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Disampaikan oleh :
dr. I G A G Utara Hartawan, SpAn MARS
Approach to the hypotensive patient


Specific treatments
Definition of Shock
Inadequate oxygen delivery to meet
metabolic demands
Results in global tissue hypoperfusion and
metabolic acidosis
Shock can occur with a normal blood
pressure and hypotension can occur
without shock
Understanding Shock
Inadequate systemic oxygen delivery
activates autonomic responses to maintain
systemic oxygen delivery
Sympathetic nervous system
NE, epinephrine, dopamine, and cortisol release
Causes vasoconstriction, increase in HR, and increase of cardiac
contractility (cardiac output)
Renin-angiotensin axis
Water and sodium conservation and vasoconstriction
Increase in blood volume and blood pressure
Understanding Shock
Cellular responses to decreased systemic oxygen
ATP depletion ion pump dysfunction
Cellular edema
Hydrolysis of cellular membranes and cellular
Goal is to maintain cerebral and cardiac perfusion
Vasoconstriction of splanchnic, musculoskeletal,
and renal blood flow
Leads to systemic metabolic lactic acidosis that
overcomes the bodys compensatory mechanisms
Global Tissue Hypoxia
Endothelial inflammation and disruption
Inability of O2 delivery to meet demand
Lactic acidosis
Cardiovascular insufficiency
Increased metabolic demands
Multiorgan Dysfunction
Syndrome (MODS)
Progression of physiologic effects as
shock ensues
Cardiac depression
Respiratory distress
Renal failure
Result is end organ failure
Approach to the Patient in Shock
Cardiorespiratory monitor
Pulse oximetry
Supplemental oxygen
IV access
ABG, labs
Foley catheter
Vital signs including rectal temperature
Physical exam (VS, mental status, skin color,
temperature, pulses, etc)
Infectious source
Coagulation studies
Further Evaluation
CT of head/sinuses
Lumbar puncture
Wound cultures
Acute abdominal series
Abdominal/pelvic CT or US
Cortisol level
Fibrinogen, FDPs, D-dimer
Approach to the Patient in Shock
History Physical examination
Recent illness Vital Signs
Fever CNS mental status
Chest pain, SOB Skin color, temp, rashes,
Abdominal pain sores
Comorbidities CV JVD, heart sounds
Resp lung sounds, RR,
oxygen sat, ABG
Toxins/Ingestions GI abd pain, rigidity,
Recent hospitalization or guarding, rebound
surgery Renal urine output
Baseline mental status
Is This Patient in Shock?
Patient looks ill
Altered mental status
Skin cool and mottled or
hot and flushed
Weak or absent
peripheral pulses Yes!
SBP <110 These are all signs and
Tachycardia symptoms of shock
Do you remember how to
quickly estimate blood pressure 60

by pulse?

If you palpate a pulse, 70

you know SBP is at 80
least this number

Goals of Treatment

control work of Breathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation
Determine need for intubation but remember:
intubation can worsen hypotension
Sedatives can lower blood pressure
Positive pressure ventilation decreases preload
May need volume resuscitation prior to
intubation to avoid hemodynamic collapse
Control Work of Breathing
Respiratory muscles consume a significant
amount of oxygen
Tachypnea can contribute to lactic acidosis
Mechanical ventilation and sedation
decrease WOB and improves survival
Optimizing Circulation
Isotonic crystalloids
Titrated to:
CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr (30 ml/hr)
Improving heart rate
May require 4-6 L of fluids
No outcome benefit from colloids
Maintaining Oxygen Delivery
Decrease oxygen demands
Provide analgesia and anxiolytics to relax muscles
and avoid shivering
Maintain arterial oxygen saturation/content
Give supplemental oxygen
Maintain Hemoglobin > 10 g/dL
Serial lactate levels or central venous oxygen
saturations to assess tissue oxygen extraction
End Points of Resuscitation
Goal of resuscitation is to maximize survival
and minimize morbidity
Use objective hemodynamic and physiologic
values to guide therapy
Goal directed approach
Urine output > 0.5 mL/kg/hr
CVP 8-12 mmHg
MAP 65 to 90 mmHg
Central venous oxygen concentration > 70%
Persistent Hypotension
Inadequate volume resuscitation
Cardiac tamponade
Hidden bleeding
Adrenal insufficiency
Medication allergy
Practically Speaking.
Keep one eye on these patients
Frequent vitals signs:
Monitor success of therapies
Watch for decompensated shock
Let your nurses know that these patients
are sick!
Types of Shock
What Type of Shock is This?
68 yo M with hx of MVC and DM Types of Shock
presents to the ER with abrupt
onset of diffuse abdominal pain Hypovolemic
with radiation to his low back. The Septic
pt is hypotensive, tachycardic,
afebrile, with cool but dry skin Cardiogenic
Hypovolemic Shock Obstructive
Hypovolemic Shock
Hypovolemic Shock
Bowel obstruction, pancreatitis
Neglect, environmental (dehydration)
GI bleed
Massive hemoptysis
AAA rupture
Ectopic pregnancy, post-partum bleeding
Hypovolemic Shock
Establish 2 large bore IVs or a central line
Normal Saline or Lactate Ringers
Up to 3 liters
O negative or cross matched
Control any bleeding
Arrange definitive treatment
Evaluation of Hypovolemic Shock
CBC As indicated
ABG/lactate CXR
Pelvic x-ray
Abd/pelvis CT
BUN, Creatinine Chest CT
Coagulation studies GI endoscopy
Type and cross-match Bronchoscopy
Vascular radiology
Degree of Bleeding

