Week 3 Flashcards

1
Q
  1. Explain the distinction between the peripheral venous compartment and the central venous compartment.
A

Peripheral venous compartment is a large and diverse peripheral section and the central venous compartment is a smaller intrathoracic section that includes the venae cavae and the right atrium

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2
Q
  1. Name the systemic vascular that space most directly determines cardiac filling pressure.
A

Central venous compartment, central venous pressure is cardiac filling pressure

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3
Q
  1. Compare the volume of the unfilled systemic vascular circuit and the actual volume of blood that occupies this space in a typical young, health adult, and calculate the mean circulatory pressure resulting from the additional volume of blood.
A

3.5 is the total systemic circuit volume, normally however the systemic circuit contains about 4.5L of blood and this is somewhat inflating, giving a pressure of about 7mmHg which would exist throughout the system in the absence of flow

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4
Q
  1. List the two major factors that affect mean circulatory filling pressure.
A

The two major factors that affect mean circulatory filling pressure are the circulating blood volume and the state of the peripheral venous vessel tone (more effective than arterioles because of veins huge volume, veins being the only that really affect filling pressure)

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5
Q
  1. Explain how the flow-induced distribution of blood volume affects the pressures in systemic arteries and veins, and explain in particular why the pressure in the veins tends to remain close to the mean circulatory filling pressure that would be measured in the absence of flow.
A

The flow caused by the cardiac pumping action does tend to shift some of the blood volume from venous to arterial side, causing arterial side pressures to increase above the mean circulatory pressure while pressures on the venous side decrease below it. Because veins are about 50 times more compliant than arteries the flow induced decrease in venous pressure is only 1/50th as large as the accompanying increase in arterial pressure. Even with flow, peripheral vein pressure usually stays close to mean circulatory filling pressure.

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6
Q
  1. Explain the technical distinction between cardiac output and venous return, and state how their magnitudes compare when a person is in a stable cardiovascular situation (i.e., remaining at a consistent activity level like sitting continuously at rest).
A

In any stable situation, venous return must equal cardiac output or blood will accumulate in the circuit. In situations where they are not equal (in transitions), the central venous compartment is changing in volume and pressure.

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7
Q
  1. Review the relationship between cardiac filling pressure and cardiac output.
A

Greater filling pressure increases SV and cardiac out put via the stretch/contractility relationship (starling). Central venous pressure has a positive effect on cardiac output and a negative effect on venous return. Following a transient change, the central venous pressure changes to a point where they return to equal.

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8
Q
  1. Draw a graph that shows the normal relationship between central venous pressure and venous return, and indicate a point on the graph where the mean circulatory filling pressure is indicated.
A

Central venous pressure is always automatically driven to a value that makes cardiac output equal to venous return. Venous return increases as central venous pressure decreases. Changes in venous resistance can influence the slope of the venous function curve and if central venous pressure declines below intrathoracic pressure, the veins in the thorax collapse and tend to limit venous return. If the pressure of the central venous system is rises to the to the pressure of the peripheral system (generally close to the circulatory filling pressure, than venous return stops (NO FLOW)) Cause and effect only works in the direction of central venous pressure causes changes in venous return, and not the reverse.

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9
Q
  1. List three factors that can increase the peripheral venous pressure.
A

Changes in volume of blood within the elastic vessels will increase peripheral venous pressure, changes in circulating blood volume produce larger changes in the volume of veins due to their huge compliance. Changes in venous tone produced by increasing or decreasing the activity of sympathetic vasoconstrictor nerves will alter the venous pressure. Any increase in forces compressing veins from the outside also increases venous pressure (ie. Exercising or wearing elastic stockings)

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10
Q
  1. Draw a graph showing how a change in peripheral venous pressure changes the relationship between central venous pressure and venous return.
A

Increasing peripheral venous pressure shifts the whole curve up and to the right and decreased peripheral venous pressure shifts the venous function curve down and to the left. Altering peripheral venous pressure changes the relationship between central venous pressure (volume directly proportional) and venous return

