ACUTE SEVERE

HYPOTENSION AND SHOCK:

DIAGNOSIS, ASSESSMENT,
TREATMENT

Plan of discussion

Definitions
Initial Assessment
Stages of Shock
Physiologic Determinants of Shock
Types of Shock
Common Features of Shock
Management
Take Home Points

Definitions
Shock is a physiologic state characterized
by systemic reduction in tissue perfusion,
resulting in decreased tissue oxygen
delivery
Poor tissue perfusion

Stages / Spectrum of Shock

Pre-shock: compensated/warm shock
Body is able to compensate for perfusion
Up to ~10% reduction in blood volume
Tachycardia to cardiac output & perfusion

Shock
Compensatory mechanisms overwhelmed
See signs/symptoms of organ dysfunction
~20-25% reduction in blood volume

End-organ dysfunction (multiple system

organ failure/MSOF)
Leading to irreversible organ damage/death

Physiologic Determinants
Global tissue perfusion is determined by:
Cardiac output (CO)
CO = Heart rate (HR) times Stroke Volume (SV)
SV = function of Preload, Afterload, Contractility

Systemic vascular resistance (SVR)

Variables: Length, Inverse of Diameter, Viscosity

Etiology of Shock
Hypovolemic shock
Hemorrhage
Burns
Diarrhea
Vomiting
Peritonitis

Vasogenic
Psychogenic
Anaphylactic
Septic

Cardiogenic
Pulmonary embolism
Cardiomyopathy
Cardiac contusion
Cardiac tamponade
Acute myocardial infarction
Arrhythmia
Acute valvular disease
Aortic dissection

Types of Shock
Hypovolemic shock from preload
Hemorrhage
Fluid Loss (Vomiting, Diarrhea, Burns)

Cardiogenic shock pump failure or SV

MI, arrhythmia, aortic stenosis, mitral regurg
Extracardiac obstructive causes such as PE,
tension pneumothorax, tamponade

Distributive (vasodilatory) shock - SVR

Septic, anaphylactic, and neurogenic shock
Pancreatitis, burns, multi-trauma via activation
of the inflammatory response

Common Features of Shock

Hypotension (not an absolute requirement)
SBP < 90mm Hg, not seen in pre-shock

Cool, clammy skin

Vasoconstrictive mechanisms to redirect blood
from periphery to vital organs
Exception is warm skin in early distrib. shock

Oliguria (kidney perfusion)

Altered mental status (brain perfusion)
Metabolic acidosis

Clinical exam
History to determine etiology
Bleeding (recent surgery, trauma, GI bleed)
Allergies or prior anaphylaxis
Sx consistent with pancreatitis, EtOH history
Hx of CAD, MI, current chest pain/diaphoresis

Physical examination
Mucous membranes, JVD, lung sounds,
cardiac exam, abdomen, rectal (blood), neuro
exam, skin (cold & clammy or warm)

Labs/Tests directed toward suspected dxs

Understanding Shock
Mechanisms of Response to Severe Stress
Distribution of regional blood flow
Oxygen transport mechanisms
Temperature
Anaerobic metabolism
Ventilation
Oxygen extraction
Blood hemoglobin concentration

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
delivery
ATP depletion ion pump dysfunction
Cellular edema
Hydrolysis of cellular membranes and cellular
death
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
Result:
Lactic acidosis
Cardiovascular insufficiency
Increased metabolic demands

Multiorgan Dysfunction
Syndrome (MSOF)
Progression of physiologic effects as
shock ensues:

Cardiac depression
Respiratory distress
Renal failure
Disseminated intravascular coagulation (DIC)

Result is end organ failure

Approach to the Patient in Shock

ABCs

Cardiorespiratory monitor
Pulse oximetry
Supplemental oxygen
IV access
ABG, labs
Foley catheter
Vital signs including temperature

Diagnosis
Physical exam (VS, mental status, skin color,
temperature, pulses, etc)

