Shock & Exercise - Quiz 11 🫀

Question 1

What is the definition of Shock?

Answer 1

Inadequacy of blood flow which results in inadequate delivery of oxygen and nutrients throughout the body to the extent that the tissues are damaged

Question 2

What is the “Last-Ditch Stand”

Answer 2

When the brain lacks O₂ & increased CO₂, it activates extreme stimulation of SNS as last effort to keep the MAP from falling too low

Question 3

What is the end result of Circulatory Shock?

Answer 3

Further Tissue Deterioration

The shock itself leads to more shock!

That is, the inadequate blood flow causes the body tissues to begin deteriorating, including the heart and circulatory system. This deterioration causes an even greater decrease in cardiac output, and a vicious cycle ensues, with progressively increasing circulatory shock, less adequate tissue perfusion, more shock, and so forth until death. It is with this late stage ofcirculatory shock that we are especially concerned, because appropriate physiological treatment can often reverse the rapid slide to death.

Question 4

What causes Shock? What two factors can severely reduce cardiac output?

Answer 4

• Shock is from inadequate Cardiac Output

Two Types of Factors that can severely reduce cardiac output:
* Cardiac Abnormalities effecting pump
* Factors decreasing venous return

Question 5

How can you have Circulatory Shock even with Normal Cardiac Output? (2)

Answer 5

Excessive Metabolic Rate

&

Abnormal Tissue Perfusion

Question 6

How much blood can be lost before going into Hemorrhagic/Hypovolemic shock?

Answer 6

> 10% will causes decreases in Cardiac Output & MAP

Greater blood loss usually diminishes the cardiac output first and later the arterial pressure, both of which fall to zero when about 40 to 45 percent of the total blood volume has been removed.

Question 7

What happens during the Sympathetic Reflex to shock? (3)

Answer 7

1. Arterioles constrict = Increased PVR
2. Veins constrict = adequate venous return
3. Increased HR

The arterial pressure is maintained at or near normal levels in the hemorrhaging person longer than is the cardiac output. The reason for this difference is that the sympathetic reflexes are geared more for maintaining arterial pressure than for maintaining cardiac output. They increase the arterial pressure mainly by increasing the total peripheral resistance, which has no beneficial effect on cardiac output; however, the sympathetic constriction of the veins is important to keep venous return and cardiac output from falling too much,in addition to their role in maintaining arterial pressure.

Question 8

How is blood flow to the Brain & Heart affected by the Sympathetic Reflex during shock?

Answer 8

No Constriction in Brain or Heart

Autoregulation maintains Blood flow through the Heart and Brain as long as MAP > 70 mmHg

Question 9

What are the Compensatory Mechanisms in Hemorrhage? (6)

Answer 9

• Baroreceptors
• Chemoreceptors
• Cerebral Ischemic Response
• Endogenous Vasoconstrictors
• Reabsorption of Tissue Fluids
• Salt and Water Conservation

Question 10

How do Baroreceptors work?

Answer 10

Located in Carotid Sinus & Aortic Arch

Senses pressure changes and alters SVR, HR & Contractility accordingly.

Tachycardia and Positive Inotropy = ↑ cardiac output. ↑ in CO and SVR lead to a partial restoration of arterial pressure.

Question 11

In Shock, where is vasoconstriction most prominent? 3

Answer 11

Vasoconstriction is most prominent in:

Cutaneous vascular bed
Skeletal muscle vascular bed
Splanchnic vascular bed

Vasoconstriction is slight or absent in:
Cerebral circulation
Coronary circulation

The reduced cardiac output is redistributed to favor flow through the brain and heart

Baroreceptors are sensitive to the rate of pressure change as well as to the steady or mean pressure. Therefore, at a given mean arterial pressure, decreasing thepulse pressure(systolic minus diastolic pressure) decreases the baroreceptor firing rate. This is important during conditions such ashemorrhagic shockin which pulse pressure as well as mean pressure decreases. The combination of reduced mean pressure and reduced pulse pressure amplifies the baroreceptor response.

Question 12

How do the Peripheral Chemoreceptors respond to Severe Hypotension?

Answer 12

Decreased organ blood flow leads to acidosis activating the chemoreceptors.

Further increases SNS response & respiration to increase BP

Reduced organ blood flow caused by vasoconstriction and reduced arterial pressure, leads to systemic acidosis that is sensed bychemoreceptors. The chemoreceptor reflex further activates the sympathetic adrenergic system thereby reinforcing the baroreceptor reflex. When the hypotension is very severe (e.g., mean arterial pressures <50 mmHg) and the brain becomes ischemic, this can produce a very intense sympathetic discharge that further reinforces the other autonomic reflexes.

