Lecture 4 - shock Flashcards

1
Q

review Preload = Central Venous Pressure (range, low, high, indication, _____ _____ where we expect ___ _______?, which shock state would we be concerned with fluid overload?

A

Range- 0-10mmHg

Low = Hypovolemia
High = Normo/Hypervolemia

Why?- Monitor Fluid status in patients who are prone to volume depletion or Volume overload

Major surgeries where we expect 3rd spacing:
Shock States where we may be concerned with fluid overload (Mainly Cardiogenic)

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2
Q

Afterload = SVR = Systemic Vascular Resistance (measured with, range, low, high, indication, which shock would see elevation in SVR, which shock would see low in SVR)

A

Measured with Invasive hemodynamics like the EV1000, Vigileo, etc

Range- 700-1500 Dynes
Low = Vasodilation
High = Vasoconstriction
Why?- Monitor bodies response to disease state and subsequent therapy

Cardiogenic shock- expect to see elevations, medical mgmt. would reduce SVR
Septic shock- Low SVR, medical mgmt. would increase SVR

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3
Q

review Contractility

A

Difficult to measure directly, use other determinants to assess contractility
- Ie. If SVR is high, and Preload is high, but CO is Low- what type of shock would we expect?
- You don’t know yet!

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4
Q

Arterial BP (what, more accurate than, used to monitor (3))

A

1) Invasive blood pressure monitoring
- More accurate than a sphygmomanometer, exists in realtime

2) Used to monitor:
- Response to vasopressor/dilator therapy
- Response to shock state treatment
- Labile blood pressure

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5
Q

Shock Syndrome (what, results in, imbalance between, leads to, no what what the underlying cause of shock, all shock will…)

A
  • Acute, widespread impaired tissue perfusion
  • Results in cellular, metabolic, and hemodynamic alterations
  • Imbalance between cellular oxygen supply and cellular oxygen demand
  • Often results in multiple organ dysfunction syndrome (MODS)
  • No matter what the underlying cause of shock, all shock will result in the same outcome if not treated early.
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6
Q

Etiology of Shock States (3 + 3 types)

A

1) Hypovolemic: Loss of circulating or intravascular volume

2) Cardiogenic: Impaired ability of heart to pump

3) Distributive: Mal-distribution of circulating blood volume
types: Septic, anaphylactic, or neurogenic

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7
Q

Shock Syndrome-Pathologic Process (4 stages)

A

Initial: Insult occurs (bacteria in blood)

Compensatory: Body is maintaining tissue perfusion. Heart rate may be elevated with normal BP. Start to see a decrease in urine output/production (KEY: WANT TO CATCH IN THIS PHASE)

Progressive: Heart rate elevated, BP drops, urine output significant decreased. Team starts to initiate fluid boluses, vasopressors. Lactic acid levels increase (anaerobic metabolism)

Refractory: Multiple organ failure. Unable to maintain tissue perfusion despite aggressive measures. (MODS OCCURS)

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8
Q

Pathophysiology: Initial stage

A

Decreased CO → tissue perfusion is threatened

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9
Q

Pathophysiology: Compensatory stage (_________ mechanisms to maintain.. (3), mediated by ______, 3 responses, ________ mechanisms may normalize -> elevations in (2))

A

1) Homeostatic mechanisms to maintain cardiac output, blood pressure, tissue perfusion
- Mediated by sympathetic nervous system:
a) Neural response
b) Hormonal response
c) Chemical response

2) Compensatory mechanisms may normalize hemodynamics:
- Elevation in HR, SVR

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10
Q

Global Indicators of Progressive Shock: (5)

A
  • Serum lactate levels increased
  • Arterial base deficit levels (acidosis)
  • Serum bicarbonate levels decreased
  • pH decreases
  • Central or mixed venous oxygen saturation levels
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11
Q

Pathophysiology: Progressive stage (_______ mechanisms begin to _____, switch from _______ to ________ ________ -> _______ ____ production), increased (3) -> what? (2), what begins during this stage?)

