Dr.

RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.

1
Term “choc” – French for “push” or impact was
first published in 1743 by the physician LeDran
Belief – symptoms arose from fear or some
other form of altered cerebral function
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
• 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
Progression of physiologic effects as shock ensues
Cardiac depression
Respiratory distress
Renal failure
DIC
Result is end organ failure
• History • Physical examination
• Recent illness • Vital Signs
• Fever • CNS – mental status
• Chest pain, • Skin – color, temp, rashes,
sores
• Abdominal pain • CV – heart sounds
• Comorbidities • Resp – lung sounds, RR,
• Medications oxygen sat, ABG
• Toxins/Ingestions • GI – abd pain, rigidity,
guarding, rebound
• Recent hospitalization or
surgery • Renal – urine output
• Baseline mental status
• Infectious source
Cardiorespiratory monitor
Pulse oximetry
Supplemental oxygen
IV access
ABG, lab investigations-CBC, Chemistries, Lactate
Coagulation studies, Cultures
Foley catheter
CT of head/sinuses
Lumbar puncture
Wound cultures
Acute abdominal series
Abdominal/pelvic CT or US
Cortisol level
Fibrinogen, FDPs, D-dimer
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
 Type Preload CO PVR SVR

Hemmorrhagic

Anaphylactic
/
Cardiogenic

Septic
(Hyperdynamic)
Septic
(Hypodynamic)

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Non-hemorrhagic Hemorrhagic
Vomiting GI bleed
Diarrhea Trauma
Bowel obstruction, Massive hemoptysis
pancreatitis Abdominal Aortic
Burns Aneurysm
Environmental rupture(AAA)
(dehydration) Ectopic pregnancy,
post-partum bleeding
Airway Breathing Circulation
Establish 2 large bore IVs or a central line
Crystalloids
Normal Saline or Lactate Ringers-Up to 3 liters
Packed Red Blood Cells
O negative or cross matched
Control any bleeding
Arrange definitive treatment
TBW (42 L) = 2/3 of body weight (70 kg).

ICF (28 L) = 2/3 of TBW.

ECF (14 L) = 1/3 of TBW.

Interstitial fluid (ISF, 10.5 L) = ¾ of ECF

Intravascular fluid (IVF, 3.5 L) = ¼ of ECF.

“Crystalloids”
Normal saline (just NaCl).
Lactated ringers
Plasmalyte-balanced crystalloid solution with
multiple electrolye solution
Normosol-solution of balanced electrolytes in water
for injection.
Last 3 have K+ and other stuff (acetate, Mg++, etc.)
Crystalloids enter entire ECF: ISF (3/4 of ECF) and IVF
(1/4 of ECF).
3 or 4:1 for replacement of blood loss with crystalloid
Colloids only enter IVF (in short term– 16 hour half-
time for entrance into ISF)
1:1 replacement of blood loss with colloid
Blood trasfusion
Packed red cells- increase O2 carrying capacity
Plasma-fresh frozen plasma contains all stable
proteins-albumin, globulin and clotting factors
Normal human serum albumin-reduce edema,
hypovolemic shock
DEXTRAN-isolated from beet root
Inhibit rouleaux formation
HYDROXYETHYL STARCH-resistant to hydrolysis by
amylase, maintains blood volume longer
POLYVINYL PYROLIDINE (PVP)-synthetic water soluble
hydrophilic polymer
Gelatin polymers-HAEMACCEL-polypeptide dissolved
in electrolyte
DEXTROSE-5% in water
Vasoactive drugs are an important pharmacologic
defense in the treatment of shock.
May be required to support BP in the early stages of
shock.
These agents may be needed to:
Enhance CO through the use of inotropic agents
Increase SVR through the use of vasopressors

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 1

Drug Receptor CO SVR Dose Range

Epinephrine , β1, (β2) 2-10 µg/min

Norepinephrine , β1 0- 2-20 µg/min
Dopamine β1, DR, (α ) 1 - 30
Dobutamine β1 , β2 2 - 20
Phenylphrine  0 20-200µg/min
Vasopressin Angiotensin III 0- 5 - 20
Amrinone PDI 2 -15
(µg/kg/min)
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 2