Parameter I II III IV

Blood loss (ml) <750 7501500 15002000 >2000

Blood loss (%) <15% 1530% 3040% >40%

Pulse rate (beats/min) <100 >100 >120 >140

Blood pressure Normal Decreased Decreased Decreased

Respiratory rate (bpm) 1420 2030 3040 >35

Urine output (ml/hour) >30 2030 515 Negligible

CNS symptoms Normal Anxious Confused Lethargic

Infusion Rates
Access Gravity Pressure

18 g peripheral IV 50 mL/min 150 mL/min

16 g peripheral IV 100 mL/min 225 mL/min
14 g peripheral IV 150 mL/min 275 mL/min
What Type of Shock is This?
An 81 yo F resident of a nursing Types of Shock
home presents to the ED with
altered mental status. She is Hypovolemic
febrile to 39.4, hypotensive with a Septic
widened pulse pressure,
tachycardic, with warm extremities Cardiogenic
Septic Obstructive
Two or more of SIRS criteria
Temp > 38 or < 36 C
HR > 90
RR > 20
WBC > 12,000 or < 4,000
Plus the presumed existence of infection
Blood pressure can be normal!
Septic Shock
Sepsis (remember definition?)
Plus refractory hypotension
After bolus of 20-40 mL/Kg patient still has
one of the following:
SBP < 90 mm Hg
MAP < 65 mm Hg
Decrease of 40 mm Hg from baseline
Pathogenesis of Sepsis

Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.
Septic Shock
Clinical signs:
Hyperthermia or hypothermia
Wide pulse pressure
Low blood pressure (SBP<90)
Mental status changes
Beware of compensated shock!
Blood pressure may be normal
Ancillary Studies
Cardiac monitor
Pulse oximetry
CBC, Chem , coags, LFTs, lipase, UA
ABG with lactate
Blood culture, urine culture
Foley catheter (why do you need this?)
Treatment of Septic Shock
2 large bore IVs
NS IVF bolus- 1-2 L wide open (if no
Supplemental oxygen
Empiric antibiotics, based on suspected
source, as soon as possible
Treatment of Sepsis
Antibiotics- Survival correlates with how quickly the
correct drug was given
Cover gram positive and gram negative bacteria
Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or
Imipenem 1 gram IV
Add additional coverage as indicated
Pseudomonas- Gentamicin or Cefepime
MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infections- Clindamycin or
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic Cefepime or Imipenem
Persistent Hypotension
If no response after 2-3 L IVF, start a
vasopressor (norepinephrine, dopamine,
etc) and titrate to effect
Goal: MAP > 60
Consider adrenal insufficiency:
hydrocortisone 100 mg IV
Early Goal Directed Therapy

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.
Treatment Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.
What Type of Shock is This?
A 55 yo M with hx of AMI, DM Types of Shock
presents with crushing
substernal CP, diaphoresis, Hypovolemic
hypotension, tachycardia and Septic
cool, clammy extremities
Cardiogenic Obstructive
Cardiogenic Shock
Defined as: Signs:
SBP < 90 mmHg Cool, mottled skin
CI < 2.2 L/m/m2 Tachypnea
PCWP > 18 mmHg Hypotension
Altered mental status
Narrowed pulse pressure
Rales, murmur
What are some causes of cardiogenic shock?

