Shock, Sepsis

Question 1

Widespread abnormal cellular metabolism that occurs when oxygenation and tissue perfusion needs are not met to the level necessary to maintain cell function.

Answer 1

Shock. Also defined as a clinical syndrome that results from inadequate tissue perfusion and low blood perfusion creating an imbalance between the delivery of and requirement for oxygen and nutrients that support cellular function resulting in cellular injury and inadequate tissue function.

Question 2

What does adequate perfusion depend on?

Causes of shock?

Answer 2

Adequate volume of blood for the heart to pump (preload). Effective pumping by the heart (CO). Constriction and dilation of the vasculature (SVR/afterload) which needs to be appropriate to what’s going on in the body. Unobstructed pathway for blood flow.
Volume, amount, contents, pump, distribution

Question 3

All forms of shock involve what? Variables that influence O2 transport include?

Answer 3

Involve impaired delivery of O2 to the tissues. Variables: O2 delivered to tissues, O2 consumption by tissues, O2 extraction ratio (the percent of available O2 the cell is capable of taking in, how much the body needs compared to what’s actually available)

Question 4

O2 delivery depends on?

Answer 4

Blood flow (CO), perfusion. Amount of hgb available to carry O2. Percentage of arterial O2 hgb saturation. Enough blood with enough Hgb with enough O2 in it. The body normally provides 3-4 times more O2 than needed for normal metabolism

Question 5

Represents the body’s demand for O2 and is reflection of the body’s metabolism. Due to reduction in blood flow or uneven distribution of blood.

Answer 5

O2 consumption. Decreased is common in all forms of shock. The magnitude of the O2 consumption deficit has been correlated with mortality rates.
Due to reduction in blood flow: hypovolemic, cariogenic, obstructive (perfusion)
Or due to uneven distribution of the blood: septic, anaphylactic, neurogenic

Question 6

Provides an estimate of the balance between tissues O2 demand or consumption and O2 supply/delivery.

Answer 6

O2 extraction ratio. Also provides an indication of the ability of the tissues to extract and use the O2 delivered.

Question 7

What are possible causes of hypo-perfusion and hypoxia?

Answer 7

Volume: not enough perusing or wrong type (decreased Hct, Hgb, increased fluid/plasma). Pump ineffective. Vasculature is ineffective (dilated out). Volume isn’t where it needs to be. Obstruction in the blood’s pathway.

Question 8

Indicator of perfusion in capillary beds. Shows average of pressure in the vessels.

Answer 8

MAP: mean material pressure. 1 systolic + 2 diastolic all divided by 3. Want 60 or higher. Does not indicate oxygenation.

Question 9

What are the types of shock? Earliest indicator of shock?

Answer 9

Hypovolemic, the most common. Cariogenic (inadequate pump, like HF). Distributive (ineffective vasculature) which can be: Neural. Chemical (anaphylaxis, sepsis, capillary leak). Obstructive.
Hr is the earliest indicator because the body is using it to compensate.

Question 10

Stage in symptomatic shock but the body has no decreased O2 or perfusion.

Answer 10

Compensatory. Either volume, pump, or vasculature is compromised but the body compensates quickly because it’s capable of correcting it. Tachy, lightheaded, etc. Eg, donating blood.

Question 11

Stage in shock wherein the cells aren’t receiving O2, leads to metabolic acidosis.

Answer 11

Progressive shock.

Question 12

Stage in shock with cell damage all over the body, including organs. Organ and cell death.

Answer 12

Irreversible/refractory. Pt will die, no recovery. Even with reversing the cause, organs start failing. Provide comfort measures.

Question 13

Explain MAP/SBP, HR, and RR in compensatory stage of shock?

Answer 13

MAP/SBP: Increases initially, drops long term. Increased HR, usually by 10-15 bpm. Increased RR, deeper to pull more O2. Preload increases with respirations.

Question 14

Explain MAP/SBP, HR, and RR in progressive stage of shock?

Answer 14

Decreased MAP, SBP, increased DBP. Narrowing pulse pressure. Increasing tachycardia, except paced and beta blocked. Tachypnea, decreased status that exhaustion happens. Probably eventually go into reparatory failure.

