Shock and Sepsis Flashcards
What is shock?
Broad term that describes a physiologic state where O2 delivery to the tissues is inadequate to meet metabolic requirements, causing global hypoperfusion
Difference between compensated and uncompensated shock?
Compensated - normal BP with inadequate perfusion
Uncompensated - hypotension and inability to maintain normal perfusion
4 types of shock?
- Hypovolemic (most common)
- Cardiogenic
- Distributive
- Obstructive
Physiology and examples of hypovolemic shock?
Decreased circulatory volume; hemorrhage or fluid loss
Physiology and examples of cardiogenic shock?
Impaired heart pump function; ACS, valve failure, dysrhythmias
Physiology and examples of distributive shock?
Pathologic peripheral blood vessel vasodilation; sepsis, anaphylaxis, neurogenic
Physiology and examples of obstructive shock?
Non-cardiac obstruction to blood flow; pulmonary embolism, tension pneumothorax, tamponade
Important history in the presentation of shock?
Obvious bleeding (trauma or anatomic source - GI, vaginal, ENT), decreased PO intake, fluid loss due to vomiting, diarrhea, excess urination, ostomy, etc. suggest hypovolemic shock
Chest pain, SOB, leg swelling, syncope may indicate ACS, CHF, PE
Sudden onset of hives, face or body swelling
Infectious signs (fever, cough, abdominal pain, headache)
May have only non-focal vague symptoms like weakness, AMS, malaise
Physical exam findings important in shock?
BP (should not be the sole marker, as early shock may have normal or elevated BP and normal HR)
Tachycardia
Cool, pale, cyanotic, decreased capillary refill, dry mucous membranes, confusion, AMS, coma, thready pulses, tachypnea
Arrhythmias, JVD, dependent edema
What is the shock index?
HR/systolic BP
Normal index ranges from 0.5-0.7
> 1.0 indicate decreased LV function, associated with higher mortality
Dx testing in suspected shock?
Suspected etiology should guide testing
CBC and coags (anemia/blood loss, infection, coagulability)
Electrolytes
BUN/Cr, UA, LFTs
CXR, EKG
Lactate (degree of hypoperfusion)
Urine pregnancy test
ABG for O2/pH, central venous O2 measurement, SVR, CO through special venous catheters
If suspecting sepsis - blood, sputum, pelvic, or wound cultures, head CT and LP, targeted imaging
If suspecting cardiogenic - enzymes, echo
If suspecting obstructive - CT or V/Q scan (PE), echo (tamponade)
Distinguish between the 4 types of shock based on HR, CVP, contractility, and SVR.
All will have increased HR
CVP increased in cardiogenic +/- obstructive. CVP decreased in hypovolemic and distributive.
Contractility decreased in cardiogenic. Others are variable.
SVR increased in cardiogenic, hypovolemic, and obstructive 2/2 tamponade and PE. SVR decreased in distributive and obstructive 2/2 tension PTX.
Common lab findings in shock?
Anemia, disordered platelets/coags
Elevated or depressed WBCs with left shift
Elevated lactate or decreased serum bicarb (shift to anaerobic metabolism and tissue hypoperfusion)
Evidence of end organ damage
Rx shock?
ABCs
IV access through large bore peripheral lines or a CVP, give boluses of crystalloids - be careful with rapid fluid administration in patients with cardiogenic shock and pulmonary edema. Blood products may be needed. If volume resuscitation does not improve the HDS, vasoactive medications (epinephrine, norepinephrine, dopamine, vasopressin) may be needed.
Monitor fluid status (urinary catheter, intraarterial BP measurements, CVP monitoring)
Aggressive Rx of underlying cause
Rx underlying causes of shock?
Hypovolemia 2/2 hemorrhage - surgical or interventional control
Sepsis - early goal-directed therapy and aggressive ABX Rx
Cardiogenic shock - emergent angiography or surgical procedures (bypass, valve repair, IABP)
Obstructive shock due to PE - anticoagulation or thrombolysis, tamponade - drainage
Define successful resuscitation from shock.
