Lecture 4 - shock Flashcards
review Preload = Central Venous Pressure (range, low, high, indication, _____ _____ where we expect ___ _______?, which shock state would we be concerned with fluid overload?
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)
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)
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
review Contractility
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!
Arterial BP (what, more accurate than, used to monitor (3))
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
Shock Syndrome (what, results in, imbalance between, leads to, no what what the underlying cause of shock, all shock will…)
- 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.
Etiology of Shock States (3 + 3 types)
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
Shock Syndrome-Pathologic Process (4 stages)
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)
Pathophysiology: Initial stage
Decreased CO → tissue perfusion is threatened
Pathophysiology: Compensatory stage (_________ mechanisms to maintain.. (3), mediated by ______, 3 responses, ________ mechanisms may normalize -> elevations in (2))
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
Global Indicators of Progressive Shock: (5)
- Serum lactate levels increased
- Arterial base deficit levels (acidosis)
- Serum bicarbonate levels decreased
- pH decreases
- Central or mixed venous oxygen saturation levels
Pathophysiology: Progressive stage (_______ mechanisms begin to _____, switch from _______ to ________ ________ -> _______ ____ production), increased (3) -> what? (2), what begins during this stage?)
- 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
Pathophysiology: Refractory stage (3)
- Unresponsive to therapy
- Irreversible with the development of MODS
- Death is final outcome
Stages of shock - NCLEX+HESI (3 stages)
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.
Consequences of shock (neuro) (3)
Mental status changes
Sympathetic Nervous system dysfunction
Thermal dysregulation
Consequences of shock (cardiac) (2)
Pump failure
Micro embolism of cardiac circulation
Consequences of shock (pulmonary) (2)
ALI/ARDS
Respiratory failure
Consequences of shock (renal) (1)
Acute Tubular Necrosis: ↑BUN, Cr, ↓Urine output
Consequences of shock (GI) (3)
Hepatic failure -> increase liver enzymes, bilirubin, ↓ albumin, clotting protein
Pancreatic failure -> increase amylase, lipase, ↓ insulin production
GI tract failure -> Gastric immotility, SBO/ileus
Consequences of shock (hematologic) (1)
DIC
Goal of Treatment (2)
Improvement of tissue perfusion
- Adequate pulmonary gas exchange: Oxygen therapy, Ventilatory support
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
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
types of shock (4)
1) Hypovolemic
2) Cardiogenic
3) Distributive:
- Anaphylactic
- Neurogenic
- Septic
4) Obstructive:
- Cardiac Tamponade
- Tension Pneumothorax
Hypovolemic Shock (3)
- Inadequate fluid volume in the intravascular space
- Decreased tissue perfusion
- Most common form
Hypovolemic Shock: Assessment and diagnosis
(4 classes, what are the percentage and mL of fluid loss)
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)
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)
Hypovolemic Shock: Medical management (3)
Correct hypovolemia
Restore tissue perfusion
Prevent complications
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
Cardiogenic Shock (what, etiology (3))
Failure of heart to pump blood effectively
etiology:
Primary ventricular ischemia
Structural problems
Dysrhythmias
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
Cardiogenic Shock: Pharmacologic support (5)
Inotropic agents
Vasopressor (sometimes)
Diuretics
Vasodilators once blood pressure stabilized (Lower SVR comparative to Contractility)
Antidysrhythmics
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
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
Anaphylactic Shock (3)
Distributive shock
Immediate hypersensitivity reaction
Life-threatening event
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
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
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
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
Neurogenic Shock: Assessment and diagnosis (4)
Hypotension
Bradycardia
Warm, dry skin
Hypothermia due to peripheral heat loss
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
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
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
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
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
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
qSOFA (3)
Altered Mental Status
Fast Resp Rate
Low BP
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
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
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)
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
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
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.)
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)
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
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
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
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
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
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)
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
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
MODS Hematologic system dysfunction (4)
Thrombocytopenia, coagulation abnormalities, anemia
Disseminated intravascular coagulation (DIC)
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
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
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
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
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.
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
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
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.
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)
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
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
remember that PCWP is a surrogate pressure for left atrial and left ventricular preload
wedge pressure
cardiogenic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high
SV - REALLY low
SVR - high
PCWP - high
O2 - low
distributive shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high
SV - high
SVR - REALLY low
PCWP - low
O2 - high then low
hypovolemic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - high
SV - REALLY low
SVR - high
PCWP - low or no change
O2 - high
neurogenic shock (HR/SV/SVR/PCWP/MIXED VENOUS O2)
HR - low
SV - dont know
SVR - REALLY low
treatment options: cardiogenic
insult: decreased CO
tx: inotropes
- afterload REDUCTION
- diuresis
- INcreased contractility
treatment options: distributive (A,S,N)
insult: decreased SVR
tx:
- volume then vasopressors
treatment options: hypovolemic
insult: decreased volume
tx:
- volume then vasopressors if unable to maintain MAP with volume
