Shock VT

Slide 1
SHOCK
DOOMSDAY
1
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Slide 2
Vicken Y. Totten
 Shock lecture
 Thanks to David Cheng MD
 And all who taught me

Slide 3
Definition
SHOCK:
inadequate organ
perfusion to meet
the tissue’s
oxygenation
demand

PATHOPHYSIOLOGY OF SHOCK
Slide 4
SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & cells swell
membranes becomes more permeable
electrolytes & fluids seep in & out of cell
Cells Die in Many Organs Death

Slide 5
Stages of shock
 Compensated /Early Shock
– Vasoconstriction  (renin & carotid sinus baroceptor
– Increase in HR and RR <- sympthatic activation)
– Normotensive usually <- (aldosterone/ADH Na+/h20
retention)
 Decompensated / late Shock
– Cool, clammy , hypotenisve.
– Vital organ preservation
– Worsening LOC
– Continued increase in HR and RR <-----(Chemreceptor
respose to metabolic acidosis)
 Irreversible-
– HR and RR drop Multi Organ Failure Impending death)

Slide 6
Symptoms of Shock
General Symptoms Specific Symptoms
 Anxious  Fevers / Rigors (sepsis)

 Dizziness  SSCP (cardiogenic)
 Weakness
 Wheezing (anaphylaxis)
 Faintness
 Thirsty  Trauma pain
 “I am sick” (hypovolemia)

Slide 7
Early Signs of Shock in

Non Complicated Patients
 WARM EARLY STAGE / PRESHOCK

 Need high index of suspicion b/c lack of signs
+/- tachycardia
+/- orthostatics (HR more sensitive than BP)
+/- pulse pressure narrowing
+/-restless

Slide 8
“Hypoperfusion can be
present in the absence of
significant hypotension.”
(Don’t only relay on BP for
diagnosisng shock)
-fccs course
8
Slide 9
Signs of Late Shock

Hypotension
COLD LATE STAGE

 Cold, clammy and pale skin
 Rapid, weak, thready pulse
 Rapid breathing (blow off CO2 met acidosis)
 Cyanotic
 AMS->Coma
 Anuria

Slide 10
End Stage Clinical effects
 Cardiovascular  GI
– Myocardial – Ischemic bowel
depression  Hepatic
– Vasogenic effects – Increased LFT’s, liver failure
 Hematologic
 Pulmonary – Neutropenia,
– ARDS Thrombocytopenia
 Renal – DIC (Gm- > Gm+)
– ARF  CNS
– coma

Slide 11
Multiple Organ Dysfunction Syndrome

Number of Mortality (%)
Organs
0 0.8
1 6.8
2 26.2
3 48.5
4 68.8
5 83.3
*Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837
Slide 12
Circumferential
Subendocardial
Infarction due
to Shock
Slide 13
Shock
Lung

Slide 14
Acute congestion of liver due to shock

Slide 15
Acute tubular necrosis of the kidney due to shock

Slide 16
Intestinal mucosal hemorrhages due to shock

Slide 17
Adrenal gland hemorrhage due to shock

Slide 18
Remember
 History and Physical often limited by patient’s
condition
 Patient presentation can be variable secondary

to
– Severity of the perfusion defect
– Underlying cause
– Prior organ dysfunction
 Exam should be tailored to be performed

quickly with highest yield for uncovering the
cause of shock.
Slide 19
Components (fluids, pump,

pipes)

Slide 20
 Components:
– Blood (fluid)
– Heart (pump)
– Blood Vessels
(pipes)

Slide 21
Types of Shock
Hypovolemic (fluids)
Cardiogenic (pump)
Redistributive (pipes)
(septic, neurogenic, anaphylactic)
Slide 22
Adequate circulating blood

volume depends on 3
components;
A minor impairment in one
can be compensated for by
the other 2 for a limited time.
Prolonged or severe
impairments will lead to
SHOCK.
22
Slide 23
An Approach to Shock – Know

this!
BP = SVR x CO
BP = blood pressure
CO = cardiac output (pump & fluids)
SVR = systemic vascular resistance (pipes)

Slide 24
An Approach to Shock
If the blood pressure is low, then either the:

CO is low
or
SVR is low
or
BOTH

Slide 25
Low SVR
There are only a few causes of low SVR.