Infectious source
Labs:

CBC
Chemistries
Lactate
Coagulation studies
Cultures
ABG

Further Evaluation

CT of head/sinuses
Lumbar puncture
Wound cultures
Acute abdominal series
Abdominal/pelvic CT or US
Cortisol level
Fibrinogen, FDPs, D-dimers

Approach to the Patient in Shock

History

Recent illness
Fever
Chest pain
Abdominal pain
Comorbidities
Medications
Toxins/Ingestions
Recent hospitalization or
surgery
Baseline mental status

Physical examination
Vital Signs
Mental status
Skin color, temp,
rashes, sores
CV JVD, heart sounds
Resp lung sounds, RR,
oxygen sat
GI abd pain, rigidity,
guarding, rebound
Renal urine output

Treatment of Shock: Goal

TO RESTORE NORMAL TISSUE PERFUSION
Blood pressure
Pulse
Respirations
Skin Appearance
Sensorium
Urine output (30-50 cc per hour)
Hemoglobin 8-10 gm or Hematocrit 24-30

Management
Correct underlying disorder if possible and
then direct efforts at increasing the blood
pressure to increase oxygen delivery to
the tissues.
Maintain a mean arterial pressure of 60
(1/3 systolic + 2/3 diastolic)
Keep O2 sats >92%, intubate if necessary

Swan-Ganz Catheter

AF/SCUB/2011

Correction of hypotension
Normal Saline should be administered
anytime a patient is hypotensive.
If possible give blood as it replaces
colloid.
Vasopressors
Inotropic agents for cardiogenic shock
Intra-aortic Balloon Pump for cardiogenic

Autonomic Drugs in Shock

Vasoactive Agent Receptor Activity

Agent

a1

a2

b1

b2

++++

++

Dopamine

++/+++

++++

++

++++

Epinephrine

++++

++++

++++

+++

Norepinephrine

+++

+++

+/++

Phenylephrine

++/+++

Dobutamine

Dopa

Intra-Aortic Balloon Pump

AF/SCUB/2011

SHOCK Registry JACC Sept. 2000, Supp. A

Spectrum of Clinical Presentations

Mortality

Respiratory
Distress

Hypotension

21%
1.4%

22%
70%

5.6%

60%

28%
65%

Hypoperfusion

Management of Cardiogenic
Shock
Attempt to correct problem and increase
cardiac output by diuresing and providing
inotropic support. IABP is utilized if
medical therapy is ineffective.
Catheterization if ongoing ischemia

Utility of IABP in Shock Pts.

Observed clinical benefits:
Improved acid-base status
Improved urine output
Improved mentation
Improved overall hemodynamics
All this, however, does not add up
to improved survival
without Flow Restoration

Risk Factors for Cardiogenic Shock Due to

AMI-mediated LV Dysfunction

Age > 65
Female gender
Large infarction
Anterior infarction
Prior infarction
DM

Post-mortem study of Shock

hearts
At least 40% of the myocardium infarcted
in the aggregate (old and new injury)
80% have significant LAD disease
2/3 have severe 3VD

Outcomes of Cardiogenic Shock

Historic mortality 60-80%
More recently reported mortality numbers
67% in the SHOCK trial registry
56% in GUSTO-I
(v.s. 3% in Pts. without shock)

Outcomes of Cardiogenic Shock

The ST pattern in Cardiogenic shock:
15-30 % Non-ST elevation MI
Older
Mortality: 77%

70-85% ST elevations MI/ New LBBB

Mortality: 53-63%

Outcomes of Cardiogenic Shock

The SHOCK registry
Similar mortality in the two groups
62.5% in non-ST elevation
60.4% with ST elevation

AF/SCUB/2011

Management of Septic Shock

Early goal directed therapy

Identification of source of infection
Broad Spectrum Antibiotics
IV fluids
Vasopressors
Steroids ??
Recombinant human activated protein C (Xygris)
Bicarbonate if pH < 7.1

Initial Resuscitation of Septic Shock

Secure airway if respirations ineffective or patient unable to
protect his airway.

