Shock Flashcards
End result of all types of shock
*Impaired tissue perfusion/oxygenation
*Impaired cellular metabolism (from the impaired perfusion/oxygenation)
*Names of stages of shock, in order
1 - initial
2 - compensatory (early)
3 - progressive (decompensated)
4 - refractory (irreversible)
What occurs during stage 1: Initial stage of shock
Subclinical hypoperfusion
*No overt clinical manifestations
Decreased O2 delivery and/or O2 extraction (from hgb)
Decreased CO detectible by hemodynamic monitoring
What occurs with stage II (Compensatory) shock
(Body is now trying to improve situation, so will see s/s)
Occurs in response to sustained decreased CO in stage 1
*S/S are evident
Compensatory mechanisms restore tissue perfection
*Shock may be reversed with adequate interventions
During stage 2 of shock, how does the SNS respond?
The SNS is activated (Epi and norepi are activated)
Combined action of epi and norepi preserves CO and perfusion to the heart and brain *Temporarily
How does the endocrine system compensate in stage 2 of shock?
RAAS activates, ultimately causing
Renin release, which causes body to *hold onto salt and water, which increases fluid volume (increased blood volume)
How does chemical compensation occur during stage 2 of shock?
Chemoreceptors detect the decrease in PaO2, causing RR to increase to increase O2
This causes respiratory alkalosis
Also causes cerebral vessels to constrict, resulting in cerebral ischemia
*Cardiovascular clinical manifestations of compensatory shock
*SBP > 90
HR 101-150
Pulses weak, rapid
Skin cool, pale, moist
*Neuro clinical manifestations of compensatory shock
Decreased LOC (first indication something is wrong)
- Anxious, then restless, then irritable, then lethargic then drowsy
*Pupils dilated but reactive to light (think fight or flight response)
*Respiratory clinical manifestations of compensatory shock
RR > 20 / min
Pattern deep and rapid (hyperventilation/hyperpnea), which causes:
* PCO2 <35 mmHg
PO2 < 60 mmHg
HCO3 22-24 (not compensatory yet, so early in process. Can still intervene)
*Renal clinical manifestations of compensatory shock
*UOP < 30 mL/hr
Hypernatremia (b/c of RAAS)
Concentrated urine (body trying to hold onto volume to keep BP up)
*GI clinical manifestations of compensatory shock
Hypoactive bowel sounds (fight or flight)
Hyperglycemia (caused by counterregulatory hormones)
What occurs during stage 4 of shock (Refractory Shock)?
Pooling of blood in capillary beds
Inadequate perfusion of vital organs
Multisystem organ failure (SIDS, MODS)
*Shock is so profound and severe that *Death is imminent
Types of shock
Hypovolemia
Cardiogenic
Obstructive
Distributive
Definition of hypovolemic shock
Inadequate blood volume to fill intravascular space
External losses causing hypovolemic shock
Hemorrhage (Most common cause)
Diarrhea
Vomiting
Massive diuresis (Ex: DI, DKA, HNKS)
Loss of plasma (burns/wounds)
Internal losses causing hypovolemic shock
Internal hemorrhage (ex: liver laceration, severe GI bleed)
3rd spacing (ascites)
Increased capillary permeability (sepsis, allergic reaction, burns)
Patho of hypovolemic shock
Decreased circulating blood volume
Causes decreased venous return (decreased preload)
Which causes decreased ventricular filling
Which causes decreased stroke volume and cardiac output
Which causes *decreased tissue perfusion
Which causes * impaired cellular metabolism
Symptoms of hypovolemic shock
Hypotension
Tachycardia
Oliguria
Cool, pale skin
Decreased cardiac output, CI, PAP, PAWP
Increased systemic vascular resistance
Management of hypovolemic shock
*Identify and treat the cause
*Fluid therapy (3:1 rule) (Replace 3 times as much as what was lost)
Prevention of hypovolemic shock
Strict I&O (hourly for every pt, esp with foley)
Monitor for bleeding (low hct, hgb, platelets)
Report abnormal findings
Identify patients at risk
What is cardiogenic shock?