They ALL cause vasodilation:
•Septic
shock
•Neurogenic (spinal cord injury) shock
•Anaphylaxis Shock
•Vasodilator (antihypertensive)
Posioning

Slide 26
How do you assess SVR?

Look at and feel the patient!
Low SVR has the features:

• warm !!!
• pink
• Bounding pulses
• hyperdynamic heart (fast and
pounding)

Slide 27
What if the SVR is high?
• Pale
• Poor cap refill (>2 seconds)
• Cool arms/legs (>2 degree C difference)
• Thready pulses (narrow pulse pressure (incr DBP))
Cause of shock (low BP) is then:
low CO

Slide 28
What are factors of CO?
CO = HR x SV
CO = cardiac output
HR = heart rate
SV = stroke volume

Slide 29
HR Problems
• Heart Rate problems are easy to diagnose
• Rate: bradycardia versus tachycardia

Low SV (stroke volume)
Slide 30
Most difficult to diagnose

and manage

Slide 31
Stroke Volume depends on

Preload--is the ventricle full?
Hypovolemic Shock
Obstructive Shock (ie Tension PTX, Tamponade)
Cardiac function
SqueezeContractility– can the ventricle contract?
Can blood get out?  Valve function:
normal?
regurgitation?
stenosis?

Slide 32
Perfusion (blood pressure) depends on:
BP = CO x SVR
CO = HR x SV
SV = preload & cardiac contractility-valve

Slide 33
Components of BP summary
Myocardial
Contractility
Stroke Volume Preload
Cardiac Output Afterload
Blood
Pressure Heart Rate
Systemic Vascular
Resistance

Slide 34
Why Monitor?
 Essential to understanding their disease
 Describe the patient’s physiologic status

– Serial monitoring
 Facilitates diagnosis and treatment of shock

Slide 35
Monitoring clinical shock parameter

Noninvasive ：
 Blood pressure (SBP, MAP)
 Urine output
 Heart rate
 Shock index
Invasive ：
 Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO2I,
VO2I, SvO2
 Arterial catheter: ABP, Serum lactate, Base deficit

Slide 36
Diagnosis of Shock
 MAP < 60 or decrease

of 20 from baseline
 systolic BP  90
  systolic BP > 40 mm
Hg from the patient’s
baseline pressure
 Shock index (HR>SBP)
 Clinical s/s of
hypoperfusion of vital
organs

Slide 37
Mean Arterial Pressure
 MAP is the mean perfusion pressure for the tissues

– Most require a MAP of 60 or greater!
 Dependent only on the elastic properties of the

arterial walls and the mean blood volume in the
arterial tree
 MAP = (2 x DBP) + SBP

3

Slide 38
Pulse Pressure=SBP-DBP
The difference between the systolic (fxn of
ejection fraction) and diastolic pressures (function
of SVR and distensibility (elastic recoil) of the aorta
 Wide  Narrow
– Normal 30-50 mmHg – May indicate an increase
– Commonly seen with fever, in vascular resistance with
anemia, exercise and decreased stroke volume
hyperthyroidism (ie aortic stenosis or
– AR (aortic regurgitation) is decreased intravascular
also a cause volume)

Slide 39
Invasive Markers
 Global Markers
– Base Deficit
– Lactate
 Regional Markers
– Gastric pH
– Sublingual CO2

Slide 40
Base Deficit
 Inadequate tissue perfusion leads to tissue

acidosis
 Amount of base required to titrate 1 L of
whole arterial blood to a pH of 7.4
 Normal range +3 to –3 mmol per L
 Elevated base deficit correlates with the
presence and severity of shock

Slide 41
Base Deficit
 Inadequate tissue perfusion leads to tissue

acidosis
 Amount of base required to titrate 1 L of
whole arterial blood to a pH of 7.4
 Normal range +3 to –3 mmol per L
 Elevated base deficit correlates with the
presence and severity of shock

Slide 42
Initial Lactate
Weil and Afifi. (Circulation 1970)