Question 15

Explain MAP/SBP, HR, and RR in refractory/irreversible stage of shock?

Answer 15

Hypotensive. Tachycardia, arhythmias. Respiratory failure.

Question 16

Explain skin, UO, mentation, and acid/base in compensatory stage of shock?

Answer 16

Skin has diaphoresis, possibly asymptotic. Decreased urinary output (baroreceptors near the kidneys produce ADH because they sense a drop in perfusion), vasoconstriction decreases kidney perfusion. Fluid retention. At first hyper awareness, very fight or flight, long term anxiety, restlessness, lightheaded. Normal pH. Late acid/base: the bicarb is decreased but still normal.

Question 17

Explain skin, UO, mentation, and acid/base in progressive stage of shock?

Answer 17

Pale and diaphoretic in early, mottling for skin in late. Decreased urine output with increased concentration. Confusion, agitation, anxiety, then progressive decline into coma. Hypoxic and acidotic. Anaerobic metabolism increase lactic acid, decreased pH. Maybe give bicarb.

Question 18

Explain skin, UO, mentation, and acid/base in irreversible/refractory stage of shock?

Answer 18

Skin is mottled and cold with terrible capillary refill, possibly necrosis. Urine output is little if at all. Coma. Raging metabolic acidosis (giving bicarb may not be effective at this point).

Question 19

Caused by a loss of whole blood, plasma or interstitial fluids in such quantities that the body’s metabolic needs can no longer be met. The problem is loss of volume, not enough or the right type circulating. Pathophysiology?

Answer 19

Hypovolemic shock. Causes are whole blood loss, plasma loss, dehydration, burns (oozing, 3rd spacing).
Decrease in venous return (pre-load) which results in decreased SV which means decreased CO which results in anaerobic metabolism and lactic acid production which causes myocardial depression (compensatory). Decreased CO leads to decreased coronary artery perfusion, inadequate cellular perfusion which leads to increased susceptibility to infections and hemorrhage which results in organ damage (refractory).

Question 20

Skin and fluid s/s in hypovolemic shock?

Answer 20

Skin is the least reliable indicator. Cool, pale due to vasoconstriction. Decreased cap refill. Clammy, moist skin due to epinephrine and norepinephrine. Increased thirst caused by the thirst mechanism being activated due to increased serum osmolality. Urine output falls due to vasoconstriction and decreased GFR. ADH released to retina fluid.

Question 21

Heart and respiratory for hypovolemic shock?

Answer 21

Tachycardia is a very early sign (the SV decreases so HR increases to compensate). Increased rate and depth of respiration to improve blood O2, blow off CO2, increase right heart filling volume to increase pressure, compensate for impending acidosis.

Question 22

Labs, mental, and hemodynamic for hypovolemic shock?

Answer 22

Labs really depend but focus a lot on h/h and electrolytes.
Hyperalert initially, LOC will initially improve but then decrease over time.
CVP: central venous pressure, reflects the preload. Will be low (2-10 is normal) because of the poor preload.
MAP: depends on their current status. Drops as shock progresses

Question 23

What is the most important intervention for hypovolemic shock due to blood loss?

Answer 23

Stop the loss and restore circulating blood volume. Replace what was lost, how much and what type (RBCs, electrolytes, plasma, saline?)? Administer enough to correct problems, like improving BP, UO, HR. Can cause fluid overload if overdone.

Question 24

What type of IV fluids are used for hypovolemic shock?

Answer 24

Lots of saline in most cases to just help volume. Crystalloid solutions: RL, NS. Liver converts the RL into bicarb. Provides intravascular expansion. IV solution may be or may not be all that is needed, depends on what was lost. Do not use D5W (initially isotonic but the glucose gets used by the body which causes hypotonicity)
Only when they are stable do you give them something to drink, until then just IV fluids.

Question 25

Things in fluids given for hypovolemic shock.

