NURS 2873 - CONCEPT – PERFUSION EXEMPLAR - SHOCK

S1 — What concept and exemplar are covered in this lecture?

The concept is perfusion and the exemplar is shock.

S1 — Who is listed as the lecturer on the title slide?

Edna McQuesten, MSN, RN.

S2 — What is perfusion?

Perfusion is the flow of blood through arteries and capillaries that delivers nutrients and oxygen to cells.

S2 — Why is perfusion essential for life?

Blood flowing through arteries and capillaries delivers oxygen and nutrients to cells; this exchange is essential for life.

S3 — Why is perfusion interrelated with nearly all exemplars?

All cells in the body depend on perfusion to transport oxygen and nutrients.

S4 — What disease processes are examples of impaired or absent tissue perfusion?

TIA/stroke, MI, dysrhythmias, valvular disease, congenital heart defects, PE, ischemic bowel, and PAD.

S4 — What happens as perfusion moves from optimal to impaired to absent?

Normal oxygen/nutrient exchange becomes impaired; with no perfusion, tissue death occurs.

S5 — How does the lecture define shock?

A syndrome characterized by decreased tissue perfusion and impaired cellular metabolism.

S5 — What phrase summarizes shock?

“Inadequate Tissue Perfusion.”

S5 — What oxygen/nutrient problem occurs in shock?

There is an imbalance between oxygen/nutrient supply and demand.

S5 — What is hypoperfusion in the lecture?

A state in which demand for oxygen and nutrients exceeds supply at the microcirculatory level.

S6 — What are the four stages of shock in order?

Initial, compensatory, progressive, and refractory.

S7 — Why is the initial stage of shock often hard to recognize?

It is usually not clinically apparent.

S7 — What metabolic change occurs at the cellular level during the initial stage?

Metabolism changes from aerobic to anaerobic.

S7 — What builds up during anaerobic metabolism in the initial stage of shock?

Lactic acid.

S7 — Which organ must remove the lactic acid that builds up in shock?

The liver.

S7 — Why is lactic-acid removal impaired during the initial stage of shock?

The process requires oxygen, but oxygen is unavailable because tissue perfusion is decreased.

S8 — What activates the SNS during the compensatory stage of shock?

Baroreceptors in the carotid and aortic bodies respond to decreased blood pressure and activate the SNS.

S8 — What classic sign of shock is emphasized in the compensatory-stage notes?

A drop in blood pressure.

S8 — What vascular response occurs after SNS activation in compensatory shock?

Vasoconstriction.

S8 — Which vital organs are preferentially perfused during compensatory shock?

The heart and brain.

S8 — Which nonvital areas have blood flow diverted or shunted during compensatory shock?

Kidneys, GI tract, skin, and lungs.

S9 — How does SNS stimulation affect the myocardium during compensatory shock?

It increases myocardial oxygen demand.

S9 — What happens when blood is shunted away from the lungs during compensatory shock?

Physiologic dead space increases.

S9 — What gas-exchange problem results from increased physiologic dead space?

Ventilation-perfusion (V/Q) mismatch.

S9 — What happens to arterial oxygen levels during compensatory shock?

They decrease.

S9 — What happens to the rate and depth of respirations during compensatory shock?

Both increase.

S9 — Why do respirations increase during compensatory shock?

Shunting from the lungs increases dead space, causing V/Q mismatch and lower arterial oxygen, so ventilation increases.

S10 — What happens to GI motility during compensatory shock?

GI motility becomes impaired.

S10 — What complication does impaired GI motility put the patient at risk for?

Paralytic ileus.

S10 — What skin finding is typical of decreased blood flow in compensatory shock?

Cool, clammy skin.

S10 — What skin finding is the septic-shock exception?

A septic patient may be warm and flushed.

S11 — What does decreased renal blood flow activate during compensatory shock?

The renin-angiotensin system.

S11 — What conversion occurs in the renin-angiotensin system during compensatory shock?

Angiotensin I is converted to angiotensin II.

S11 — What vascular effect is associated with angiotensin II in the lecture?

Vasoconstriction.

S11 — How does the renin-angiotensin response affect venous return?

It increases venous return to the heart.

S11 — What hormone release is stimulated during the renin-angiotensin response?

Aldosterone.

S11 — What happens to sodium reabsorption during this compensatory response?

Sodium reabsorption increases.

S11 — What hormone is stimulated by increased sodium reabsorption according to the lecture?

ADH from the posterior pituitary gland.

S12 — Can the body still compensate for tissue-perfusion changes in the compensatory stage?

Yes.

S12 — What happens if the cause of shock is corrected during the compensatory stage?

The patient may recover with little or no residual effects.

S12 — What happens if the cause of shock is not corrected during the compensatory stage?

The patient enters the progressive stage.

S13 — When does the progressive stage of shock begin?

When compensatory mechanisms fail.

S13 — What happens to BP and MAP in the progressive stage?

Both decrease because BP-regulating mechanisms can no longer compensate.

S13 — Why does BP drop in progressive shock according to the notes?

Cardiac output decreases.

S13 — What happens to organ perfusion during progressive shock?

All organs suffer from hypoperfusion.

S13 — Where should a patient in progressive shock be cared for?

The ICU for advanced monitoring and treatment.

S14 — What are the distinguishing features of progressive shock?

Decreased cellular perfusion and altered capillary permeability.

S14 — What happens to protein when capillary permeability increases?

Protein leaks into the interstitial space.

S14 — What does protein/fluid leakage into the interstitial space cause?