A
  • Compensatory mechanisms begin to fail
  • Switch from aerobic to anaerobic metabolism → lactic acid production
  • Increased vascular permeability, tissue edema, and decline in tissue perfusion:
    a) Fluid immediately third spaces when administered
    b) Systemic inflammatory response (SIRS)
  • Irreversible damage begins
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12
Q

Pathophysiology: Refractory stage (3)

A
  • Unresponsive to therapy
  • Irreversible with the development of MODS
  • Death is final outcome
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13
Q

Stages of shock - NCLEX+HESI (3 stages)

A

Initial + Compensatory, non-progressive stage (Stage 1)- Insult to compensatory mechanisms to maintain hemodynamics

Intermediate, progressive phase (Stage 2)-Need for support with fluid and medications to maintain tissue perfusion

Final, irreversible stage (Stage 3)-Multi-organ failure.

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14
Q

Consequences of shock (neuro) (3)

A

Mental status changes
Sympathetic Nervous system dysfunction
Thermal dysregulation

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15
Q

Consequences of shock (cardiac) (2)

A

Pump failure
Micro embolism of cardiac circulation

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16
Q

Consequences of shock (pulmonary) (2)

A

ALI/ARDS
Respiratory failure

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17
Q

Consequences of shock (renal) (1)

A

Acute Tubular Necrosis: ↑BUN, Cr, ↓Urine output

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18
Q

Consequences of shock (GI) (3)

A

Hepatic failure -> increase liver enzymes, bilirubin, ↓ albumin, clotting protein

Pancreatic failure -> increase amylase, lipase, ↓ insulin production

GI tract failure -> Gastric immotility, SBO/ileus

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19
Q

Consequences of shock (hematologic) (1)

A

DIC

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20
Q

Goal of Treatment (2)

A

Improvement of tissue perfusion
- Adequate pulmonary gas exchange: Oxygen therapy, Ventilatory support

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21
Q

Shock Syndrome: Medical Management (main)

1) adequate ____ _____ and ____ (5)

2) optimal ____ _______
- ____ _____ avoided until pH less than ____
- treat (3)

3) _______ support
- as ______ as possible, ________ requires ________
- tailored to individual needs
- tight _______ control

A

Improvement of tissue perfusion:

1) Adequate cardiac output and hgb
- Fluid management
- Vasoconstrictors
- Vasodilators
- Positive inotropes
- Antidysrhythmics

2) Optimal metabolic environment
- Sodium bicarbonate avoided until pH less than 7.1
- Treat infection, reperfusion therapy, support organs to prevent further anaerobic metabolism

3) Nutritional support
- As early as possible, enteral requires MAP >60 (too low, blood shunt away from gut, risk of gastric immotility)
- Tailored to individual need
- Tight glucose control

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22
Q

types of shock (4)

A

1) Hypovolemic

2) Cardiogenic

3) Distributive:
- Anaphylactic
- Neurogenic
- Septic

4) Obstructive:
- Cardiac Tamponade
- Tension Pneumothorax

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23
Q

Hypovolemic Shock (3)

A
  • Inadequate fluid volume in the intravascular space
  • Decreased tissue perfusion
  • Most common form
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24
Q

Hypovolemic Shock: Assessment and diagnosis

(4 classes, what are the percentage and mL of fluid loss)

A

Class I
- Fluid volume loss up to 15% total body fluid
- Up to 750 mL fluid loss

Class II
- Fluid volume loss 15% to 30% total body fluid
- Fluid loss 750 to 1500 mL

Class III
- Fluid volume loss 30% to 40% total body fluid
- Fluid loss 1500 to 2000 mL

Class IV
- Fluid volume loss greater than 40% total body fluid
- Fluid loss > 2000 mL
Refractory (organ failure d/t much organ loss)

