-T interval (Normally 0.35sec)

Front 3

Heart Rate Calculation

Back 3

R-R interval = 0.83 sec
Heart rate = (60 sec)/(0.83 sec) = 72 beats/min min beat

Front 4

Mean Vector Through the Partially Depolarized Heart

Back 4

Septum depol.s 1st, then the endocardial walls of the vents, spreading outward to exterior vents, then up from the apex to the base.

Front 5

Einthoven’s triangle & law.

Back 5

Sum of leads I+III always equals the potential of lead II

Front 6

Bipolar limb leads

Back 6

Bipolar means that the EKG is recorded from two electrodes on the body (which is really a bag of salt water).
Left arm is -0.2mv with respect to the average of the rest of the body
Rt arm is +0.3mv so lead I demonstrates a positive potential of 0.5mv

Front 7

Lead I

Back 7

The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left arm.

Front 8

Lead II

Back 8

The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left leg.

Front 9

Lead III

Back 9

The negative terminal of the electrocardiogram is connected to the left arm, and the positive terminal is connected to the left leg.

Front 10

Einthoven’s Law

Back 10

states that the electrical potential of any limb equals the sum of the other two (+ and - signs of leads must be observed).
If lead I = 1.0 mV, Lead III = 0.5 mV, then Lead II = 1.0 + 0.5 = 1.5 mV

Front 11

Precordial chest leads (Chest Leads V1- V6)

Back 11

heart surface is close to these leads.
records potential of the cardiac musculature right under the lead
tiny irregularities in the ventricular surface (particularly the anterior wall), will show up
V1 and V2 are usually negative because the electrode is nearer the “base” (top) of the heart. As depolarization of the vents occurs, movement is away from the top.
Vice versa for the bottom leads

Front 12

Augmented Unipolar Limb Leads aVR,
aVL, and aVF

Back 12

For aVR the +
electrode is the right arm, and the -
electrode is the left arm + left leg; aVL +
electrode is left arm; aVF + electrode is left foot.
Augmented unipolar leads measure resistances in the body.

Front 13

Biplolar Limb Leads

Back 13

I Right arm and left arm
II Right arm and left leg
III left arm and left leg

Front 14

Unipolar limb Leads

Back 14

AVR Right arm
AVL Left arm
AVF Left leg

Front 15

Unipolar Chest leads

Back 15

V1 4th intercostal space to the right of the sternum
V2 4th intercostal space to the left of the sternum
V3 5th intercostal space to the left of the sternum
V4 5th intercostal space in line with the middle of the clavicle
V5 5th intercostal space to the left of V4
V6 5th intercostal space in line with the middle of the axilla

Front 16

Vector Analysis

Back 16

The current in the heart flows from the area of depolarization to the polarized areas, and the electrical potential generated can be represented by a vector, with the arrowhead pointing in the positive direction.
The length of the vector is proportional to the voltage of the potential.
The generated potential at any instant can be represented by an instantaneous mean vector.
The normal mean QRS vector is 59o.

Front 17

Lead Axis

Back 17

The axis of lead I is zero degrees because the electrodes lie in the horizontal direction on each of the arms.
The axis of lead II is +60 degrees because the right arm connects to the torso in the top right corner, and left leg connects to the torso in the bottom left corner.
The axis of lead III is 120 degrees.

Front 18

Voltages are measured form the

Back 18

peak of R to the bottom of S

Front 19

Q wave is present if

Back 19

left side of the septum depolarizes first

Front 20

First area to repolarize is near

Back 20

the apex of the heart.
Last areas, in general, to depolarize are the first to repolarize.

Front 21

Repolarized areas will have a ________ charge first;

Back 21

Repolarized areas will have a + charge first; therefore, a + net vector occurs and a positive T wave.

Front 22

Atrial depolarization is_________ than in ventricles.

Back 22

Atrial depolarization is slower than in ventricles, so first area to depolarize is also the first to repolarize. This gives a negative wave in leads I, II, and III.

Front 23

define mean electrical axis.

Back 23

Draw a perpendicular line from the end of each vector, and the intersection

Front 24

The mean electrical axis averaged over the entire period of depolarization is +_____o

Back 24

The mean electrical axis averaged over the entire period of depolarization is +59o

Front 25

Axis deviations are caused by

Back 25

Changes in heart position: left shift caused by expiration, lying down and excess abdominal fat pushing up on diaphragm. Also, left ventr. hypertrophy

Front 26

Hypertrophy of left ventricle (left axis shift)

Back 26

caused by hypertension, aortic stenosis or aortic regurgitation causes slightly prolonged QRS and high voltage.