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11
Q

Central venous pressure determines both _______ and ________

A

cardiac output and venous return

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12
Q
  1. Provide an explanation for why central venous pressure (the pressure determining the filling of the right ventricle) can be assumed to determine the stroke volume and cardiac output from the left ventricle.
A

Because the right and left heart beat at the same rate, the volume pumped by the right side can be assumed pumped by the left side

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13
Q
  1. Using a graph that simultaneously plots cardiac output and venous return vs central venous pressure (Figure 28-5), explain why an initial change in central venous pressure will result in changes that eventually bring it back to the point where the two plots intersect.
A

Increased central venous pressure > increased right ventricular stroke volume >increased output of the right heart > temporarily right heart output is greater than left> blood accumulates in the pulmonary vasculature and rises left atrial pressure> increased left ventricular filling. Central venous pressure is always inherently driven to the value that makes cardiac output and venous return equal, so cardiac output and venous return always stabilize at levels where the cardiac function and venous function curves intersect

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14
Q
  1. Explain in stepwise fashion how cardiac output can be sustained after a hemorrhage by the combined effect of adjustments in cardiac and peripheral venous function.
A

Decrease in venous pressure, cardiac output would decrease and venous return would increase. The volume of venous compartment is increasing and this would produce a growing central venous pressure. Subnormal cardiac output evokes a number of compensatory mechanisms: increase the activity of cardiac sympathetic nerves to arteries or veins. There are separate influences on cardiac output and venous return, creating multiple operating points for the central venous pressure.

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15
Q

During hemorrhage, cardiac output is preserved at the expense of ______ ______ pressure.

A

central venous (until ECF is restored)

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16
Q
  1. Explain how observation of a patientÕs jugular vein could provide a diagnostic indicator of congestive heart failure.
A

Patients with abnormally high central venous pressure must have a depressed cardiac function curve, a right-shifted venous function curve or both. High central venous pressures are common with patients suffering congestive heart failure and this high central venous pressure would be apparent in jugular vein distension while upright (or at a height where jugular vein is 7cm higher than the right ventricle)

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17
Q

Low central venous pressure could mean? (two things)

A

increased cardiac function or decreased blood volume/venous tone

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18
Q
  1. Describe how central venous pressure is monitored in critical care situations, explain the two possible causes of abnormally low central venous pressure, and state which of the two is observed clinically to be the most common cause.
A

In critical care situations, central venous pressure is often monitored continuously via catheter inserted in a peripheral vein and advanced centrally until its tip is in the central venous compartment (or even into the lung artery to get left atrium pressure). Two possible causes of abnormally low central venous pressure is due to increased cardiac function curve or a left shifted venous function curve (which is normally observed as a result of low blood volume or lack of venous tone)

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19
Q
  1. Explain the need for systemic arterial blood pressure to be regulated at a level that is neither too high nor too low.
A

Arterial pressure must remain high enough to deliver blood to organs but not to high to cause unnecessary demands on the heart and vessels. Appropriate systemic arterial blood pressure is the single most important requirement for the proper function of the cardiovascular system

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20
Q
  1. Name the reflex that is the single most important mechanism providing short-term regulation of systemic arterial pressure.
A

The arterial baroreceptor reflex is the single most important mechanism providing short-term regulation of arterial pressure

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21
Q
  1. List the five general components of a reflex pathway, and then describe how the components involved in reflex control of systemic arterial pressure fit into that model.
A

Sensory pathways (arterial baroreceptors), afferent pathways (cranial nerves to the medulla), integrating centers in CNS efferent pathways (cardiovascular sympathetic and cardiac parasympathetic) and effector organs (heart and peripheral blood vessels)

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22
Q
  1. Describe the anatomical locations of the preganglionic autonomic cell bodies that initiate the efferent pathways involved in controlling arterial pressure.
A

Within in the central nervous system (lateral horn) for the sympathetic and in the brainstem for the parasympathetic