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25
Hypovolemic Shock: Hemodynamic assessment what happens to CO, CI, CVP, PAWP, SVR?
Cardiac output decreased Cardiac index decreased Central venous pressure decreased Pulmonary artery occlusion pressure decreased Systemic vascular resistance increased (threat to perfusion -> releases catecholamines)
26
Hypovolemic Shock: Medical management (3)
Correct hypovolemia Restore tissue perfusion Prevent complications
27
Hypovolemic Shock: Nursing management (4) what can mass blood transfusions precipitate? (3) what is in packed RBCs that bind with blood to stop clotting cascade?
Prevent hypovolemic shock Minimize fluid losses Enhance volume replacement I&O’s (treat I/O) Maintain surveillance for complications - Blood transfusion reactions - mass blood transfusions can precipitate hypothermia, acidosis, hyper K, sodium citrate in blood binds with blood to stop clotting cascade
28
Cardiogenic Shock (what, etiology (3))
Failure of heart to pump blood effectively etiology: Primary ventricular ischemia Structural problems Dysrhythmias
29
Cardiogenic Shock: Medical management (goals (3), what device, what procedure, other mechanical circulatory assist devices (2))
goals: Treat underlying cause of pump failure Enhance the effectiveness of the pump Improve tissue perfusion Intra-aortic balloon pump Early revascularization Mechanical circulatory assist devices - Ventricular assist device (LVAD) - Extracorporeal membrane oxygenation
30
Cardiogenic Shock: Pharmacologic support (5)
Inotropic agents Vasopressor (sometimes) Diuretics Vasodilators once blood pressure stabilized (Lower SVR comparative to Contractility) Antidysrhythmics
31
Cardiogenic Shock: Nursing management (5)
Prevention of cardiogenic shock Limit myocardial oxygen consumption Enhance oxygen supply Precise monitoring and management of hemodynamics Surveillance for complications related to intra-aortic balloon pump
32
46-year-old female diagnosed the day prior with a saddle pulmonary embolism (big ole’ clot that blocks blood to multiple branches off the pulmonary artery), she was started with a weight-based heparin bolus and is now on a continuous drip. The following day in the stepdown unit, Vitals are: BP 114/72, HR 89, RR 18, Temp 98.7 F While cardiology is rounding, she begins to decompensate, Vitals are: BP 71/42, HR 130, RR 24, Temp 98.7F Which of the following interventions should be expected? A. Thrombolytic Therapy B. Percutaneous Embolectomy (Clot retrieval) C. 1L NS D. Begin CPR
C. 1L NS
33
Anaphylactic Shock (3)
Distributive shock Immediate hypersensitivity reaction Life-threatening event
34
Anaphylactic Shock: Medical management 1) goals (3) 2) therapy 3) pharm interventions (5)
Goals: - Remove antigen - Reverse effects of biochemical mediators - Promote adequate tissue perfusion Oxygen Pharmacologic intervention: - Epinephrine (dilates airways, constricts vasculature) - Diphenhydramine (benadryl, releases biochemical affects) - Pepcid (gi upset) - Corticosteroids - Fluid replacement
34
Anaphylactic Shock 1) etiology (1) 2) Antigens (6) 3) what kind of antigen response
Etiology: - Severe antibody-antigen reaction - Antigens: Foods, Food additives Diagnostic agents Biologic agents Environmental agents Drugs, Venoms ACE-I, bee sting, etc. - IgE-mediated or non–IgE-mediated
34
Neurogenic Shock 1) what kind of shock, 2 2) etiology (2)
Distributive shock Loss or suppression of sympathetic tone Rarest form of shock Etiology - Disruption of sympathetic nervous system - Usually seen in spinal cord injury, but not the same as spinal cord shock
34
Anaphylactic Shock: Nursing management (6)
- Prevention of anaphylactic shock - Note all allergies - Facilitate ventilation - Enhance volume replacement - Promote comfort and emotional support - Maintain surveillance for complications
35
Neurogenic Shock: Assessment and diagnosis (4)
Hypotension Bradycardia Warm, dry skin Hypothermia due to peripheral heat loss
36
Neurogenic Shock: Hemodynamic assessment what happens to CO, CI, CVP, SVR
Cardiac output decreased Cardiac index decreased Central venous pressure decreased Systemic vascular resistance decreased
