Shock Flashcards
What is shock?
A life-threatening condition that results from __________
inadequate tissue perfusion.
Creates an imbalance between the delivery of oxygen and nutrients that are needed to support cellular function.
Shock affects ALL body systems
It can develop very rapid or very slow
It all depends on the underlying cause
-
-
Effective cardiac pump
Adequate vasculature / circulatory systems
Sufficient blood volume
-
-
Hypoperfusion
Hypermetabolism
Activation of the inflammatory response
The body calls on all homeostatic mechanisms to prevent and/or reverse shock;
however, if these compensatory mechanisms fail, the result is ____________
organ dysfunction and death
Pathophysiology of Shock
Cellular changes:
Cells lack adequate blood supply
produce energy through _________
____ intracellular environment
normal cell function ceases
_____
Vascular changes:
Regulatory mechanisms stimulate vasodilation or vasoconstriction in response to mediators released by the cell, communicating need for _____
anaerobic metabolism
acidotic
cell death
O2 & nutrients
Pathophysiology (cont.): Blood pressure regulation
-
-
All 3 must respond to maintain adequate BP
Best expressed through Mean Arterial BP (MAP):
MAP = __________
Tissue and organ perfusion depend on MAP of at least _____
If unable to calculate MAP through complicated measures, most BP measurement devices estimate a MAP
blood volume
cardiac pump
vasculature
Cardiac Output x Peripheral Resistance
65 mmHg
Pathophysiology (cont.):BP regulation & kidneys
Kidney regulate BP by
releasing: renin which converts angiotensin I to II (this acts as a ________)
This leads to the release of aldosterone
which promotes __________
_____ then
stimulates release of ____
which causes further retention of H20 to raise blood volume and Bp
This process can take ______
Important to catch early: medications, fluid bolus, blood products to treat
vasoconstrictor)
Na and H20 retention
Hypernatremia
ADH
hours to many days
The 3 stages of shock
3 stages:
Shock can be identified as early or late
it is important to understand the physiologic responses to divide it into the appropriate stage for treatment
The chance of survival greatly improves if _______
EBP states that aggressive therapy should occur within _____ for best outcome and survival
Stage I: Compensatory Stage
Stage II: Progressive Stage
Stage III: Irreversible Stage
diagnosed early
3 hours
Stage I: Compensatory stage
BP remains within normal limits
Increased HR and increased contractility maintain adequate cardiac output
Increased RR
SNS
release of epinephrine and norepinephrine
body shunts blood to vital organs (away from skin, kidneys, and GI tract)
cool, pale skin
Decreased urinary output (due to release of ADH and aldosterone)
Altered LOC
First sign of altered LOC- agitation, restlessness
Respiratory alkalosis <35 PCO2 (due to hyperventilation)
Stage I: Compensatory stageNursing mgmt
Identify ____ before progression
-
Monitor _______
Reduce _______
Promote ______
the cause
Fluid replacement
Vasopressors
tissue perfusion
anxiety
safety
Stage II: Progressive stage
Mechanisms that regulate BP can no longer compensate and the MAP falls below normal limits
BP: Systolic < ____
Neuro:
HR > ___
RR:
Acid/base: PaC02 >
Skin:
Urine output: <
Metabolic acidosis
______ is considered part of this stage (see later in ppt)
90 mmHg
Neuro: Declining mental status, confusion
HR > 150 bpm
RR: rapid, shallow respirations, and possibly crackles
Acid/base: PaC02 > 45 mm Hg - reflects hypoventilation
Skin: mottled, petechiae
Urine output: < 0.5 mL/kg/hr
Metabolic acidosis
MODS is considered part of this stage (see later in ppt)
Stage II: Progressive stageNursing mgmt
Client is typically moved into an ICU setting for this stage
Hemodynamic monitoring:
May include more invasive monitoring
ECG monitoring
ABG gases
Serum electrolyte levels
Respiratory support:
Up to mechanical ventilation
Fluid volume maintenance/replacement:
Up to dialysis
Assess for physical and mental status changes that can occur very quickly
Stage III: Irreversible stage
Severe organ damage past the point of survival
BP remains low, despite treatment
Renal and liver dysfunction
Respiratory dysfunction, despite O2 delivery/ interventions
Cardiac dysfunction, cannot maintain adequate MAP for perfusion
Worsening metabolic acidosis r/t __________
Leads to __________
lactic acidosis
(by product of anareobic resp.
multiple organ dysfunction syndrome
Stage iii: irreversible stage nursing mgmt.