Question 13

Blood flow is preferentially redistributed to which body organs in shock states?

Answer 13

The reduced cardiac output is redistributed to favor flow through the brain and heart

Question 14

How does the Reabsorption of Tissue Fluids happen in shock?

How much fluid can be reabsorbed at the capillary level to help maintain blood volume?

Answer 14

Hypotension & Vasoconstriction causes a drop in Hydrostatic Pressure and net fluid reabsorption from interstitium into capillaries up to 1L/hr

Can cause Hemodilution = ↓Hct

Hypotension, combined with constriction of precapillary resistance vessels (small arteries and arterioles), causes a fall in capillary hydrostatic pressure. This pressure normally drivesfiltration of fluidfrom the blood, across the capillary endothelium, and into the interstitial space. When capillary hydrostatic pressure is reduced, less fluid leaves the capillaries, and when the pressure falls sufficiently low as occurs following moderate-to-severe blood loss, net reabsorption of fluid can occur from the tissue interstitium back into the capillary plasma. Although this reabsorbed fluid does not contain cells, it does contain electrolytes and some protein, and therefore increases the plasma volume. This reabsorbed fluid leads to hemodilution of the blood; therefore, red cell hematocrit falls in response to this fluid shift. This mechanism can cause up to 1 liter/hour of fluid to be withdrawn from interstitial spaces back into the plasma.

Question 15

How does the Kidney come into play during Shock?

Answer 15

• Kidneys release more
  
  • Angiotensin II - Vasoconstriction
  • Aldersterone - Salt & Water Reabsorption to increase blood volume
  • Stimulates Vasopressin Release
  • Important for long-term recovery

The kidneys release more renin following hemorrhage leading to increased circulating levels ofangiotensin II and aldosterone. This causes vascular constriction, enhanced sympathetic activity, stimulation ofvasopressinrelease, activation of thirst mechanisms, and very importantly, increased renal reabsorption of sodium and water to increaseblood volume. This renal mechanism is particularly important in the long-term recovery from blood loss.

Question 16

What is Circulatory Decompensation or Progressive Shock?

Answer 16

When the body’s compensation mechanisms is not enough to maintain a sufficent MAP to perfuse organs and leads to irreversible shock where everything fails.

Cardiac Depression

Vasomotor Failure

Acidosis

Blood Clotting Abnormalities
Initially, hypercoaguability
Later, hypocoaguability and fibrinolysis

Reticulo-endothelial System
Impaired Immune System
Endotoxins
Macrophages release Shock Mediators

CNS Depression
Endogenous Opioids
Decreased sympathetic outflow

Cellular Deterioration
Active transport of ions decreases
Cells swell
Mitochondrial activity decreases
Lysosomes release their contents
Cellular metabolism of nutrients becomes greatly depressed

Low Flow States Cause Enhanced:
Leukocyte-endothelial adhesion
Platelet-platelet adhesion
This results in:
Reduced organ perfusion
Stimulation of inflammatory processes

Question 17

What is Cardiogenic Shock?

Answer 17

Impaired coronary blood flow resulting from hypotension causes myocardial hypoxia and acidosis, which depress cardiac function and cause arrhythmias

Question 18

What is Symptathetic Escape?

Answer 18

Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion.
Loss of precapillary vascular tone increases capillary hydrostatic pressure and capillary fluid filtration, which reduces plasma volume

Question 19

Systemic inflammatory response

Answer 19

Endotoxins released into systemic circulation from the ischemic gastrointestinal tract lead to cytokine production, and enhanced formation of nitric oxide and oxygen free radicals, which cause vasodilation, cardiac depression, and organ injury

Question 20

What are the Rheological (flow) effects of Progressive Shock?

Answer 20

Reduced microcirculatory flow causes blood viscosity within tissues to increase, which further reduces perfusion
Plugging of the microcirculation by leukocytes and platelets, and intravascular coagulation reduce organ perfusion

Question 21

What does Metabolic acidosis do to Shock?

Answer 21

Acidosis depresses cardiac muscle and vascular smooth muscle contraction, which further decreases arterial pressure

Question 22

What is Cerebral Ischemia/Hypoxia?

Answer 22

Loss of sympathetic outflow from a hypoxic medulla leads to vasodilation, which further reduces arterial pressure and cerebral perfusion

Question 23

What are the Stages of Shock?

Answer 23

• Non-Progressive/Compensated
  
  • ​Body can compensate to full recovery
• Progressive
  
  • W/o therapy, shock gets worse til death
• Irreversible
  
  • Nothing you can do, patient will die

Question 24

Hypotension Map

Answer 24

Question 25

What are treatments for Hypotension?

