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SHOCK

1
Definition
SHOCK: inadequate
organ perfusion to
meet the tissue’s
oxygenation
demand
shock
 Inadequate tissue perfusion due to one
or more of the following cause
 - Heart-pump failure
 - blood volume decrease
 - Arterial resistance
 - Decrease venous bed capacity
PATHOPHYSIOLOGY OF SHOCK
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


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)
STAGES OF SHOCK
ASSESSMENT OF SHOCK
•Assess LOC- most important indicator of cerebral
perfusion
 •WOF: increasing lethargy
 •Monitor arterial BP; IF (+) Compensation BP is
elevated, decrease in BP may occur in the late stage
 •Narrowing pulse pressure- early in shock
 •Pulse quality is thready
 •Urine output is decreased
 •Capillary refill greater than 2 sec.
 •Skin is pale ashen gray, mottled cool and clammy
 •Excessive thirst if with intact LOC
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
-fccs course

10
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
End Stage Clinical effects

 Cardiovascular  GI
 Myocardial depression  Ischemic bowel

 Vasogenic effects  Hepatic


 Increased LFT’s, liver failure
 Pulmonary
 ARDS  Hematologic
 Neutropenia,
 Renal Thrombocytopenia
 ARF  DIC (Gm- > Gm+)
 CNS
 coma
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.
Components (fluids, pump,
pipes)
 Components:
 Blood (fluid)
 Heart (pump)
 Blood Vessels
(pipes)
Types of Shock
Hypovolemic (fluids)

Cardiogenic (pump)

Redistributive (pipes)
(septic, neurogenic, anaphylactic)
classification
HYPOVOLEMIC
 ▫Significant fluid loss from intravascular space may be
due to hemorrhage, burns, G.I losses, fluid shift
CARDIOGENIC
 ▫Pump failure mechanism most common cause M.I
 ▫Any restriction of cardiac perfusion will lead to
cardiogenic shock
CIRCULATORY/ DISTRIBUTIVE
SEPTIC
 ▫Results from accumulation of toxins and bacteria in the
blood
NEUROGENIC- brain hypoxia in origin
ANAPHYLACTIC- caused by toxic allergic reaction
Shock
 Identifying the patient in shock
 Exam findings
 The “other” look
○ Supreme Court Justice Potter Stewart
 Hemodynamics
○ SBP
○ MAP
○ CVP
○ SvO2
○ PCWP
 Lactate?
Shock
 Cardiogenic
 AMI, Cardiomyopathy,
Valvular Disease,
Myocarditis,
Arrhythmia
 Hypovolemic
 Fluid loss, internal or
external
 Obstructive
 Pneumothorax,
Cardiac Tamponade,
Acute PE
 Distributive
 Sepsis, Anaphylaxis
20
An Approach to Shock – Know this!

BP = SVR x CO
BP = blood pressure
CO = cardiac output (pump & fluids)
SVR = systemic vascular resistance (pipes)
An Approach to Shock
If the blood pressure is low, then either
the:
CO is low
or
SVR is low
or
BOTH
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
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)
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
What are factors of CO?

CO = HR x SV
CO = cardiac output
HR = heart rate
SV = stroke volume
HR Problems
• Heart Rate problems are easy to diagnose

• Rate: bradycardia versus tachycardia


Low SV (stroke volume)

Most difficult to diagnose


and manage
Stroke Volume depends
Preload--is the ventricle full?
on
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?
Perfusion (blood pressure) depends on:

BP = CO x SVR
CO = HR x SV
SV = preload & cardiac contractility-valve
Components of BP summary
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Why Monitor?

 Essential to understanding their disease

 Describe the patient’s physiologic status


 Serial monitoring

 Facilitates diagnosis and treatment of shock


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
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
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
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 in
 Commonly seen with fever, vascular resistance with
anemia, exercise and decreased stroke volume (ie
hyperthyroidism aortic stenosis or decreased
 AR (aortic regurgitation) is also
intravascular volume)
a cause
Invasive Markers
 Global Markers
 Base Deficit
 Lactate

 Regional Markers
 Gastric pH
 Sublingual CO2
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
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
Initial Lactate
Weil and Afifi. (Circulation 1970)
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
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
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.
Sublingual CO2
 Decrease gut perfusion
 Gastric tissue = esophagus = sublingual
tissue
 Non-invasive, hand held monitor
 Rapid measurement
 Sensitive marker of decreased blood
flow
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
Direct arterial pressure
A-line
Pulmonary Artery Catheter
 INDICATIONS
 volume status
 cardiac status

 COMPLICATIONS
 technical
 anatomic
 physiologic
Swan-Ganz Catheter
PLACEMENT
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.
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
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


PA Insertion

20

15

10

5
RA = 5 RV = 22/4 PA 19/10 PAOP(wedge) = 9

0
CVP
 CVP of SVC at level of right atrium
 pre-load “assessment”
 normal 4 - 10 mm Hg
PAOP (wedge)

 End expiration
 Wedge adjustment with positive pressure
 Measured PAOP - ½ PEEP = “real PAOP”
Vascular Resistance
PULMONARY (PVR)
SYSTEMIC (SVR)