Answer 25

Albumin is a large protein and volume expander, helps pull fluid back into circulation. Used once the pt is stabilized, not used in active shock cause it can cause ARDS!
Hespan (hetastarch) has no blood products, also a plasma volume expander with large starch molecules. Cheaper than blood products. For Jehovah’s witnesses.
Plasma, FFP. Clotting factors in it, so for clotting disorders. Mainly used for ascites, burns. Saline first followed with FFP. Give blood products though for major whole blood loss!

Question 26

Pharmacological cardio support for hypovolemic shock?

Answer 26

Improve left ventricular function by administering inotropic agents like dopamine, dobutamine, and digoxin. Improve preload by administering fluids or vasoconstrictors (after the volume is replaced) like dopamine, norepinephrine, neo-synephrine

Question 27

Dopamine dosages?

Answer 27

Renal/mesenteric dilation (uncommon, lowest dose): 0.5-2mcg/kg/min
Inotropic-beta (increase CO, more common): 2-10 mcg/kg/min. If just bradycardia then 5-10 (inotropic range, not for vasoconstriction)
Vasoconstriction-alpha: >10 mcg/kg/min
Not given above 20 cause it’ll cause severe vasoconstriction, cuts off circulation. Dose determines effect.
Go-to when the issue is with CO or BP after hypovolemic shock.

Question 28

Secondary interventions for hypovolemic shock?

Answer 28

Correct acid/base, may give bicarb if shock not reversed fairly quickly. Monitor for fluid-overload rebound, although overload is better than shock (may give diuretic if needed). Meet nutritional needs with a high caloric intake. Provide emotional support. Elevate legs for better return (shock position, flat with legs up to drain blood from the legs back to the core circulation).

Question 29

Caused whenever the heart’s pumping ability becomes impaired resulting in a decreased CO. Basically HF.

Answer 29

Cardiogenic shock. Caused by any condition that causes dysfunction of the ventricles (though left is the most important because it’s the main pump) due to ischemia, structural problems, or dysrhythmias, basically same causes as HF. Different from HF because there’s compromised perfusion, the same because of decreased BP and O2, with crackles.
When the pt has a decreased BP, listen to lungs to determine whether hypovolemic or cardiogenic shock cause cardio will have crackles and edema.

Question 30

Interventions for cardiogenic shock?

Answer 30

Oxygenation, increase O2 attached to Hgb. Correct any dysrhythmias, hypervolemia, hypovolemia. Inotropic meds are the primary intervention to get the heart working better. Decrease left ventricular workload. Vasodilators to increase after load mildly (NTG is preferred, vasodilator peripheral and coronary arteries). Intra-aortic balloon pump. VAD: ventricular assist device.

Question 31

Pathophysiology of distributive/circulatory shock?

Answer 31

Vasculature is the issue, not the pump or volume. Event causes vasodilation. Inflammatory response in vessels. Misdistribution of the blood (it’s all there but in the wrong places). Decreased pre-load leads to decreased CO. Inadequate perfusion leads to anaerobic metabolism and acidosis which then causes the heart to be involved too.

Question 32

The three kinds of distributive/circulatory shock?

Answer 32

Neurogenic, neural induced.
Chemically induced: Sepsis, anaphylaxis, capillary leak (fluid oozes out into the third space)
Obstructive

Question 33

Type of distributive shock that occurs due to massive vasodilation as a result of loss of the sympathetic tone. Causes?

Answer 33

Neurogenic shock. When sympathetic tone is lost, all that is left is vagal stimulation which decreases HR. Sympathetic counteracts it usually.
Caused by spinal cord injury(T6) and above, spinal anesthesia (these two are the most common causes!). Drugs such as ganglionic blocking agents or barbiturates, brain damage to the medulla (which is rare).

Question 34

HR, temp, and extremities in neurogenic shock?

Answer 34

HR decreased due to loss of sympathetic nervous stimulation, so vagus nerve takes over. Bradycardia along with the low BP is specific to neurogenic shock (cause there should be tachycardia with a low BP).
Extremities are warm and pink originally because of vasodilation (1st hour or so) but then get colder later on cause the blood isn’t actually moving around. Temp is unregulated and hypothermia cause blood isn’t being warmed at the core. BP is decreased like all the shock.