Myocardial contusion
Aortic or mitral stenosis
Acute aortic insufficiency
Pathophysiology of Cardiogenic Shock

Often after ischemia, loss of LV function

Lose 40% of LV clinical shock ensues
CO reduction = lactic acidosis, hypoxia
Stroke volume is reduced
Tachycardia develops as compensation
Ischemia and infarction worsens
Ancillary Tests
CBC, Chem 10, cardiac enzymes,
coagulation studies
Treatment of Cardiogenic Shock
Goals- Airway stability and improving
myocardial pump function
Cardiac monitor, pulse oximetry
Supplemental oxygen, IV access
Intubation will decrease preload and result
in hypotension
Be prepared to give fluid bolus
Treatment of Cardiogenic Shock
Aspirin, beta blocker, morphine, heparin
If no pulmonary edema, IV fluid challenge
If pulmonary edema
Dopamine will HR and thus cardiac work
Dobutamine May drop blood pressure
Combination therapy may be more effective
PCI or thrombolytics
RV infarct
Fluids and Dobutamine (no NTG)
Acute mitral regurgitation or VSD
Pressors (Dobutamine and Nitroprusside)
What Type of Shock is This?
A 34 yo F presents to the ER after dining
at a restaurant where shortly after eating
Types of Shock
the first few bites of her meal, became Hypovolemic
anxious, diaphoretic, began wheezing,
noted diffuse pruritic rash, nausea, and a Septic
sensation of her throat closing off. She
is currently hypotensive, tachycardic and Cardiogenic
ill appearing. Anaphylactic
Anaphalactic Shock
Anaphylactic Shock
Anaphylaxis a severe systemic
hypersensitivity reaction characterized by
multisystem involvement
IgE mediated
Anaphylactoid reaction clinically
indistinguishable from anaphylaxis, do not
require a sensitizing exposure
Not IgE mediated
Anaphylactic Shock
What are some symptoms of anaphylaxis?