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23
Q
  1. Describe the location and mechanism of functioning of the arterial baroreceptors.
A

Barorecptors are in the walls of the aorta (arch) and the carotid arteries (bifurcation of common to internal and external). They are mechanoreceptors that sense arterial pressure indirectly from the degree of stretch of the elastic arterial walls. In general increased stretch causes increased firing, both the absolute change and the rate of change are Ômeasured.Õ

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24
Q
  1. Draw a diagram that demonstrates how baroreceptors respond differently to constant pressure vs pulsatile pressure.
A

The presence of pulsating pressure increases the baroreceptor firing rate at any given level of mean arterial pressure

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25
Q
  1. Explain the significance of the shape of the baroreceptors firing vs arterial pressure curve, particularly in the region near the normal mean arterial pressure.
A

The changes in mean arterial pressure near the normal value of 100 mmHg produce the largest changes in baroreceptor discharge rate. Near 100 it takes very little change in pressure to change firing of the receptors

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26
Q
  1. Describe what happens to the baroreceptors firing rate if arterial pressure remains elevated above normal over a period of several days.
A

If arterial pressure remains above normal over a period of several days, the arterial baroreceptor firing rate will gradually return to normal (adapts and therefore is not a good mechanism for long term changes). This causes a shift to the right of the pulsatile curve.

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27
Q
  1. State the name of the general region of the brain involved in reflex regulation of the cardiovascular system. (Not the specific nuclei.)
A

medulla oblongata in medullary cardiovascular centers

28
Q
  1. Describe the effect of increased and decreased baroreceptors input on activity of (1)spinal sympathetic excitatory tracts, (2) spinal sympathetic inhibitory tracts, and (3) parasympathetic preganglionic neurons.
A

. Increased input from the arterial baroreceptors tends to inhibit the activity of the spinal sympathetic excitatory tract, stimulate the activity of the spinal sympathetic inhibitory tract and stimulate the activity of the parasympathetic preganglionic nerves. A simultaneous decrease in tonic activity of cardiovascular sympathetic nerves and increase in tonic activity of cardiac parasympathetic nerves occurs in arterial baroreceptor discharge.

29
Q
  1. Describe the events initiated by arterial baroreceptors responding to a decrease in mean arterial blood pressure, which mediate the negative feedback process that returns blood pressure toward normal.
A

Increased arteriolar tone, increased venous tone, increased cardiac contractility and increased heart rate contribute to changing the TPR and CO

30
Q
  1. List locations other than systemic arteries having mechanoreceptors and/or chemoreceptors that elicit cardiovascular reflex responses, and describe the cardiovascular variables they monitor.
A

Cardiopulmonary (blood volume detectors) receptors are mechano and chemo receptors in the atria, ventricles coronary vessels and lungs (cardiopulmonary receptors) sense the pressure (or volume) in the atria and central venous pressure by stretch. Not all of these mechanisms are for MAP homeostasis, these generally act by changing the set-point of the baroreceptor reflex. Increased firing in this system leads to inhibition of long-term mechanisms that increase blood volume (renal controls)

31
Q
  1. Describe the locations of chemoreceptors that influence cardiovascular function, list the chemical changes detected by them, and explain their effects on systemic arterial pressure.
A

Chemoreceptors are located in the carotid bodies and the arch of the aorta as well as central chemoreceptors located within the central nervous system. The increase firing in response to low oxygen, low pH (high CO2). This reflex stimulates sympathetics to increase MAP and stimulates respiration. Cerebral ischemia is detected by central chemoreceptors (near CV control centers), which produces sympathetic vasoconstriction and cardiac stimulation.