37
Neurogenic Shock: Medical management 1) goals (3) 2) other interventions (3)
Goals - Remove cause of neurogenic shock - Prevent cardiovascular instability - Restore tissue oxygenation and perfusion - Fluid resuscitation - Vasopressors - Warming measures
38
Neurogenic Shock: Nursing management (5)
1) Prevent of neurogenic shock - Immobilization of spinal cord injuries - Slight elevation of the head of the bed after spinal anesthesia 2) Treat hypovolemia 3) Maintain normothermia 4) Monitor for dysrhythmias 5) Deep venous thrombosis prevention
39
SIRS- Systemic Inflammatory Response Syndrome (what, will accompany any _____ ______ _______, examples of when SIRS can occur (6))
nonspecific, can exist as a result of any inflammatory response - Will accompany any progressive shock state - Ischemia, infection, trauma, inflammation, burns, pancreatitis
40
SIRS 3 stages 1) 1 2) 2 3) 2
Stage 1: - Cytokine production following insult/injury. Cellular inflammatory response initiated -> Local inflammation to support tissue repair and leukocyte recruitment Stage 2: - Cytokine release into blood stream to improve local response  Growth factor stimulation, macrophage and platelet production. - During normal inflammatory response, pro-inflammatory mediators would drop off at this point Stage 3: - Loss of homeostasis leads to systemic inflammation. Wide spread activation of reticular endothelial system leads to loss of circulatory integrity. - Relative hypovolemic shock and end-organ dysfunction
41
SIRS Criteria requires at least 2 of the following clinical findings (4)
TEMP >38C, <36C HR >90 bpm RR >20 or PaCo2 of less than 32 WBC >12,000 or <4,000 or >10% Immature Band Cells
42
qSOFA (3)
Altered Mental Status Fast Resp Rate Low BP
43
Severe Sepsis and Septic Shock (what, which type of shock and how?)
Microorganisms invade the body, initiating a systemic inflammatory response Distributive shock: maldistribution of blood flow to the tissues
44
Severe Sepsis and Septic Shock: Etiology (4)
Microorganisms: - Gram-negative and gram-positive aerobes - Anaerobes - Fungi - Viruses Endogenous sources - ex: perforated bowels (goes in perineal cavity) Exogenous sources - ex: anything we put in patient -> important to get lines out Secondary infections are not uncommon
45
Severe Sepsis and Septic Shock: Assessment and diagnosis (based on 3 conditions)
Diagnosis based on identification of three condition: - Suspected infection - Two or more clinical indications of the systemic inflammatory response syndrome (SIRS) - Evidence of at least one organ dysfunction (impaired renal, AMS, Diff. breathing)
46
Clinical Manifestations of Shock (early septic shock (warm/compensatory)) (8)
Increased HR Full, Bounding Pulse Pink, warm, flushed skin Increased resp rate Increased temp Increased CO/CI Decreased PaCO2 Increased ScvO2
47
Clinical Manifestations of Shock (Late Septic Shock (Cold/Progressive)) (7)
Increased HR, decreased BP Crackles Markedly decreased U/O Decreased SVR Decreased PAOP Decreased PaO2, HCO3 Decreased ScvO2
48
Severe Sepsis and Septic Shock: Medical mgmt (what type of therapy and 3 indications) ______ _______ Directed therapy - _______/________ infection - reverse... - promote... 1) secure _________, correct ________ 2) _________ administration early via IV access - iniitial bolus of ___________ for patients in septic shock (within ___ hours of presentation) - what other intervention? 3) ___________ therapy within ___ hour how do you draw blood cultures?
Early Goal Directed Therapy (EGDT) - Control/Eliminate infection - Reverse pathophysiologic response - Promote metabolic support 2) Secure airway, correct hypoxemia 3) Fluid administration via early IV access - Initial bolus of 30ml/kg for patients in septic shock (within 3 hours of presentation) - Vasopressors 4) Antibiotic therapy – Empiric Abx for suspected organism (within 1 hour) - Broad spectrum until cultures provide further guidance - Vanco + 3rd or 4th gen cephalosporin –OR- beta-lactamase inhibitor (Piperacillin-tazobactam) Antifungals when appropriate (voriconazole) tip: - blood cultures -> anaerobic/aerobic from 2 separate sites, 15 minutes apart (accessible site: sputum, urine, wounds, surgical sites, central lines, etc.)
