NURS 350 - Shock

shock overview

• oxygen needed for organs, tissues, and cells to function properly

• lungs - oxygenate blood

• CV system - deliver oxygen and remove waste

• shock = inadequate oxygen/perfusion - cell dysfunction

• body-wide response - organs compensate or fail (hypoxia)

types of shock

• hypovolemic shock

  • total body fluid decrease

  • hemorrhage

  • loss of circulating blood volume

  • decreased preload and stroke volume - MAP

  • causes: dehydration, hemorrhage

• cardiogenic shock

  • pump failure - decreased CO and MAP

  • large MI, cardiac arrest

• distributive shock

  • fluid shifted from central vascular space

    • blood shifts into tissues/interstitial space

    • vasodilation and capillary leakage - decreased SVR, SV, CO, MAP

  • sepsis: infection-induced organ dysfunction; most common distributive shock

  • anaphylaxis: severe allergic reaction causing widespread vasodilation

• obstructive shock

  • cardiac function decreased by noncardiac factors (indirect pump failure)

  • pulmonary embolism, tension pneumothorax

gas exchange and tissue perfusion

• shock overview

  • impaired perfusion and gas exchange - decreased oxygen delivery to tissues

  • commonly a result of cardiovascular problems

  • can occur in any setting (acute care, LTC, sepsis, infections)

  • untreated shock - cell death, MODS, death

• factors affecting perfusion (MAP)

  • blood volume

  • cardiac output - CO

  • vascular bed integrity/capillary function

key features of shock

• CV symptoms

  • decreased cardiac output and decreased BP

  • increased pulse rate

  • diminished peripheral pulses

  • narrowed pulse pressure

  • dysrhythmias

• respiratory symptoms

  • increased RR

  • decreased PaCO2 then increased PaCO2

• GI symptoms

  • decreased motiliy

• hepatic symptoms

  • increased liver enzymes, ammonia, and bilirubin

• neuromuscular symptoms

  • early: restlessness and anxiety

  • late: decreased CNS activity, sluggish pupils

• kidney symptoms

  • decreased or absent urinary output

  • serum creatinine, BUN and SG

• endocrine symptoms

  • hyperglycemia early, hypoglycemia late

• integumentary system

  • warm - cool - cold - mottled - cyanotic

• hematologic symptoms

  • decreased hemoglobin and platelets

  • increased d-dimer and bleeding times

shock overview

• mean arterial pressure (MAP) and perfusion

  • increased blood volume or increased CO - increased MAP

  • decreased blood flow or decreased CO - decreased MAP

  • vascular bed size inversely r/t MAP

• vessel changes

  • vasodilation - decreased BP, slower blood flow

  • vasoconstriction - increased BP, faster blood flow

• sympathetic nervous system

  • maintains vessel “sympathetic tone”

  • increases SNS stimulation - vasoconstriction - increased MAP

  • decreased SNS stimulation - vasodilation - decreased MAP

• organ perfusion

  • blood flow shifts based on oxygen demand

  • skin/muscles tolerate hypoxia longer

  • heart, brain, liver, pancreas highly sensitive to hypoxia

adaptive responses and events during shock

1. initial stage

   1. decreased tissue perfusion

   2. anaerobic metabolism

   3. no obvious s/s of shock

2. compensatory stage

   1. sympathetic stimulation

   2. increased HR, RR, DBP

   3. decreased pulse pressure, SBP, O2 sat

   4. decreased urine output

   5. decreased perfusion to non-vital organs

   6. vasoconstriction

3. progressive stage

   1. hypotension, weak pulse

   2. anoxia and ischemia of nonvital organs

   3. hypoxia of vital organs

4. refractory stage

   1. severe hypotension despite vasopressors

   2. severe tissue hypoxia with ischemia and necrosis

   3. MODS - microthrombi - death

hypovolemic shock - patho

• patho

  • loss of circulating blood volume - decreased MAP

  • possible RBC loss - decreased oxygen delivery to tissues

  • decreased perfusion and oxygenation - anaerobic cellular metabolism

• compensation

  • baroreceptors detect decreased MAP

  • brain activates compensatory mechanisms

  • blood shunted to vital organs

• progression of shock

  • continue hypoperfusion - increased lactic acid and harmful metabolites

  • causes acidosis, tissue damage, depressed cardiac function

  • early treatment = reversible damage

• severe/untreated shock

  • prolonged hypoxia - cell death and organ failure

  • progresses to MODS

  • end-stage shock may become irreversible

hypovolemic shock

• etiology

  • too litle circulating blood volume - MAP decreased which prevents total body perfusion and gas exchange