Comfort measures
-Ensure all are involved & provide comfort
-Inform family about the importance of seeing, touching, and talking to client
Inform family/loved ones regarding prognosis
-Discuss living wills
-Advanced directives
-Any other written/verbal wishes
-Ethics committee, if needed, to assist in making difficult care decisions
Engaging palliative care
Clinical manifestations:stages of shock
Blood pressure:
Compensatory- Normal
Progressive- Systolic <90 mm Hg; MAP < 65 mm Hg
Requires fluids resuscitation to support blood pressure
Irreversible- Requires mechanical or pharmacologic support
Clinical manifestations:stages of shock
Heart rate
Compensatory: >100 bpm
Progressive: >150 bpm
Irreversible: Erratic
Clinical manifestations:stages of shock
Respiratory status
compensatory: >20 breaths/min
PaCO2 < 32 mm Hg
Progressive: Rapid, shallow respirations; crackles
PaO2 <80 mm Hg
PaCO2 >45 mm Hg
Irreversible: Requires intubation and mechanical ventilation and oxygenation
Skin
Copensatory: cold, clammy
Progressive: Mottled, petechiae
Irreversible:
Jaundice
Urinary output
Compensatory: decreased
Progressive: <0.5 ml/kg/hr
Irreversible: Anuric; requires dialysis
(lack of urine production.)
Mentation
Compensatory: confusion and/or agitation
Progressive: lethargy
Irreversible: Unconscious
Acid-base balance
Compensatory: Resp. alkalosis
PaCO2 <32
Progressive: Metabolic acidosis
Paco2 >45
Irreversible: Profound acidosis
Types of Shock
CHAIN
Cardiogenic
Hypovolemic
Anaphylactic
Infectious (sepsis)
Neurogenic
Hypovolemic shock
Most common type of shock
characterized by ____________
External _______
Internal _______
Sequence of events
decreased intravascular volume
External fluid losses
Internal fluid shifts
Risk factors for hypovolemic shock:
External:
External:
Trauma
Surgery
Vomiting
Diarrhea
Diuresis
Diabetes insipidus
Internal:
Hemorrhage
Burns
Ascites
Peritonitis
Dehydration
Necrotizing pancreatitis
Hypovolemic shock:care mgmt
______:
#1 concern
IV access:
Pharmacologic therapy:
Reverse cause of dehydration:
Monitor for s/s hypervolemic complications with frequent assessments:
Fluid replacement:
IV
at least 2 sites
IO (intraosseous or CVAD)
Pharmacologic therapy:
vasopressors
(nausea, vomiting, diarrhea, hyperglycemia)
Antiemetics, antidiarrheal, insulin, desmopressin)
Desmopressin- used as an antidiuretic for diabetes insipudis
Listen to lungs, JVD, difficulty breathing, electrolyte imbalance—fluid overload
Hypovolemic shock: fluids
Crystalloids:
0.9 % Sodium Chloride
Lactated Ringers
Colloids:
Albumin (5%, 25%) - Rapidly expands plasma volume
Blood Products- Plasma, packed red blood cells, and platelets
Hypovolemic shock: visual aid
See slide
Plasma loss through burns
Hemorrhage
Decreased body fluids
GI loss- bleeding, vomiting, diarrhea
Diabetes insipidus
Diuresis
Cardiogenic shock
Impaired ability for the heart to contract and pump blood…which causes inadequate O2 for heart and tissue
Two types:
Coronary-
Anterior wall Mis put at greater risk for b/c more damage to left ventricle
Non-coronary
hypocalcemia, hypoxemia, cardiomyopathy, tamponade, dysrhythmias
Cardiogenic shock:
Risk factors:
S&S:
Older age
Heart failure
Previous heart attack (higher for women)
Coronary artery disease
high blood pressure
Diabetes
Angina
Fatigue
Feelings of doom
Dsrythymias
Increased RR, tachycardia, low BP
Pale skin
Weak pulse
SOB
Cardiogenic shock: care mgmt
Limit myocardial damage and preserve healthy myocardium
Improve cardiac function by increasing ________ and decreasing ______ (or both!)
Correct underlying cause…
Coronary:
Non-coronary:
If cause of cardiogenic shock is from cardiac arrest, ______ and _____
cardiac contractility
ventricular afterload
resuscitate client and keep cool (therapeutic hypothermia); WHY?
