exam 1 lecture 8

Question 1

circulatory shock

Answer 1

1. Hypovolemic
2. Cardiogenic
3. Distributive, vasodilatory
   a. Neurogenic
   b. Septic*
4. Obstructive (e.g. pulmonary
   embolism, tamponade) – sometimes grouped with cardiogenic shock

Question 2

hypovolemic shock

Answer 2

loss of extracellular fluid and electrolytes. The initial effect is a fall in MFP, a corresponding shift of the vascular function curve, a fall of preload, and a fall of cardiac output

Question 3

hypovolemic shock includes

Answer 3

hemorrhage, burns, vomiting and diarrhea, anaphylactic shock, trauma

Question 4

response to hypovolemic shock

Answer 4

Rapid reflexive responses aimed at restoring
cardiac output and mean arterial pressure.

Slower hormonal responses aimed at 
   restricting fluid excretion and returning the 
   blood volume back to normal.

Conservation of body fluid: operates mainly through the renal-body fluid system.

Replenishing lost fluid operates via drinking and metabolic water production.

Enhanced salt appetite to replace electrolytes

Question 5

hormonal symptoms to hypovolemia

Answer 5

thirst, increased salt appetite, oliguria

Question 6

sympathetic activation symptoms to hypovolemia

Answer 6

tachycardia, cold msot skin, pallor, oliguria

Question 7

symptoms of hypovolemia b/c of lack of oxygen

Answer 7

increased respiratory rate, lactic acidosis, dulled perceptions

Question 8

compensation baroreceptor response

Answer 8

Arteriolar vasoconstriction (adrenergic)

Increases systemic vascular resistance either by direct innervation or via epinephrine and norepinephrine released by the adrenal medulla.

Particularly notable in cutaneous and splanchnic circulations. In severe hemorrhage, there is renal vasoconstriction and potential renal failure.

Not in coronary or cerebral circulations

Question 9

compensation baroreceptor response

Answer 9

Heart: Increased rate (chronotropy), myocardial conontractility (inotropy) and rate of relaxation (lusitropy). Also increased dromotropy.

Question 10

compensation baroreceptor response

Answer 10

Venous capacitance reduced: Sympathetic venoconstriction is supplemented by reverse stress relaxation of the veins and venules as a result of reduction of intraluminal pressure.

This is “relative hypervolemia” and will tend to maintain MFP

Question 11

slow compensation.

Answer 11

Kidneys: increased water and sodium conservation. Renin controls the renin-angiotensin-aldosterone system, and therefore the production of angiotensin II and aldosterone. There is also increased secretion of ADH and decreased secretion of ANF.

Question 12

slow compensation

Answer 12

movement of fluids into circulation compartment, and replenishing lost fluid and salt

Question 13

compensatory mechanism

Answer 13

operate by negative feedback (without clincial intervention, may be recovery from hemorrhage)

Question 14

decompensatory mechanism

Answer 14

operate by positive feedback (no recovery, need clinical intervention)

Question 15

examples of DC mechanism

Answer 15

cardiac failure (coronary flow inadequate)
acidosis (oxygen lack generates lactic acid)
reduced cerebral blood flow
blood clotting phenomena
depression of phagocytosis of monocyte-
derived cells (e.g. Kupffer cells)
intestinal ischemia/reperfusion injury
(“cardiotoxin”, endotoxic shock)

Question 16

active hyperemia in exercise

Answer 16

Locally produced factors (such as CO2 & H+) cause vasodilation and increased blood flow in the active muscles-> Cardiac output is therefore directed toward the active muscles, where it is needed, and away from the viscera, where it is not.

Question 17

changes in exercise

Answer 17

Sympathetic (adrenergic):
heart β1, arterioles (skin, viscera) alpha-1,
veins alpha-1 (vascular function curve)
Venous “pump”
central venous pressure increases,
increasing cardiac output according to
Starling Law
cerebral circulation unchanged
increase flow in coronary circulation, increase flow in active muscles, cutaneous circulation

Question 18

during exercise

Answer 18

cardiac output=increases

SVR=decreases, EDV=increases, MAP=increases, atreriovenous oxygen difference= increases as does oxygen consumption

Question 19

pulmonary circuit

Answer 19

low resistance circuit.

Question 20

3 zones of blood flow in lungs

Answer 20

zone 1= no blood flow
zone 2=intermittent flow (flow at systole)
zone 3=continuous flow throughout systole and diastole (constant flow)

Question 21

ventilation perfusion mismatch

Answer 21

failure to match ventilation and blood flow, occurs in pulmonary diseases

Question 22

ways to determine perfusion

Answer 22

V/Q scan or angiography (gold standard)

Question 23

PVR

Answer 23

PVR decreases as pulmonary arterial pressure rises-> flow through it can increase 5-6 times in response to less than doubled pulmonary arterial pressure (not proportional to pressure like in a rigid tube)

Question 24

hypoxic pulmonary vascontriction

Answer 24

occurs in fetus, in adults: shunts poorly ventilated alveoli to regions that are better ventilated, HPV can lead to pulmonary hypertension and right ventricular hypertrophy

Question 25

pulmonary hypertension

Answer 25

most causes are secondary to increased resistance to flow through pulmonary vascular bed, if PVR or PAW elevated, Pa will be

Question 26

some cases of PHT

Answer 26

high altitude, hypoventilatory diseases, chronic bronchitis, asthma, CF, adult respiratory distress syndrome

Question 27

consequences of PHT

Answer 27

right ventricular overload, right ventricular hypertrophy

Question 28

treatments of PHT

Answer 28

infused prostacyclins, calcium channel blockers, NO, endothelin receptor blockers,

Question 29

pulmonary edema

Answer 29

cardiogenic edema (increased LA pressure), and increased capillary permeability (from bacterial infection or toxins)

Question 30

AV anastomoses (shunts)

Answer 30

control flow into the heat exchanging subpapillary plexuses in the hands, feet, ears, face

Question 31

metabolic factors that affect cerebral blood flow

Answer 31

(active hyperemia) Co2, pH, potassium, adenosine, prostoglandins

Question 32

splanchnic circulation

Answer 32

This circulation is important in the response to circulatory shock – involving both arteriolar and venous alpha-adrenergic vasoconstriction

Question 33

flow rate of splanchnic circulation influenced by

Answer 33

sympathetic
  mechanical influences
  GI hormones such as CCK
  catecholamines
  vasopressin
  angiotensin II

Question 34

portal hypertension

Answer 34

normally: pressure in portal vein is lower than hepatic veins and vena cavae, resistance to flow in liver is very low. Elevated intrahepatic resistance= portal hypertension

Question 35

consequences of Portal hypertension

Answer 35

Formation of portosystemic shunts: bypasses develop wherever the systemic and the portal circulation have common capillary beds.
High pressure portal blood is shunted into the systemic venous system, causing dilation of veins in the rectum (hemorrhoids) and the cardioesophageal junction (esophageal varices).

Question 36

consequences of portal hypertension

Answer 36

Abdominal edema and ascites: The rise of portal venous pressure (P1) elevates the capillary hydrostatic pressure in the gastrointestinal tract, pancreas,and spleen. Abdominal edema occurs initially, followed by fluid leaving the tissues and accumulating in the peritoneal cavity.

Question 37

septic shock

Answer 37

ischemia caused by splanchnic vasoconstriction followed by reperfusion causes injury, allowing bacteria to invade the circulation: Myocardial depression
Hypovolemia from edema caused by permeabilization of capillaries (endotoxins) 
Relative hypovolemia (capacity), fall of TPR from activation of inducible NOS (iNOS).