Drug CO SVR Dose Range

Nifedipine 0- 0.5 - 10

Nitroglycerin 0- 3-5
Nitroprusside 0- 0.5 - 5
Prostacyclin 10 - 40

(µg/kg/min)

20
An endogenous precursor of norepinephrine with
multiple dose-related effects
stimulates alpha, beta and dopaminergic receptors.
Low Dose (0.5 - 3 µg/kg/min)
Predominantly dopaminergic (DR) effects
Enhanced blood flow to renal and splanchnic beds
Moderate Dose (5 -10 µg/kg/min)
Positive inotropic effects (1)
High Dose (>10 µg/kg/min)
a-actions (vasoconstriction)

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DRUG Common Uses
Phenylephrine Septic Shock, neurogenic
shock
Norepinephrine Septic shock
Epinephrine Anaphylaxis, ACLS, septic
shock
Dopamine Renal Insufficeny, septic
shock, cardiogenic shock
Dobutamine Cardiogenic shock (CS)
Isoproterenol bradycardia due to heart
block, effects HR
Milrinone Cardiogenic shock- in those
who don’t respond to
dobutamine
 Epinephrine—catecholamine. Low doses stimulates
beta receptors (so increases CO), causes
bronchodilation as well. Larger doses act on alpha
receptors.
 Drug of choice in anaphylaxis. Prevents release of
histamine, so reverses vasodilation and
bronchoconstriction.
 Can be given IV, subcut or even via ETT.
Isoxsuprine(isoproterenol)—synthetic catecholamine.
Works exclusively on beta receptors. Increases heart
rate, myocardial contractility and variable BP effects.

Limited usefulness as vasopressor. Increases myocardial

oxygen consumption and decreases coronary flow.
Causes cardiac dysrhythmias.
Milrinone—used in combination with other agents in
cardiogenic shock.
Increases cardiac output and decreases SVR without
increasing heart rate or myocardial oxygen
consumption.
Improved CO then increases renal perfusion, thus
urinary output with decrease in circulating volume and
decreased cardiac workload.
Norepinephrine—catecholamine.
Primarily alpha 1 stimulation but also beta1 receptors.
Useful in cardiogenic and septic shock.
Does cause reduced renal blood flow so limits its long
term use.
Phenylephrine—adrenergic that stimulates alpha
receptors. Longer duration of action than
epinephrine. Reduction of renal and mesenteric blood
flow limits prolonged use.
 Neosynephrine (phenyleprine)—adrenergic that
stimulates alpha receptors. Longer duration of
action than epinephrine. Reduction of renal and
mesenteric blood flow limits prolonged use.
Two or more of Criteria-Systemic Inflammatory
Response Syndrome (SIRS)
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!
Sepsis 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
MAP = [(2 x diastolic)+systolic] / 3
High fever
Diffuse rash with desquamation on the palms and
soles over subsequent 1-2 weeks
Hypotension (may be orthostatic) and evidence of
involvement of 3 other organ systems
Streptococcal TSS more frequently presents with focal
soft tissue inflammation and less commonly is
associated with diffuse rash.
Streptococcus pyogenes (group A Streptococcus)
S aureus
• 2 large bore IVs
• NS IVF bolus- 1-2 L wide open (if no
contraindications)
• Supplemental oxygen
• Empiric antibiotics, based on suspected source, as
soon as possible
Antibiotics- Survival correlates with how quickly the
correct drug was given
Cover gram positive and gram negative bacteria
 Zosyn(piperacillin+ tazobactum) 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 Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic – Cefepime or Imipenem
Vasoactive Drugs in Sepsis and Usual Hemodynamic Responses