32
Q
  1. Explain what occurs during the Cushing reflex (aka, CushingÕs phenomenon).
A

Increase in arterial pressure that parallels a rise in intracranial pressure occurs to sustain blood flow to the brain. CushingÕs syndrome cause extremely increased arterial pressure (strong activation of sympathetic centers) in response to high CO2 and low pH of cerebral ischemia. With the strong sympathetic activation, you also get parasympathetic activation as a compensatory mechanism and reflex bradycardia

33
Q
  1. Describe the cardiovascular effects associated with emotional responses to embarrassment (blushing), danger (fight-or-flight), and extreme stress (vasovagal syncope).
A

Corticohypothalimc pathways originate in the cerebral cortex and reach the medullary cardiovascular centers- loss of sympathetic vasoconstrictor activity only to particular cutaneous vessels causes blushing. The alerting reaction increases sympathetic tone in pupillary dilation, increased skeletal muscle tenseness and increase in blood pressure. Extreme stress in some individuals can lead to fainting (vasovagal syncope) due to a large increase in sympathetic tone which leads to decreased cerebral blood flow

34
Q
  1. Propose a mechanism to explain the slight increase in mean arterial pressure (and in respiration rate) that occurs during voluntary exercise.
A

Central command increases mean arterial pressure and respiration rate during voluntary exercise. This can work as a feedforward mechanism. Descending motor pathways that activate skeletal muscle groups also recruit both respiratory and CV control centers to increase breathing, sympathetic activity, cardiac output and MAP to accommodate physical activity

35
Q
  1. Describe the variability in the effects of different types of pain on mean arterial blood pressure.
A

Superficial pain causes an increase in blood pressure (similar to alerting response). Deep pain from viscera or joints causes decreased sympathetic tone (which may contribute to shock in a vasovagal-like response).

36
Q
  1. Explain the Òrenal-MAP set pointÓ model of long-term regulation of arterial pressure.
A

In the long term, mean arterial pressure is whatever it needs to be to maintain an appropriate blood flow through arterial pressure via effects on renal function. Because baroreceptors adapt, they canÕt determine the long-term set point so renal control of fluid balance becomes important (Renal-MAP set point theory)

37
Q
  1. List the steps of the cause/effect mechanisms connecting an increase in blood volume to a change in arterial pressure.
A

Increase in blood volume means increased peripheral venous pressure and a right shift of venous function curve. This leads to an increase in central venous pressure and increase in cardiac output, furthermore, increase in arterial pressure (compensation).

38
Q
  1. Explain how arterial blood pressure affects urinary output rate, and describe how that relationship participates in the negative feedback control of arterial blood pressure.
A

A decrease in arterial pressure causes a decrease in urinary output rate and thus an increase in blood volume. In a healthy person, there is a very tight control of fluid through urinary output. (steep relationship between arterial pressure and urine output)

39
Q
  1. Correctly complete this phrase: ÒIn the long term, the arterial pressure must be that which makes the urinary output rate equal to the ___________________.Ó
A

Fluid intake rate

40
Q
  1. Draw a graph showing the urine output rate vs the mean arterial pressure for a healthy person.
A

steep relationship in a healthy person between MAP and urinary output

41
Q
  1. List the two general categories of effects that alter cardiovascular variables after a disturbance alters arterial pressure from normal.
A

. Variable that change due to the effect of the disturbance and variables that change due to compensatory response of the arterial baroreceptor reflex/ renal fluid balance mechanisms

42
Q
  1. Describe the change in pressure occurring in veins, capillaries, and arteries of the feet when a person goes from a recumbent to a standing position.
A

In a standing individual, additional cardiovascular pressure differences exist between the heart and other regions. Going from incumbent to standing increases venous transmural pressure, distends the compliant peripheral veins and greatly increases peripheral venous volume by as much as 500mL in a normal adult The increase in capillary transmural hydrostatic pressure causes a tremendously high transcapilary filtration rate although flow remains the same at every level. Bulk flow can cause edema of the lower extremities.

43
Q
  1. Describe the effect of sympathetic firing on blood pressures and distribution in the lower extremity of a standing individual.
A

Arteriole constriction can cause a greater pressure drop across arterials, but this has a limited effect on capillary pressure because venous and capillary pressure remains extremely high.