Slide 43
Lactate and Outcomes

Adult Patients A peak blood
lactate level
of >4.0 mmol/L
was identified as a
strong
independent
predictor of
mortality
and morbidity
and suggests that
tissue
hypoperfusion
Demmers Ann Thorac Surg 70:2082-6:2000
Slide 44

Slide 45
Gastric Intramucosal pH
 Blood flow is not uniformly distributed to all tissue

beds
 Regions with inadequate tissue perfusion may exist
while global markers are ‘normal’
 Gut mucosa among the first to be affected during
shock and the last to be restored to normal
 Intramucosal pH falls when perfusion becomes
inadequate

Slide 46
Sublingual capnometry:
A new noninvasive measurement for diagnosis and
quantitation of severity of circulatory shock
hypercarbia is a universal indicator of critically reduced

tissue perfusion.
Slide 47
Sublingual CO2
 Decrease gut perfusion

– Gastric tissue = esophagus = sublingual tissue
 Non-invasive, hand held monitor
 Rapid measurement
 Sensitive marker of decreased blood flow

Slide 48
Sublingual capnometry:
A new noninvasive measurement for diagnosis and
quantitation of severity of circulatory shock
P SL CO2
provides a
prompt
indication of the
reversal of
tissue
hypercarbia
when
circulatory
shock is
reversed
Slide 49
Direct arterial pressure

A-line

Pulmonary Artery Catheter
Slide 50
 INDICATIONS
– volume status
– cardiac status
 COMPLICATIONS
– technical
– anatomic
– physiologic

Slide 51
Swan-Ganz Catheter

Slide 52
PLACEMENT

Slide 53
Correct PA-C Position
 From the RIJ approach, the RA is entered at

approximately 25 cm, the RV at approximately
30 cm, and the PA at approximately 40 cm; the
PCWP can be identified at approximately 45
cm.
Slide 54
Standard Parameters
 Measured  Calculated
– Blood pressure – Mean BP
– Pulmonary A. – Mean PAP
pressure – Cardiac Index
– Heart rate – Stroke volume
– Cardiac Output index
– Stroke volume – SVRI
– Wedge pressure – LVSWI
– CVP – BSA

Slide 55
Why Index?
 Body habitus and size is individual
 “Indexing” to patient with BSA allows for

reproducible standard
PATIENT A PATIENT B
 60 yo male  60 yo male
 50 kg  150 kg
 CO = 4.0 L/min  CO = 4.0 L/min
 BSA = 1.86  BSA = 2.64
CI = 2.4 L/min/m2 CI = 1.5 L/min/m2

Slide 56

Slide 57
PA Insertion
20
15
10
5
RA = 5 RV = 22/4 PA 19/10 PAOP(wedge) = 9
0
Slide 58
CVP
 CVP of SVC at level of right atrium
 pre-load “assessment”
 normal 4 - 10 mm Hg

Slide 59
PAOP (wedge)
 End expiration
 Wedge adjustment with positive pressure
– Measured PAOP - ½ PEEP = “real PAOP”

Slide 60
Vascular Resistance
PULMONARY (PVR)
SYSTEMIC (SVR)
MAP - CVP
x 80 MPAP - PAOP
C0 x 80
CO
 SVR = vasoconstriction
 SVR = vasodilation
PVR = constriction
PE, hypoxia
Vascular resistance = change in pressure/blood flow

Slide 61
Cardiac Cycle
PVR
MPAP pulmonary PCWP
RVSW Right ventricle Left ventricle LVSW
CVP MAP
systemic
SVR

Slide 62
Swan Ganz interpretation
Etiology CO PCWP SVR

cardiogenic decreased increased increased
hypovolemic decreased decreased increased
distributive increased decreased decreased

Slide 63
Too Many Numbers

Slide 64
Definitions
 O2 Delivery - volume of gaseous O2

delivered to the LV/min.
 O2 Consumption - volume of gaseous O2
which is actually used by the tissue/min.
consumption > demand = anaerobic metabolism

Slide 65
Mixed venous oxygen saturation
 Reflects difference between oxygen delivery

and consumption
 Normal – 65-75%
 Measurement taken from the distal port of a
PA catheter

Slide 66
SvO2: Low Values (< 60%)
  CO/CI
 SV/SVI
  Hgb
  SaO2
  O2 consumption

Slide 67
SvO2: High Values (> 75%)