When >40% of LV function is lost, results in pump failure; cardiac output cannot meet tissue demands
Causes of cardiogenic shock
*MI (most common cause)
Post-cardiac surgery
Dysrhythmias
Valvular heart disease
Cardiomyopathy
Patho of cardiogenic shock
- Myocardial damage: compensatory mechanisms cause further detriment to myocardium
- Decreased pumping ability
- Decreased stroke volume and decreased cardiac output
(Volume is normal, but heart can’t pump to perfuse properly) - *Decreased tissue perfusion
- *Impaired cellular metabolism
Symptoms of cardiogenic shock
Hypotension
Tachycardia
Tachypnea
Oliguria
Cool, pale skin
Decreased cardiac output, decreased cardiac index
*Increased Pulmonary artery pressure, increased PAWP
Increased SVR
Management of cardiogenic shock
Goal = restore force of contraction: Improve CO and decrease workload
Positive inotropic agents (mid-range dopamine)
Afterload reducing agents (vasodilators: nitros)
Preload reducing agents (diuretic: furosemide)
Mechanical assist devices (rarely)
Prevention of cardiogenic shock
Minimize size of infarct
PTCA
Fibrinolytics not recommended anymore
CABG
What is obstructive shock?
AKA extracardiac obstructive shock
Occurs as result of physical impairment to adequate blood flow
Obstruction of heart or great vessels impedes venous return or prevents effective pumping action
Three categories of obstructive shock
Impaired diastolic filling (causes decreased CO)
Increased RV afterload (has to work harder to push blood into lungs)
Increased LV afterload (aortic valve malfunction)
Causes of impaired diastolic filling leading to obstructive shock
Tamponade (pericardial sac has increase in pericardial fluid)
Tension pneumo
Pericarditis
Compression of great veins
Causes of increased RV afterload, leading to obstructive shock
PE
Pulmonary HTN
PEEP
Causes of increased LV afterload leading to obstructive shock
Aortic dissection
Aortic stenosis
Abdominal distention
Systemic embolization
Patho of obstructive shock
Mechanical obstruction
Causes decreased ventricular filling or pumping
Which causes decreased cardiac output
Which causes hypotension
Which causes *Decreased tissue perfusion
And *impaired cellular metabolism
Symptoms of obstructive shock
Hypotension
Tachycardia
Tachypnea
Oliguria
Decreased CO
Increased PAP
Increased PCWP
Decreased SvO2
Management of obstructive shock
Relieve obstruction (according to cause)
Ex: pericardiocentesis or needle thoracentesis
Prevention of obstructive shock
Early reduction of long-bone fracture (femur)
TEDs
SCDs
Prophylactic anticoagulant therapy
What is distributive shock?
AKA Vasogenic
Widespread *vasodilation and *decreased SVR
Causing abnormal distribution of intravascular volume and relative hypovolemia
Three types of distributive shock
Neurogenic
Anaphylactic
Septic
What is neurogenic shock?
Nervous system disturbance effecting vasomotor center, creating SNS disruption.
Results in:
- vasodilation
- loss of vasomotor tone
- impaired thermoregulation
Etiology of neurogenic shock
High *SCI
Deep general anesthesia
Spinal anesthesia
Venous patho of neurogenic shock
Massive vasodilation so:
- decreased venous return
- decreased filling (preload)
- decreased cardiac output
- *decreased tissue perfusion
- *impaired cellular metabolism
Arterial patho of neurogenic shock
Massive vasodilation so:
- decreased SVR (afterload)
- decreased BP
- *decreased tissue perfusion
- *impaired cellular metabolism
Symptoms of neurogenic shock
Hypotension
*Bradycardia
*Hypothermia
Decreased CO
Decreased PAP, decreased PAWP
*Decreased SVR
Management of neurogenic shock
*Maintain airway, immobilize pt
*ID and correct problem:
- intubate and ventilate (high SCI)
- vasopressors (to decrease vessel size)
- atropine (for bradycardia)
- slow rewarming (too fast will cause vasodilation)
- DVT prophylaxis (b/c lots of blood pooling, high risk for clots)
Prevention of neurogenic shock
Properly immobilize spine (of spinal injury pt)
Elevate HOB with spinal anesthesia
What is anaphylactic shock?