Question 35

How is neurogenic shock treated?

Answer 35

Fluids because of the preload crash, the body perceives hypovolemia because the blood isn’t going back to the heart so fluids give the heart volume to work with. Vasoconstricting drugs to take over SNS job to get blood back into circulation. O2 like all forms of shock.
Dopamine (Inotropin) 10-20 mcg/kg for acidosis because the heart needs help. Norepinephrine (Levophed) as a pure vasoconstrictor.

Question 36

Explain the pathophysiology of hypovolemic shock?

Answer 36

A decreased blood volume/plasma loss will cause a decrease in venous return (pre-load) which results in decreased CO. The CO results in anaerobic metabolism/lactic acid production which causes myocardial depression (acidosis compromises the cardiac pump) and decreased coronary artery perfusion (could cause ischemia). Inadequate cellular perfusion which leads to an increased susceptibility to infection and hemorrhage which results in organ damage (refractory).

Question 37

S/s of cardiogenic shock?

Answer 37

Decreased CO, cardiac index is adjusted for the size of the person. Decreased BP, diminished peripheral pulses. Skin is pale, moist, and cyanotic. UO is decreased cause poor kidney perfusion. LOC depends on the acidotic state and BP. HF with decreased EF.
When the pt has a decreased BP, listen to the lungs to determine whether it’s cardiogenic shock, because they’ll have pulmonary edema with crackles.

Question 38

Catheter with inflatable balloon at the end. Inserted through the femoral artery, threaded toward the heart, the balloon is positioned in the descending thoracic aorta where coronary arteries come off. Uses internal counter pulsation through the regular inflation and deflation of the balloon to augment the pumping action of the heart.

Answer 38

Intra-aortic ballon pump (IABP). Assistive device sort of like an artificial heart. Hyperperfuses the heart while it’s healing.
Inflates during diastole, increasing pressure in aorta and therefore increasing blood flow through the coronary and peripheral arteries. Deflates just before systole, lessening pressure in aorta before left vent contraction, decreasing amount of resistance the heart has to overcome to eject blood and decreasing lvent workload.

Question 39

Shock involving a sudden life-threatening hypersensitivity reaction to an antigen. There’s enough fluid but it’s in the wrong places. Characterized by massive vasodilation and increased capillary permeability (causes hives). Pathophysiology?

Answer 39

Anaphylactic shock a type of chemical distributive shock. Chemical mediators cause vasodilation, capillary permeability, bronchoconstriction, increased coronary permeability, bronchospasm. Shock from profound vasodilation and and low CO. Death can result from severe hypoxemia secondary to bronchoconstriction or from cardiovascular collapse.

Question 40

Treatment for anaphylactic shock?

Answer 40

Treat the anaphylaxis first! Use all three: epinephrine, diphenhydramine, and corticosteroids. Also give vasodilators and extra fluid to take care of the cardiac component. The shock component is vasodilation and CO.

Question 41

Pt. becomes hypovolemic by loss of fluid into the interstitial tissues.

Answer 41

Capillary leak. Caused by burns, ascites, sepsis, peritonitis, severe malnutrition, hyperglycemia. Treatment is the same as hypovolemic shock.

Question 42

Type of distributive shock wherein heart muscle is within normal limits but shock still occurs.

Answer 42

Obstructive shock. Heart muscle is unable to pump due to a secondary obstruction, unable to fill. Fix the obstruction.
Ex: peritonitis, cardiac tamponade, pneumothorax, etc.

Question 43

Explain glucose metabolism and fluid shifting complications of all types of shock?

Answer 43

Pt may become hyperglycemic to meet the increased demands of energy, pancreas stops the insulin production.
Water moves into the cells taking Na with it. This movement of water further decreases the circulating blood volume and leads to cellular edema and disruption of metabolic activity.

Question 44

Explain the brain and kidney complications of all types of shock?