Answer 25

Give Blood

Epi/Norepi

Head Down Position

Oxygen

Glucocorticoids

Blood and Plasma Transfusion
Sympathomimetic Drugs
Epinephrine
Norepinephrine
Treatmentby the Head-Down Position.
Head about 12 inched below feet
Oxygen Therapy.
less beneficial than one might expect,is not inadequate oxygenation of the blood but inadequate transport of the blood after it is oxygenated.
Treatmentwith Glucocorticoids.
adrenal cortex hormones frequently increase the strength of the heart in the late stages ofshock;
stabilize lysosomes
might aid in the metabolism of glucose by the severely damaged cells.

Question 26

What are the Decompensatory Mechanisms?

Answer 26

Cardiac & CNS Depression
Acidosis
Vasomotor Failure
Abnormal Clotting
Reticulo-Endothelial System
Cellular Deterioration
Low Flow States

Question 27

What are the Positive Feedback Decompensatory Mechanisms?

Answer 27

↓CO & Contractility

↓MAP & O2 Transport

Vasodilation

Tissue Hypoxia

Question 28

What happens on the Cellular Level that leads to Irreversible Shock?

Answer 28

Depletion of high-energy phosphates

Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock
The high-energy phosphate reserves in the tissues of the body, especially in the liver and heart, are greatly diminished in severe shock. Essentially all the creatine phosphate has been degraded, and almost all the adenosine triphosphate has downgraded to adenosine diphosphate, adenosine monophosphate and, eventually, adenosine. Much of this adenosine then diffuses out of the cells into the circulating blood and is converted into uric acid, a substance that cannot re-enter the cells to reconstitute the adenosine phosphate system. New adenosine can be synthesized at a rate of only about 2% of the normal cellular amount an hour, meaning that once the high-energy phosphate stores of the cells are depleted, they are difficult to replenish.
Thus, one of the most devastating end results in shock, and the one that is perhaps most significant for development of the final state of irreversibility, is cellular depletion of these high-energy compounds.

Question 29

What is the Rate of Blood Flow through muscles during Excercise for a nonathlete and an athelete?

Answer 29

Normal:
3 – 4 ml/min/100 g of muscle

Extreme exercise in the well-conditioned athlete:
50 -80 ml/min/100 g of muscle

Thecardiac outputoften must increase to four to five times normal in the nonathlete, or to six to seven times normal in the well-trained athlete, to satisfy the metabolic needs of the exercisingmuscles.

Question 30

How does capillary recruitment help deliver oxygen to muscle tissues during exercise?

Answer 30

Increase surface area for diffusion
&
Shorten the distance for diffusion

Question 31

What causes Low Blood flow to muscles during muscle contraction?

Answer 31

Muscle contraction compresses blood vessels

Can stop blood flow, but also rapidly weakens contraction

Question 32

What is the status of some Muscle Capillaries at rest vs. during exercise?

Answer 32

At Rest: Some Capillaries have no flow

During Exercise: All capillaries open, increases surface area 2-3x & enhances o2 diffusion

Duringrest, somemusclecapillaries have little or noflowingblood, butduring strenuousexercise, all the capillaries open. This opening of dormant capil­laries diminishes the distance that oxygen and other nutrients must diffuse from the capillaries to the contractingmusclefibers and sometimes contributes a twofold to threefold increased capillary surface area through which oxygen and nutrients can diffuse from thebloodto the tissues.

Question 33

What causes the tremendous amount of blood flow to the muscles during exercise?

Answer 33

The tremendous increase inmuscle blood flowthat occursduringskeletalmuscle activity is caused mainly by chemicals acting directly on themusclearterioles to cause dilation.

• Vasodilation d/t release of
  
  • Adenosine (ATP)
  • Lactic Acid
  • Potassium
• Blood flow can increase 20x
• Decrease oxygen in muscles greatly enhances flow.

The arteriolar walls cannot maintain con­traction in the absence of oxygen and because oxygen deficiency causes release of vasodilator substances. Adenosine may be an important vasodilator substance.

These factors include (1) potassium ions, (2) adeno­sine triphosphate (ATP), (3) lactic acid, and (4) carbon dioxide.

Question 34

What factors helps oxygen unloading from Hgb to muscle tissues during exercise? (5)

Answer 34

Contracting muscle avidly extracts oxygen from the blood

This is facilitated by
Right-ward shift of oxyhemoglobin dissociation curve
Reduced pH
Lactic acid
Increased pCO2
Increased temperature

Question 35

What factor Greatly enhances blood flow to the muscle?

Answer 35

Decreased Oxygen in Muscle

Question 36

How does Epi and Norepi play a role in Blood Flow to the Muscles?

