Shock Flashcards

1
Q

What is the definition of shock?

A
  • State of cellular and tissue hypoxia
  • Acute circulatory failure
  • Initially reversible ( but must be treated to prevent irreversible organ dysfunction)
  • “Undifferentiated shock” refers to the situation where shock is recognized but the cause is
    unclear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does cellular hypoxia cause?

A

1) Cell membrane ion pump dysfunction -> intracellular edema -> leakage of intracellular
contents into extracellular space -> inadequate regulation of intracellular pH similar PP to cerebellar hypoxia)

2) Ultimately results in acidosis, endothelial dysfunction, stimulation of inflammatory and
anti-inflammatory cascades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Components of the shock graph (oxygen consumption vs oxygen delivery) and physiology

A

Supply independent phase:
- Tissue oxygen consumption (VO₂) is maintained at a constant level despite decreasing oxygen delivery (DO₂)
- Body compensates by ^ oxygen extraction from the blood

Supply dependent phase:
- Once oxygen delivery (DO₂) falls below a critical threshold, tissue oxygen consumption (VO₂) becomes dependent on oxygen delivery
- The reduced oxygen delivery leads directly to reduced oxygen consumption -> causing cellular dysfunction and energy failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Formulas in oxygen delivery and extraction ratio

A

DO2 (oxygen delivery) =
CO (cardiac output) x
CaO2 (arterial O2 content)

ER (Extraction ratio) = VO2 (oxygen consumption)
/ DO2

Note: tf lower ER is better as it means tissues are able to meet its metabolic needs within having to extract more o2 from the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the causes of High ER?

A

OH CRAP, Shock!

Oxygen (hypoxia, high altitude, lung disease)
Hemoglobin (anemia)

Contractility
Rhythm
Afterload
Preload

Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of very low ER?

A

Hyperoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of high VO2?

A
  • Fever and inflammatory states
  • Increased metabolic rate
    ~ Hyperthyroidism, adrenergic drugs, hyperthermia
  • Increased muscular activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of decreased VO2?

A
  • Decreased muscular activity
    ~ Analgesia/sedation, muscle paralysis, ventilator support
  • Decreased metabolic rate
    ~ Hypothyroidism, hypothermia
  • Antipyretics
  • Hyponutrition
  • Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the stages of shock?

A

[Pre-shock]
- Not many changes yet
- Compensatory mechanisms to dec tissue perfusion
~ Tachycardia, mild ^ in SBP and hyperlactatemia
- Body goes into supply-dependent phase

[Shock]
- Compensatory mechanisms become overwhelmed
- Organ dysfunction begins

[End-organ dysfunction]
- Anuria (no urine) and acute renal failure develops
- Acidemia further depresses CO
- Hypotension becomes severe, often resistant to ionotropes
- Multi organ failure(MOF) and death follows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the s/s of organ dysfunction?

A
  • Symptomatic tachycardia
  • Dyspnea
  • Restlessness
  • Diaphoresis (^ sweat)
  • Metabolic acidosis
  • Hypotension
  • Oliguria
  • Cool + clammy skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the compensatory mechanisms (through sympathetic nervous system) to maintain BP when a px is in shock?

A

1) ^ CO
- ^ HR + SV
- ^ sympathetic tone
~ Causes constriction of venous circulation (^ in preload inc CO)

2) Maintain normovolemia
- ^ sympathetic tone
~ Causes constriction of arterial circulation (redistributes blood to vital organs)

3) Stimulate adrenal gland
- ^ secretion of adrenaline, noradrenaline and cortisol
~ ^ arterial and venous tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the compensatory mechanisms (through RAAS) to maintain BP when a px is in shock?

A

1) Maintaining normovolemia
- Aldosterone ^ sodium reabsorption in the kidneys
~ ^ CO
- Angiotensin II causes vasoconstriction

2) Renal protective actions
- Angiotensin II preferentially constricts the efferent
arteriole to maintain GFR and prevent pre-renal
AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the s/s differences in compensated and uncompensated shock?

A

Comp vs Uncomp

Alert w some irritability VS Altered mental state

Tachycardia + hypotension in uncomp

Tachypnea + ARDS in uncomp

Decreased urine output VS prerenal azotemia, metabolic acidosis, anuria

Nausea, anorexia VS Hypoactive bowel sounds

Hyperglycemia vs hypoglycemia

Warm extremities VS Cold extremities w slowed capillary refill

Decreased venous PO2 VS elevated lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Systemic Inflammatory Response Syndrome (SIRS) and how is it related to shock?

