Shock Flashcards
Shock Types
Arterial blood flow inadequate to meet tissue needs for O2. Tissue perfusion depends on CO and SVR with CO depending on preload, contractility and afterload and; SVR depending on viscosity, vessel length and diameter, ie SVR = vL/r4.
Shock Types
Hypovolemic – decreased CO and PCWP (CVP
Shock Types
Distributive (vasodilatory - “warm shock”) – increased CI (> 4.0 L/min/m2) with decreased SVR (
Clinical shock markers
- SBP 1.0 mmol/L
A 56 year old alcoholic patient with cirrhosis and ascites presents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. This patient has which type of shock? A. Hypovolemic B. Cardiogenic C. Distributive D. Septic D. Obstructive
A. Hypovolemic
A 56 year old alcoholic patient with cirrhosis and ascites presents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. Which parameter will be found? A. Decreased CVP (normal 0-5 mmHg) B. Increased CI (normal 2.0-4.0 L/min/m2) C. Increased PCWP (normal 4-12 mmHg) D. Decreased SVR (normal 800-1500 dyne-sec-cm-5)
A. Decreased CVP (normal 0-5 mmHg)
What are other causes of hypovolemic shock?
Burns Diarrhea Vomiting Nephrotic Syndrome
What is treatment for Hypovolemic Shock
Hypovolemic shock: CVP
A 52 y/o female diabetic presents with dyspnea and BP of 65/50. History is positive for an old MI. The patient is on a loop diuretic, an aldosterone antagonist, an ACE inhibitor, and a beta blocker. Heart rate is 140. The skin is cool and clammy and the patient is restless. There are bilateral basilar crackles and the neck veins are distended. This patient most likely has which type of shock?
A. Hypovolemic
B. Cardiogenic
C. Distributive
D. Septic
E. Obstructive
B. Cardiogenic*
* CVP > 18 mm Hg and Cardiac Index
Describe how to treat a patient with Cardiogenic Shock
inotropic agents that produce vasodilation as well as increased HR and O2 consumption. 2 and 3 are more related to acute LV failure rather than cardiogenic shock.
- Upright, O2, Fluid bolus (CVP to 15 -18 mmHg), NIPPV
- Low BP – dobutamine# (initial 0.5-1 mcg/kg/min with maintenance of 2-20 mcg/kg/min) or milrinone# with intraaortic balloon counterpulsation
- Normal or high BP – IV nitroglycerin or nitroprusside with IV loop diuretic/furesomide
- AF – esmolol or cardioversion
- Post MI – antiplatelets, norepinephrine* or dopamine** if hypotensive – MAP to 65 mm Hg) (dobutamine or milrinone# for those with vasoconstriction and not as severe hypotension, ie. BP 80 mm Hg)
- IABP, CABG, or PCI
*vasopressor with some inotropic properties. **alpha agonist with some inotropic effects but increases PCWP.
A 46 y/o female with lung cancer presents with dyspnea and cough. Heart sounds are distant and lungs are clear. Neck veins are distended. BP is 60/40. EKG is shown.
This patient has (a)(an):
A. CHF.
B. cardiomyopathy.
C. myocardial infarction.
D. pericardial tamponade.
E.ventricular septal rupture.
D. pericardial tamponade.
EKG shows Electrical alterans- every other complex is a different size. In otherwords, you have a normal complex and then decreased, normal and then decreased.
Electrical Alterans is a marker for pericardial effusion.
What is Beck’s triad for Cardiac Tamponade
- Distended neck veins
- Distant heart sounds
- Distressed BP (Hypotension)
TEE shows an echo free space anterior and posterior to the left ventricular wall. This represents which type of shock?
A.Distributive
B.Neurogenic
C.Obstructive
D.Hypovolemic
E.Anaphylactic
C. Obstructive
What are other causes of obstructive shock?
Tension pneumothorax
Pericardial disease
Disease of pulmonary circulation (PE)
Cardiac tumor (myxoma)
Left atrial mural thrombus
Obstructive valvular disease
A 25 y/o HIV patient presents with cough, fever of 39 C* and *heart rate of 98* beat/min. *Respiratory rate is 26 breaths/min* with WBC of 9,000 cells/mm3 with *15% bands. Glucose is 145 mg/dL.
This patient most likely has:
A. Systemic Immune Response Syndrome.
B. sepsis.
C. severe sepsis.
D. pancreatitis.
E. vasculitis
A. Systemic Immune Response Syndrome. (SIRS)
What is SIRS?