 Sepsis
 AV shunts/fistulae

Slide 68
Oxycalculations

Slide 69
Break Time…

Slide 70
Goals of Shock
Resuscitation
 Restore blood pressure
 Normalize systemic perfusion
 Preserve organ function

Slide 71
Parameters of Adequate
Resuscitation
Urine output (0.5 - 1.0 ml/kg/hr)
acceptable renal perfusion
Reversal of lactic acidosis (nl. pH)
improved perfusion
Normal mental status
adequate cerebral perfusion

Slide 72
SHOCK: an EMERGENCY !!!
Goal RAPIDLY RESTORE TISSUE PERFUSION
• Recognize it !!!
•Immediate stabilization: ABC

……. SHOTGUN approach
Normalization of BP, pulse, UOP
Hemodynamic parameters
Restoration of aerobic
metabolism, elimination of tissue
acidosis, repayment of O2 debt
•Treat the cause
Slide 73
“Shock is a symptom of its

cause.”
-fccs course
73
Slide 74
In general, treat the

cause...

Management
Slide 75
 ABC’s
– Maintain airway
– Decrease work of breathing & Optimize 02
– Circulation & Control Hemorrhage includes:
• Direct pressure
• Pressure points
• Fluids & Drugs
 Must address and treat:

– PRELOAD
– AFTERLOAD
– PUMP
Re-assess every 5-15 minutes

(the sicker the patient, the shorter the interval
Slide 76
Management priorities
in hypoperfused states
Priority # Physiology to Intervention Parameter to target PAC Avoid
improve targets
1 Volume Fluids CVP 10-15 DO2 Low Sao2
See CXR
2 Pressure Vasopressor SBP? 100 or within 20-25 Low SV, DO2
torr High HR,
MBP ? 80 of patient's Nl Resistances
3 Flow Inotrope Signs of perfusion DO2 Low BP, SV,

Resistances
BP potency: Dopamine...NE…Vasopressin/Phenylephrine
When in doubt, try a little more volume

Slide 77
Hypovolemia

Slide 78
Time
Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV)
allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal

Slide 79
Classes of Hypovolemic Shock

Slide 80
Clinical Signs of Acute

Hemorrhagic Shock
% Blood loss Clinical Signs

< 15 Slightly increased heart rate
15-30 Increased HR, increased DBP (narrow pp),

prolonged capillary refill, flat neck veins
30-50 Above findings plus: hypotension,

confusion, acidosis, decreased urine output
> 50 Refractory hypotension, refractory

acidosis, death
Slide 81
Hypovolemic Shock
 Causes  Signs
– hemorrhage   cardiac output
– vomiting   PAOP/CVP
– diarrhea   SVR
– dehydration
– third-space loss
– burns

Slide 82
Treatment - Hypovolemic
 Reverse hypovolemia & hemorrhage control
 Crystalloid vs. Colloid
– 1 L crystalloid  250 ml colloid
• Watch for fluid overload by reassessing lung sounds
• 3:1 Rule (3cc crystalloid for 1cc bld loss)
• Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused
• Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus
– Colloids: (ex: albumin)
• Will increase osmotic pressure, watch for pulm edema
• Remain in vascular space longer (several hrs)
• NOT increase survival
 prbc sooner than later
– 500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4%
– Increases oxygen carrying capacity
– Used with acute hemorrhaging (mntn Hct 24% and Hgb 8g /dL)
NOT FOR VOLUME

– FFP for coagulopathy (all factors)
– Factor vii
– PLT for thrombocytopenia
 Pressors?

Slide 83
Resuscitation
 Transport times < 15 minutes showed
pre-hospital fluids were ineffective,
however, if transport time > 100 minutes
fluid was beneficial.
 Penetrating torso trauma benefited from

limited resuscitation prior to bleeding
control. Not applicable to BLUNT
victims.