A
  • Exaggerated defense response to a noxious stressor
  • Mostly found in septic shock cases

Diagnostic criteria (at least 2)
- <36deg C or >38deg C
- RR >20 (or PaCO2 <32mmHg)
- HR > 90
- WBC is <4000m^3 or >12000m^3 or >10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the sepsis continuum/progression?

A

1) Infection
- Invasion of normally sterile tissue

2) SIRS
- Infection
overcomes the body’s
local defense mechanism
- Induces a body-wide
response

3) Sepsis
- Infection ± SIRS + Organ
dysfunction
- Dysregulated immune response occurs due to intensity of infection
- Injury to tissues and
organs

4) Septic Shock
- Sepsis + refractory
hypotension
- Profound circulatory,
cellular, and metabolic
abnormalities

5) Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How to diagnose shock?

A

1) Lab studies
- To determine the degree of end-organ perfusion
- Lactate > 2 mmol/L
- Renal panel – AKI as evidenced by creatinine
- Liver function tests(LFT) – transaminitis suggestive of ischemic hepatitis
- Troponin – raised with MI
- ABG/VBG

2) Point-of-care Ultrasound Studies (POCUS)
- Usually for px with undifferentiated shock
- Do Focused Assessment with Sonography for Trauma(FAST) +
Echocardiography
- Perihepatic, perisplenic, pelvic, pericardial, pneumothorax, pleural effusion
- Or Rapid Ultrasound in Shock (RUSH)

17
Q

What is the general management of shock? (Airway and breathing)

A
  • Supplemental o2
  • Advanced airway maneuvers if:
    ~ Severe hemodynamic compromise
    ~ Hypercapnic respiratory failure
    ~ Hypoxemic respiratory failure
18
Q

What is the general management of shock? (Circulation)

A
  • Establish vascular access and obtain blood samples for testing
  • Begin hemodynamic monitoring
    ~ Telemetry, SpO2, BP
    ~ May or may not do an arterial line
  • Provide hemodynamic support
    ~ Fluid resus (colloids or crystalloids)
    ~ Do passive leg raise test if fluid responsiveness is in doubt
    ~ Determine need for vasopressors, inotropes or blood transfusions
  • Insert urine catheter for renal perfusion monitoring
19
Q

What are colloids and crystalloids in IV solutions for fluid resuscitation?

A

Colloids vs crystalloids

Large insoluble molecules (eg starch, protein) VS Electrolytes

Small volumes given VS Large volumes

Lower risk of edema VS Higher

Slower perfusion VS Faster

Albumin, Dextran VS NaCl, Lactated Ringers, D5W

20
Q

Inotropes vs vasopressors

A

Inotropes:
- Increases CO, which may indirectly improve BP
- Increase myocardial contractility (stroke volume)
- Targets heart

Vasopressors:
- Directly increases blood pressure by vasoconstriction
- Increase vascular tone (blood pressure)
- Targets BV

21
Q

When are certain inotropes and vasopressors given?

A
  • Vasopressors when the problem is low BP
  • Inotropes when the problem is low CO
  • After px is adequately hydrated

Vaso:
- Norepinephrine (1st choice for septic, cardiogenic and hypovolemic shock)
- Epinephrine (1st choice for anaphylatic shock)
- Dopamine (alternative for septic shock in some px)

Ino:
- Dobutamine (1st choice for cardiogenic shock w low CO and normal BP)

22
Q

What is the general management of shock? (Disability and Exposure)

A
  • POCUS
  • CXR (to rule out pneumothorax)
  • ECG
  • ABG
  • Labs
  • Adrenaline and antihistamines for anaphylaxis
  • Needle thoracostomy for tension pneumothorax
  • Corticosteroids for adrenal crisis
23
Q

What are the types of shock?

A

1) Distributive (severe peripheral BV dilation -> inadequate perfusion / dec SVR)
- Septic
- Non-septic

2) Cardiogenic (failure of heart to pump effectively despite normal blood volume)
- Cardiomyopathic
- Arrhythmogenic
- Mechanical

3) Hypovolemic
- Hemorrhagic
- Non-hemorrhagic

4) Obstructive (Obstruction to blood flow -> dec CO)
- Pulmonary vascular
- Mechanical

5) Mixed/uknown

24
Q

What are the most common causes of septic shock (Distributive)?

A
  • Gram negative bacteria
  • Fungi
  • Viruses
25
Q

What is the management for sepsis?