First- Pruritus, flushing, urticaria appear

Next- Throat fullness, anxiety, chest tightness, shortness of

breath and lightheadedness

Finally- Altered mental status, respiratory distress and circulatory

Anaphylactic Shock
Risk factors for fatal anaphylaxis
Poorly controlled asthma
Previous anaphylaxis
Reoccurrence rates
40-60% for insect stings
20-40% for radiocontrast agents
10-20% for penicillin
Most common causes
Anaphylactic Shock
Mild, localized urticaria can progress to full anaphylaxis
Symptoms usually begin within 60 minutes of exposure
Faster the onset of symptoms = more severe reaction
Biphasic phenomenon occurs in up to 20% of patients
Symptoms return 3-4 hours after initial reaction has cleared
A lump in my throat and hoarseness heralds life-
threatening laryngeal edema
Anaphylactic Shock- Diagnosis
Clinical diagnosis
Defined by airway compromise, hypotension, or
involvement of cutaneous, respiratory, or GI
Look for exposure to drug, food, or insect
Labs have no role
Anaphylactic Shock- Treatment
Angioedema and respiratory compromise require immediate
IV, cardiac monitor, pulse oximetry
IVFs, oxygen
Second line
H1 and H2 blockers
Anaphylactic Shock- Treatment
0.3 mg IM of 1:1000 (epi-pen)
Repeat every 5-10 min as needed
Caution with patients taking beta blockers- can cause severe
hypertension due to unopposed alpha stimulation
For CV collapse, 1 mg IV of 1:10,000
If refractory, start IV drip
Anaphylactic Shock - Treatment
Methylprednisolone 125 mg IV
Prednisone 60 mg PO
H1 blocker- Diphenhydramine 25-50 mg IV
H2 blocker- Ranitidine 50 mg IV
Albuterol nebulizer
Atrovent nebulizer
Magnesium sulfate 2 g IV over 20 minutes
For patients taking beta blockers and with refractory hypotension
1 mg IV q5 minutes until hypotension resolves
Anaphylactic Shock - Disposition
All patients who receive epinephrine
should be observed for 4-6 hours
If symptom free, discharge home
If on beta blockers or h/o severe
reaction in past, consider admission
What Type of Shock is This?
A 41 yo M presents to the ER Types of Shock
after an MVC complaining of
decreased sensation below his Hypovolemic
waist and is now hypotensive, Septic
bradycardic, with warm
extremities Cardiogenic
Neurogenic Obstructive
Neurogenic Shock
Neurogenic Shock
Occurs after acute spinal cord injury
Sympathetic outflow is disrupted leaving
unopposed vagal tone
Results in hypotension and bradycardia
Neurogenic Shock
Loss of sympathetic tone results in warm
and dry skin
Shock usually lasts from 1 to 3 weeks
Any injury above T1 can disrupt the
entire sympathetic system
Higher injuries = worse paralysis
Neurogenic Shock- Treatment
Remember c-spine precautions
Fluid resuscitation
Keep MAP at 85-90 mm Hg for first 7 days
Thought to minimize secondary cord injury
If crystalloid is insufficient use vasopressors
Search for other causes of hypotension
For bradycardia
Neurogenic Shock- Treatment
Used only for blunt spinal cord injury
High dose therapy for 23 hours
Must be started within 8 hours
Controversial- Risk for infection, GI bleed
What Type of Shock is This?
A 24 yo M presents to the ED Types of Shock
after an MVC c/o chest pain and
difficulty breathing. On PE, you Hypovolemic
note the pt to be tachycardic, Septic
hypotensive, hypoxic, and with
decreased breath sounds on left Cardiogenic
Obstructive Obstructive
Obstructive Shock
Obstructive Shock
Tension pneumothorax
Air trapped in pleural space with 1 way valve,
air/pressure builds up
Mediastinum shifted impeding venous return
Chest pain, SOB, decreased breath sounds
No tests needed!
Rx: Needle decompression, chest tube
Obstructive Shock
Cardiac tamponade
Blood in pericardial sac prevents venous
return to and contraction of heart
Related to trauma, pericarditis, MI
Becks triad: hypotension, muffled heart
sounds, JVD
Diagnosis: large heart CXR, echo
Rx: Pericardiocentisis
Obstructive Shock
Pulmonary embolism
Virscow triad: hypercoaguable, venous injury,
Signs: Tachypnea, tachycardia, hypoxia
Low risk: D-dimer
Higher risk: CT chest or VQ scan
Rx: Heparin, consider thrombolytics
Obstructive Shock
Aortic stenosis
Resistance to systolic ejection causes
decreased cardiac function
Chest pain with syncope
Systolic ejection murmur
Diagnosed with echo
Vasodilators (NTG) will drop pressure!
Rx: Valve surgery
Type of Insult Physio Compen Compensation Compensation