Front 27

Hypertrophy of right ventricle (right axis shift)

Back 27

caused by pulmonary hypertension, pulmonary valve stenosis, interventricular septal defect. All cause slightly prolonged QRS and high voltage.
Deep inspiration, standing up, and in tall individuals and giraffes

Front 28

Bundle branch block-

Back 28

left bundle branch block causes left axis shift because right ventricle depolarizes much faster than left ventricle. QRS complex is prolonged. This differentiates Bundle branch block from hypertrophy

Front 29

If sum of voltages of Leads I, II &III is greater than _____ mV, this is considered to be a high voltage EKG.

Back 29

If sum of voltages of Leads I, II &III is greater than 4 mV, this is considered to be a high voltage EKG.
Usually, total voltages vary between 0.5 and 2.0 mV
Most often caused by increased ventricular muscle mass (hypertension, marathon runner).

Front 30

Decreased voltages in standard limb leads

Back 30

Cardiac muscle abnormalities (old infarcts causing decreased muscle mass and scaring , low voltage EKG, and prolonged QRS).
Conditions surrounding heart (fluid in pericardium, pleural effusions, emphysema) short circuits the voltage and it’s dissipated throughout the body.
Anterior-posterior rotation of apex of heart.

Front 31

Prolonged QRS

Back 31

Cause is prolonged conduction of cardiac impulse through ventricles.
Normal QRS = 0.06 - 0.08 sec.
One cause is cardiac hypertrophy.
One cause is a Purkinje system block.
If QRS exceeds 0.12 sec, usual cause is conduction block.

Front 32

Unusual QRS

Back 32

Can be caused by local conduction blocks which may cause multiple QRS peaks. Lead III esp. shows double Rs in ventricles or areas firing at different times d.t. failure of Purkinjes

Front 33

Current of injury

Back 33

Damaged cardiac muscle remains partially or totally depolarized all the time.
Current flows between damaged depolarized tissue and ‘normal’ polarized cardiac cells all the time
Injured muscle emits negative charges throughout each heart beat.
Causes of current of injury: (1) local ischemia (most common), (2) mechanical trauma, (3) infection.

Front 34

the J point is

Back 34

Under normal conditions, the J point is the junction of QRS complex and ST segment.
Under normal conditions, PR segment is considered the baseline for the entire tracing.

Front 35

Axis of the current of injury

Back 35

At the end of the S wave the ventricles are fully depolarized. This is the J point.
The difference between the J point and the T-P segment is the current of injury.
Plot the voltages of the current of injury on the coordinates of the three leads to determine the electrical axis.
The negative end of the vector originates in the injured or ischemic area.

Front 36

Prolonged QRS

Back 36

Cause is prolonged conduction of cardiac impulse through ventricles.
Normal QRS = 0.06 - 0.08 sec.
One cause is cardiac hypertrophy.
One cause is a Purkinje system block.
If QRS exceeds 0.12 sec, usual cause is conduction block.

Front 37

Unusual QRS

Back 37

Can be caused by local conduction blocks which may cause multiple QRS peaks. Lead III esp. shows double Rs in ventricles or areas firing at different times d.t. failure of Purkinjes

Front 38

Current of injury

Back 38

Damaged cardiac muscle remains partially or totally depolarized all the time.
Current flows between damaged depolarized tissue and ‘normal’ polarized cardiac cells all the time
Injured muscle emits negative charges throughout each heart beat.
Causes of current of injury: (1) local ischemia (most common), (2) mechanical trauma, (3) infection.

Front 39

the J point is

Back 39

Under normal conditions, the J point is the junction of QRS complex and ST segment.
Under normal conditions, PR segment is considered the baseline for the entire tracing.

Front 40

Axis of the current of injury

Back 40

At the end of the S wave the ventricles are fully depolarized. This is the J point.
The difference between the J point and the T-P segment is the current of injury.
Plot the voltages of the current of injury on the coordinates of the three leads to determine the electrical axis.
The negative end of the vector originates in the injured or ischemic area.