MAP - CVP
x 80 MPAP - PAOP x 80
C0
CO

 SVR = vasoconstriction
PVR = constriction
 SVR = vasodilation
PE, hypoxia

Vascular resistance = change in pressure/blood flow


Cardiac Cycle
PVR

MPAP pulmonary PCWP

RVSW Right ventricle Left ventricle LVSW

CVP MAP
systemic

SVR
Swan Ganz interpretation

Etiology CO PCWP SVR


cardiogenic decreased increased increased

hypovolemic decreased decreased increased

distributive increased decreased decreased


Too Many Numbers
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


Mixed venous oxygen saturation
 Reflects difference between oxygen
delivery and consumption
 Normal – 65-75%
 Measurement taken from the distal port
of a PA catheter
SvO2: Low Values (< 60%)

  CO/CI
 SV/SVI

  Hgb

  SaO2

  O2 consumption
SvO2: High Values (> 75%)
 Sepsis

 AV shunts/fistulae
Oxycalculations
Break Time…
Goals of Shock
Resuscitation
 Restore blood pressure

 Normalize systemic perfusion

 Preserve organ function


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
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


-fccs course

71
In general, treat the cause...
Management
 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
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


Hypovolemia
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
Classes of Hypovolemic Shock

Class I Class II Class III Class IV


Blood Loss < 750 750-1500 1500-2000 > 2000

% Blood Vol. < 15% 15 – 30% 30 – 40% > 40%

Pulse < 100 > 100 > 120 > 140

Blood Pressure Normal Normal Decreased Decreased

Pulse Pressure Normal Decreased Decreased Decreased

Resp. Rate 14 – 20 20 – 30 30 – 40 > 40

UOP > 30 20 – 30 5 – 15 negligible

Mental Status sl. Anxious mildly anx confused lethargic

Fluid crystalloid crystalloid blood blood


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
Hypovolemic Shock
 Causes  Signs
 hemorrhage   cardiac output
 vomiting   PAOP/CVP
 diarrhea   SVR
 dehydration
 third-space loss
 burns
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?
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.
Role of PASG?
 Higher mortality rate in penetrating thoracic,
cardiac trauma

 Role undefined in rural, blunt trauma

 Splinting role
Cardiogenic Shock
 Mech
 defect in cardiac function (lost > 40% Fxn)

 Signs
  cardiac output
  PAOP/CVP
  SVR
  left ventricular stroke work (LVSW)
Cardiogenic Shock

 Myocardial failure (MI)


 Severe Arrhythmia
 Severe Valvular dysfunction

 Reduction in cardiac output:


 >Decreased oxygen delivery
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
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
Coronary Perfusion Pressure

Coronary PP = DBP - PAOP

coronary perfusion =  P across coronary a.

GOAL - Coronary PP > 50 mm Hg


Treatment of Cardiogenic 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
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
Intra-Aortic Balloon Pump
Distributive Shock
 Types
 Sepsis
 Anaphylactic
 Acute adrenal insufficiency
 Neurogenic

 Signs
 ± cardiac output
  PAOP
 SVR
Anaphylaxis
Anaphylactic Shock

 Rapid onset
 Diffuse vasodilation mechanism from
histamine & bradykinin
 Edema from increased capillary permeability

 Bronchoconstriction
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
Diagnosis

 Historyand physical alone make the diagnosis


 Lab values serve no role
 Histamine levels are elevated for about 30 min,
tryptase for several hours.
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
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
Septic Shock
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)
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
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
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
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.
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)
Surviving Sepsis
 Initially conceived
following the Rivers
trial and before
ProCESS.
 Quality improvement
in the care of sepsis
 1 hour bundle
○ Measure lactate,
obtain cultures, start
antibiotics, fluid
resuscitate (30cc/kg)
and start
vasopressors
Neurogenic shock
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.
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
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 O2 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
Obstructive Shock
 Causes
 Cardiac Tamponade
 Tension Pneumothorax
 Massive Pulmonary Embolus

 Signs
  cardiac output
  PAOP/CVP
  SVR

 Treatment
Needle decompression
Embolectomy / TPA
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)
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
Vasopressors & Inotropic Agents

 Norepinephrine
 Dopamine

 Epinephrine
 Dobutamine

 Amrinone
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
Dobutamine

 -agonist

 5 - 20 g/kg/min

 potent inotrope, variable chronotrope

 caution in hypotension (inadequate volume)


may precipitate tachycardia or worsen
hypotension
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.
Epinephrine
 - and -adrenergic effects

 potent inotrope and chronotrope

 dose 1 - 10 g/min

 increases myocardial oxygen consumption


particularly in coronary heart disease
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
vasopressin

 V1 vascular smooth muscle receptor


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