Unit 4 - Wk 3 Physiology

Front 1

Compliance Equation

Back 1

C = dV/dP

Volume must start completely full to affect pressure; can only be measured after the system is full

Front 2

Capacitance

Back 2

Filling the container; you can only start to measure it after the system is full

Front 3

Total Peripheral Resistance Equation

Back 3

TPR = Arterial - Venous = 92 - 2 = 90; takes 90 mmHg to push blood through peripheral capillaries by minute

Front 4

Shows us what happens if you change the capacitance of a system (decreased capacitance = decreased venous pressure, etc)

Back 4

Compliance

Front 5

Back 5

CO maintained by retention of wtaer in moderate HF; but increased fluid volume can cause the heart to fail even further into severe HF; the body will retain even MORE water and this cycle will continue until death

Front 6

How does an increase in total peripheral resistance effect MAP, CVP, CO or patient weight?

Back 6

Front 7

How does increased CO effect MAp, CVP, CO and pt weight?

Back 7

Blood pumps from venous side to arterial side, decreased CVP and increases CO and MAP. Doesnt effect pt weight

Front 8

How does increased venous compliance affect MAP, CVP, CO and pt weight?

Back 8

Equivalent o increasing the volume of container

Front 9

How does decreased blood volume effect MAP, CVP, CO and pt weight?

Back 9

Less blood = less weight = less CVP = less venous return = decreased CO = decreased MAP

Front 10

How will a decrease in total peripheral resistance affect MAP, CVP, CO and pt weight?

Back 10

Decreased TPR doesnt change pt weight, CVP increases bc blood can flow easier from arterial to venous side; increased venous return = increased cardiac output; heart pumps against decreased afterload so mean arterial pressure decreases

Front 11

How will decreased cardiac output effect MAP, CVP, CO and pt weight?

Back 11

No change in pt weight, CO obv decreases, decrease CO = decrease CVP bc less side moved from venous side to arterial side, MAP will decrease

Front 12

How would decreased venous compliance effect MAP, CVP, CO and pt weight?

Back 12

Increase in CVP (decrease container size); increased venous return; increased cardiac output; MAP increases due to increased CO

Front 13

Mean Arterial Blood Pressure Equation

Back 13

MAP = (Systolic - Diastolic)/3 + Diastolic

MAP = (CO)(TPR) + CVP (shows us how we might effect MAP using beta blockers or calcium channel blockers)

MAP = Arterial Blood Volume/Arterial Compliance

Front 14

Arterial Blood Volume Equation

Back 14

ABV = (Total Blood Volume)(.12)

ABV = (MAP)(Arterial Compliance)

Front 15

Total Peripheral REsistance Equation

Back 15

TPR = (MAP - CVP)/CO

(92-2)/

Front 16

Central Venous Blood Pressure (CVP) Equation

Back 16

CVP = Venous Blood Volume/Venous Compliance

CVP = MAP - (CO)(TPR)

Front 17

Venous Blood Volume Equation

Back 17

VBV = (CVP)(Venous Compliance)

VBV = total Blood volume(2/3)

Front 18

Pulmonary Resistance Equation

Back 18

PR = (Pulmonary Artery Pressure - Pulmonary Vein Pressure)/CO

Front 19

Arterial Compliance Equation

Back 19

AC = dAV/dAP

Front 20

Venous Compliance

Back 20

VC = dVV/dVP

Front 21

Blood Flow Through the Systemic Capillaries Equation

Back 21

It is equal to cardiac output

Front 22

Blood Flow Through the Pulmonary Capillaries

Back 22

Equal to CO

Front 23

How does blood loss alone affect the curve?

Back 23

Front 24

Effect of exsanguination + sympathetic activation

Back 24

Also get a simultnaeous increase in TPR, which causes vascular function curve to become less steep; we will also see venoconstriction

Front 25

Effect of sympathetic activity and increased TPR and venoconstriction during exanguination on the curves

Back 25

You can see it's trying to push back to normal/increase CO

If blood loss isn't much or tx is given, you can return to normal, if the loss continues you end up in hemorrhagic shock

Front 26

Shock

Back 26

System can no longer respond; venodilation in the face of decreased blood volume

Front 27

Shock

Back 27

Hypodynamic stage of shock: heart is failing bc its not responding to sympathetic activity and Vascular curve shifts left cuz venoconstriction can no longer be maintained

Now CO is unable to sustain life of the system

Front 28

Effect of fight or flight on curves

Back 28

Increased CO, increased pressure/performance of vascular system

Front 29

Effects of nitroglycerin

Back 29

Venodilation (increased venous compliance), vasodilation (slight), increased cardiac function (reflex-slight)

Front 30

Effects of nitroglycerin

Back 30

Venodilation (increased venous compliance), vasodilation (slight), increased cardiac function (reflex-slight)

Front 31

21 yo in ED 30 min after MVC; femoral artery laceration; estimated he has lost 1.5L blood; what condition is produced by the blood loss after compensation has occured

Back 31

A decrease in blood volume, an increase in TPR and an increase in HR

Front 32

45 yo w in clinic; arterial bp = 180/110; blood volume is normal; what describes the cause of her condition?