Normalization of hemodynamic status (BP, HR, urine output)
Lactate decreases by half in the first few hours
Normal volume status restored
Maximal tissue oxygenation
Resolution of acidosis and return to normal metabolic parameters
Anaphylaxis is a clinical diagnosis. It is highly likely when any one of what 3 criteria are fulfilled?
- Acute onset (minutes to hours) of an illness with involvement of the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen tips/tongue/uvula)
AND at least one of the following:
A. respiratory compromise (dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
B. reduced BP* or associated symptoms of end-organ dysfunction (eg, hypotonia, collapse, syncope, incontinence) - 2+ of the following that occur rapidly after exposure to a likely allergen for that patient:
A. Involvement of the skin-mucosal tissue
B. Respiratory compromise
C. Reduced BP or associated symptoms
D. Persistent GI symptoms (eg, crampy abdominal pain, vomiting) - Reduced BP* after exposure to a known allergen for that patient (minutes to several hours):
A. Infants and children - low systolic (age specific) or greater than 30% decrease in systolic
B. Adults: systolic <90 or >30% decrease from baseline
Management of anaphylaxis?
ABCs Stop the exposure Epinephrine IV fluids (1L isotonic NS bolus over 5-10 minutes; up to 7L needed in severe cases) Secondary agents
What is the single most effective action in anaphylaxis?
Epinephrine
MOA epinephrine that are needed in anaphylaxis?
Alpha 1
Beta 1
Beta 2
Cutaneous vasoconstriction + skeletal muscle vasodilation
Dosing of epinephrine in anaphylaxis?
- 3-0.5 mg (1:1000) IM in the anterolateral thigh Q5-15 minutes
- 1 mg (1:10,000) IV over 5 minutes for cases refractory to IM or if critical (hypotensive, unable to talk, exchanging minimal/no air)
What does 1:1000 and 1:10,000 mean?
1: 1000 -> 1 mg in 1 mL
1: 10,000 -> 1 mg in 10 mL
IM or IV? Location of administration?
Nearly all adverse outcomes are a result of IV administration
IM achieves significantly more rapid and higher peak concentration of epi compared to SQ -> almost no difference between SQ/IM in the deltoid, but large difference when given in the anterolateral thigh due to higher blood flow
Secondary agents that may be used in anaphylaxis?
H1 blocker - diphenhydramine - 50 mg IV, onset 1-3 hours
H2 blocker - ranitidine 50 mg IV (decreases urticaria in emergency setting, no effect on edema or vitals)
Steroids - dexamethasone 10 mg IV or methylprednisolone 125 mg IV, onset 4-6 hours
O2
Glucagon - 1-5 mg IV over 5 minutes
Purpose of steroids in anaphylaxis?
Prevent creation of newly synthesized mediators, may assist in preventing prolonged or biphasic anaphylaxis
Purpose of glucagon in anaphylaxis?
Patients taking beta-blockers may have blunted response to exogenous epinephrine
If these patients have refractory bronchospasm or hypotension, consider glucagon
Pediatric doses of epinephrine in anaphylaxis?
- 01 mg/kg IM (1:1000) up to adult dosing
0. 01 mg/kg IV (1:10,000) over 5-10 minutes up to adult dosing
Pediatric doses of IV fluids in anaphylaxis?
Bolus 20 cc/kg up to 100 cc/kg
Pediatric doses of benadryl in anaphylaxis?
1 mg/kg
Pediatric doses of ranitidine in anaphylaxis?
1 mg/kg
Pediatric doses of methylprednisolone in anaphylaxis?
1-2 mg/kg IV
Classic presentation of sepsis?
Elderly patient with multiple comorbidities with fever, tachycardia, tachypnea, and/or hypotension with AMS coming in from a nursing home, leukocytosis, pneumonia or UTI on CXR or UA
However, patients will present with one or maybe no abnormal vitals, non-specific symptoms, mild delirium, appear well but with a history of fever, rigors, or confusion earlier in the day
SIRS criteria?
2/4:
- Fever >38.3C (100.4) or <36C (96.8)
- HR>90
- RR>20 or PaCO2 <32 mmHg
- WBC >12 or <4 or >10% bands
Define sepsis.
2/4 SIRS + infection (may be obvious such as pneumonia on history, physical or CXR, or suspected such as fever + abdominal pain)
Define severe sepsis.
