test 3

Question 1

What is circulatory shock

Answer 1

 Inadequate blood flow through body resulting in tissue damage because
they are not receiving enough oxygen and other needed nutrients and
metabolic wastes are not being removed.

Question 2

Circulatory shock involves what tissues

Answer 2

 Involves ALL tissues of body including cardiovascular system.

Question 3

what happens to bp during circulatory shock

Answer 3

 Blood pressure may or may not fall

Question 4

positive feedback mechanisms

Answer 4

-whatever the controller is as it starts going up, it starts creating an increase

Question 5

treatment of circulatory shock

Answer 5

 need to catch problem before it has spiraled out of

control

Question 6

Low output failure

Answer 6

 Abnormalities that decrease ability of heart to pump blood (OUTPUT PROBLEMS)
-Cardiogenic shock caused by cardiac problems
 Abnormalities that decrease venous return (INPUT PROBLEMS)
-Most common form is loss of circulating blood volume
-Decreased venous tone and accumulation of fluid in veins
-Obstruction to blood flow (myxoma)

Question 7

high output failure

Answer 7

 Cardiac output normal or even higher than normal yet tissues not receiving enough blood flow

• High metabolic rates (systemic septicemia)
• Abnormal tissue flow patterns (shunting)

Question 8

Stages of Shock

Answer 8

 Nonprogressive stage (Compensated stage)
 Progressive stage
 Irreversible stage

Question 9

Nonprogressive stage (Compensated stage)

Answer 9

 Normal compensatory mechanisms able to stabilize patient and can lead to full recovery without external intervention

Question 10

Progressive stage

Answer 10

 Without external intervention patient will die

Question 11

Irreversible stage

Answer 11

 Does not matter if external intervention is applied, the patient will die

Question 12

“Common” Types / Causes of Shock:

Answer 12

 HYPOVOLEMIA (hemorrhagic shock most common)
 Neurogenic (increased vascular capacity i.e. increased compliance)
 Anaphylactic / histamine
 Septic

Question 13

decrease in CBV does what to sympathetic compensatory mechanisms

Answer 13

 Increase SVR
 Increase HR & contractility
 Increase arterial & venous tone
-keeps P and CO good

Question 14

decrease in CBV without Without sympathetic response

Answer 14

-patient would die after losing 15 to 20% of CBV versus 30 to 40% loss with mechanisms intact

Question 15

Second plateau in BP waveform

Answer 15

-CNS ischemic response kicks in

Question 16

Big increase in SVR diverts remaining CO to

Answer 16

-heart and brain

 Cerebral and coronary blood flow remains close to normal as long as BP above 70 mmHg

Question 17

Progressive versus Nonprogressive

Answer 17

 All groups where blood pressure stayed above 45 mmHg survived
-Compensatory mechanisms kept patient alive
 All groups where blood pressure dropped below 45 mmHg died
-The greater the blood loss, the quicker
death occurred
-Compensatory mechanisms not able to
stop deterioration of circulatory function

Question 18

Compensatory Mechanisms Maximum activation within 30 seconds

Answer 18

 Baroreceptors; Chemoreceptors; CNS ischemic response
 Reverse stress-relaxation of blood vessels
 Increased release of epinephrine and norepinephrine from adrenal medulla and resulting increase in heart rate and increase in arterial and venous tone

Question 19

Compensatory Mechanisms Maximum activation within 10 minutes to an hour

Answer 19

 Increased release of renin and angiotensin II production
 Increased release of aldosterone
 Increased release of anti-diuretic hormone

Question 20

Compensatory Mechanisms Maximum activation within 1 to 48 hours

Answer 20

 Increased water reabsorption from intestinal tract
 Movement of interstitial fluid into the capillaries (increased CBV)
 Increased retention of salt and water by kidneys
 Increased stimulation of thirst centers & salt appetite

Question 21

how does positive feedback affect Cardiovascular Deterioration

Answer 21

 Positive feedback mechanisms lead to further deterioration

Question 22

At “low” levels of shock which mechanism overrides the other and what happens when levels of shock increase

Answer 22

• normal compensatory mechanisms (negative feedback) over ride the positive feedback mechanisms.
• As level of shock increases, balance between negative feedback and positive feedback mechanisms shift
• If treatment initiated soon enough patient can be saved.