49
Severe Sepsis and Septic Shock: LABS (5) and tests (2)
labs: - CBC w/ differential, chem, liver function, coags (including D-Dimer) - Suggests severity and provides baseline in following response - Lactate - ABGs - Peripheral blood cultures. *** BEFORE ABX*** -> Anaerobic and aerobic from 2 separate sites 15 min apart ( And other potential readily accessible sites- sputum, urine, wounds, surgical sites, central lines, etc. - IMAGING- X-ray and CT - Eliminate sources of infection (if necessary)
50
Severe Sepsis and Septic Shock: Nursing management (9)
- Identify the sepsis syndrome (qSOFA, SIRS criteria) - Give fluids - Give medications (vasoactive agents, antibiotics, rhAPC and other drugs) - Prevent complications - Prevent other infections - Monitor patient’s response to therapy - Maintain MAP 65-70mmHg, CVP 8-12, ScvO2 >70% - Observe for complications - Collaborative management
51
65-year-old female presenting with weakness, fatigue, palpitations and altered mental status- brought in via EMS HR 170 bpm (In Atrial fibrillation with Rapid ventricular response on monitor- Afib w/rvr). BP 72/40, RR 30, Pulse ox 92% on RA, temp 103.1 Which of the following would be expected intervention? A: Cardiovert with 200J B: 1L bolus of NS, followed by Vasopressor drip C: Cardiovert with 360J D: Defibrillate with 360J E: Your shift is over in 30 min so let someone else worry about it.
B
52
Shock Can Lead to _________ exam: what is it? cause?
a: MODS “Multiorgan dysfunction is the progressive physiological failure of several organ systems in acutely ill patients following an acute threat to systemic homeostasis such that homeostasis cannot be maintained without intervention.” Cause is unknown, but any shock state can result in MODS
53
Multiple Organ Dysfunction Syndrome: Gi dysfunction (GI tract contains approximately _____ to ______ of the ________ tissue of the entire body, mechanisms linking _______ ____ to ______ organ dysfunction -> (3))
Gastrointestinal tract contains approximately 70% to 90% of the immunologic tissue of the entire body Mechanisms linking gastrointestinal tract to latent organ dysfunction: - Hypoperfusion - Translocation of gastrointestinal bacteria - Colonization
54
Multiple Organ Dysfunction Syndrome: hepatobiliary dysfunction (what, _____ and ______ can lead to liver failure, with _______ in liver enzymes)
Selective changes in carbohydrate, fat, and protein metabolism in response to SIRS Shock liver and posttraumatic hepatic insufficiency can lead to liver failure - Elevations in Liver enzymes
55
Multiple Organ Dysfunction pulmonary dysfunction (frequently..., _____ organs affected in progression from ____ to _____, what 2 conditions is result?
Frequently early target organ First organ affected in progression from SIRS to MODS Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)
56
MODS Renal dysfunction: (______ highly vulnerable to ________ injury, ____ or _____ s/d to decreased _________ and ________, use of __________ drugs intensifies ______ ________, what condition results?)
Kidney highly vulnerable to perfusion injury Oliguria or anuria secondary to decreased perfusion and hypotension Use of nephrotoxic drugs intensifies renal dysfunction Acute renal failure
57
MODS Cardiovascular dysfunction (initial response, what occurs as MOD progresses, what follows after? (2))
Initial cardiovascular response is myocardial depression Cardiac failure as MODS progresses Cardiogenic shock and biventricular failure follow
58
MODS Hematologic system dysfunction (4)
Thrombocytopenia, coagulation abnormalities, anemia Disseminated intravascular coagulation (DIC)
59
Collaborative Management of High-Risk Patients: Prevention, detection, and treatment of infections (6)
Medical/surgical interventions to remove sources of infection or contamination Appropriate antibiotics Prevention of skin breakdown Early nutritional support Strict adherence to standards of practice to prevent infection Prevention of ventilator-associated pneumonia - oral care - subglottic suction - positioning - adequate staffing