Meet criteria for sepsis + have sepsis-induced organ dysfunction or tissue hypoperfusion
CMS defines end-organ dysfunction as follows:
- SBP<90 or MAP<70 or SBP decrease >40 or <2SD below normal for age or known baseline
- Cr >2.0 or urine output <0.5 mL/kg/hr for >2 hours
- Bilirubin >2 mg/dL
- Platelet count <100,000
- Coagulopathy (INR>1.5 or aPTT>60)
- Lactate >2 mmol/L
Define septic shock.
Persistently low BP despite fluid administration (30 mL/kg)
Diagnostic testing for sepsis revolves around what 2 things?
- Risk stratification
2. Investigation of potential sources of infection
How is risk stratification done?
Lactate - marker of anaerobic glycolysis during periods of insufficient O2 delivery (low levels correlate with low mortality, high levels correlate with high mortality); must be tested immediately, as delays can falsely elevate
How is investigation of infectious source done?
CBC with diff, CMP, PT/INR/PTT, blood cultures x2, UA with culture and sensitivity, CXR
Optional depending on suspected source - 3rd blood culture (endocarditis), CSF (meningitis), arthrocentesis (septic arthritis), wound cultures, etc.
How is therapeutic intervention assessed?
Reduction in lactate after therapy
Rx sepsis
Administer antimicrobials at the earliest possible time. However, it is appropriate to obtain necessary data (CXR, UA, etc.) to determine the most likely cause so that the most appropriate drugs can be selected
Source control (promptly remove potentially infected devices when feasible)
3 hour bundle
Lactate measurement
BCx obtained before antimicrobial administration
Administration of broad-spectrum ABX
Administration of 30 mL/kg IV crystalloid for hypotension or lactate 4+ (use caution in ESRD, CHF, and ESLD where this may be deleterious)
6 hour bundle
Administer vasopressors for hypotension that does not respond to fluids in order to achieve a MAP 65+
Reassess and document volume status after fluid administration for patients with hypotension that does not respond to fluids or lactate 4+ mmol/L
Repeat lactate measurements for patients with initial lactate 4+
ABCs of sepsis care?
- Early recognition
- Prompt IVFs
- Prompt ABX
SEP-1 CMS measure - 3 hour bundle
Measure lactate
BCx prior to ABX
Administer broad-spectrum ABX
Administer 30 mL/kg crystalloid for hypotension or lactate 4+
SEP-1 CMS measure - 6 hour bundle
Apply vasopressors for hypotension not responsive to initial fluids to maintain MAP 65+
Re-measure lactate if initial elevated
If persistent hypotension after fluids or initial lactate 4+, reassess volume status and tissue perfusion and document findings according to the following:
Either - repeat focused exam by licensed practitioner including vitals, CP, capillary refill, pulse and skin findings
OR 2 of the following - measure CVP, measure ScvO2, bedside CV US, dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
Review LUMC ED Non-Invasive Sepsis Guidelines (first main goal)
- Initiate sepsis order set.
- Think of source control and send cultures.
- Initiate broad-spectrum ABX within 1 hour
- Supplemental O2; if hypoxemic despite NRB, intubate and switch to invasive guidelines
- Establish 2 large bore IVs and give IVF bolus isotonic crystalloid 30 mL/kg bolus
Main goal: fluid resuscitation
How is fluid resuscitation assessed in LUMC ED Non-Invasive Sepsis Guidelines?
Dynamic IVC US - keep giving 500-1000 mL boluses until there is <30% change in IVC size with inspiration
OR
Clinically assess for improvement in end organ perfusion:
-Is HR, MAP, UOP, mental status improving? If yes to any, check for volume overload (JVD, rales, worsening O2 sats). If no evidence of volume overload, give another 500-1000 CC bolus.
Most patients will require ___L of fluid during initial resuscitation
4-6
Review LUMC ED Non-Invasive Sepsis Guidelines (second goal following fluid resuscitation)?
Measure MAP. If <65, start vasopressors and switch to invasive guidelines. If 65+, move on.
Review LUMC ED Non-Invasive Sepsis Guidelines (third goal following adequate MAP?)