Shock logic sation Heart Rate Contractility

Cardiogenic Heart fails to CO BaroRc

pump blood SVR
Obstructive Heart pumps CO BaroRc
well, but the SVR
outflow is
Hemorrhagic Heart pumps CO BaroRc
well, but not SVR
volume to
Distributive Heart pumps SVR CO
well, but
there is No Change - No Change -
peripheral in neurogenic in neurogenic
vasodilation shock shock
Usually the first therapeutic strategy,
particularly hypovolemic or distributive
Not all patients will respond to fluid
loading with a significant increase in
cardiac output
If the heart is working on the terminal
(flat) portion of the FrankStarling curve,
increased preload may not result in a
significant increase in SV
FrankStarling curve
1. Crystalloids
Comprise electrolytes (with or without dextrose)
and water
Cross semipermeable membranes easily - rapidly
distributed through the intravascular and
extravascular spaces (1L = 20% in vascular space)
Time for fluid equilibration across the body
compartments depends on:
osmolality of the fluid
solute clearance
integrity of the vascular endothelium
Example: Isotonic Saline (NaCl 0,9%/ NS), Ringer
Lactat (RL), Ringer Asetat, Ringer Fundin
Problems: NS can produce hyperchloremic acidosis,
RL can inactive the anticoagulant and promote the
formation clots in donor blood
Isotonic saline
Isotonic 0,9%)
saline has a higher sodium
concentration (154vs 140 mEq/L), much
higher chloride concentration (154 vs 103
mEq/L), a much lower plasma (5,7 vs 7,4),
and slightly higher osmolality (308vs 290
mOsm/L ) than plasma
Disadvantage isotonic saline : can
produce hyperchloremic acidosis (by the
high chloride concentration). Saline
induce acidosis after large volume
isotonic saline infused and it is usually
has no adverse consequences.
Lactate Ringers
Solution/ RL/Hartmanns
Lactate ringers solution / Hartmanns
solution contains : Na 130 mEq/L, Cl 109
mEq/L, lactate 28 mEq/L, K 4 mEq/L, and
Ca 3 mEq/L. the addition of lactate similary
requires a reduction in chloride
Disadvantage : ringers solution can bind
to certain drug an reduce their effectivness
(aminocaproic acid, amphotericin,
ampicillin, thiopental). RS also bind to
citrated anticoagulant in blood product and
Lobo, D.N., Lewington, A.J.P., Allison, S.P. 2013. Basic Concepts of Fluid and Electrolyte Therapy.
Germany: Bibliomed
2. Colloids
Containing large molecules that do not pass
through a semipermeable membrane
Remain in the circulation for longer, have a
smaller volume of distribution - more effective
at increasing intravascular volume than the
same volume of crystalloid (1 L = 80% still in
Naturally occurring colloids: human albumin,
plasma protein fraction, fresh frozen plasma,
and immunoglobulin
Semisynthetic: gelatins, starches and dextran
Albumin 4% (40g/L; 260 mOsm/L) is iso-oncotic
and infusion rapidly increases circulating
volume (1L=70% still in vascular space). The
effect can be lost after just 12 hours.
Provided in glass bottles that limit the speed of
infusion and the increment in plasma volume
lasts only a few hours
Concentrated (20%) albumin is available in
smaller volumes (100 mL), increases
circulating fluid volume by drawing fluid from
the interstitial. This process takes time and
concentrated albumin is not a useful
resuscitation fluid
Contain a carbohydrate polymer (starch) as their
oncotic molecule and differ according to the type
and molecular size of the starch used (high starch
450.000 D, medium starch 200.000 D, low starch
70.000 D)
Degradation by serum amylase, and cleared by the
Duration of oncotic effect is related to the size of the
starch molecule and clearance rates. The effect
usually is lost by 24 hours.
As the plasma expander, 6% hetastarch is
equivalent to 5% albumin
Use in patients with septic shock has been
associated with increased risk of death, renal
impairment and bleeding risk (by inhibitions of
factor VIII and von Willebrand factor and impaired
platelet adhesiveness; in high MW and in large
The use of blood is essentially limited to
shock from acute blood loss or for
correcting anemia that may be
contributing to impaired O2 delivery
(improve Oksygen carrying capacity)
Lobo, D.N., Lewington, A.J.P., Allison, S.P. 2013. Basic Concepts of Fluid and Electrolyte Therapy.
Germany: Bibliomed
Lobo, D.N., Lewington, A.J.P., Allison, S.P. 2013. Basic Concepts of Fluid and Electrolyte Therapy.
Germany: Bibliomed
Crystalloid vs Colloid ??
Which is the better for resuscitation fluid? STILL
Cheap, easy to administer, and replete intravascular
and extravascular fluid
Problem: generally requires 3-4 times the volume
needed when using colloids, tendency to interstitial
edema, and electrolyte alteration
Restore circulating volume more quickly, persist for
longer and seem less likely to lead to interstitial edema
Problem: more expensive, have a greater risk of side
effects and in critically ill patients can accumulate in
the interstitial, contributing to persistent interstitial
dextrose solution
Solutions like 5% dextrose and dextrose
saline are not meant for resuscitation
as parenteral nutrition; not as plasma
expander (less than 10% volume dextrose
remain in the vascular space).
Adverse effect: increase osmolarity,
cellular swelling (D5W), hyperglycemia,
aggravation of ischemic brain injury,
hyperlcatatemia in critical ill patient,
cellular dehydration (D5NS)

cardiac index 3 l/min/m2

systemic oxygen delivery (do2) > 500 ml/m
systemic oxygen uptake (vo2) > 100 ml/m
arterial lactate < 2 mmol/l or base deficit >
The End

Any Questions?