Approach to shock

2.  Shock is a physiologic state characterized by
a significant reduction of systemic tissue
perfusion, resulting in decreased oxygen
delivery to the tissues.

3.  cell membrane ion pump dysfunction
 intracellular edema
 leakage of intracellular contents into the
extracellular space
 inadequate regulation of intracellular pH

4.  alterations in the serum pH
 endothelial dysfunction
 redox state
 further stimulation of inflammatory and
antiinflammatory cascades

5.  sequential cell death
 end-organ damage
 multi-system organ failure
 death.
 Initially reversible
 rapidly become irreversible

6.  Cryptic = hidden or silent
 Inadequate oxygen delivery leading to shock can
occur despite the patient being hypertensive or
normotensive and clinicians should not wait for
the presence of hypotension before aggressively
attempting to reverse shock and restore
adequate tissue perfusion.
 Early evaluation of serum lactate can assist in
identifying “cryptic shock” (normal blood
pressure accompanied by tissue level
hypoperfusion).

7.  Systemic tissue perfusion is determined by
the cardiac output (CO) and systemic vascular
resistance (SVR):
 ●CO is the product of heart rate and stroke
volume.
 The stroke volume is related to preload,
myocardial contractility, and afterload
 ●SVR is governed by the vessel length, blood
viscosity, and vessel diameter

8.  Decreased systemic tissue perfusion is a
consequence of diminished CO, SVR, or both. The
CO or SVR may be elevated in shock if the other
is disproportionately low.
 As an example, SVR is decreased out of
proportion to the elevation of the CO in
hyperdynamic shock .
 Complex interactions between humoral and
microcirculatory processes cause patchy regional
blood flow and reduced effective tissue perfusion
 This results in derangement of cellular metabolic
processes.

9.  Hypovolemic
 Cardiogenic
 Distributive.

10.  ↓preload due to intravascular volume loss.
 leading to ↓ CO & compensatory ↑SVR
 ↓ PCWP is decreased.

11.  Due to severely decreased SVR.
 Compensatory ↑CO
 The PCWP may be low or normal
 Septic
 Adrenal crises
 Neurogenic (spinal shock)
 Anaphylactic
 PCWP : DD hypovolemic from cardiogenic shock .

12.  An example, in septic shock :
 hypovolemic component (due to decreased
oral intake, insensible losses, vomiting,
diarrhea)
 cardiogenic component (due to sepsis-
related myocardial dysfunction)
 distributive component (due to the effects of
inflammatory and antiinflammatory cascades
on vascular permeability and vasodilation).

13.  Preshock
 Shock
 End-organ dysfunction.

14.  warm shock or compensated shock.
 rapid compensatory homeostatic
mechanisms for diminished tissue perfusion
 Signs : tachycardia, peripheral
vasoconstriction, and either a modest ↑ ↓
systemic blood pressure

15.  Overwhelmed compensatory mechanisms
 S/S signs of organ dysfunction appear.
 tachycardia, dyspnea, restlessness, diaphoresis, metabolic
acidosis, oliguria, and cool clammy skin.
 ↓25% in effective arterial blood volume in hypovolemic shock
 ↓ cardiac index to ≤2.5 L/min/m2 in cardiogenic shock,
 activation of innumerable mediators of the systemic
inflammatory response syndrome (SIRS) in distributive shock.

16.  ⇊ urine output : ARF
 Acidemia decreases the cardiac output and
alters cellular metabolic processes
 restlessness evolves into agitation,
obtundation, and coma.

17.  Hypotension
 Oliguria
 abnormal mental status
 metabolic acidosis
 in some patients, cool and clammy skin.

18.  Hypotension occurs in the majority of shock patients.
 absolute hypotension (eg, systolic BP<90 mmHg)
 relative hypotension (eg, a drop in systolic BP>40 mmHg).
 Relative hypotension explains, in part, why a patient may be
in shock despite having a high or normal BP.

19. Pathogenesis:
 shunting of renal blood flow to other vital
organs
 intravascular volume depletion
 both.

20.  orthostatic hypotension
 poor skin turgor
 absent axillary sweat
 dry mucous membranes.