44
Q
  1. Describe the effect of the skeletal muscle pump on blood pressures and distribution in the lower extremity of an upright, exercising person.
A

A standing person requires the skeletal muscle pump to maintain flow, which if decreased affects central blood volume, stroke volume, cardiac output and arterial pressure. The skeletal pump expels both venous blood and lymph form an area of skeletal muscle which allow the one-way valve to partially support the weight of the fluid, therefore capillary pressure and transcapillary fluid filtration rate are dramatically reduced for some period after skeletal muscle contraction.

45
Q
  1. List the primary disturbances (uncompensated) of cardiovascular variables that occur in a standing person, and list the compensatory responses elicited by the medullary cardiovascular centers.
A

An increase in arterial and venous pressures in the lower extremities causing signaling in the arterial and cardiopulmonary baroreceptor

46
Q
  1. List the factors that explain why the arterial blood pressure of a standing person might be slightly overcompensated compared to the normal pressure of a recumbent person.
A

Heart rate and total peripheral resistance are greater when and individual stands. Average arterial baroreceptor discharge rate can actually decrease in spite of a small increase in mean arterial pressure if there is a simultaneously sufficient large decrease in pulse pressure. Cardio pulmonary receptors may interpret signals and re-set the set point. Mean arterial pressure determined by sphymomanometry from the arm of a standing individual overestimates the mean arterial pressure actually being sensed by the baroreceptors in the carotid sinus because of they are higher than the pressure in the arm.

47
Q
  1. Describe the changes in cardiovascular system function that occur when an individual is subjected to long-term bed rest.
A

First is a shift in the fluid from the lower extremeities to the upper portions of the body (increase in central venous pressure), which can cause distention of the head and neck veins, facial edema, nasal stuffiness and decreases in calf girth and leg volume. The increase in ventral blood volume stimulates the cardiopulmonary mechanoreceptors which influence renal function by neural and hormonal pathways to reduce sympathetic drive and promote fluid loss. In a few days the patient can become hypovolemic because their normal coping mechanisms upon standing are not as effective. (must exercise orthostatic reflex before returning patient completely upright)

48
Q
  1. Explain the function of the respiratory pump (thoracoabdominal pump).
A

Because of one way valves the negative pressure created on inspiration transiently increases the pressure gradient between the peripheral and central venous pools and causes venous return to the central venous pool. Transient changes in cardiopulmonary receptor activity cause variable firing of parasympathetics and variable heart called Òrespiratory arrhythmiaÓ

49
Q
  1. Describe the valsava maneuver, and its effect on blood pressures and flow.
A

Valsalva maneuver is normally performed by forced expiration against a closed glottis, which leads to a decrease in venous return and arterial blood pressure. This evokes a compensatory reflex increase in heart rate and peripheral vasoconstriction. After the maneuver, HR momentarily drops then increases due to the venous blood moving rapidly into the central venous pool, increasing stroke volume, cardiac output and arterial pressure. Dangerous for people at risk for a cerebral vascular accident because it can lead to vascular rupture of weakened blood vessels.

50
Q
  1. Describe the major change in blood volume during pregnancy, and why it occurs.
A

There is nearly a 50% increase in circulating blood volume during pregnancy. The placenta is a low resistance organ (highly vascular organ) added in parallel so it decreases TPR by about 40%

51
Q
  1. Explain how blood flow through the fetal heart and great vessels is different from the postnatal state, and the changes occurring at birth that cause the transition.
A

Very little blood flows into the pulmonary artery because of the vascular resistance of the collapsed fetal lungs. The fetal right and left heart work in parallel to pump blood through the systemic organs and the placenta due to shunts like the foramen ovale and the ductus arteriousus. At birth there is a decrease in pulmonary vascular resistance which decreases pulmonary pressure. At the same time there is growing systemic pressure (resistance increases due to the loss of the placenta), reversing the flow through the atria. Ductus arteriosus closes and the foramen ovale gradually seals. There is also an increased pressure afterload on the left ventricle and decreased on the right ventricle. Babies have higher heart rates and lower arterial pressures than adults; by adolescence they are near adult values.