SIRS
Dysregulated inflammation related to autoimmune disorders, pancreatitis, vasculitis, VTE, burns, surgery, etc.
Same category as sepsis.
know this, it will be on the Final
What is the usual acid base imbalance in a patient with SIRS?
Respiratory Alkalosis
SIRS: RR > 20 bpm, or PCO2 < 32 mm Hg
What labs should be ordered for SIRS, Sepsis, or Distributive Shock?
Labs in SIRS, sepsis, or distributive shock:
CMP
ABGs
Type and crossmatch
Coagulation parameters
Lactate
Blood cultures
A gram stain sputum is obtained on the above patient and shows clusters of a gram positive cocci. One may now diagnose:
A. SIRS
B. sepsis
C. septic shock
D. severe sepsis
E. refractory septic shock
B. sepsis
What do the organisms release that cause these patients to go on to shock?
Pathogen-Associated Molecular Patterns (PAMPs), ie. glycolipids, glycoproteins, lipoproteins, peptidoglycans, lipopolysaccharides, mannoproteins, DNA, RNA, etc. which activate Pattern Recognition Receptors to release cytokines and chemokines and thus produce Shock/MOF/Death.
What causes Initiation of Host Response
•Initiation of Host Response
–Pathogen Associated Molecular Patterns (PAMPs)
–Pattern Recognition Receptors
in the attached image:
LP- Lipoproteins
PG- Peptidoglycan
LTA- Lipoteichoic acid
LPS- Lipopolysaccharide
What causes the same events in non septic patients with SIRS?
Lipoteichoic acid (adhesin)
What do these products cause?
Activation of Pattern Recognition Receptors
–MyD88 / NF-kB Signaling
- Pro-inflammatory Cytokines
- Vascular Adhesion Molecules
•Pro-Inflammatory Cytokines Involved in triggering of the Innate Immune Response
•Pro-Inflammatory Cytokines Involved
–Tumor Necrosis Factor (TNF-a)
•Stimulates the recruitment and activation of neutrophils and monocytes
–Leads to the production of IL-1
- Activates vascular endothelial cells to express cellular adhesion molecules
- Can induce extrinsic apoptosis
–IL-1
•Similar to and redundant of TNF
–IL-6
•Similar to and redundant of TNF
What are the general variables that cause one to recognize impending shock?
Sepsis/SIRS
Infection plus:
General variables
TPR changes –T > 38.3C (101 F) or < 36C; HR > 90 bpm; RR > 20 bpm or PCO2 > 32mmHg
Glucose > 140 mg/dL
Altered mentation
Edema of > 20mL/kg over 24 hours
NOTE: MEMORIZE TPR AND WHITE COUNT FOR FINAL!!!!
What are the inflammatory and hemodynamic variables?
Sepsis*
Inflammatory variables
WBC > 12,000 with bandemia > 10%; WBC < 4,000
Increased CRP and procalcitonin (increased CD 64)
Hemodynamic variables
SBP* < 90 mmHg; MAP < 65 mmHg
*These worsen with development of severe sepsis
What are the organ dysfunction variables?
Sepsis
_Organ Dysfunction variables*_
PaO2/FiO2 < 300 (<250)
Urine output < 0.5 mL/kg/hr
Creatinine increase > 0.5 mg/dL (> 2 mg/dL)
INR > 1.5 or PTT > 60 seconds
Ileus
Platelets < 100,000 microl-1
Bilirubin > 4 mg/dL
Hyperprolactinemia > 1 mmol/L (tissue hypoxia)
Decreased capillary refill (tissue hypoxia)
Increased serum lactate
*These worsen with development of severe sepsis
Severe sepsis may be diagnosed in the above patient with evidence of significant dysfunction in how many organs?
A. 1
B. 2
C. 3
D. 4
E. 5
Sever Sepsis is one step before Septic Shock
A. 1
Most common evidence of severe organ dysfunction are:
ARDS, ARF, and DIC; or serum lactate > 4 mmol/L.
End-Organ Damage
–Microcirculatory damage / disorder
- Central Nervous System
- Lungs
- GI
- Liver
- Kidney
The above patient is considered to have developed _septic shock*_ when unable to maintain a mean arterial pressure > 60 mmHg after:
A.activated protein C.
B. fluid resuscitation.
C. calcium channel blockers.
D. sodium bicarbonate.
E .antibiotics.