Back 32

Increased total peripheral resistance

Front 33

60 yo during hip operation; concern for DVT; a drug given to decrease venous compliance; what describes the effect that this drug will have on the cardiovascular system

Back 33

Increased mean arterial pressure; it would do this by causing a venoconstriction which would push more blood to heart, increase CO and increase MAP

Front 34

Relationship of resistance to radius

Back 34

Resistance of a vessel is inversely proportional to the fourth power of the radius

Front 35

How quickly will unconsciousness occur in total cessation of blood flow to the brain?

Back 35

5-10 seconds

This occurs because lack of oxygen delivery to the brain cells shuts down most metabolism in these cells

Front 36

Three metabolic factors with potent effects in controlling cerebral blood flow

Back 36

1. carbon dioxide concentration
2. hydrogen ion concentration
3. oxygen concentration

Front 37

Back 37

Arterial PC02 and cerebral blood flow

Front 38

Back 38

Arterial PC02 and cerebral blood flow

Front 39

Hydrogen Ion Conc and Cerebral Blood Flow

Back 39

H+ increases cerebral blood flow (bc H+ decreases neuronal activity); increased flow carries hydrogen ions, carbon dioxide, and other acid forming substances away from brain tissue

Loss of carbon dioxide removes carbonic acid and brings H+ back to normal

Front 40

Oxygen Deficiency as a Regulator of Cerebral Blood Flow

Back 40

If blood flow to the brain ever becomes insufficient to supply this needed amount of oxygen, the oxygen deficiency mechanism for causing vasodilation immediately causes vasodilation, returning the brain blood flow and transport of oxygen to the cerebral tissues to near normal.

Front 41

Back 41

Autoregulation of Cerebral Blood Flow

Front 42

Is the brain capable of anaerobic metabolism?

Back 42

No; One of the reasons for this is the high metabolic rate of the neurons, so that most neuronal activity depends on second-by-second delivery of oxygen from the blood.

Front 43

What is the main supply of energy for brain cells?

Back 43

Glucose derived from blood; As is true for oxygen, most of this is derived minute by minute and second by second from the capillary blood, with a total of only about a 2-minute supply of glucose normally stored as glycogen in the neurons at any given time.

Front 44

Cushing Reaction

Back 44

CNS ischemic response that results from increased pressure of the CSF around the brain in the cranial vault; when CSF pressure rises to equal the arterial pressure, it compresses the whole brain as well as the arteries in the brain and cuts off blood supply to the brain. This initiates a CNS ischemic response that causes arterial pressure to rise

Front 45

How would increased preload affect the pressure volume loop?

Back 45

Increases in preload = increased EDV = increased venous return; causes an INCREASE IN STROKE VOLUME (frank starling); increased SV is reflected in increased width of PVL

Front 46

How would an increase in afterload affect the PVL?

Back 46

Increased afterload = increase in aortic pressure; the ventricle must eject blood against a higher pressure resulting in decreased SV; the decreased SV = decreased width of pressure volume loop; decreased stroke volume results in an increase in end systolic volume

Front 47

How does increased contactility affect PVL?

Back 47

The ventricle develops greater tension than usual during systole, causing an increase in stroke volume; the increase in stroke volume results in a decrease in end diastolic volume

Front 48

What is 1 -> 2?

Back 48

Isovolumetric contraction; cycle begins during diastole at 1; LV is filled with blood from left atrium and (EDV); ventricular pressure is low because muscle is relaxed; one xcitation the ventricle contracts and ventricular pressure increases; mitral valve closes when the left V pressure is greater than left A pressure; bc all valves are closed, no blood can be ejected from the ventricle (isovolumetric)

Front 49

What is 2 -> 3?