Answer 36

• Epinephrine
  
  • Alpha: Vasoconscriction in Non-Active Muscles, Renal & Splanchnic vessels
  • Beta-2: Mild Vasodilation in skeletal muscles
• Norepinephrine
  
  • Alpha: Vasoconstriction in Non-Active Muscles, Renal & Splancnic vessels

Question 37

How much is Oxygen Consumption increased during Exercise?

Answer 37

60x

Question 38

How is the Heart affected during exercise?

Answer 38

↑Sympathetic & ↓Parasympathetic

↑Cardiac Output: ↑HR, ↑Inotropy, ↑CVP, ↑Lusitropy

↓SVR
↑ Cardiac output
*↑ heart rate (↑ sympathetic and ↓ parasympathetic activity)
*↑ stroke volume (↑ CVP, ↑ inotropy, ↑ lusitropy)

↑ Mean arterial pressure and pulse pressure
*CO increases more than SVR decreases
*↑ stroke volume increases pulse pressure
↑ Central venous pressure
*Venous constriction (↑ sympathetic activity)
*Muscle pump activity
*Abdominothoracic pump
↓ Systemic vascular resistance
Metabolic vasodilation in active muscle and heart
Cutaneous vasodilation (↓ sympathetic activity)
Vasoconstriction in splanchnic, nonactive muscle, and renal circulation (↑ sympathetic activity).

Question 39

How does the change in Cardiac Output correlate to Heart Rate during exercise?

Answer 39

The increase in cardiac output observed with exercise is correlated principally with an increase in heart rate.

The increase in stroke volume in exercise is only about 10 to 35%

The increased level of the cardiac output curve is easy to understand. It results almost entirely from sympathetic stimulation of the heart that causes (1) increased heart rate, often up to rates as high as 170 to 190 beats/min, and (2) increased strength of contraction of the heart, often to as much as twice normal.

Cardiac output increases approximately in proportion to the degree of exercise

Increased cardiac output is essential to supply the large amounts of oxygen and other nutrients needed by the exercising muscles

The ability of the circulatory system to provide increased cardiac output for delivery of oxygen and other nutrients to the muscles duringexerciseis equally as important as the strength of the muscles themselves in setting the limit for continued muscle work.

Question 40

How does the Heart maintain its stroke volume at the high Heart Rates of exercise? 5

Answer 40

• Abdominothoracic & Skeletal muscles increase venous return to maintain CVP & Preload
• Venous Constriction/Decreased Venous Compliance
• Increased Atrial Inotropy for atrial filling
• Increased Ventricle Inotropy to squeeze out more blood
• Enhanced Ventricle Relaxation for better filling

Question 41

What factors enhance Venous Return during Exercise?

Answer 41

• Sympathetically-mediated constriction of Capicitance Vessels
• ↓SVR in Muscles
• Contracting Muscles help pump venous blood back to heart
• Deeper & Faster breathing decreases intrathoracic pressure to enhance cardiac blood flow

The mean systemic filling pressure rises tremendously at the onset of heavyexercise. This effect results partly from the sympathetic stimulation that contracts the veins and other capacitative parts of the circulation. In addition, tensing of the abdominal and other skeletal muscles of the body compresses many of the internal vessels, thus providing more compression of the entire capacitative vascular system, causing a still greater increase in mean systemic filling pressure.

The slope of the venous return curve rotates upward. This upward rotation is caused by decreased resistance in virtually all the blood vessels in active muscle tissue, which also causes resistance to venous return to decrease, thus increasing the upward slope of the venous return curve.

Question 42

Does the Mean Arterial Pressure increase or decrease from Exercise?

Answer 42

Arterial blood pressure rises during exercise
Despite considerable reduction in Systemic Vascular Resistance (SVR) in the body musculature

The increase in cardiac output is proportionally greater than the decrease in SVR
Ohm’s Law: MAP = CO x SVR

The vasoconstriction in the inactive tissues is important for maintaining normal or increased blood pressure during exercise

Increase in Cardiac Output is more than the decrease in SVR

MAP increases even though SVR decreases

(1) vasoconstriction of the arterioles and small arteries in most tissues of the body except the brain and the active muscles, including the heart, (2) increased pumping activity by the heart, and (3) a great increase in mean systemic filling pressure caused mainly by venous contraction.

Question 43

What is the importance of an Increased MAP during Exercise?

Answer 43

Increased Pressure stretches vessel walls to increase blood flow up to 20x

&

Increased pressure also increases Perfusion Pressure

Question 44

What effect does the SNS have on the kidneys, splanchnic beds and inactive muscles during heavy exericse?

Answer 44

Sympathetic-mediated vasoconstriction of the arterioles increases the resistance in the:
Kidneys
Splanchnic beds
Inactive muscle

This diverts blood away from these areas