60
Collaborative Management of High-Risk Patients: Maintenance of tissue oxygenation (what may be augmented in health care setting?, how to manage hypoperfusion and organ hypoxemia (6))
Supply is independent oxygen consumption - may be augmented in healthcare settings Hypoperfusion and organ hypoxemia - Fluid resuscitation - Monitor arterial lactate - Mechanical ventilation - Temperature and pain control - Rest - Maintain normal hematocrit – Hgb >7
61
Nursing Management of High-Risk Patients (what kind of support, hyper_____ with (3), ____ route preferred)
Nutritional/metabolic support - Hypermetabolic with severe weight loss, cachexia, and loss of organ function - Enteral route preferred
62
Experimental Approaches in SIRS and MODS (4)
Continuous venovenous hemofiltration Immunomodulatory strategies to prevent the conversion from SIRS to bacterial sepsis, septic shock, and MODS Pharmacologic approaches that inhibit neutrophil function Other therapies
63
Disseminated Intravascular Coagulation (what (2), etiology (DIC is a _______ complication, extrinsic pathway, intrinsic pathway)
Imbalance between the natural procoagulant and anticoagulant systems (abnormal blood clotting throughout the body’s blood vessels. You may develop DIC if you have an infection or injury that affects the body’s normal blood clotting process.) Unregulated thrombin activity, profuse fibrin production from fibrinogen, microvasculature thrombi, platelet consumption, and microangiopathic hemolytic anemia etiology: - DIC is a secondary complication (septic, certain cancers) - Extrinsic pathway is activated by damage to the endothelial lining of blood vessels. - Intrinsic pathway is activated when subendothelial tissue is exposed to the bloodstream and circulating factor XII comes in contact with the exposed tissue.
64
Severe Sepsis and Septic Shock (what plays a big role in regulating the inflammatory response)
*Activated protein C plays a big role in regulating the inflammatory response
65
Clinical Presentation DIC (3)
Systemic ischemia from the thrombi formation Minor or major hemorrhage - demarcation cyanosis: arterial blood clot in one extremity, acute, no signs until all platelets consumed
66
Assessment DIC (7)
Complete history Acute or chronic presentation Low-grade bleeding Unexpected thrombotic events Signs and symptoms of inappropriate clotting Demarcation cyanosis Bleeding from the nose, gums, lungs, gastrointestinal tract, surgical sites, injection sites, and intravascular access sites; hematuria; petechial rashes.
67
Care of the Patient DIC (6)
Onset is sudden and acute. Constant reassessment Dyspnea Hypotension Ischemic bowel (Gi bleed) Signs and symptoms of the onset of shock (looks like shock)
68
Laboratory Studies DIC (5)
Platelets (low) Fibrinogen (low) PT (high) PTT (high) d-dimer (high) -> measure of clot being broken down, will increase if it is
69
Management DIC (9)
Eliminate the causative agent. Antibiotic or antifungal therapy for sepsis Antineoplastic therapy Fluid replacement Oxygen Resolution of low-flow states Activated protein C Heparin therapy FFP, cryoprecipitate, RBC
70
remember that PCWP is a surrogate pressure for left atrial and left ventricular preload
wedge pressure
71
cardiogenic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high SV - REALLY low SVR - high PCWP - high O2 - low
72
distributive shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high SV - high SVR - REALLY low PCWP - low O2 - high then low
73
hypovolemic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high SV - REALLY low SVR - high PCWP - low or no change O2 - high
74
neurogenic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - low SV - dont know SVR - REALLY low
75
treatment options: cardiogenic
insult: decreased CO tx: inotropes - afterload REDUCTION - diuresis - INcreased contractility
76
treatment options: distributive (A,S,N)
insult: decreased SVR tx: - volume then vasopressors
77
treatment options: hypovolemic
insult: decreased volume tx: - volume then vasopressors if unable to maintain MAP with volume