Slide 84
Role of PASG?
 Higher mortality rate in penetrating thoracic, cardiac
trauma
 Role undefined in rural, blunt trauma
 Splinting role

Slide 85
Cardiogenic Shock
 Mech
– defect in cardiac function (lost > 40% Fxn)
 Signs
  cardiac output
  PAOP/CVP
  SVR
  left ventricular stroke work (LVSW)

Slide 86
Cardiogenic Shock
 Myocardial failure (MI)

 Severe Arrhythmia
 Severe Valvular dysfunction
 Reduction in cardiac output:

– >Decreased oxygen delivery

Slide 87
Symptoms of Cardiogenic
Shock
 Skin: progressive peripheral vasoconstriction
results in cool, moist, pale skin with mottling
 CHF Sx
– JVD, HJR, APE, pedal edema
 Heart:
– Sounds: d/t enlargement and congestion you can
hear murmurs or S3 or S4
– Pulse: rapid rate and thready/weak pulse
 BP: decreased BP and MAP
 UO: decreases early d/t decreased renal
perfusion

Slide 88
Cardiogenic Shock
 Assess for:
– Signs of heart failure
– Signs of tamponade
– Cardiac dysrrhythmia
– Myocardial infarction
– Tachycardia
– Muffled heart sounds or third heart sound
– Engorged neck veins with hypotension
– Dyspnea
– Edema in feet and ankles

Slide 89
Coronary Perfusion
Pressure
Coronary PP = DBP - PAOP
coronary perfusion =  P across coronary a.
GOAL - Coronary PP > 50 mm Hg

Treatment of Cardiogenic
Slide 90
Shock
 Increase oxygen supply to the heart
– Decrease O2 consumption (pain meds/sedation)
– Increase O2 delivery (Mech vent, reperfusion of the
coronary arteries)
 Maximize the cardiac output
– Mntn normal rhythm (dysrhythmics, pacing,
cardioversion)
– Diastolic Vasopressors (dopamine, epi, norepi,
vasopressin)
– Improve myocardial contractility--Inotropes
• dobut and amrinone
 Decrease the afterload (workload of the LV)
– IABP
– LVAD

Slide 91
The Failing Heart

 Improve myocardial function, C.I. < 3.5 is a risk
factor, 2.5 may be sufficient.
 Fluids first, then cautious pressors
 Remember aortic DIASTOLIC pressures drives

coronary perfusion (DBP-PAOP = Coronary
Perfusion Pressure)
 If inotropes and vasopressors fail, intra-aortic

balloon pump & LV assist devices

Slide 92
Intra-Aortic Balloon Pump

Slide 93
Distributive Shock
 Types
– Sepsis
– Anaphylactic
– Acute adrenal insufficiency
– Neurogenic
 Signs
– ± cardiac output
  PAOP
 SVR

Slide 94
Anaphylaxis

Slide 95
Anaphylactic Shock
 Rapid onset
 Diffuse vasodilation mechanism from
histamine & bradykinin
 Edema from increased capillary permeability
 Bronchoconstriction

Slide 96
Symptoms
Onset within seconds and
progression to death in minutes
 Cutaneous manifestations
– urticaria, erythema, pruritis, angioedema
 Respiratory compromise
– stridor, wheezing, bronchorrhea, resp.
distress
 Circulatory collapse
– tachycardia, vasodilation, hypotension
 CNS
– apprehension->ams->coma

Slide 97
Diagnosis
 History and physical alone make the

diagnosis
 Lab values serve no role
– Histamine levels are elevated for about 30 min,
tryptase for several hours.

Slide 98
Treatment
 Remove the antigen
 ABC’s
 IV Fluids, O2, cardiac monitor, pulse ox
 First line Rx:
– Epinephrine
– For severe bronchospasm, laryngeal edema, signs
of upper airway obstruction, respiratory arrest or
shock: IV epi
• 100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in
10 mL of NS, give over 5-10 min)
– If less severe, can give 0.3-0.5 mL 1:1000 SC

Slide 99
Treatment
 2nd line:
– H1 blocker: Diphenhydramine 25-50 mg IV
– H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)
– Steroids (Methylprednisolone 125 mg IV or Prednisone
40-60 mg po)
– Albuterol
– For patients taking Beta-blockers with refractory
hypotension, think about glucagon