Cardiogenic shock: pharm therapy
Dobutamine:
Nitroglycerin:
Dopamine:
Norepinephrine, Epinephrine, Milrinone, Vasopressin, and Phenylephrine
Antiarrhythmics
Increases the strength of myocardial activity and improving cardiac output
Decreases pulmonary and systemic vascular resistance (decreased afterload)
Dobutamine:
Venous vasodilator, reduces preload
Higher doses can cause arterial vasodilation
Frequently used in combo with dobutamine
Nitroglycerin:
May be used with dobutamine and nitroglycerin to improve tissue perfusion
Doses greater than 8 mcg/kg/min can cause vasoconstriction
Can also increase HR past therapeutic levels
Dopamine:
Distributive shock
Occurs when:
this displacement leads to
relative hypovolemia due to blood not returning to the heart
Which leads to inadequate tissue perfusion
intravascular blood pools in peripheral blood vessels
3 types of distributive shock:
Anaphylactic
Neurogenic
Septic Shock
Distributive shock:Anaphylactic shock
Severe allergic reaction to: antibodies the body has already produced (for example: ________)
Antigen-antibody reaction
-causes mast cells release vasoactive substances (histamine and bradykinin)
-activates inflammatory cytokines
-vasodilation and capillary permeability
____ onset of symptoms
Signs/symptoms…what would you expect?
blood transfusion reactions
Acute
Anaphylactic shock clinical assessment:
Severe-
Generalized flushing
Diffuse erythema
Difficulty breathing (laryngeal edema)
Bronchospasms
Hypotension
Dysrhythmias
Severe – respiratory distress, rapid onset hypotension, neurologic compromise, cardiac arrest
Distributive shock:Anaphylactic shock Care mgmt
Remove causative agent (for example, discontinuing an antibiotic)
Establish adequate IV access
Fluid replacement
Vasopressors
Diphenhydramine (Benadryl)
Nebulized medications:
Albuterol (Proventil)
Maintain/establish airway
Distributive shock:Neurogenic shock
Vasodilation occurs as a result of a loss of balance between _______ and _______ stimulation.
What effect does SNS and PNS stimulation have on smooth muscle?
Drastic decrease in _____ and ____
Inadequate BP results in insufficient perfusion of tissues and cells
parasympathetic and sympathetic
Parasympathetic wins- more vasodilation
SVR and bradycardia
Distributive shock:Neurogenic shock causes & s/s
Causes:
S/S:
Spinal cord injury
Spinal anesthesia
Other related diseases that cause nervous system damage
Short courses of neurogenic shock: syncope
Similar to parasympathetic stimulation
Dry, warm skin
Hypotension
Bradycardia***
Distributive shock:Neurogenic shock care mgmt
Goal of treatment is restore ________ (could be a surgical procedure, proper positioning)
Keep HOB _____ (especially when anesthetic agent has been given-this will prevent it from spreading up the cord)
In spinal cord injury, great caution with _____ the client
Support CV and Neuro function
Higher incidence of _________ may be implemented
Monitor for s/s of ______ which could lead to hypovolemic shock
sympathetic tone
> 30 degrees
moving/mobilizing
VTE; DVT prophylaxis
internal bleeding
Distributive shock: septic shock
Defined as: “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality.”
Most common type of Distributive Shock*****
Caused by widespread infection or Sepsis
Distributive shock: septic shock
-
-
Most common bacteria: _______
Sepsis is defined as: “life threatening organ dysfunction caused by __________
Both sepsis and septic shock incidences have continued to rise despite all the aggressive treatments / therapies
Bloodstream (bacteremia), most commonly CVAD’s
Lungs (pneumonia)
Urinary tract (urosepsis); most commonly urinary catheters
gram negative
a dysregulated host response to infection”.
Distributive Shock:Septic Shock risk factors
Invasive lines and procedures
Indwelling medical devices
Increased number of antibiotic-resistant microorganisms
Increasing number of older population
Septic shock: S&S
Early stages of sepsis:
Progression to septic shock:
BP – may remain WNL or respond to fluid therapy
Tachycardia
Hyperthermia
Fever
Warm flushed skin with bounding pulses
Elevated RR
Subtle changes in mental status
Decreased urine output
Hypotension – not responding to fluids
Skin is cool , pale, and mottled
Tachycardia
Tachypnea
Oliguria
nonresponsive
Distributive Shock:Septic Shock reduction/prevention
Strict infection control practices:
Hand hygiene
CLABSI prevention
Early removal of indwelling/invasive devices
Protocols to reduce VAP
Wound debridment
Early ambulation with pneumonia
Distributive shock:sepsis/septic shock labs
Labs:
Lactic acid (lactate): derived from muscle cells and erythrocytes; common marker used for sepsis
C-reactive protein (CRP): present during inflammatory process
Procalcitonin: substance produced in response to bacterial infections and tissue injury. Sepsis marker that is MOST studied.