21.  Due to vasoconstriction

22.  early distributive shock prior to the onset of
compensatory vasoconstriction
 terminal shock due to failure of compensatory
vasoconstriction.

23.  ⇩ lactate clearance by liver, kidneys & skeletal muscle
 Lactate production may increase due to anaerobic
metabolism if shock progresses to circulatory failure and
tissue hypoxia, which can worsen the acidemia.

24.  – Depending upon the cause :
 hematemesis, hematochezia, melena,
vomiting, diarrhea, or abdominal pain.
 There may be evidence of blunt or
penetrating trauma,
 The patient may be postoperative.

25.  ⇩ skin turgor (in younger patients), dry skin
 dry axillae
 dry tongue & oral mucosa.
 postural hypotension
 ⇩ JVP
Occasionally :
 Anemia
 ⇈ amylase and lipase

26.  Depending upon the cause.
 dyspnea, chest pain, or palpitations.
 H/O of CV disease.
 Lung : diffuse crackles
 cardiac :new murmur, gallops, or soft heart sounds.
 ⇧ JVP and CVP
 ⇩ distal arterial pulses
 CXR : pulmonary congestion or pulmonary edema
 ECG : recent or current ischemia
 ⇧ Cardiac enzymes.
 Echo may demonstrate the etiology.

27.  Depending upon the cause
 dyspnea, productive cough
 dysuria, hematuria
 chills, myalgias, rashes, fatigue, malaise
 headache, photophobia, pain
 recent ingestion.
 O/E: fever, tachypnea, tachycardia,
leukocytosis, an abnormal mental status, or
flushing.

28. Causes:
Hemorrhage-induced –
 penetrating trauma, GI bleeding, ruptured
hematoma, hemorrhagic pancreatitis, fractures,
or a ruptured aneurysm.
Fluid loss-induced
 diarrhea, vomiting, heat stroke, inadequate
repletion of insensible losses, burns, and "third
spacing".
 Third-space losses are common postop & if
intestinal obstruction, pancreatitis, or cirrhosis.

29.  myopathic
 Arrhythmic
 Mechanical
 extracardiac (obstructive).

30.  Massive PE
 Tension pneumothorax
 Severe constrictive pericarditis
 Pericardial tamponade
 Severe pulmonary hypertension: Eisenmenger's
 They may present clinically as hypovolemic shock
when their primary physiologic disturbance is
decreased preload, rather than pump failure.

31.  Resuscitative efforts should NOT be delayed
for history, physical examination, laboratory
testing, or imaging.


32.  The patient's baseline medical status
 recent complaints
 food and medicine allergies
 recent changes in medications, potential
acute or chronic drug intoxication
 preexisting diseases
 immunosuppressed states
 hypercoagulable conditions.

33.  neither sensitive nor specific for identifying
the cause of shock.

34.  CBC : leukocytosis and/orbandemia >10% (sepsis)
 Basic chemistry (sodium, potassium, chloride, serum
bicarbonate)
 RFT :urea & creatinine
 liver function tests
 amylase, lipase
 INR, PTT
 fibrinogen, fibrin split products or dimer, cardiac
enzymes (troponin or CK mb)
 ABG
 Toxicology screen
 lactate level.
 Type and crossmatch should be performed for
patients who are at risk for significant bleeding

35. Causes:
 increased production ( anaerobic metabolism)
 mitochondrial derangements affecting oxygen
utilization
 decreased clearance due to hepatic dysfunction.

36.  CXR
 abdominal X-ray for intestinal obstruction
 abdominal CT
 ECG
 Echocardiogram
 urinalysis
 Gram stain of material from sites of possible
infection (sputum, urine, wounds) may give early
clues to the etiology of infection while cultures are
incubating.
 Blood should be taken from two distinct
venipuncture sites

37.  Hemodynamic measurements
 titration of vasopressors
 guide fluid resuscitation
 cardiac output
 pulmonary artery occlusion pressure: PAWP
 SVR
 never been shown to improve outcomes

38.  35 to 60 %
 higher in cardiogenic shock; 60 to 90 %