Slide 100
Septic Shock

Slide 101
SEPSIS
 Systemic Inflammatory Response (SIRS)

manifested by two or > of following:
– Temp > 38 or < 36 centigrade
– HR > 90
– RR > 20 or PaCO2 < 32
– WBC > 12,000/cu mm or > 10% Bands (immature
wbc)

Slide 102
Risk factors of Sepsis
 Extreme age: <1 and >65 years

 Surgical / invasive procedures
 Malnutrition
 Chronic illness
– DM, CRF, Hepatitis
 Compromised immune status
– AIDS, immunosuppressives, EtOH, malignancies
 Drug resistant organisms

Slide 103
What is Sepsis?
 SIRS  Sepsis  Severe Sepsis  Septic
Shock
 Sepsis is the combination of the Systemic
Inflammatory Response Syndrome (SIRS) & a
confirmed or presumed infectious etiology.
 Severe Sepsis: SIRS criteria, source of infection and
infection-induced organ dysfunction or hypoperfusion
abnormalities (sepsis + lactic
acidosis/oliguria/AMS/etc.)
 Septic Shock: SIRS criteria, source of infection, and
hypotension not reversed with fluid resuscitation and
associated with organ dysfunction or hypoperfusion
abnormalities
Slide 104
Septic Shock
 Bacterial, viral, fungal infection
 “Warm shock” is early stage

– Fever, tachycardia, tachypnoea,
leucocytosis,
– inadequate oxygen extraction (High
SvO2, Metabolic acidosis) in infected
tissues
 “Cold shock” is late stage

Septic/Inflammatory Shock
Slide 105
Signs: Early– warm w/ vasodilation, often adequate urine

output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Early—hyperglycemia, respiratory

alkylosis, hemoconcentration,
WBC typically normal or low.
Late – Leukocytosis, lactic acidosis
Very Late– Disseminated Intravascular
Coagulation & Multi-Organ
System Failure.

Slide 106
Septic Shock TX
 Prompt volume replacement - fill the tank
 Early antibiotic administration - treat the cause
 If MAP < 60
– Dopamine = 2 - 3 g/kg/min
– Norepinephrine = titrate (1-100 g/min)

Neurogenic shock
Slide 107

Slide 108
Neurogenic Shock
 Essential derangement:
paralysis of the
sympathetic chain which
controls vascular tone from
injury to thoracic or
cervical level spinal cord
injury.
 Produces decreased SVR
from loss of vascular tone
and bradycardia from
unopposed
parasympathetic input to
SA node.
Slide 109
Neurogenic (Vasogenic) Shock
 Caused by:
– Spinal cord injury loss of SNS
 Massive venous pooling & arteriolar dilatation
 Signs and Symptoms:
– Hypotension without tachycardia
– Warm pink skin from cutaneous vasodilation
– Low BP w/ minimal response to fluids
– Accompanying Neurologic deficit
 Spinal shock is not Neurogenic shock

– Spinal Shock: the temporary loss of spinal reflex activity
that occurs below a total or near total spinal cord injury

Slide 110
Treatment of Neurogenic
Shock
 Increase vascular tone and improve CO
– Increase preload with fluids
• CVP
• PAWP
– Increase vascular tone
• Vasopressors
– Maintain heart rate
• Treat bradycardia if symptomatic
– Maintain adequate oxygenation
• Watch with SCI because of the disruption of O 2 to the medulla
– Initiate therapy to prevent DVT
• Sluggish venous flow will increase risk factors
– Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4
mg/kg/hr x 23 hours)
• There are contradicting studies, all of which have flaw
 The symptoms of neurogenic shock typically last 1-3 weeks
Slide 111
Obstructive Shock
 Causes
– Cardiac Tamponade
– Tension Pneumothorax
– Massive Pulmonary Embolus
 Signs
  cardiac output
  PAOP/CVP
  SVR
 Treatment
Needle decompression
Embolectomy / TPA

Slide 112
Adrenal Crisis
Distributive Shock
 Causes
– Autoimmune adrenalitis
– Adrenal apoplexy = B hemorrhage or infarct
 This is suspected when patient is non-

responsive to fluids, vasopressors and
antibiotics.
 Electrolytes may reveal hypoNa+ & hyperK+
 Steroids may be lifesaving in patient who is
unresponsive to fluids-inotropic-vasopressor
(hydrocortisone 100mg IV)
Slide 113
Vasopressor Agents?
 Augments contractility, after preload established,
thus improving cardiac output.
 Risk tachycardia and increased myocardial oxygen

consumption if used too soon
 Rationale, increased C.I. improves global perfusion