Severe allergic reaction
Caused by repeated exposure to an antigen (normally, but not always)
Patho of anaphylactic shock
Causes release of vasoactive substances (causes redness and swelling)
Leads to massive vasodilation, causing decrease in BP, decreased tissue perfusion
Capillary permeability increases so intravascular volume decreases
Symptoms of anaphylactic shock
Hypotension
Tachycardia
Tachypnea and *wheezing
Dyspnea
*Stridor
*Urticaria, *pruritus
*Angioedema
Cyanosis
Decreased CO and CI
Decreased SVR
Decreased SvO2
Management of anaphylactic shock
Intubate and ventilate
Bronchodilators (albuterol)
Steroids (to decrease edema and inflammation)
Antihistamines (to block chem. mediators causing the prob)
Sympathomimetics (*Epi = drug of choice)
Prevention of anaphylactic shock
Careful history for allergies
Diligent monitoring for:
- IV antibiotic reactions, esp with first doses
- Monitor for blood transfusion reaction
What is septic shock?
Component of continuum of progressive clinical insults to include:
SIRS
Sepsis
MODS
What is SIRS?
(Systemic inflammatory response syndrome)
Exaggerated defense response to noxious stressor to localize and then eliminate the endogenous or exogenous source of the insult
Examples of noxious stressors that could cause SIRS
Infection
Trauma
Surgery
Acute inflammation
Ischemia
Reperfusion
Malignancy
What is sepsis?
“Overwhelming infection”
Life threatening organ dysfunction caused by dysregulated host response to infection
What is MODS?
Organ dysfunction in acutely ill clients
What is septic shock?
Subset of sepsis where circulation and cellular metabolism are impaired enough to cause increased mortality
Causes of septic shock
*Gram-negative bacteria (Ex: *E. Coli & *pseudomonas)
Gram-positive bacteria (Ex: strep & staph)
Viruses (Ex: covid)
Fungi
Which type of shock can nurses have the biggest impact in preventing?
Septic shock (by preventing infection)
Screening tools to detect sepsis
SIRS criteria
Vital signs
Signs of infection
qSOFA criteria
NEWS
MEWS
What is qSOFA criteria?
Quick Sequential Organ Failure Assessment
Scoring = 1 point for each of 3 criteria:
(1) respiratory rate ≥ 22 breaths/min
(2) altered mental status
(3) systolic blood pressure (SBP) ≤ 100 mm Hg.
A qSOFA score ≥ 2 is suggestive of sepsis
Describe the continuum of sepsis and the S/S in each stage
Infection - fever
Sepsis - fever, increased HR, increased RR, increased or decreased WBC
Severe sepsis - hypotension, increased lactate, acute lung injury
Septic shock - vasopressors required, lactate higher
MODS - progressive dysfunction of 2 or more body systems as a result of SIRS
*Early symptoms of septic shock
HR, pulse, BP, skin, LOC, UOP, temp
Tachycardia
Bounding pulses
BP normal or low
Skin warm, flushed
Hyperpnea
Irritable, confused
Oliguria
*Hyperthermia
*Late symptoms of septic shock
Tachycardia
Pulses weak/thready
Hypotension
Narrow pulse pressure
Skin cool, pale
Lethargy to coma
Anura
*Hypothermia
Hemodynamic symptoms of septic shock in early vs. late phases CO/CI, RAP/PAP/PCWP, SVR, SvO2
Early:
- *increased CO/CI
- decreased RAP/PAP/PCWP
- decreased SVR
- increased SvO2
Late:
- *decreased CO
- decreased SvO2
Diagnostic assessment cues (lab values) of early vs. late septic shock acid/base bal, PT/PTT, platelets, WBCs, glucose, BUN/Cr, lactate
Early:
- *respiratory alkalosis
- increased PT, PTT
- decreased platelets
- *increased WBC count
- increased glucose
Late:
- *metabolic acidosis
- increased PT, PTT
- decreased platelets
- *decreased WBC count
- decreased glucose
- increased BUN, Cr
- *increased lactate
What is the surviving sepsis campaign?