Answer 44

The decrease in blood flow to the brain leads to cerebral hypoxia which can lead to either seizures or cerebral infarction. Assess for anxiety, restlessness, changes in LOC, lethargy, stupor, coma.
Vasoconstriction compromises blood flow to the kidney leading to acute tubular necrosis. High K+, decreased erythropoetin and UO. Assess for oliguria.

Question 45

Myocardial complications of all types of shock?

Answer 45

Decrease in CO leads to decrease in perfusion which leads to myocardial failure. This leads to altered cell membrane potential which leads to an increase incidence of dysrhythmias. Arrhythmias and lack of contractility cause high K+.

Question 46

How does shock affect the peripheral circulation?

Answer 46

Initially there is a vasoconstrictive response in an attempt to increase circulating blood volume. Fluid moves from the interstitial space to the intravascular space to restore volume. Eventually the compensatory mechanisms fail and the body attempts to maintain blood flow to the heart and brain at the expense of the other organs, called shunting.

Question 47

Complications of shock for the GI?

Answer 47

Gut immunity goes down cause it’s not being perfused. Infarcts cause the gut to open up and spill contents into the peritoneum, causing peritonitis r/t shock.
When the blood vessels constrict the bowels are more affected than any other system with blood being shunted away.

Question 48

Hepatic complications of shock? Pulmonary?

Answer 48

The decreased blood flow to the liver leads to hepatic hypoxia. Proteins like albumin aren’t made, toxin buildup, decreased clotting factors, creates bicarb, dumps glucose into the blood which isn’t good for thin capillaries. Pancreas can’t make insulin or digestive enzymes when the pt needs more nutrients.
ARDS can result, pneumonia, VAP

Question 49

Explain DIC in shock?

Answer 49

Global inappropriate microcirculation clotting in the capillaries. Paradoxical bleeding, factors used up and bleeding in weird ways. Caused by anything that puts someone into severe shock or sepsis. Inflammatory response to a ton of things can cause it. Results in decreased perfusion and decreased LOC because of brain bleeds. Keep them from anything that can cause any form of bleeding whatsoever.

Question 50

Lab values found in DIC?

Answer 50

Severely decreased platelets. Elevation of D-dimer shows presence of clotting (it’s the waste product from clotting). Increased PT/PTT/TT because the clotting time tends to be longer and longer. Fibrin (which helps make the clots) crashes, with little to none as time goes on. FDP (fibrin degeneration product) skyrockets.

Question 51

Treatment for DIC?

Answer 51

Correct the underlying cause and secondary effects. Replace what’s missing: volume, RBC, FFP, clotting factored. Heparin therapy to attempt to save clotting factors, stop inappropriate clotting when caught early on.

Question 52

Systemic response to an overwhelming inflammatory process caused by an infection. Immune repose activates cytokines and mediators associated with inflammation, leading to poor tissue perfusion and capillary leaking in to third spaces. Coagulation system is activated inappropriately. Progression?

Answer 52

Sepsis.

1. Systemic inflammatory response syndrome: SIRS
2. Sepsis (>= 2 SIRS critters plus infection)
3. Severe sepsis: organ dysfunction
4. Septic shock and MODS

Question 53

SIRS criteria?

Answer 53

2 or more of: Temp > 38C/100.4F or < 36C/96.8F. HR > 90bpm. RR >20/min or PaCO2 <32 mmHg. WBC > 12,000 or <4,000 and/or 10% bands.
The physiologic presentation is similar to sepsis but no source of infection found.

Question 54

Infection associated with organ dysfunction hypotension, and/or hypoperfusion. SBP <90 or MAP <65, or a drop in SBP >40 from baseline BP. Will respond to fluid resuscitation. Inappropriate clotting.
Manifestations of hypoperfusion?

Answer 54

Severe sepsis.

Tachypnea, oliguria, actue alterations in cognition and/or affect, lactate >= 4mmol/L.

Question 55

Severe sepsis with hypotension despite adequate fluid replacement and perfusion abnormalities that may include: lactic acidosis, oliguria, acute alteration in mental status.

Answer 55

Septic shock.Requires vasopressor support regardless of adequate fluid replacement.