Slide 114
Vasopressors & Inotropic

Agents
 Norepinephrine
 Dopamine
 Epinephrine
 Dobutamine
 Amrinone

Slide 115
Dopamine
 Low dose (0.5 - 2 g/kg/min) = dopaminergic
 Moderate dose (3-10 g/kg/min) = -effects
 High dose (> 10 g/kg/min) = -effects
 SIDE EFFECTS
– tachycardia
– > 20 g/kg/min  to norepinephrine

Slide 116
Dobutamine
 -agonist
 5 - 20 g/kg/min
 potent inotrope, variable chronotrope
 caution in hypotension (inadequate volume)

may precipitate tachycardia or worsen
hypotension

Slide 117
Norepinephrine
 Potent -adrenergic vasopressor
 Some -adrenergic, inotropic, chronotropic
 Dose 1 - 100 g/min
 Unproven effect with low-dose dopamine to protect

renal and mesenteric flow.

Slide 118
Epinephrine
 - and -adrenergic effects
 potent inotrope and chronotrope
 dose 1 - 10 g/min
 increases myocardial oxygen consumption

particularly in coronary heart disease

Slide 119
Amrinone
 Phosphodiesterase inhibitor, positive inotropic
and vasodilatory effects
 increased cardiac stroke output without an

increase in cardiac stroke work
 most often added with dobutamine as a second

agent
 load dose = 0.75 -1.5 mg/kg  5 - 10 g/kg/min

drip
 main side-effect - thrombocytopenia

Slide 120
vasopressin
 V1 vascular smooth muscle receptor

vasoconstriction
 0.01-0.04 units/min
 Risk: coronary, mesenteric ischemia,
hyponatremia, skin necrosis

Slide 121
Calcium Sensitisation by
Levosimendan
 Enhanced
Enhanced contractility
contractility of
of myocardial
myocardial cell
cell
by amplifying
by amplifying trigger
trigger for
for contraction
contraction with
with
no
no change in total
change in total intracellular
intracellular Ca
Ca2+
2+
 Clinical
Clinical trials
trials status

Slide 122
Endpoints?
 ACS / ATLS - restoration of vital signs and

evidence of end-organ perfusion
 Swan-guided resuscitation
– C.I.  4.5, DO2I  670, VO2I  166
 Lactic Acid clearance
 Gastric pH

Don’t forget...
Slide 123
Shock: “rude unhinging of the

machinery of life.”
-Samuel D. Gross, 1872
123
Slide 124
??????????? For the human

speaker

Shock VT

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Slide 1

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Cell function ceases & cells swell

membranes becomes more permeable

electrolytes & fluids seep in & out of cell

Cells Die in Many Organs Death

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General Symptoms Specific Symptoms

 Anxious  Fevers / Rigors (sepsis)

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Early Signs of Shock in

 WARM EARLY STAGE / PRESHOCK

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Signs of Late Shock

COLD LATE STAGE

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End Stage Clinical effects

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Multiple Organ Dysfunction Syndrome

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Acute congestion of liver due to shock

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Acute tubular necrosis of the kidney due to shock

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Intestinal mucosal hemorrhages due to shock

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Adrenal gland hemorrhage due to shock

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 Patient presentation can be variable secondary

 Exam should be tailored to be performed

Components (fluids, pump,

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Adequate circulating blood

An Approach to Shock – Know

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If the blood pressure is low, then either the:

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There are only a few causes of low SVR.

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How do you assess SVR?

Low SVR has the features:

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What if the SVR is high?

Cause of shock (low BP) is then:

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What are factors of CO?

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• Heart Rate problems are easy to diagnose

• Rate: bradycardia versus tachycardia

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Most difficult to diagnose

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Stroke Volume depends on

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Perfusion (blood pressure) depends on:

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Stroke Volume Preload

Cardiac Output Afterload

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 Essential to understanding their disease