Performance improvement program that includes sepsis screening for acutely ill/high risk pts
SOP (protocol) for treatment
**Possible interventions for septic shock
For all pts: isotonic crystalloids (*LR or NS depending on meds)
Vasopressors - Norepi = vasopressor of choice
Antibiotics
Treat hyperglycemia > 180 mg/dL
Stress ulcer prophylaxis (with PPI)
Pharmacologic VTE prophylaxis (Lovenox)
**Prevention of septic shock
Good hand hygiene
Monitor temp, WBC
Standard precautions
Keep pt clean
Oral & airway care
Catheter and wound care
*ID high risk patients
Examples of pts at high risk for sepsis
Basically anyone in CC unit, but:
> 65 yrs
Compromised immunity
Co-morbidities
*Desired outcomes for pts with septic shock
CVP 8-12 mmHg
MAP 65 mmHg *if on vasopressor
UOP > or equal to 0.5 mL/kg/hr
SvO2 65%
Possible interventions for Initial Resuscitation of septic shock
*Medical emergency
Begin treatment/resuscitation immediately
*At least 30mL/kg crystalloid for hypotension in first 3 hrs (more if Bp is worse)
Suggested guidelines for initial resuscitation of septic shock
Using dynamic (direct) measure to guide fluid resuscitation
Guiding resuscitation to decrease high lactate
*Using cap refill as adjunct to other measures
Admit to ICU within 6 hrs if required
Hemodynamic management of septic shock
- *Crystalloids as first line fluid for everyone (LR or NS)
- No starches or gelatins (nothing with sugar)
- Norepinephrine, vasopressin, epi *IN THIS ORDER (add a drug as opposed to escalating the dose)
- Use peripheral line rather than waiting for central access
- Invasive BP monitoring (art line instead of BP cuff)
Recommendation for ventilation for pts with septic shock
*HFNC
If ARDS, follow current guidelines for ARDS
When should a pt with septic shock be fed and how?
Start enteral feeding if tolerated within 72 hours
Long-term outcomes/goals for pts with septic shock
Discussion of goals with pt/family within 72 hrs of onset
Palliative care consultation when appropriate
Support group referral as appropriate upon discharge
Written/verbal discharge education
VAP bundle for prevention of sepsis
HOB elevation 30-45 degrees
Sedation vacations QD
Sedation protocol
Avoid intubation
Toothbrushing daily
Physical conditioning
Early enteral nutrition
Change vent circuit only when necessary
5 moments for hand hygiene to prevent sepsis
Before pt contact
Before aseptic task
After body fluid exposure
After pt contact
After contact with pt surroundings
In general, what are the problems for all types of shock?
Decreased tissue perfusion related to decreased circulating blood volume, decreased myocardial contractility, and widespread vasodilation
Baseline measurements that should be obtained for all types of shock
RAP
PAOP/PCWP
When monitoring fluid volume in a patient with shock, which patient responses should be monitored?
PA pressures (PA catheter to judge fluid replacement)
Vital signs
Urine output
*Body weight (would be best measurement, but rarely accurate)
*LOC
Guidelines for treating shock with crystalloids
LR or NS
3:1 rule (replace with 3 mL for every mL of blood loss)
Colloids for treatment of shock
Hypertonic fluids that pull fluid from 3rd space into vascular space to increase BP
No evidence that colloids are a good treatment
Positioning for pts with shock
*Avoid trendelenburg position (tricks the baroreceptors!)
HOB 20-30 degrees
FOB elevated
Pt should be turned frequently
Types of mechanical interventions for cardiogenic shock
Intra-aortic balloon pump
Ventricular assist device
Benefits of intra-aortic balloon pump
Inflated diastole, deflated systole:
Increased coronary artery perfusion
Decreased afterload
Potential complications of intra-aortic balloon pump
Thromboembolism
Decreased perfusion to extremities
Nursing interventions for ventricular assist device
Maximize O2 delivery & reduce O2 consumption (limit activity)
Positioning
Maintenance of body temp
Nutritional support
Maintenance of skin integrity
Psychological support
Potential complications for a ventricular assist device
Cerebral edema
DIC
Leukopenia
ARDS
Acute renal failure
Decreased liver function
MODS