Front 41

Current of injury in acute (recent) anterior wall infarction.

Back 41

Current of injury in acute (recent) anterior wall infarction. Bipolar limb leads negative, drawn horizontally from the J point, indicates anterior wall.
Chest lead from the J point is strongly negative – indicating anterior wall injury

Front 42

Horizontal J point line shows

Back 42

positive deviation – posterior wall injury

Front 43

The T-P segment shows a current of injury following ___________

Back 43

acute coronary thrombosis.
This current of injury improves over several weeks when at rest.
However, exercise may cause ischemia of this recovered area, resulting in a current of injury.

Front 44

Ventricular repolarization usually occurs in the __________ direction as depolarization which causes an upright T wave in the three standard leads.

Back 44

Ventricular repolarization usually occurs in the opposite direction as depolarization which causes an upright T wave in the three standard leads.
Prolongation of repolarization may change the T wave axis.

Front 45

T wave abnormalities

Back 45

Left bundle branch block causes a late depolarization and thus a late repolarization of the left ventricle
(Just after right ventricle is
repolarized and left is still depolarizing. This gives right
axis deviation and an inverted
T wave in lead I.)
Mild ischemia particularly in the apex of the heart prevents apex from repolarizing first. Thus, the T wave inverts
Digitalis toxicity prolongs depolarization in certain parts of the heart and can cause a biphasic T wave.

Front 46

Where is the Q wave

Back 46

It is the first downward deflection in the QRS

Front 47

When can Q waves appear?

Back 47

within hours of artery occlusion, but usually not within the first 2 hours of symptoms. Q waves do not always go away p the MI resolves

Front 48

Q wave criteria for acute MI

Back 48

The Qwave is more than0.04 sec wide
There are abnormalities in the T waves and /or ST segments

Front 49

Isoelectric Line

Back 49

Also known as the badeline, is best determined by drawing a line between the end of T and begtinning of the P wave. This line will be used as a reference point to measure ST segment elevation

Front 50

The J Point

Back 50

The J point is used to measure ST segment changes. The ability to identify the J point is crucial to determining ST segment changes. It is found where the S wave makes its sharp deviation toward T

Front 51

ST elevation

Back 51

Fireman's cap , this finding is associated with mocardial injury or infarct. It is measured 1mm to the right of the J point and it must be 1mm or greater in elevation from the isoelectric line before we consider it to be elevated.

Front 52

Stokes-Adams syndrome

Back 52

Fainting from transient complete AV block (3rd degree heart block). Ventricles stop contracting for 5-30 sec because of overdrive suppression meaning they are used to atrial drive.
Patient faints because of poor cerebral bloodflow
Then, ventricular escape occurs with A-V nodal or A-V bundle rhythm (15-40 beats /min).
Pacemakers connected to right ventricle are provided for these patients.

Front 53

Incomplete intraventricular block

Back 53

Impulse is sometimes blocked and sometimes not in peripheral portions of Purkinje system resulting in abnormal QRS waves. Purkinje can’t fire during its refractory phase and misses a beat
Electrical alterans
Can be caused by ischemia, myocarditis, and digitalis toxicity

Front 54

Causes of ectopic foci are

Back 54

(1) Local areas of ischemia
(2) Calcified plaques
(3) Toxic irritation of A-V node, Purkinje system or myocardium by drugs, nicotine or caffeine

Front 55

AV nodal, AV bundle premature contractions

Back 55

P wave early and inverted—high A-V junction
P wave missing—mid A-V junction
P wave late and inverted—low A-V junction
Impulse travels backward into atria

Front 56

Relationship between Pressure, Flow, and Resistance

Back 56

Q=P/R
Flow (Q) through a blood vessel is determined by:
1) The pressure difference (P) between the two ends of the vessel
2) Resistance (R) of the vessel

Front 57

Peripheral vascular resistance

Back 57

= blood pumped out of the heart every second. It averages 100mls. PVR
Heart generates about 100 mm Hg pressure.
Resistance of the entire systemic circulation is 100ml/100mmHg or 1PRU – peripheral resistance unit.
If all the vessels constrict, PRU can be as high as 4. In shock PRU can drop to 0.2
Pulmonary pressure: Mean pulm art press = 16mm Hg. Mean left atrial press = 2mm Hg. Net pulm press = 14mm Hg.
C.O = 100 ml / sec. Pulm vasc resistance = 0.14PRU about 1/7th of the systemic resistance

