CR09 - Integrative Functions of CV System II

What is cardiogenic shock?

Impaired cardiac function leading to inadequate perfusion.

What is hypovolemic shock?

Reduced blood volume resulting in circulatory failure.

What is septic shock?

Systemic inflammatory response causing widespread vasodilation.

What is anaphylactic shock?

Severe allergic reaction triggering vasodilation and fluid shifts.

What is neurogenic shock?

Loss of autonomic control leading to unopposed vasodilation.

What is the immediate cardiovascular effect of massive hemorrhage?

Hypotension.

What rapid reflex response is elicited by hemorrhage-induced hypotension?

Baroreceptor reflex.

What nervous system is activated during hemorrhage?

The sympathetic nervous system.

What renal hormone system is activated during hemorrhage?

Kidney release of renin. (RAAS)

What is the overall goal of the body’s response to hemorrhage?

To compensate for blood loss and increase cardiac output.

What is the initial hemodynamic consequence of hemorrhage?

↓ Blood volume → ↓ cardiac output and ↓ arterial pressure.

Which reflex is the primary compensatory mechanism for decreased arterial pressure?

The baroreceptor reflex.

Which baroreceptors detect decreased arterial pressure during hemorrhage?

Carotid sinus baroreceptors.

How do baroreceptors respond to decreased arterial pressure?

By increasing sympathetic outflow and decreasing parasympathetic outflow.

What cardiac effects result from increased sympathetic activity during hemorrhage?

↑ Heart rate and ↑ contractility.

What vascular effects result from increased sympathetic activity?

↑ Total peripheral resistance due to arteriolar constriction.

Which vascular beds experience arteriolar constriction during hemorrhage?

Skeletal, splanchnic, and cutaneous vascular beds.

Which vascular beds are NOT constricted during hemorrhage?

Coronary and cerebral vascular beds (maintain blood to the heart and brain)

What happens to veins during hemorrhage compensation?

Venoconstriction occurs, leading to increased venous return.

What is the role of peripheral chemoreceptors during hemorrhage?

Carotid and aortic body chemoreceptors detect hypoxia → increase sympathetics to heart and blood vessels.

What is the role of central chemoreceptors during hemorrhage?

Cerebral ischemia (if present) causes an increase in PCO2 → increased sympathetic outflow to peripheral vasculature → vasoconstriction

What is the result of arteriolar constriction?

Causes decreased capillary pressure (Pc) → increased capillary fluid absorption, which helps restore blood volume.

What hormones are released from the adrenal medulla during hemorrhage?

Epinephrine and norepinephrine.

What is the role of epinephrine and norepinephrine during hemorrhage?

They supplement sympathetic effects on the heart and blood vessels.

What stimulates RAAS activation during hemorrhage?

Decreased renal perfusion pressure.

What is the role of RAAS in response to hemorrhage?

ANG II → vasoconstriction → increased TPR

Aldosterone → increased NaCl reabsorption → increased blood volume

What triggers ADH release during hemorrhage?

Atrial receptors detecting decreased blood volume.

What is the effect of ADH release during hemorrhage?

ADH acts on the renal collecting duct, increasing H2O absorption → increased blood volume.

What is shock?

A hemodynamic disturbance characterized by systemic hypoperfusion resulting in inadequate oxygen delivery to vital organs.

What are the major classifications of shock?

Cardiogenic, hypovolemic, distributive, septic, anaphylactic, and neurogenic.

Can shock evolve from one type to another?

Yes.

What types of shock are classified as distributive?

Septic, anaphylactic, and neurogenic.

What defines the compensation (non-progressive) stage of shock?

15–25% fluid loss with compensatory mechanisms restoring MAP without intervention.

What defines the decompensation (progressive) stage of shock?

25–35% fluid loss with failure of compensatory mechanisms requiring intervention.

What defines irreversible shock?

>35% fluid loss with severe cellular and tissue injury.

What conditions are associated with irreversible shock?

Hypoxic and ischemic cell injury, myocardial infarction, intestinal ischemia, acute tubular necrosis.

What is the outcome of irreversible shock?

Death is inevitable despite therapy.

What causes cardiogenic shock?

Mechanisms that reduce the CO, including cardiac pump failure, impaired diastolic filling (preload), or an obstruction of the outflow (afterload)

What are examples of issues that cause cardiogenic shock?

• Decreased preload

• Mechanical obstruction of venous return

• Impaired diastolic dilatation of ventricles

• Contractile insufficiency

• Valvular obstruction

• Valvular insufficiency

What does decreased CO lead to in cardiogenic shock?

Decreased BP and peripheral edema → reduced perfusion to kidneys, lungs, heart, brain → heart tries to compensate with tachycardia

What causes hypovolemic shock?