Systemic
Cardiac Blood
Drug Dose Vascular
Output Pressure
Resistance

Dopamine* 2.5-20 mcg/kg/min + + +

Norepinephrine† 0.05-2 mcg/kg/min + ++ ++

Epinephrine 0.05-2 mcg/kg/min ++ ++ +

Phenylephrine 2-10 mcg/kg/min - ++ ++

Dobutamine‡ 2.5-10 mcg/kg/min + +/- -

• Defined as: • Signs:
• SBP < 90 mmHg • Cool, mottled skin
• CI < 2.2 L/m/m2 • Tachypnea
• PCWP > 18 mmHg • Hypotension
• Pulmonary Arterial • Altered mental status
Wedge pressure • Narrowed pulse
pressure
• Rales, murmur
AMI
Sepsis
Myocarditis
Myocardial contusion
Aortic or mitral stenosis, HCM
Acute aortic insufficiency
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
Goals- Airway stability and improving myocardial
pump function
Cardiac monitor, pulse oximetry
Supplemental oxygen, IV access
Intubation will decrease preload and result in
hypotension -fluid bolus
AMI
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(Percutaneous Coronary Intervention) or thrombolytics
RV infarct
Fluids and Dobutamine (no NTG)
Acute mitral regurgitation or VSD
Pressors (Dobutamine and Nitroprusside)
Correct hypotension:
Fluid resuscitation to correct hypovolemia
Inotropic or Vasopressor support:
Dobutamine
Milrinone
Norepinephrine
Dopamine
Epinephrine
Oxygenation
If MI – ASA, Heparin, and Revascularization
If arrhythmia – correct arrhythmia
If extracardiac abnormality – reverse or treat cause
 Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm Edema
Most likely major underlying disturbance?

Acute Pulmonary Hypovolemia Low-output Arrhythmia

Edema cardiogenic shock
Brady Tachyc
Administer
Administer cardia ardia
Fluids
Furosemide
Blood transfusions
Morphine
Cause-specific See Sec. 7.7 in
Oxygen intubation
interventions Check Blood Pressure ACC/AHA Guidelines
Nitroglycerin
for patients with
Dopamine
STEMI
Dobutamine
Systolic BP Systolic BP
Check Blood Pressure (>100 mm (NO Systolic BP Systolic BP (<70 mm
Hg) signs/sympto (signs/symptoms Hg + signs/symptoms
ms of shock) of shock) of shock)
Systolic BP
(>100 mm Hg) Nitroglycerin Dobutamine Dopamine Norepinephrine

Further Diagnostic/Therapeutic Considerations (for non-hypovolemic

shock)
ACE Diagnostic / Therapeutic
Inhibitors Pulmonary artery catheter, Intra-aortic balloon pump,
echo, angiography, etc Reperfusion revascularization 41
• 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
Pruritus, flushing, urticaria appear

Throat fullness, anxiety, chest tightness,

shortness of breath and lightheadedness

Finally- Altered mental status, respiratory

distress and circulatory collapse
ABC’s
Angioedema and respiratory compromise require
immediate intubation
IV, cardiac monitor, pulse oximetry
IVFs, oxygen
Epinephrine
Second line
Corticosteriods
H1 and H2 blockers
Epinephrine
0.3 mg IM of 1:1000
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
Corticosteroids
Methylprednisolone 125 mg IV
Prednisone 60 mg PO
Antihistamines
H1 blocker- Diphenhydramine 25-50 mg IV
H2 blocker- Ranitidine 50 mg IV
Bronchodilators
Albuterol nebulizer
Atrovent nebulizer
Magnesium sulfate 2 g IV over 20 minutes
Glucagon
For patients taking beta blockers and with refractory
hypotension
1 mg IV q5 minutes until hypotension resolves
• Occurs after acute spinal cord injury
• Sympathetic outflow is disrupted leaving
unopposed vagal tone
• Results in hypotension and bradycardia
• Spinal shock- temporary loss of spinal reflex activity
below a total or near total spinal cord injury (not the
same as neurogenic shock, the terms are not
interchangeable)
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
A,B,Cs
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
Atropine
Pacemaker
Methylprednisolone
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
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
Confirmation -CXR
Rx: Needle decompression, chest tube
Cardiac tamponade
Blood in pericardial sac prevents venous return to
and contraction of heart
Related to trauma, pericarditis, MI
Beck’s triad: hypotension, muffled heart sounds, JVD
Diagnosis: large heart CXR, echo
Rx: Pericardiocentisis
Pulmonary embolism
Virchow’s triad: Hypercoagulability. Hemodynamic
changes (stasis, turbulence) Endothelial
injury/dysfunction.
Signs: Tachypnea, tachycardia, hypoxia
Low risk: D-dimer
Higher risk: CT chest
Rx: Heparin, consider thrombolytics
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
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