Risk factors for septic shock = bacteremia, age, diabetes, cancer, immunosuppression,
recent invasive procedure.
B. fluid resuscitation.
Distributive shock, including septic shock, anaphylaxis, or adrenal insufficiency is characterized by:
A. decreased CO.
B. increased PCWP.
C. SVR < 800 dynes.s/cm-5.
D. decreased mixed venous oxygen saturation.
C. SVR < 800 dynes.s/cm-5.
In septic shock a redistribution of oxygen delivery or inability of tissues to extract O2 can actually lead to a high central oxygen saturation of greater than 70%, in the presence of increased serum lactate. Ultimately, however, the CVOS may drop and require fluid, RBCs*, and vasopressors to maintain it above 70%.
How do we treat shock?
Early Sepsis Protocol
Nine steps to be done within 2 hours for patients with infection, SIRS, and dysfunction of one organ.
- Serum lactate
- Two sets of blood cultures
- Two 18 gauge lines
- Start antibiotics
- Give 2 liters NS
- CBC and BMP
- O2 sat > 90%
- Start norepinephrine if shock is present.
- Transfer for lactate > 4 mmol/L, Systolic BP < 90 mm Hg, or MAP < 60-70 after 2 liters of NS.
Discuss Early Goal Directed Therapy.
Septic shock - EGDT
Early Goal Directed Therapy. Problem is O2 utilization (ScvO2)
- Fluids: need to maintain CVP at 8-12 mm Hg. Give 30mL/kg of crystalloid (1-2 liters over 30-60 minutes). May need 4-6 liters total.
- Vasopressors. Need to maintain MAP at > 65 mm Hg and cardiac index at 2-4 liters/min2. Use _Norepinephrine* 5-20 mcg/min_ (mainly alpha agonist/vasopressor; as is phenylephrine which is pure alpha and therefore good in extreme tachycardia).
If norepinephrine fails, go to epinephrine (mainly beta agonist/inotropic effect). May also consider Vasopressin 0.03 units/min (potentiates norepinephrine).
- Need to maintain central venous O2 saturation at > 70%. For < 70% give _PRBC**_ to obtain hemacrit of 30%**. If still < 70%, then dobutamine as ionotropic therapy??
- Hope to reduce lactate by 20% in first 2 hours. (Increased glycolysis, inhibition of pyruvate dehydrogenase, and impaired liver function, all increase lactate levels)
*dopamine (5-20 ug/kg/min) results in more arrhythmias, but may be used in bradycardia and “cold shock”. Moderate dose = beta effects – high dose = alpha. Use epinephrine first in anaphylactic shock.
*dopamine (5-20 ug/kg/min) results in more arrhythmias, but may be used in bradycardia and “cold shock”. Moderate dose = beta effects – high dose = alpha. Use epinephrine first in anaphylactic shock.
** Generally do not transfuse for Hb > 7 gm or hematocrit > 21%
Is anything equivalent to EGDT?
Septic Shock
Maintain glucose < 180 mg/dL
Steroids?
Usual Care versus EGDT
The treatment of septic shock should be based on Usual Care in deference to Early Goal Directed Therapy (EGDT). In other words, provider directed usual care is as good as EGDT, if based on rapid recognition,* early antibiotics, and aggressive fluid resuscitation. This rather than necessarily placing central line for CVP and CvO2.
*56% of sepsis-related deaths were in people with normal BP and normal or intermediate serum lactate levels (< 4 mmol/L) - NEJM Oct 1, 2014.
Which antibiotics are used in Ususal Care vs EGDT?
A patient presents with septic shock. In addition to early recognition and immediate fluid resuscitation:
- Obtain cultures and remove vascular devices.
- Begin vancomycin (may use daptomycin, linezolid, or ceftaroline) and cefotaxime (may use cefotetan, cefepime, cefoperazone, ceftazidime, pipericillin-tazobactam, ticarcillin-clavulanate, meropenem, or imipenem). Must cover MRSA, Pseudomonas, and Gm negatives with ESBL activity.
Renoprotective effect for acetaminophen in severely septic patients.
No long-term benefit of adrenaline in cardiac arrest outside the hospital – contracts vessels in gut, liver, and kidneys. On the other hand, faster administration of epinephrine (one to three minutes) in people who arrest in the hospital with a non-shockable rhythm (asystole or PEA) have increased survival.