52
Q
  1. Explain the shift in the QRS axis that occurs from birth into childhood.
A

Pulmonary vascular resistance decreases precipitously at birth due to remodeling of alveolar vessels. Distinct difference between right and left ventricular mass and wall thickness develop only after birth converting from right ventricle dominance to left ventricle dominance due to increased afterload of the left ventricle. Bonus: heart murmurs occur in 50% of healthy children, most without any associated pathology.

53
Q
  1. List some of the age-dependent alterations in the function of the heart and blood vessels.
A

Cardiac changes include: decrease in the resting and max cardiac index, a decrease in the maximum heart rate, an increase in the contraction and relaxation times of the heart muscle, an increase in the myocardial stiffness during diastole a decrease in number of functional myocytes and an accumulation of pigment in the myocardial cells; vascular changes include a decrease in capillary density in some tissues, a decrease in arterial and venous compliance and an increase in total peripheral vascular resistance and increase in pulse pressure. Arterial baroreceptor-induced responses to changes in blood pressure are blunted with age due to decrease in receptor responsiveness, decreased norepinephrine, and sympathetic response

54
Q
  1. List functional differences in the cardiovascular system between males, premenopausal females, and postmenopausal females.
A

Premenapausal women have lower left ventricular mass to body mass ratio, which may reflect a lower cardiac afterload in women. This may result form lower arterial pressure, greater aortic compliance and improved ability to induce vasodilatory mechanisms because of estrogenÕs protective effects. After menopause these gender differences disappear, in fact, older women with ischemic heart disease often have a worse prognosis than men. Women have lower intrinsic heart rates and longer QT intervals than do men, they are at greater risk for developing long Q-T intervals and torsades de points. They are twice as likely as men to suffer atrioventricular nodal reentry tachycardias.

55
Q
  1. Draw a diagram that summarizes influences on the medullary cardiovascular centers and how they affect sympathetic outputs that regulate systemic arterial blood pressure.
A

things that increase the set point: response to exercise, alerting reaction, cerebral ischemic response, cushing reflex, increase in CO2 arterial pressure, decrease in central venous pressure or cutaneous pain

56
Q

Discuss the EKG elements of supra ventricular tachyardia

A

rhythm originates in the atria so there will be a p wave preceding each QRS (which will be narrow) (supra ventricular abnormality)

57
Q

Discuss the EKG elements of first degree block.

A

prolonged PR interval (supra ventricular abnormality)

58
Q

Discuss the EKG elements of second degree block

A

not all P wayne are followed by QRS complex as conduction pathway may still be in refractory (supraventricular abnormality)

59
Q

Discuss the EKG elements of third degree block

A

P wave (at regular intervals) register completely in completely different time than the QRS complex (bradycardia ventricular rhythm) as action potentials are being initiated by different locations (supra ventricular abnormality)

60
Q

Discuss the EKG elements of atrial fibrillation.

A

Very irregular QRS complexes with no regular P waves. (supra ventricular abnormality)

61
Q

Discuss the EKG elements of bundle branch block.

A

QRS complex is split with two R waves due to the varying timing of the ventricle depolarization; the later R wave belongs to the ventricle with a bundle block (slower depolarization); compare lead and direction of deflection to determine right and left bundle blocks (ventricular abnormality)

62
Q

Discuss the EKG elements of premature ventricular contraction.

A

(PVC) because the contraction is from an ectopic cell, it causes a very wide QRS complex (AP travels very slowly) (ventricular abnormality)

63
Q

Discuss the EKG elements of ventricular tachycardia.

A

Repeating and wide QRS complex, QRS complex originates in the ventricle. (ventricular abnormality)

64
Q

Discuss the EKG elements of long QT syndrome with torsades des pointes.

A

elongated QT segments that degenerate into V-tach of varying magnitudes. (ventricular abnormality)

65
Q

Discuss the EKG elements of ventricular fibrillation

A

random and irregular depolarization of ventricles, resulting in a very squiggly line and poor blood pumping