Increased systemic interstitial edema.

S14 — What is anasarca?

Diffuse, profound edema.

S14 — Which solid organs/tissues are specifically said to be affected by fluid leakage and worsening perfusion?

Liver, spleen, GI tract, lungs, and peripheral tissues.

S14 — What happens to cardiac output and blood pressure as progressive shock worsens?

Cardiac output decreases, causing blood pressure to decrease.

S14 — What peripheral assessment findings can result from sustained hypoperfusion?

Weak peripheral pulses and ischemia of distal extremities.

S15 — What major assessment change indicates brain hypoperfusion in progressive shock?

Changes in mental status.

S15 — What happens to cerebral perfusion pressure in progressive shock?

It decreases.

S15 — What happens to cerebral blood flow in progressive shock?

It decreases.

S15 — How does brain hypoperfusion affect responsiveness?

Responsiveness to stimuli decreases.

S15 — What neurologic condition may result from brain hypoperfusion?

Delirium.

S16 — Why does myocardial hypoperfusion worsen during progressive shock?

Cardiac output falls, lowering BP and coronary, cerebral, and peripheral perfusion.

S16 — What rhythm complication can occur from myocardial hypoperfusion?

Dysrhythmias.

S16 — What ischemic cardiac problem can occur in progressive shock?

Myocardial ischemia.

S16 — What symptom characterizes myocardial ischemia in the lecture?

Chest pain.

S16 — What major cardiac event may occur during progressive shock?

Myocardial infarction.

S16 — What is the stated end result of severe myocardial hypoperfusion?

Complete deterioration of the cardiovascular system.

S17 — What happens to fluid in the lungs during progressive shock before it enters the alveoli?

Fluid moves from the pulmonary vasculature into the interstitium.

S17 — What two pulmonary problems are associated with this interstitial fluid shift?

Pulmonary edema and bronchoconstriction.

S18 — What happens when fluid moves into the alveoli during progressive shock?

Edema develops and the V/Q mismatch worsens.

S18 — What respiratory findings are listed when alveolar edema worsens?

Tachypnea, crackles, and increased work of breathing.

S19 — What happens to the GI mucosal barrier during progressive shock?

It becomes ischemic because GI blood supply decreases.

S19 — What complications can an ischemic GI mucosal barrier cause?

Ulcers and GI bleeding.

S19 — Why does GI hypoperfusion increase infection risk?

It increases the risk of bacteria migrating from the GI tract into the blood.

S19 — How does GI hypoperfusion affect nutrition?

It decreases the ability to absorb nutrients.

S20 — What does prolonged kidney hypoperfusion cause?

Renal tubular ischemia.

S20 — What renal complication may result from renal tubular ischemia?

Acute kidney injury.

S20 — What types of drugs can worsen AKI during progressive shock according to the notes?

Certain antibiotics, diuretics, and anesthetics.

S20 — What happens to urine output with renal hypoperfusion?

It decreases.

S20 — What renal laboratory values rise with progressive kidney hypoperfusion?

BUN and serum creatinine.

S20 — Why does metabolic acidosis occur with progressive kidney hypoperfusion?

The kidneys cannot adequately excrete acids, especially lactic acids, or reabsorb bicarbonate.

S21 — How does progressive shock affect liver metabolism?

The liver becomes unable to adequately metabolize drugs and waste.

S21 — Why can jaundice occur during liver hypoperfusion?

Bilirubin accumulates.

S21 — Why do liver enzymes rise during progressive shock?

Liver cells die.

S21 — What immune/clotting consequence occurs as liver function is lost?

The liver loses its immune-organ role, increasing the risk for DIC and significant bleeding.

S22 — What is the final stage of shock?

The refractory stage.

S22 — What happens to anaerobic metabolism in refractory shock?

It is exacerbated.

S22 — What happens to lactic acid during refractory shock?

It accumulates.

S22 — How does lactic-acid accumulation affect capillary permeability?

It helps increase capillary permeability.

S22 — What moves out of the vascular space as capillary permeability increases in refractory shock?

Fluid and plasma proteins move into the interstitial space.

S22 — What two severe circulatory/oxygenation findings occur in refractory shock?

Profound hypotension and hypoxemia.

S22 — Which failing organs are specifically named as affecting other organs in refractory shock?

Liver, lungs, and kidneys.

S22 — Why is recovery unlikely in refractory shock?

Compensatory mechanisms are overwhelmed and organ-system failure affects other organs.

S22 — If the lecture is split into two sections, where does the speaker suggest stopping the first section?

After the refractory-stage discussion.

S23 — What topic is introduced after the four stages of shock?

Classifications of shock.

S24 — What are the four main categories of shock?

Cardiogenic, hypovolemic, distributive, and obstructive shock.

S24 — What two forms of hypovolemia are included under hypovolemic shock?

Absolute hypovolemia and relative hypovolemia.

S24 — What three types are included under distributive shock?

Neurogenic, anaphylactic, and septic shock.

S25 — What is the basic pathophysiology of cardiogenic shock?

Systolic or diastolic dysfunction of the heart’s pumping action reduces cardiac output.

S25 — IMAGE: What circulation labels are shown on the cardiogenic-shock heart diagram?

“To lungs” and “From lungs,” with red indicating oxygenated blood and blue indicating unoxygenated blood.

S25 — What is systolic dysfunction?

Inability of the heart to pump blood forward.

S25 — Which ventricle is generally affected by systolic dysfunction in the lecture, and why?

The left ventricle because systolic pressure is greater on the left side of the heart.