Patients with hypotension not responding promptly to acute

volume expansion should also be intubated to prevent
respiratory arrest.

Supplemental O2
Fluid resuscitation- follow BP, respiration, pulse, mental status,
and CVP to assess response.
If circulatory status fails to improve after 2-3 L or signs of fluid
overload develop consider vasoactive agents.
Consider placing a PAC as this will allow better titration of
hemodynamic drugs and assessment of circulatory status.

Resuscitation (cont.)
Dopamine in low doses (2-5 mcg/kg/min) as this will not only
improve perfusion pressure but may help preserve renal function.
The dose can then be titrated upward or NE added to achieve and
maintain a MAP of at least 60 mm Hg.
Blood cultures and initial laboratory values which assess end organ
function should be sent
Early institution of appropriate antibiotic therapy is crucial. Delay in
initiating antibiotics or initiation of antibiotic therapy which does not
cover the offending agent are associated with a worse outcome.

This initial resuscitation should ideally be accomplished within

1 hour.

Corticosteroids in septic shock

The use of corticosteroids in severe sepsis and
septic shock as an adjunctive therapy is
controversial.
Low dose corticosteroids (200-300mg/day)
has reported earlier reversal of shock and
improved survival. Or increase in superinfection
related mortality.
Especially patients showed no response to
corticotropin test.

Management of Hypovolemic
Shock
Correct bleeding abnormality
If PT or PTT elevated then plasma
Aggressive Fluid replacement with 2 large
bore IVs or central line.
Pressors are last line, but commonly
required.

AF/SCUB/2011

Clinical Signs of Acute Hemorrhage

Class % Blood
Loss

Clinical Signs

Up to 750 ml Slight increase in HR; no change in BP

(15%)
or respirations

II

750-1500 ml Increased HR and respirations;

(15-30%)
increased diastolic BP; anxiety, fright or
hostility

III

1500-2000
Increased HR and respirations; fall in
ml (30-40%) systolic BP; significant AMS

IV

>2000
(>40%)

Severe tachycardia; severe lowering of

BP; cold, pale skin; severe AMS

Treatment Goals
Directed at adequate oxygenation and
ventilation

STOP THE BLEEDING

Maintain circulation with fluid replacement

Treatment
Maintain body temperature
IV fluid administration- 2 large bore IVs
Perform serial neurological exams every 5
minutes
Perform vital signs every 5 minutes
Transport to medical facility

AF/SCUB/2011

Schematic
LVEDP elevation
Hypotension
Decreased coronary
perfusion
Ischemia
Further myocardial
dysfunction
Neurohormonal
activation
Vasoconstriction
Endorgan hypoperfusion

Medical Stabilization of Shock Pts.

Figure out the volume status, Swan if in doubt

Air way
Judicious afterload reduction
Maintain AV synchrony
Dont tolerate Afib
Dual chamber pacing if A-V block present
Correct Acid-Base disturbances
Maintain BP ( IABP and/or Pressors).

SHOCK Trial
Whether
EARLY REVASCULARIZATION improves
survival among patients with
cardiogenic shock?

SHOCK Trial:
Primary end point, 30 days mortality
66.4%
63%

56%
50%

52.4%

Mortality

47%

Revasc.
Med Rx

Diff.=9%
P=0.11

Diff.=13%
P=0.027

Diff.=14%
P<0.02

Take Home Points

Shock = poor tissue perfusion/oxygenation
Know difference btw compensated/uncomp.
shock

3 types, based on pathophysiology of

shock:
Hypovolemic due to decreased preload
Cardiogenic due to decreased SV or CO
Distributive due to decreased SVR

Know the common signs of shock:

Oliguria, AMS, cool/clammy skin, acidosis