Back 49

Ventricular Ejection; the aortic valve opens at point 2 when pressure in the LV exceeds pressure in the aorta; blood is ejected into the aorta and ventricular volume decreases; the volume that is ejected in this phase is the STROKE VOLUME; thus, stroke volume can be measured graphically by the width of the pressure volume loop; the volume remaining in the left ventricle at point 3 is the end systolic volume

Front 50

What is 3 -> 4?

Back 50

Isovolumetric relaxation; at point 3, the ventricle realxes. When ventricular pressure decreases to less than aortic pressure, the aortic valve closes. Bc all of the valves are closed again, ventricular volume is constant (isovolumetric) during this phase

Front 51

What is 4 -> 1?

Back 51

Ventricular filling
Once left ventricular pressure decreases to less than left atrial pressure, the mitral valve opens and filling of the ventricle begins; during this phase, ventricular volume increases to about 140 ml (EDV)

Front 52

What is 4 -> 1?

Back 52

Ventricular filling
Once left ventricular pressure decreases to less than left atrial pressure, the mitral valve opens and filling of the ventricle begins; during this phase, ventricular volume increases to about 140 ml (EDV)

Front 53

Metabolic Hypothesis/Vasodialator Theory

Back 53

Tissue produces a vasodilatory metabolite that regulates flow (adenosine in the coronary circulation when ATP is degraded due to decreased oxygen)

The dilation of the arterioles is produced when the concentration of these metabolites increases in the tissue. The arterioles constrict if the tissue concentration decreases

Front 54

Oxygen Lack Theory

Back 54

Smooth muscle requires oxygen to remain contracted; when 02 conc in tissue rises above a certain level, the sphincters presumably close until the tissue cells consume excess oxyge

When the excess oxygen is gone and levels fall, the sphincters open to begin cycle again

Front 55

Vasomotion

Back 55

Cyclical opening and closing of precapillary sphincters and metarterioles several times a minute

Front 56

Reactive Hyperemia

Back 56

Same as metbaolic hypothesis

Lack of flow sets in motion factors that cause vasodilation

Front 57

Capillary blanch times greater than 2 seconds may indicate what?

Back 57

Dehydration, shock, peripheral vascular disease, hypothermia

Front 58

Myogenic Hypothesis

Back 58

Increased perfusing pressure causes stretch of the arteriolar wall and the surrounding smooth muscle

Bc an inherent property of smooth muscle is to contract when stretched, the arteriole radius decreases and flow does not increase significantly

This explanation cannot stand alone unless overcompensation to the stretch occurs

Front 59

endothelium derived relaxing factor (nitric oxide)

Back 59

rapid flow of blood through the arteries causes shear stress on endothelial cells = release of nitric oxide; NO increases the diameters of the upstream arterial blood vessels whenever microvascular blood flow increases downstream

Front 60

Oxygen and VEGF

Back 60

Vascular Endothelial Growth Factor promotes new vessel growth due to decreased oxygen

Front 61

Vasoconstrictor Agents

Back 61

norepinephrine, epinephrine, angiotensin II, vaospresin, endothelin

Front 62

Vasodilator Agents

Back 62

Bradykinin, Histamine

Front 63

hr < 60 bpm

Back 63

bradycardia

Front 64

hr > 100 bpm

Back 64

tachycardia

Front 65

hr > 250 bpm

Back 65

flutters; organized electrical contraction but not effective flow

Front 66

hr > 350 bpm

Back 66

fibrillations; random electrical events; not existant flow

Front 67

Back 67

Wiggers; know it

Front 68

Back 68

Find R wave on dark line; can calculate rate by looking where next R rate falls

300,150,100,75,60,50

Front 69

What's the rate?

Back 69

100

Front 70

What's the rate?

Back 70

150

Front 71

What's the rate?

Back 71

60

Front 72

Back 72

First degree heart block

Front 73

Back 73

Mobitz 2* heart block; normal PR interval but P wave is not followed by QRS; not every Q wave generates QRS contraction

Occurs BELOW THE AV NODE

Front 74

Back 74

Wenckebach; second degree AV conduction block; PR interval increases until the last P wave is not followed by QRS (PR lengthening NOT seen in mobitz)

Wenckebach is usually located in the AV node

Front 75

Back 75

Third degree heart block; total separation of atrial and ventricular contractions

Varied number of P's between QRST; multiple P waves with no QRST waves

Rate of QRST is often around 40 bpm

Front 76

Back 76

Bundle branch block; note rabbit ear appearance of R wave

Front 77

Back 77

Wolf Parkinson White Syndrome;

Front 78

Back 78

Premature Ventiruclar Contraction