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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
• Recent illness
• Fever
• Chest pain,
• Abdominal pain
• Comorbidities
• Medications
• Toxins/Ingestions
• Recent hospitalization or
surgery
• Baseline mental status
• Physical examination
• Vital Signs
• CNS – mental status
• Skin – color, temp, rashes,
sores
• CV – heart sounds
• Resp – lung sounds, RR,
oxygen sat, ABG
• GI – abd pain, rigidity,
guarding, rebound
• Renal – urine output
• 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
10
Type Preload CO PVR SVR
Hemmorrhagic
Anaphylactic
Cardiogenic
Septic
(Hyperdynamic)
Septic
(Hypodynamic)
/
Non-hemorrhagic
Vomiting
Diarrhea
Bowel obstruction,
pancreatitis
Burns
Environmental
(dehydration)
Hemorrhagic
GI bleed
Trauma
Massive hemoptysis
Abdominal Aortic
Aneurysm
rupture(AAA)
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
18
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
19
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  20-200µg/min
Vasopressin Angiotensin III 5 - 20
Amrinone PDI 2 -15
Drug Receptor CO SVR Dose Range
0 -
(µg/kg/min)
1
0
20
Nifedipine 0 - 0.5 - 10
Nitroglycerin 0 - 3 - 5
Nitroprusside 0 - 0.5 - 5
Prostacyclin 10 - 40
2
Drug CO SVR Dose Range
(µg/kg/min)
21
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)
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
Drug Dose
Cardiac
Output
Blood
Pressure
Systemic
Vascular
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 + +/- -
• Signs:
• Cool, mottled skin
• Tachypnea
• Hypotension
• Altered mental status
• Narrowed pulse
pressure
• Rales, murmur
• Defined as:
• SBP < 90 mmHg
• CI < 2.2 L/m/m2
• PCWP > 18 mmHg
• Pulmonary Arterial
Wedge pressure
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
Edema
Hypovolemia Low-output
cardiogenic shock
Arrhythmia
Administer
Furosemide
Morphine
Oxygen intubation
Nitroglycerin
Dopamine
Dobutamine
Administer
Fluids
Blood transfusions
Cause-specific
interventions Check Blood Pressure
Brady
cardia
Tachyc
ardia
Check Blood Pressure
Systolic BP
(>100 mm Hg)
Systolic BP
(NO
signs/sympto
ms of shock)
Systolic BP
(signs/symptoms
of shock)
Systolic BP (<70 mm
Hg + signs/symptoms
of shock)
See Sec. 7.7 in
ACC/AHA Guidelines
for patients with
STEMI
ACE
Inhibitors
Nitroglycerin Dobutamine Dopamine Norepinephrine
Systolic BP
(>100 mm
Hg)
Further Diagnostic/Therapeutic Considerations (for non-hypovolemic
shock)
Diagnostic / Therapeutic
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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Class drug therapy of shock

  • 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
  • 2. 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
  • 3. • 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
  • 4.
  • 5. Progression of physiologic effects as shock ensues Cardiac depression Respiratory distress Renal failure DIC Result is end organ failure
  • 6. • History • Recent illness • Fever • Chest pain, • Abdominal pain • Comorbidities • Medications • Toxins/Ingestions • Recent hospitalization or surgery • Baseline mental status • Physical examination • Vital Signs • CNS – mental status • Skin – color, temp, rashes, sores • CV – heart sounds • Resp – lung sounds, RR, oxygen sat, ABG • GI – abd pain, rigidity, guarding, rebound • Renal – urine output
  • 7. • Infectious source Cardiorespiratory monitor Pulse oximetry Supplemental oxygen IV access ABG, lab investigations-CBC, Chemistries, Lactate Coagulation studies, Cultures Foley catheter
  • 8. CT of head/sinuses Lumbar puncture Wound cultures Acute abdominal series Abdominal/pelvic CT or US Cortisol level Fibrinogen, FDPs, D-dimer
  • 10. 10 Type Preload CO PVR SVR Hemmorrhagic Anaphylactic Cardiogenic Septic (Hyperdynamic) Septic (Hypodynamic) /
  • 11. Non-hemorrhagic Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Environmental (dehydration) Hemorrhagic GI bleed Trauma Massive hemoptysis Abdominal Aortic Aneurysm rupture(AAA) Ectopic pregnancy, post-partum bleeding
  • 12. 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
  • 13. 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.
  • 14. “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.)
  • 15. 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
  • 16. 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
  • 17. 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
  • 18. 18 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
  • 19. 19 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  20-200µg/min Vasopressin Angiotensin III 5 - 20 Amrinone PDI 2 -15 Drug Receptor CO SVR Dose Range 0 - (µg/kg/min) 1 0
  • 20. 20 Nifedipine 0 - 0.5 - 10 Nitroglycerin 0 - 3 - 5 Nitroprusside 0 - 0.5 - 5 Prostacyclin 10 - 40 2 Drug CO SVR Dose Range (µg/kg/min)
  • 21. 21 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)
  • 22. 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
  • 23.  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.
  • 24. 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.
  • 25. 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.
  • 26. 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.
  • 27.  Neosynephrine (phenyleprine)—adrenergic that stimulates alpha receptors. Longer duration of action than epinephrine. Reduction of renal and mesenteric blood flow limits prolonged use.
  • 28. 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!
  • 29. 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
  • 30. 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
  • 31.
  • 32. • 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
  • 33. 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
  • 34. Vasoactive Drugs in Sepsis and Usual Hemodynamic Responses Drug Dose Cardiac Output Blood Pressure Systemic Vascular 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 + +/- -
  • 35. • Signs: • Cool, mottled skin • Tachypnea • Hypotension • Altered mental status • Narrowed pulse pressure • Rales, murmur • Defined as: • SBP < 90 mmHg • CI < 2.2 L/m/m2 • PCWP > 18 mmHg • Pulmonary Arterial Wedge pressure
  • 36. AMI Sepsis Myocarditis Myocardial contusion Aortic or mitral stenosis, HCM Acute aortic insufficiency
  • 37. 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
  • 38. 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
  • 39. 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)
  • 40. 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
  • 41. Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm Edema Most likely major underlying disturbance? Acute Pulmonary Edema Hypovolemia Low-output cardiogenic shock Arrhythmia Administer Furosemide Morphine Oxygen intubation Nitroglycerin Dopamine Dobutamine Administer Fluids Blood transfusions Cause-specific interventions Check Blood Pressure Brady cardia Tachyc ardia Check Blood Pressure Systolic BP (>100 mm Hg) Systolic BP (NO signs/sympto ms of shock) Systolic BP (signs/symptoms of shock) Systolic BP (<70 mm Hg + signs/symptoms of shock) See Sec. 7.7 in ACC/AHA Guidelines for patients with STEMI ACE Inhibitors Nitroglycerin Dobutamine Dopamine Norepinephrine Systolic BP (>100 mm Hg) Further Diagnostic/Therapeutic Considerations (for non-hypovolemic shock) Diagnostic / Therapeutic Pulmonary artery catheter, Intra-aortic balloon pump, echo, angiography, etc Reperfusion revascularization 41
  • 42. • 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
  • 43. Pruritus, flushing, urticaria appear Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse
  • 44. ABC’s Angioedema and respiratory compromise require immediate intubation IV, cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line Corticosteriods H1 and H2 blockers
  • 45. 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
  • 46. 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
  • 47. • 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)
  • 48. 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
  • 49. 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
  • 50. 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
  • 51. 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
  • 52. 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
  • 53. 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
  • 54. 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