Cardiovascular Physiology — Circulatory Shock

Physiologic Causes of Shock

Circulatory Shock Caused by Decreased Cardiac Output

1. Cardiac abnormalities that decrease the ability of the heart to pump blood

myocardial infarction

severe heart valve dysfunction

heart arrhythmias

2. Factors that decrease venous return

diminished blood volume

decreased vascular tone

obstruction to blood flow

Circulatory Shock That Occurs Without Diminished Cardiac Output

excessive metabolism of the body

abnormal tissue perfusion patterns

What Happens to Arterial Pressure in Circulatory Shock?

Tissue Deterioration Is the End Result of Circulatory Shock

shock itself breeds more shock.

Stages of Shock

nonprogressive stage

progressive stage

irreversible stage

Shock Caused by Hypovolemia—Hemorrhagic Shock

Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure

Sympathetic Reflex Compensations in Shock—Their Special Value to Maintain Arterial Pressure

arterioles constrict in most parts of the systemic circulation,

veins and venous reservoirs constrict

heart activity increases markedly

Value of the Sympathetic Nervous Reflexes

Greater Effect of the Sympathetic Nervous Reflexes in Maintaining Arterial Pressure than in Maintaining Cardiac Output

Protection of Coronary and Cerebral Blood Flow by the Reflexes.

Progressive and Nonprogressive Hemorrhagic Shock

Nonprogressive Shock—Compensated Shock

Baroreceptor reflexes

Central nervous system ischemic response

Reverse stress-relaxation of the circulatory system

Formation of angiotensin

Formation of vasopressin (antidiuretic hormone)

Compensatory mechanisms that return the blood volume back toward normal

“Progressive Shock” Is Caused by a Vicious Circle of Cardiovascular Deterioration

Cardiac Depression

Vasomotor Failure

Blockage of Very Small Vessels—“Sludged Blood”

Increased Capillary Permeability

Release of Toxins by Ischemic Tissue

Cardiac Depression Caused by Endotoxin

Generalized Cellular Deterioration

Active transport of sodium and potassium

Mitochondrial activity

Lysosomes

Cellular metabolism of nutrients

Tissue Necrosis in Severe Shock—Patchy Areas of Necrosis Occur Because of Patchy Blood Flows in Different Organs

shock lung syndrome.

Acidosis in Shock

excess lactic acid

Positive Feedback Deterioration of Tissues in Shock and the Vicious Circle of Progressive Shock

Irreversible Shock

Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock

creatine phosphate

adenosine triphosphate

adenosine diffuses out of the cells

Hypovolemic Shock Caused by Plasma Loss

Intestinal obstruction

Severe burns

Dehydration

excessive sweating,

fluid loss in severe diarrhea or vomiting

excess loss of fluid by nephrotic kidneys

inadequate intake of fluid and electrolytes

loss of aldosterone secretion

Hypovolemic Shock Caused by Trauma

Neurogenic Shock—Increased Vascular Capacity

Causes of Neurogenic Shock

Deep general anesthesia

Spinal anesthesia

Brain damage

Anaphylactic Shock and Histamine Shock

histamine

increase in vascular capacity

dilation of the arterioles

greatly increased capillary permeability

Septic Shock

causes of septic shock

Peritonitis caused by spread of infection from the uterus and fallopian tubes

Peritonitis resulting from rupture of the gastrointestinal system

Generalized bodily infection

Generalized gangrenous infection

Infection spreading into the blood

Special Features of Septic Shock

High fever.

Often marked vasodilation

High cardiac output

Sludging of the blood

Development of micro–blood clots (disseminated intravascular coagulation)

Physiology of Treatment in Shock

Replacement Therapy

Blood and Plasma Transfusion

Dextran Solution as a Plasma Substitute

Treatment of Shock with Sympathomimetic Drugs

neurogenic shock

anaphylactic shock

Other Therapy

Treatment by the Head-Down Position

Oxygen Therapy

Treatment with Glucocorticoids

Circulatory Arrest

cardiac arrest or ventricular fibrillation

Effect of Circulatory Arrest on the Brain

acute cerebral hypoxia

caused mainly by permanent blockage of many small blood vessels