Repeat lactate. If increasing of <10% clearance, options are as follows:
- Consider transfusion (if Hgb <7, transfuse 1 unit pRBC) OR
- Inotropes (especially if heart appears hypodynamic on echo/US); if Ca low, replete that first (500-1000 mg), if normal, administer dobutamine (2.5-20mcg/kg/min) OR
- Additional fluids (if had empiric IVF loading, give an additional L)
Continue to repeat the lactate if you do any of the above.
If 10+% lactate clearance -> move forward
Review LUMC ED Non-Invasive Sepsis Guidelines (fourth goal following adequate MAP?)
If goals achieved - dispo -> admission (ICU vs. monitored bed), periodically check MAP >65, good mental status, good UOP
Trend lactate Q2-4 hours until normal. If it rises again, restart guidelines.
If goals not achieved, continue with the above or switch to invasive guidelines.
How do the LUMC ED invasive sepsis guidelines differ (initial and fluid resuscitation)
Initially, also place full-sterile central line.
Assess fluid resuscitation using CVP as another option; other measures impacted by whether or not the patient is intubated.
How do the LUMC ED invasive sepsis guidelines differ (MAP)
Vasopressors:
- Titrate norepinephrine (0.01 mcg/kg/minute)
- Place sterile A-line
- If MAP <65 after Norepi between 0.5-0.1 mcg/kg/minute, add hydrocortisone 50 mg Q6 and vasopressin 0.04 units/minute
- Next pressor of choice - epinephrine 0.01 mcg/kg/minute (max dose 0.5 mcg/kg/min)
How do the LUMC ED invasive sepsis guidelines differ (repeat lactate)
- Also send ScvO2
- If lactate <10% clearance OR ScvO2 <70%: same options as before, as well as intubate to decrease pulmonary metabolic load (especially true in elderly patients)
- Can move forward if lactate clearance 10+% AND ScvO2 70+%
Elements of lung protective MV?
Ketamine is the preferred induction agent (1-1.5 mg/kg IV)
Etomidate is acceptable (0.3 mg/kg IV)
Low TV (consider 6 cc/kg of IBW) with goal plateau pressure <30
Analgesia + sedation per protocol
Raise HOB to 30-45 degrees to decrease aspiration risk
Traditionally, it was believed that elevated lactate is due to anaerobic metabolism as a consequence of inadequate perfusion with low O2 delivery to the tissues. This led to multiple interventions to improve O2 delivery (blood transfusion, inotropes to increase mixed venous O2 saturation, and nitroglycerine infusion for hypertensive patients). Lack of oxygen deficiency may explain why these interventions have not proven to be beneficial. Explain.
Most patients with sepsis and elevated lactate have hyperdynamic circulation with very adequate delivery of O2 to the tissues. Moreover, the lungs have been shown to produce lactate during sepsis, which couldn’t be due to hypoxemia. Now, we think it is due to endogenous epinephrine stimulating beta-2 receptors -> glycolysis -> pyruvate -> excess lactate
This may be a beneficial compensatory response, serving as a metabolic fuel for the heart and brain.
Lactate is thus really a marker of endogenous catecholamine release and is useful for detecting patients who have occult shock - patients who are maintaining their BP due to a vigorous endogenous catecholamine response.
Causes of false positive elevated lactate?
Beta-agonists (albuterol, epinephrine)
Extreme exercise
Seizures
Lactate should quickly clear after these inciting situations.
Hepatic failure can have elevated lactate from decreased clearance, but they are also prone to sepsis or hypotension.
Any shock state, dead bowel, multitude of toxicologic causes.
Define sepsis in ICU patients per Sepsis-3 (2016 JAMA)
Increase of 2+ in SOFA score
Define sepsis in ED patients per Sepsis-3 (2016 JAMA)
2+ of the new qSOFA (quickSOFA) - SBP of 100 or less, RR 22+, AMS
Define septic shock per Sepsis-3 (2016 JAMA).
Persistent hypotension require pressors to maintain MAP 65+ despite adequate volume resuscitation
Lactate 2+
Define severe sepsis per Sepsis-3 (2016 JAMA).
No longer used
What are qSOFA and SOFA?
Mortality predictors (NOT tests for sepsis)