Critical decrease in intravascular circulating blood volume (>500 mL loss).

What factors influence prognosis in hypovolemic shock?

Cause, pre-existing illness, time to diagnosis, and adequacy of therapy.

What happens if hypovolemic shock is untreated?

It is fatal.

Where is fluid lost, causing hypovolemic shock?

Through the skin, GI tract, kidneys, or intervascular space

What does loss of blood volume lead to in hypovolemic shock?

Loss of preload to the heart → decreased BP → insufficient organ perfusion → heart tries to compensate with tachycardia

What type of shock is suggested by hypotension (80/50), tachycardia (130 bpm), chest discomfort, and blurred vision?

Cardiogenic shock.

What immediate intervention is most appropriate for cardiogenic shock?

Maintain airway and breathing.

What triggers septic shock?

Severe bacterial infection releasing endotoxins.

What systemic response is activated in septic shock?

Systemic inflammatory response syndrome (SIRS).

Which mediators drive septic shock?

Cytokines and inflammatory mediators (TNF, interleukins, nitric oxide).

How do inflammatory mediators affect blood vessels?

They cause vasodilation in arterioles, capillaries, and venules, leading to pooling in the peripheral circulation.

How does septic shock affect cardiac output?

Reduced return of blood to the heart → decreased preload → decreased CO → hypotension.

What type of hypersensitivity reaction causes anaphylactic shock?

Acute, life-threatening Type I hypersensitivity

What mediates vasodilation in anaphylaxis?

Vasoactive substances released from mast cells.

What is the role of histamine in anaphylaxis?

Causes vasodilation and increased vascular permeability.

What other causes can lead to massive vasodilation?

Vasoactive drugs and narcotic overdose affecting medullary centers, causing coma with peripheral vasodilation

• Adverse drug reactions

What is the pathogenesis of anaphylactic shock?

Inappropriate mast cell activation → degranulation → histamine → vasodilation and increased vascular permeability → smooth muscle contraction in airways, inflammation, and ANS activation → anaphylaxis

What injuries can cause neurogenic shock?

Brain trauma, intracranial hemorrhage, and spinal cord injury.

What is the mechanism of neurogenic shock?

Increased pressure on vasomotor centers disrupts normal vascular control → vasodilation.

Where does vasodilation occur in neurogenic shock?

Especially in the abdominal organs, causing blood pooling in splanchic circulation/

What are the effects of neurogenic shock on blood pressure?

Vasodilation → reduced blood pressure → decreased blood flow to vital organs

What is the major risk of neurogenic shock?

Risk of shock and organ failure if blood pressure remains too low.

Does neurogenic shock result in bradycardia or tachycardia?

Bradycardia, because vasomotor areas in the brain are damaged.

What type of shock is suggested by itching, throat tightness, facial flushing, and hypotension after eye drops?

Anaphylactic shock.

What is the most appropriate immediate intervention for anaphylactic shock?

Administer epinephrine (or antihistamines for a less severe reaction).

What types of pain can cause the superficial pain response in the eye?

Corneal abrasion, foreign object, applanation tonometry, contact-lens irritation

What is the superficial pain neural response?

Activate sympathetic nervous system, inhibit parasympathetic nervous system.

What are the cardiovascular effects of the superficial pain response?

Increased BP due to:

• Vasoconstriction (increased TPR)

• Increased HR and CO

How does superficial pain relate to fight or flight?

The sympathetic response is initiated, preparing the body for action.

What can acute pain cause, and how should it be treated?

Acute pain causes transient hypertension; adequate pain control through anesthetics can minimize excessive sympathetic stimulation

What triggers the deep pain response in the eye?

Acute orbital trauma, severe inflammation, acute angle-closure glaucoma, orbital fractures.

What is the neural response to deep pain?

Activates parasympathetic nervous system, inhibits sympathetic nervous system.

What is the cardiovascular response to deep pain?

Vasodilation and bradycardia → low HR and CO → serious drop in BP (hypotension). Can contribute to shock and circulatory failure.

What type of response can severe ocular or orbital pain provoke?

A vasovagal-type cardiovascular response with symptoms of pallor and diaphoresis, dizziness, visual dimming, bradycardia, and hypotension.

How does deep pain cause pain-induced shock?

• Loss of sympathetic tone → can’t maintain BP

• Bradycardia and vasodilation → reduced perfusion to brain and vital organs

• Can lead to organ failure and death

What is the emergency response to pain-induced shock?

• Monitor BP and HR

• IV fluids and vasopressors to restore circulatoin

• Pain control (opioids, NSAIDS) to stabilize autonomic response