Distributive shock:sepsis/Septic shock treatment
Fluid replacement therapy:
Implemented to correct tissue hypoperfusion
Pharmacolgic therapy
-Broad-spectrum antibiotics
-Vasopressors
-Inotropic agents
-PRBC’s
-Neuro-muscular blockade and sedation aganets
-DVT and PUD prophylaxis
Nutritional therapy
Should be initiated 24-48 hours of admission
SIRS Criteria and stages of sepsis: visual aid
SIRS = systemic inflammatory response syndrome
SIRS= Temp>100.4, HR >90, RR>20 or PaCO2 <32
WBC’s >12,000 or <4,000
Sepsis= SIRS + Infection
Severe Sepsis= Sepsis + End organ damage
Septic Shock = Severe Sepsis + Hypotension
Sepsis bundle:
Surviving Sepsis Campaign Bundle & CMS Core measure monitoring metrics
Complete within 1 hr of patient presentation/symptoms:
-measure lactate level (remeasure if initial is >2 mmol/L
-Obtain blood cultures
-Administer broad spectrum antibx
-Begin rapid admin. Of 30 mL/kg crystalloid for hypotension or lactate >/= 4 mmol/L (within 30 min)
-Admin. Vasopressors if patient is hypotensive during or after fluid resuscitation to maintain MAP ./= 65 mmHg
Sepsis bundle cont:
Complete within 3 hr of patient presentation/symptoms
Obtain serum lactate level
Obtain blood cultures prior to admin. Antibx
Admin. Rx broad spectrum antibx
Initiate aggressive fluid resuscitation in patients with hypotension or elevated serum lactate (>/= 4 mmol/L)
Minimum initial fluid bolus of 30 mL/kg with crystalloid solutions
Complete ASAP or within the first 6 hr of patient presentation/symptoms
Begin vasopressor agents if hypotension is not improved after initial fluid bolus (MAP 70%)
-Bedside cardiovascular US
-Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
Distributive Shock: risk factors
Septic Shock:
Neurogenic Shock:
Anaphylactic shock:
Septic shock:
Immunosuppression
Extremes of age <1 and >65
Malnourishment
Chronic illness
Invasive procedures
Emergent and/or multiple surgeries
Neurogenic shock:
-Spinal cord injury
-Spinal anesthesia
-Depressant action of medications
Anaphylactic shock:
-Hx medication sensitivity
-Transfusion reaction
-hx reaction to insect bites/stings
-Food allergies
-Latex sensitivity
Vasoactive agents
Inotropic agents
Vasodilators
Vasopressor agents
Inotropic agents:
Improve contractility, increase stroke volume, increase cardiac output
Dobutamine
Dopamine
Epinephrine
Milrinone
Vasodilators
Nitroglycerin
Nitroprusside
Vassopressor agents
Norepinephrine
Dopamine
Phenylephrine
Vasopressin
Epinephrine
Quick Review of shock:
Cardiogenic =
Obstructive =
Hypovolemic =
Distributive =
Cardiogenic = heart fails to pump out blood
MI, Arrythmia, aortic stenosis, mitral regurgitation
Obstructive = cardiac pump failure due to an indirect cardiac factor: outflow is obstructed
PE, tension pneumothorax, tamponade, aortic dissection
Hypovolemic = heart pumps well, but not enough blood volume to pump
Hemorrhage, fluid loss (burns, vomiting, diarrhea)
Distributive = heart pumps well, but there is peripheral vasodilation
Pancreatitis, burns, multi-trauma via activation of the inflammatory response
Multiple organ dysfunction syndrome(MODS)
Altered organ function
Falls into _______ Phase of Shock
Dysfunction and mortality:
One organ system dysfunction=20% mortality
>4 organ systems dysfunction=60% mortality
MODS can be a complication of all forms of shock; however, is most common in ____
Stage II: Progressive
sepsis
Risk factors and s&S of Mods:
Lungs
Liver
Neuro
Renal
Advanced age
Malnutrition
Coexisting diseases / chronic illness
Immunosuppression
Surgical or traumatic wounds
Lungs
Progressive dyspnea
Respiratory failure
Liver
Elevated bilirubin and liver function tests
Neuro
Unresponsive or coma
Renal
Decreased urine output
MODS: Care mgmt
Goal is to prevent; however, if unable to, goal then becomes to reverse MODS
Frequent monitoring of diagnostics (labs, ecg monitoring…more invasive testing if needed)
- Controlling the initial event
- Promoting adequate organ perfusion
- Providing nutritional support
- Maximizing patient comfort
Stages of shock:
When do you start fluid replacement and vasopressors?
Since the body may not be able to maintain this state for long:
Compensatory
Most common type of Distributive Shock*****
Sepsis
Pulse pressure
- norm?
how to calculate?
Normal is 40 mmHg
- Systolic – diastolic = pulse pressure
- Eg: 120/80 = 40 mmHg
- Eg: 90/70 = 20 mmHg
Hypovolemic shock occurs when there is a reduction of
intravascular volume by 15-30% (750-1500 mL)
Hypovolemic shock
proper positioning
- Modified Trendelenburg (passive leg raise) head flat legs raised
- This helps promote venous blood return to the heart
Neurogenic shock
Can be caused by depressant actions of medications
Or from prolonged lack of glucose (an insulin reaction)