Front 58

Conductance

Back 58

Conductance is how well a vessel conducts. Exact opposite of resistance = (1/resistance)
Conductance is a measure of the blood flow through a vessel for a given pressure difference.
Units ml/min per mmHg

Front 59

Poiseulle’s Law

Back 59

Q =_Pr4
8l
Q =pie(change in Pressure)radius to the 4
8(viscosity of the fluid)Length of tube

Front 60

Parallel and serial resistance

Back 60

Brain, kidney, muscle, G.I, skin and coronary are arranged in parallel. So, removal of a parallel tissue – like a kidney, or any amputation – reduces conductance and increases resistance

Front 61

Effect of Vessel Diameter on Blood Flow

Back 61

The conductance of a vessel increases in proprotionto the fourth power of the radius (r4)

Front 62

Vascular Distensibility

Back 62

Vascular Distensibility is the fractional increase in volume for each mmHg rise in pressure
Veins are 8 times more distensible than arteries
Veins provide a reservoir function
Pulmonary arteries are relatively distensible and under much lower pressures than art.s. They are about 6 x as distensible as systemic art.s
Vascular Disten= Increase in volume
Increase in pressure x Original volume

Front 63

Vascular Capacitance (or compliance)

Back 63

Vascular capacitance is the total quantity of blood that can be stored in a given portion of the circulation for each mmHg.
Veins are more compliant and more distensible than arteries
Capacitance = Distensibility x volume
The capacitance of veins is 24 times that of arteries.
Vascular compliance =
Increase in volume
Increase in pressure

Front 64

Starling Forces (Part II)

Back 64

Presence of negative ions on proteins increases the colloid osmotic effect of proteins–Donnan effect.
Plasma colloid osmotic = 28mmHg
Plasma protein conc. = 7.3mg/dl
The reflection coefficient of capillaries quantitates the amount of protein that is reflected away from the capillary membrane.
Reflection coefficient of 1 means all proteins are reflected and none pass through pores, reflection coefficient of 0 means membrane is permeable to all proteins.
In general, a colloid or colloidal dispersion is a substance with components of one or two phases. A colloid mixture is a heterogeneous mixture where very small particles of one substance are distributed evenly throughout another substance. A colloid mixtures particles are between 1 nm and 1000 nanometers in diameter. Typical membranes restrict the passage of dispersed colloidal particles more than they restrict the passage of dissolved ions or molecules; i.e. ions or molecules may diffuse through a membrane through which dispersed colloidal particles will not. The dispersed phase particles are largely affected by the surface chemistry existent in the colloid.
Many familiar substances, including butter, milk, cream, aerosols (fog, smog, smoke), asphalt, inks, paints, glues, and sea foam are colloids.

Front 65

Vasodilator theory

Back 65

as cells metabolize ATP, adenosine is released into the interstitial fluid and causes cap.s and arterioles to dilate. Other possible dilators – CO2, histamine, K+ ions and H+ ions from lactic acid

Front 66

Oxygen lack theory

Back 66

or nutrient lack – smooth MM contraction in the cap. Sphincters and meta-arterioles, require Ox to sustain the contraction. As Ox drops, the sphincters begin to lose strength and open. Other dilators – drop in glucose, vitamin deficiency Bs esp: niacin, thiamine, riboflavin will cause dilation.

Front 67

Active hyperemia

Back 67

tissue is metabolically active and blood flow is high.

Front 68

Reactive hyperemia

Back 68

Blood flow is occluded for a time, then restored, flow to the tissue is high, long enough to reduce the tissue debt

Front 69

Vasoconstrictors

Back 69

Norepinephrine – powerful vaso constrictor
Epinephrine – can be a dilator in cardiac MM
not as powerful a constrictor
Angiotensin II – constricts areas. Esp small arterioles
Vasopressin (ADH) – can greatly raise BP esp after trauma
Endothelin – released after BV damage, causing vessel spasm

Front 70

Vasodilator agents

Back 70

Bradykinin – arteriole dilation and cap permeability
Histamine – “ “
Prostaglandins – “ “
Nitric oxide – as Endothelial Derived Relaxing Factor – as press in cap.s h sheer forces on endoth cells cause release of EDRF
And vessel dilates