A

Surviving sepsis campaign bundle
- Measure lactate level (remeasure if >2mmol/L)
~ ^ in lactate indicates tissue hypoxia

  • Obtain blood cultures before administering Abx
  • Administer broad-spectrum Abx within 1 hr of presentation w max dosing
    ~ Piperacillin-tazobactam & IV vancomycin
    ~ Monitor CRP, pro-calcitonin, WBC and cultures
  • Begin rapid administration of crystalloids for hypotension, or lactate
    ~ Consider colloids after resus w crystalloids has failed or edema arose
    ~ Give NS 1000 ml/30 mins
    ~ Monitor MAP >65mmHg, UO >0.5ml/kg/hr, CVP 8-12 mmHg
  • Apply vasopressors if still hypotensive
    ~ 1st choice norepinephrine
    ~ 2nd choice epinephrine or vasopressin or dopamine
26
Q

What is neurogenic shock (Distributive - non septic)?

A

1st degree injury:
- Immediate effect of trauma, especially to spinal cord

2nd degree injury:
- Within minutes to hours of injury
- Eg ischemia, hypoxia, edema

Interruption of autonomic pathways -> dec vascular resistance -> dec BP and HR
~ Bradycardia is unique to neurogenic shock

27
Q

What is the management for neurogenic shock?

A
  • C-spine stabilisation
  • Thorough neurologic exam
  • Check for bladder distention and insert IDC
  • Administer glucocorticoids within 8 hours of non-permeating traumatic spinal cord injury (TSCI)
  • Treat w fluids/blood or inotropes if needed
  • Keep MAP 85-90 mmHg
  • Treat bradycardia w atropine or external pacing
  • Provide DVT/PU prophylaxis
27
Q

What is the management of anaphylactic shock (Distributive - non septic)

A
  • Nasal endoscopy for upper airway obstruction
  • Supplemental O2
  • Intubation if airway obstruction is from angioedema
  • Give IM Adrenaline every 5-15 mins as needed
  • H1 + H2 antihistamines
  • Glucocorticoids
  • Bronchodilators is bronchospasm present

If there is refractory anaphylaxis:
- Start adrenaline infusion

28
Q

What is the pathophysiology of cardiogenic shock?

A
  • Heart dysfunction -> dec heart contractility and SV -> dec CO -> insufficient organ perfusion ->, ^ pulmonary hydrostatic pressure -> pulmonary edema
29
Q

What conditions fall under cardiomyopathic causes of cardiogenic shock?

A

MI
HF

30
Q

What conditions fall under arrhythmogenic causes of cardiogenic shock?

A

Sustained VT or heart blocks

31
Q

What conditions fall under mechanical causes of cardiogenic shock?

A

IV rupture
Ventricular wall rupture

32
Q

What is the management of cardiogenic shock?

A
  • POCUS echocardiogram
  • Regional wall motion abnormality (RWMA)
  • ECG, CXR
  • BNP, ABG

Noncongested / no fluid overload / dry and cold:
- Fluid bolus only if hypotensive
- Vasopressor only if shock persists
- Administer inotropes if hypoperfusion persists despite fluids + vasopressor

Congested / wet and cold:
- Administer inotropic therapy and add on vasopressor if needed to maintain perfusion
- Do not give anymore fluids as px is alr overloaded
- Once SBP > 90 mmHg, start diuretics and nitrates

33
Q

What is the management of hypovolemic shock?

A

If hemorrhagic:
- Arrest bleeds externally
- Transfuse ASAP
~ Use O negative if emergency
- Massive Transfusion Protocol
~ 1 unit RBC : 1 unit FFP : 1 unit PLT
- Give tranexamic acid (TXA) for severe traumatic injury

If non-hemorrhagic:
- Treat underlying reason (eg antiemetics, antidiarrheals)

34
Q

What are the causes of obstructive shock?

A

1) Pulmonary embolism or severe pulmonary artery hypertension (PAH)
- Right heart failure -> ^ RV pressure -> dec LV preload -> dec CO

2) Tension pneumothorax
- ^ intrathoracic pressure -> dec venous return -> dec CO

3) Cardiac tamponade
- ^ pericardial pressure -> right heart failure -> dec CO

35
Q

How to manage obstructive shock?

A
  • Provide immediate hemodynamic support (fluid resus)
    ~ For px who are preload-dependent
    ~ Consider vasopressors or inotropic support
  • Pericardiocentesis for cardiac tamponade
  • Thrombolytic therapy
  • Needle thoracostomy