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Cardiovascular II Exam 3 > Shock > Flashcards

Flashcards in Shock Deck (38):
1

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.

2

Shock Types

Hypovolemic – decreased CO and PCWP (CVP

3

Shock Types

Distributive (vasodilatory - “warm shock”) – increased CI (> 4.0 L/min/m2) with decreased SVR (

4

Clinical shock markers

1. SBP 1.0 mmol/L

5

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

6

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)

7

What are other causes of hypovolemic shock?

Burns Diarrhea Vomiting Nephrotic Syndrome

8

What is treatment for Hypovolemic Shock

Hypovolemic shock: CVP

9

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

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B. Cardiogenic*

 

* CVP > 18 mm Hg and Cardiac Index

10

Describe how to treat a patient with Cardiogenic Shock

1. Upright, O2, Fluid bolus (CVP to 15 -18 mmHg), NIPPV

2. Low BPdobutamine# (initial 0.5-1 mcg/kg/min with maintenance of 2-20 mcg/kg/min) or milrinone# with intraaortic balloon counterpulsation

3. Normal or high BP – IV nitroglycerin or nitroprusside with IV loop diuretic/furesomide

4. AF – esmolol or cardioversion

5. Post MIantiplatelets, 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)

6. IABP, CABG, or PCI

*vasopressor with some inotropic properties. **alpha agonist with some inotropic effects but increases PCWP.

#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.

 

11

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. 

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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.

12

What is Beck’s triad for Cardiac Tamponade

•Distended neck veins

•Distant heart sounds

•Distressed BP (Hypotension)

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13

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 

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C. Obstructive

14

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

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15

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)

 

 

16

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

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17

What is the usual acid base imbalance in a patient with SIRS?

Respiratory Alkalosis

SIRS: RR > 20 bpm, or PCO2 < 32 mm Hg

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18

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

19

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

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B. sepsis

20

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.

21

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

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22

What causes the same events in non septic patients with SIRS? 

Lipoteichoic acid (adhesin)

23

What do these products cause?

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Activation of Pattern Recognition Receptors

–MyD88 / NF-kB Signaling

      •Pro-inflammatory Cytokines

      •Vascular Adhesion Molecules

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24

•Pro-Inflammatory Cytokines Involved in triggering of the Innate Immune Response

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•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

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25

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!!!!

26

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 

27

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 

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28

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 

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Sever Sepsis is one step before Septic Shock

 

A. 1

29

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

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30

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. 

31

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%.     

32

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.

1. Serum lactate

2. Two sets of blood cultures

3. Two 18 gauge lines

4. Start antibiotics

5. Give 2 liters NS

6. CBC and BMP

7. O2 sat > 90%

8. Start norepinephrine if shock is present.

9. Transfer for lactate > 4 mmol/L, Systolic BP < 90 mm Hg, or MAP < 60-70 after 2    liters of NS.

33

Discuss Early Goal Directed Therapy.

Septic shock - EGDT

Early Goal Directed Therapy. Problem is O2 utilization (ScvO2)

1. 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.

 

2. 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). 


3. 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??

 

4. 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%

34

Is anything equivalent to  EGDT?

Septic Shock

Maintain glucose < 180 mg/dL

Steroids? 

35

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.

36

Which antibiotics are used in Ususal Care vs EGDT?

A patient presents with septic shock. In addition to early recognition and immediate fluid resuscitation:

1. Obtain cultures and remove vascular devices.

2. 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.

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38

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.