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70 Cards in this Set

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remain contracted until a few milliseconds after the end of the T repolarization wave.
The ventricular fibers
this approximates the time of ventricular contraction
Q-T interval (Normally 0.35sec)
Heart Rate Calculation
R-R interval = 0.83 sec
Heart rate = (60 sec)/(0.83 sec) = 72 beats/min min beat
Mean Vector Through the Partially Depolarized Heart
Septum depol.s 1st, then the endocardial walls of the vents, spreading outward to exterior vents, then up from the apex to the base.
Einthoven’s triangle & law.
Sum of leads I+III always equals the potential of lead II
Bipolar limb leads
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
Lead I
The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left arm.
Lead II
The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left leg.
Lead III
The negative terminal of the electrocardiogram is connected to the left arm, and the positive terminal is connected to the left leg.
Einthoven’s Law
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
Precordial chest leads (Chest Leads V1- V6)
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
Augmented Unipolar Limb Leads aVR,
aVL, and aVF
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.
Biplolar Limb Leads
I Right arm and left arm
II Right arm and left leg
III left arm and left leg
Unipolar limb Leads
AVR Right arm
AVL Left arm
AVF Left leg
Unipolar Chest leads
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
Vector Analysis
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.
Lead Axis
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.
Voltages are measured form the
peak of R to the bottom of S
Q wave is present if
left side of the septum depolarizes first
First area to repolarize is near
the apex of the heart.
Last areas, in general, to depolarize are the first to repolarize.
Repolarized areas will have a ________ charge first;
Repolarized areas will have a + charge first; therefore, a + net vector occurs and a positive T wave.
Atrial depolarization is_________ than in ventricles.
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.
define mean electrical axis.
Draw a perpendicular line from the end of each vector, and the intersection
The mean electrical axis averaged over the entire period of depolarization is +_____o
The mean electrical axis averaged over the entire period of depolarization is +59o
Axis deviations are caused by
Changes in heart position: left shift caused by expiration, lying down and excess abdominal fat pushing up on diaphragm. Also, left ventr. hypertrophy
Hypertrophy of left ventricle (left axis shift)
caused by hypertension, aortic stenosis or aortic regurgitation causes slightly prolonged QRS and high voltage.
Hypertrophy of right ventricle (right axis shift)
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
Bundle branch block-
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
If sum of voltages of Leads I, II &III is greater than _____ mV, this is considered to be a high voltage EKG.
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).
Decreased voltages in standard limb leads
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.
Prolonged QRS
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.
Unusual QRS
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
Current of injury
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.
the J point is
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.
Axis of the current of injury
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.
Prolonged QRS
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.
Unusual QRS
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
Current of injury
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.
the J point is
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.
Axis of the current of injury
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.
Current of injury in acute (recent) anterior wall infarction.
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
Horizontal J point line shows
positive deviation – posterior wall injury
The T-P segment shows a current of injury following ___________
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.
Ventricular repolarization usually occurs in the __________ direction as depolarization which causes an upright T wave in the three standard leads.
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.
T wave abnormalities
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.
Where is the Q wave
It is the first downward deflection in the QRS
When can Q waves appear?
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
Q wave criteria for acute MI
The Qwave is more than0.04 sec wide
There are abnormalities in the T waves and /or ST segments
Isoelectric Line
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
The J Point
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
ST elevation
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.
Stokes-Adams syndrome
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.
Incomplete intraventricular block
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
Causes of ectopic foci are
(1) Local areas of ischemia
(2) Calcified plaques
(3) Toxic irritation of A-V node, Purkinje system or myocardium by drugs, nicotine or caffeine
AV nodal, AV bundle premature contractions
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
Relationship between Pressure, Flow, and Resistance
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
Peripheral vascular resistance
= 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
Conductance
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
Poiseulle’s Law
Q =_Pr4
8l
Q =pie(change in Pressure)radius to the 4
8(viscosity of the fluid)Length of tube
Parallel and serial resistance
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
Effect of Vessel Diameter on Blood Flow
The conductance of a vessel increases in proprotionto the fourth power of the radius (r4)
Vascular Distensibility
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
Vascular Capacitance (or compliance)
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
Starling Forces (Part II)
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.
Vasodilator theory
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
Oxygen lack theory
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.
Active hyperemia
tissue is metabolically active and blood flow is high.
Reactive hyperemia
Blood flow is occluded for a time, then restored, flow to the tissue is high, long enough to reduce the tissue debt
Vasoconstrictors
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
Vasodilator agents
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