  • hemorrhagic shock - hypovolemic shock, decreased clotting factors

  • hypovolemia from dehydration caused by decreased fluid intake or increased fluid loss

• incidence and prevalence

  • incidence - unknown

  • common complication in ED and post-surgical patients

• health promotion/disease prevention

  • recognizing hypovolemic shock is a major nursing responsibility

hypovolemic shock - assessment

• history

  • ask about recent illness, trauma, procedures, or chronic health problems

  • I&Os, assess for areas of poor clotting and bruising

• physical assessment/ signs and symptoms

  • watch for trends in VS

  • CV changes - decreased MAP - compensatory responses

  • HR increase above baseline to maintain CO and MAP despite SV being decreaased

  • increased HR often first sign of shock

  • vasoconstriction - DBP increased but SBP remains = narrow pulse pressure

  • as shock progresses - SBP decreases and CO and RR increase

  • urinary output <300mL/hr - early shock

• skin changes

  • cool, clammy, pale/cyanotic skin

  • dry mucous membranes

  • mottling and decreased skin elasticity as shock worsens

  • slow/absent capillary refill

• neurologic changes

  • early sign: thirst

  • restlessness, anxiety, “impending doom”

  • progresses to confusion, lethargy, decreased LOC

• musculoskeletal changes

  • generalized weakness and muscle pain

  • decreased or absent deep tendon reflexes

interventions and management - hypovolemic shock

• interventions for hypovolemic shock

  • reversing the shock

  • restoring fluid volume

  • preventing complications

• nonsurgical management of perfusion

  • maintain perfusion

  • increase vascular volume

  • support compensatory mechanisms

nonsurgical management to maintain perfusion

• oxygen therapy

  • maintain O2 sats 90-96%

• IV therapy

  • crystalloids and colloids - volume replacement

  • crystalloids - NS and LR

  • colloids - PRBCs, platelets, FFP

• drug therapy

  • drugs for shock increase MAP, venous return, CO = improved perfusion

• assess

  • q15min VS, until shock controlled

  • hemodynamics, CVP via central line, pulmonary artery monitoring

drugs for hypovolemic shock

• vasoconstrictors - improve MAP by increasing peripheral resistance and increasing venous return

  • norepinephrine

  • phenylephrine

  • epinephrine

  • dopamine

  • vasopressin

• inotropes - increase contractility of heart thereby increasing CO

  • epinephrine

  • dobutamine

  • milrinone

surgical management - hypovolemic shock

• surgical management

  • traumatic injury most often the cause for hemorrhagic shock

  • other causes - GI bleeding and bleeding from surgical intervention

  • achieving hemostasis

    • apply manual pressure, ligation, tourniquet

    • topical application of pro-coagulation agents - thrombin and fibrin glue

    • injection of epinephrine

• evaluate outcomes

  • vascular volume restored with normal tissue perfusion

sepsis and septic shock - patho

• sepsis

  • extreme response to infection that can cause tissue damage, organ failure, and death

  • associated with SIRS and MODS

• normal infection response

  • infection contained to local area, should not lead to sepsis

  • WBCs release cytokines - local inflammation increases WBCs to kill invading organism

  • resulting in constricted small veins and dilating arterioles in that area, increase perfusion

  • response resolved after infection controlled

• septic shock

  • life-threatening organ dysfunction - dysregulated response to an infection

  • subset of sepsis with severe circulatory/metabolic abnormalities, increased risk of death

