Unit 4 - Wk 4 Physiology

Front 1

where are baroreceptors located?

Back 1

carotid sinus (via carotid bodies)
wall of aortic arch

Front 2

How is vasomotor tone maintained?

Back 2

Tonic stimulation of 1-2 AP's per second; if tonic contraction is not maintained there is a 50% drop in bp

Front 3

Where do you monitor flow to the head and body?

Back 3

Head = carotid bodies/sinus

Body = aortic arch

Front 4

How are signals transmitted from the carotid sinus?

Back 4

Herings nerve to the glossopharyngeal nerve to the nucleus tractus solitarius of the medulla

Front 5

How are baroreceptor signals transmitted from the arch of the aorta?

Back 5

Vagus into the nucleus tractus solitarius

Front 6

Most sensitive range for carotid sinus baroreceptors?

Back 6

60-180 mmHg

The reflex is most sensitive at 100 mmHg (as pressure increases # of impulses from carotid sinus increase which = inhibition of vasoconstrictor center and activation of the vagal center to the heart)

Front 7

Which vascular control mechanism is the fastest?

Back 7

Baroreceptors; act within a couple of seconds

Front 8

Which mechanism is effective control between 60 mmHg - 180 mmHg

Back 8

Baroreceptors

Front 9

Why don't quick vascular control repsonses (baro/chemoreceptors) respond for long term?

Back 9

Receptors reset according to the new pressure established

Baro/Chemo get blood w highest 02 and lowest C02

Front 10

Which response is faster; baroreceptors or chemoreceptors?

Back 10

Baroreceptors

Front 11

Describe the ischemic response

Back 11

Cerebral iscemia > increased C02 > VMC activated > increased symp activity > increased arterial pressure

Front 12

What is the direct affect of aldoesterone related to blood pressure?

Back 12

Stimulates the retention of sodium by the kidney (increases action of the sodium/potassium pump)

Front 13

Best definition of shock

Back 13

Inadequate perfusion of tissue (which can be caused by a ton of stuff obv)

Front 14

During shock does a pt often go acidodic or alkalotic?

Back 14

Acidotic;

Pts with a large base deficit (15 mmol) = mortality of 70%

Front 15

Acute Respiratory Alkalosis

Back 15

PC02 decreased, pH increased, HC03 depressed

H20 + C02 <- (carbonic anhydrase) -> H + HC03

Front 16

Metabolic Acidosis

Back 16

Accumultation of lactic acid because tissues are not being perfused adequately and later due to renal failure

Front 17

Anion Gap

Back 17

Degree of acidity experienced during metabolic acidosis

Na - Cl + HC03

Increased anion gap = decrease in bicarb levels

Front 18

Third Spacing of Fluid

Back 18

Movement of fluid out of cardiovascular system into the tissues/other spaces

Third spacing occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or "third" space - the nonfunctional area between cells

Often happens in shock due to increased capillary permeability

Front 19

Hemorrhagic Shock

Back 19

Loss of substantial blood volume for period of time; if rapidly returned wont produce shock

Exanguination does not equal shock; pt can die from exanguination but not be in shock; must be inadequate tissue perfusion

Wigger's Model: Decreased bp to approximately 50 mmHg for several hours

Front 20

Cardiogenic Shock

Back 20

Loss of cardiac function (pericardial, myocardial or valvular dysfunction)

Front 21

Distributive Shock

Back 21

Septic Shock;

can be induced experimentally by injection of endotoxin or lipopolysaccharide iv or injection of live bacteria

Front 22

L/P ratio = conc of protein in lymph/plasma

Back 22

If capillaries are totally permeability and unable to retain protein in circulation L/P ratio = 1

As LP ratio drops it means there is a lower conc of protein in lymphatic fluid compared to plasma

Front 23

How does cortisol affect blood pressure?

Back 23

Helps NE promote vasoconstriction

Front 24

Renin

Back 24

Released from kidneys; produces A1 from angiotensinogen; A1 (ACE) -> AII which is a potent vasoconstrictor

Front 25

In the early stages of shock would there be respiratory alkalosis or acidosis?

Back 25

A short lived respiratory alkalosis due to hyperventilation; however this is short and will become acidosis as lactate acid builds up from peripheral tissues

Front 26

Pulmonary Shock Response

Back 26

ARDS due to WBC release inflammatory mediators

Front 27

Renal Shock Response

Back 27

Acute renal failure due to decreased blood flow (so don't give antibiotics that use renal metabolism/nephrotoxicity)

Dopamine has been suggested to stimulate the cardiovascular system due to its sparing of renal blood flow

Front 28

Metabolic Shock Response

Back 28

Build up of lactic acid due to decreased tissue perfusion; glucose levels in the plasma can be either elevated or depresed; often an increase in protein catabolism that results in a negative nitrogen balance

Front 29

Inflammatory Response in Shock

Back 29

Prostaglandins, TXA2, leukotrienes

Oxygen radicals from AA pathway is activated during shock

Front 30

Tx hemorrhagic shock

Back 30

Fluids at a rapid rate to restore hemodynamic function (2-3 liters in 10 min)

If Hg conc falls below 10g/dL, blood should be given. this should be matched but if not use type 0

Front 31

Tx cardiogenic shock

Back 31

Pulmonary capillary wedge pressure; indicates how well heart is pumping blood; can put in a Swan-Ganz catheter to measure this

can give dopamine, NE, or dobutamine to increase PCWP

Lasix can help reduce fluid loads (diuretics)

Front 32

Tx septic shock

Back 32

Fluid tx to maintain pulmonary capillary wedge pressure at 15 mmHg

Oxygen support/ventilation

drugs to increase cardiac output

Antibiotics to control infection
In severe wound infection debridement or drainage may be required

Front 33

Steroids have been used as a treatment for shock in patients. This was because

Back 33

Steroids helped to reduce the movement of fluid into the interstitial space; stabilize capillary membranes

Front 34

You are treating a 21 year old male patient who was admitted to the hospital 1 hour ago for treatment of injuries sustained in a motor vehicle accident. He lost a large volume of blood. The accident apparently occurs several hours before the paramedics were called. Once the monitors are in place, you find that he has an increased heart rate, increased cardiac output, and increased respiratory rate. These data suggest that the

Back 34

Patient may be in the hyperdynamic phase of shock and will soon exhibit depressed cardiovascular parameters if treatment is unsuccessful.

Front 35

A patient is in the early stages of shock. He is hyperventilating. This can result in
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Respiratory acidosis
E. Mixed respiratory and metabolic acidosis

Back 35

Respiratory alkalosis

Front 36

A patient is in the advanced stages of shock. All treatments have failed to produce an improvement in his condition. He will most likely be in
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Respiratory acidosis
E. Mixed respiratory and metabolic acidosis

Back 36

Metabolic acidosis due to buildup of lactic acid