Question 23

Positive Feedback Mechanisms

Answer 23

 Cardiac depression
 Vasomotor failure / depression of vasomotor center
 Decreased flow leads to “sludge” in smaller blood vessels and further decrease in flow
 Increased capillary permeability due to hypoxia
 Toxin release from ischemic tissue (cell membrane breakdown)
-Histamine; serotonin; endotoxin from intestine
 Generalized cellular deterioration
-Sodium-potassium pump depressed; decreased mitochondrial activity; lysosome deterioration with hydrolase release; cellular metabolism stops
 Tissue necrosis
-Start with cells at venous end of capillaries
 Lactic acid and carbon dioxide accumulation (acidosis)
 Depletion of high-energy compounds

Question 24

Organ Deterioration

Answer 24

 Liver
-Failure of metabolic functions
-Failure of detoxification functions
 Lungs
-Development of pulmonary edema
-Impaired gas transfer
 Heart
-Step-by-step decrease in cardiac function

Question 25

Cardiac Deterioration

Answer 25

 When blood pressure falls low enough coronary blood flow decreases to point where it can provide adequate nutrition which further damages the heart  Damage to heart severe even during early stages BUT the huge cardiac reserve keeps heart from immediately reaching an inadequate level of performance  Cardiac depression probably more of a problem during later stages of shock -normal cardiac function for nearly 4 hours

Question 26

Other Cause of Hypovolemic Shock

Answer 26

```  Plasma loss (same characteristics as hemorrhagic loss but have added blood viscosity due to concentration of red cells) -intestinal obstruction -burns  Dehydration -Excess sweating -Excess diarrhea or vomiting -Inadequate fluid / electrolyte intake -Adrenal cortical destruction and subsequent decrease in aldosterone concentration  Trauma ```

Question 27

Neurogenic Shock

Answer 27

 Massive dilation of veins holds so much volume that venous return falls way below normal  Deep general anesthesia -Can depress vasomotor center to point no longer functional  Spinal anesthesia -If it extends up spinal chord and blocks sympathetic outflow  Brain damage -Especially if basal area of brain involved -Although short time of cerebral ischemia will cause large stimulation of vasomotor center, ischemia longer than 5 to 10 minutes will cause deactivation of the vasomotor center

Question 28

Anaphylactic & Histamine Shock

Answer 28

-Usually triggered by antigen-antibody reaction  Antibodies have strong interaction with antigen  Basophils / mast cells stimulated to release histamine  Histamine release

Question 29

Histamine release results in (3)

Answer 29

 Increased venous dilation (epi constrict)  Dilation of arterioles (epi constrict)  Increased capillary permeability -Loss of fluid and protein into interstitial fluid

Question 30

Septic Shock driven by

Answer 30

-bacterial infection  Gram-positive bacteria  Endotoxin-producing gram-negative bacteria

Question 31

Second biggest killer in hospitals following cardiogenic shock

Answer 31

-septic shock

Question 32

Major types of septic shock

Answer 32

 Peritonitis  Spread of skin infection  Gangrenous infection  Kidney / urinary tract infection that spreads to blood

Question 33

Features of Septic Shock

Answer 33

```  High fever  Vasodilation  Blood sludging (RBC agglutination)  Disseminated intravascular coagulation  Cardiovascular problems not seen until infection is widely spread and entrenched ```

Question 34

Treatment of Shock

Answer 34

 Volume replacement (PRBC, plasma) (hypovolemic)  Administration of sympathomimetic drugs (neurologic and anaphylactic shock, not well with hemorrhagic shock= ANS already max)  Head down position (Trendelenburg position)  Oxygen therapy (although oxygenation not problem)  Glucocorticoid administration (control glucose metabolism)- increase heart strength, stabilization of lysosomes, increase glucose metab in damaged cells)  Circulatory assist