septic shock etiology

• sepsis etiology and progression

  • infection enters bloodstream - sepsis develops if local control fails

  • widespread inflammation (SIRS) impairs perfusion and gas exchange

  • causes hormonal, vascular, and tissue dysfunction

• early sign

  • mild hypotension

  • decreased urine output

  • increased respiratory rate

  • fever, hypothermia, or normal temp

  • increased WBC count

  • early recognition/treatment improves outcomes

• progression

  • microthrombi form - hypoxia and organ dysfunction - DIC

  • creates cycle of inflammation, poor perfusion, and cell damage

  • increased lactic acid leads to metabolic acidosis

  • stress response triggers continued release of glucose - hyperglycemia

systemic inflammatory response syndrome (SIRS) criteria

• defined by the presence of 2 of the 4 criteria below

  • temperature

    • fever >38 or hypothermia <36

  • heart rate

    • tachycardia >90bpm

  • respiratory rate

    • tachypnea >20 bpm or PaCO2 <32 mmHg

  • leukocyte count

    • leukocytosis WBC >12000 or leukopenia <4000 or bandemia >10% immature bands

sepsis s/s and phases

• sepsis signs and symptoms

  • decreased O2 sat, rapid RR, decreased or absent urinary output, change in cognition and affect

• septic shock

  • require vasopressors to maintain a MAP of at least 65 mmHg and

  • have serum lactate >2mmol/L despite adequate fluid resuscitation

• phases of septic shock

  • warm shock (early/compensated phase)

    • decreased systemic vascular resistance (SVR), normal or increased cardiac output

    • warm extremities and reduction flash/rapid capillary refill

  • cold shock (late/decompensated phase)

    • increased peripheral vascular resistance to shunt blood to vital organs

    • decreased CO, cold extremities, and delayed capillary refill

    • nearly irreversible at this state, MODS and organ failure is evident

    • poor clotting/uncontrolled bleeding (consumed platelets and clotting factors)

    • severe hypovolemic shock - continued vasodilation and capillary leak

    • poor cardiac contractility from ischemia

sepsis

• incidence and prevalence

  • patients at increased risk for sepsis have decreased immunity

• conditions predisposing sepsis and septic shock

  • >80 yo, immunosuppression, invasive lines, chronic illness

• health promotion and disease prevention

  • prevention is the best strategy

  • use aseptic technique during invasive procedures

  • remove indwelling urinary catheters and IVs and wean from the vent asap

sepsis - physical assessment s/s

• early (hyperdynamic/warm phase)

  • tachycardia, increased CO and HR, BP and SV, bounding pulse

  • warm, flushed skin; pink mucous membranes

  • tachypnea to maintain oxygenation

• progressive/late (hypodynamic/cold phase)

  • decreased CO, weak/thready pulse, delayed cap refill

  • cool, clammy, mottled/cyanotic skin

  • decreased urine output, increased creatinine

• complications with progression

  • DIC - microclots - hypoxia, ischemia, bleeding

  • petechiae, eccymosis, bleeding from IV/gum sites

  • ARDS - inflammatory lung damage - respiratory failure

  • MODS - progressive failure of >2 organ systems

laboratory assessment - septic shock

• key lab findings

  • increased procalcitonin

  • increased serum lactate

  • normal/decreased WBC count with increased band neutrophils (left shift)

  • bacteria in blood positive for sepsis

  • decreased bicarbonate - metabolic acidosis

• blood and culture studies

  • blood cultures may identify bacteria

  • obtain sputum, urine, stool, would, and/or blood cultures

  • draw cultures before antibiotics if no treatment delay >45 mins

• late septic shock findings

  • decreased hemoglobin, hematocrit, platelets, fibrinogen (DIC)

  • lactate >4mmol/L linked to high mortality

intervention for septic shock

• 1 hour bundle for management of sepsis

  • measure lactate level

    • remeasure lactate if initial is >2

  • obtain blood cultures prior to administering antibiotics

  • administer broad-spectrum antibiotics

  • rapidly administer 30mL/kg IV crystalloid for hypotension or lactate >4mmol/L

  • administer vasopressors if hypotensive during or after fluid resuscitation to maintain a MAP of >65

goal outcomes with sepsis or septic shock

• with appropriate interventions, the patient with sepsis or septic shock is expected to have normal aerobic cellular metabolism

• indicators for improvement in tissue perfusion include the following:

  • ABG (pH, PaO2, and PaCO2) WNL

  • maintenance of a urine output of >0.5mL/kg/hr

  • maintenance of MAP >65

  • absence of multiple organ dysfunction syndrome

  • capillary refill < 3 seconds

  • extremities warm without mottling

anaphylaxis patho

• patho

  • severe type 1 hypersensitivity reaction

  • rapid vasodilation and bronchoconstriction after allergen exposure

  • causes decreased CO, BP, and respiratory compromise

  • medical emergency, can be fatal within minutes

• common causes

  • medications and contrast dye, foods, insect stings/bites

• prevention and patient teaching

  • avoid known allergens, wear medical alert bracelet

  • inform health care providers of allergies

  • carry emergency anaphylaxis kit with epinephrine autoinjector

anaphylaxis assessment

• early recognition

  • symptoms may begin subtly - sudden, severe, abdominal cramping, and diarrhea

  • feeling of apprehension is an early sign

  • immediate intervention is required when criteria met

• skin manifestations

  • generalized itching and urticaria

  • angioedema

  • redness, hypo/hyperpigmentation

• respiratory manifestations

  • bronchoconstriction and mucosal edema

  • congestion, rhinorrhea, dyspnea

  • wheezing, crackles, decreased breath sounds

key features of anaphylaxis

• acute reaction (minutes - hours) involving:

  • skin/mucosal symptoms

    • hives, itching, flushing, swollen lips, tongue, uvula

  • PLUS at least 1:

    • airway/breathing: respiratory compromise

    • circulation: decreased BP or associated symptoms of end-organ dysfunction (syncope, incontinence)

    • other: severe GI symptoms (cramping, vomiting)

• OR

• acute onset after allergen exposure

  • hypotension, bronchospasm, or laryngeal involvement: stridor, voice changes

medication management - anaphylaxis

• immediately administer epinephrine IM

  • repeat q5-15 minutes X3 doses PRN

  • IV epi if unresponsive to IM epi

    • epi constricts blood vessels, improved cardiac contraction and dilates bronchioles

• apply O2 via NRM and infuse NS

• administer other drugs PRN

  • albuterol

  • H1 antihistamines

  • H2 antihistamines

  • glucocorticoids

  • vasopressors

  • glucagon

drugs to treat shock

• epinephrine (adrenaline)

  • treatment of choice for anaphylactic shock

    • activates 3 types of adrenergic receptors - alpha 1, beta 1, and beta 2

      • activation of alpha 1 elicits vasoconstriction

      • activation of beta 1 increased CO and BP

        • used for heart blocks, HF, shock, cardiac arrest

      • activation of beta 2 counteracts bronchoconstriction

        • used for asthma, coup, bronchospasm

      • given IV, IM, SQ, topically, and inhaled

      • adverse effects - hypertensive crisis, tachycardia, dysrhythmias, angina, hyperglycemia, extravasation

• norepinephrine (levophed)

  • receptor specificity: alpha 1, alpha 2, beta 1

  • action: similar to epi, but no beta 2 activation

  • limited chemical indications - hypotension and cardiac arrest

  • adverse effects - tachydysrhythmias, angina, HTN, local necrosis

• isoproterenol (isuprel)

  • action - increase HR and force of contraction

  • receptor specificity: beta 1 and beta 2

  • used to manage - AV heart block, improve outcomes in cardiac arrest and increase CO and improve tissue perfusion in shock

  • IV

  • adverse effects: tachydysrhythmias, angina, and hypoglycemia in diabeics

• dopamine (intropi)

  • receptor specificity - dopamine, beta 1 and at high doses alpha 1

  • therapeutic uses - shock, HF

    • beta 1 activation increases CO - improving tissue perfusion - treat HF

    • dopamine receptor activation in kidney - dilate renal blood vessels improve renal perfusion

    • activate alpha 1 - vasoconstriction decreased renal perfusion - monitor urinary output

  • adverse effects - tachycardia, dysrhythmias and anginal pain

  • route - continuous IV infusion

  • if extravasation, treatment is phentolamine

• atropine (atropen)

  • action - competitive blockade on muscarinic receptors; no direct effect of its own

  • effects

    • heart: increase HR (used for bradycardia)

    • exocrine glands: decrease secretion from salivary glands

    • smooth muscle: relaxation of bronchi

  • route: IV, IM, SQ, topically (to the eye)

  • therapeutic use for shock: increases HR (used for bradycardia)

  • adverse effects: dry mouth, blurred vision, urinary retention, constipation, and tachycardia

  • beers criteria: potentially inappropriate for geriatrics