د/باسم السيد Management of shocked patient المحاضرة التي قدمت يوم الثلاثاء 8 ابريل 2014 في دار الحكمة بالقاهرة من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب و ضمن موديول الطوارئ و التخدير و العناية المركزة

1. Shock
D.Basem elsaid enany
Assisstant professor cardiology
AinShams university

2. Definition
SHOCK: inadequate organ perfusion
to meet the tissue’s oxygenation
demand.

3. “Hypoperfusion can be
present in the absence of
significant hypotension.”
-fccs course

4. Pathophysiology
• ATP production fails, the Na+/K+ pump
fails resulting in the inability to correct
the cell electronic potential.
• Cell swelling occurs leading to rupture
and death.
• Oxidative Phosphorylation stops &
anaerobic metabolism begins leading to
lactic acid production.

5. Clinically
• Hypotension (ie. SBP < 90mmHg or MAP <60mmHg or
reduced by >30% for last 3min)
• Oliguria (Urine output <20ml/hr or 0.3ml/kg/hr for 2
consecutive hours)
• Poor peripheral perfusion (eg. Skin is cool and clammy;
demonstrates poor capillary refill). With
cardiogenic/septic, Skin exhibits cyanosis mottling which
occurs first over knees.

6. Etiology of shock
Cardiogenic
• Acute myocardial infarction (implies >40% LV muscle
loss)Shock accompanies 6-20% of all acute MI’s ;more
common with patients with ant. MI
• Dilated cardiomyopathy
• Acute myocarditis

7. • Mechanical
– Mitral regurgitation
– Ventricular septal defect
– Left ventricular aneurysm
– Left ventricular outflow obstruction
• Metabolic and pharmacologic myocardial
depression
• Arrhythmias

8. • Extra cardiac obstructive
– Massive pulmonary embolism
– Severe pulmonary hypertension
– Pericardial obstruction
– Tension pneumothorax

9. Oligemic:
_ Hemorrhagic
Volume depletion
Adrenal insufficiency
Distributive
– Septic
– Toxic agents including adverse reaction to medications
and certain drug overdose
– Anaphylaxis
– Neurogenic

11. General Management
1. Initial Approach to patient in shock ABC
• Airway
– Indications for intubation in patients with shock
• Severe hypoxemia
• In appropriately high pCo2
Resting ventilatory muscles will permit diversion of
cardiac output to other hypoperfused organs

12. • Breathing oxygen
• Circulation
a. Immediate determination of relative intravascular volume status is
required.
– Physical Examin- sufficient to distinguish shock with volume overload (ie.
Cardiogenic shock) with pulmonary edema from shock with inadequate
volume / eg. Septic shock with low cardiac filling pressures.
– Unless there are signs of intravascular volume overload initial resuscitation
with IV fluids is generally indicated.
b. Vasopressor medications should be selected based on the cause of
shock

13. Assess Volume Status
1. An adequate pre load is prerequisite to
successful resuscitation
2. Clinical assessment is often inaccurate
3. CVP, PCWP is many circumstances.
4. Insertion of Swan Ganz catheter is
indicated in patient with hypotension
unresponsive to fluid administration or if
fluids are contraindicated

14. Replace volume
a) In the absence of clinical evidence of pulmonary
edema, an immediate fluid challenge is
indicated.
b) Often small volume of fluid can mean the
difference between inadequate LV filling
pressure and pulmonary edema.
c) Frequent small volume 250cc saline bolus are
preferable in cardiogenic shock resuscitation.

15. Management of cardiogenic shock
Definition
1. Clinical
a) Poor cardiac output
b) Tissue hypoxemia
1. Oliguria
2. Cyanosis
3. Altered mentation
4 . Cool extremities
c) Adequate blood volume

16. 2. Hemodynamic
• systolic hypotension (< 90 mm or 30mm below baseline)
• Low cardiac index (<2.2L/min/m2)
• Elevated PCWP (>18mmHg)
• The LV ejection fraction can be misleading

20. Nesiritide=a human BNP that acts mainly as a vasodilator

22. • -Dobutamine: b1 > b2 > a. It is mainly an
inotropic agent.
• -Norepinephrine: b1 > a > b2. Norepinephrine
is a potent vasoconstrictor.
• -Epinephrine: b1 = b2 > a. Potent inotrope.
• -Isoproterenol (pure b-agonist): b1 > b2. This
is a potent inotrope and chronotrope.
• (dopamine, norepenipherine….add
dobutamine, if BB milrinone as
phosphodiesterase inhibitors)

23. INTRAAORTIC BALLON PUMP
COUNTERPULSATION
 30-cm balloon attached on a large bore
catheter
 Advanced into aorta until tip is in origin of left
subclavian artery
 Balloon inflated with helium (35-40 mL) at
start of diastole when the aortic valve closes
 Balloon rapidly deflated at the start of
ventricular systole just before the aortic valve
opens

24. Intraaortic balloon pump counterpulsation

25. INTRAAORTIC BALLOON PUMP
COUNTERPULSATION
Mechanics
 Inflation of balloon increases peak diastolic
pressure and displaces blood toward the
periphery MAP and coronary blood flow
 Deflation of balloon reduces end-diastolic
pressure which reduces impedance to flow
when the aortic valve opens at the beginning
of systole ventricular afterload and
promotes ventricular stroke output

26. Indication for IABP

27. Contraindications to IABP
• Significant aortic regurgitation or significant arteriovenous
shunting
• Abdominal aortic aneurysm or aortic dissection
• Uncontrolled sepsis
• Uncontrolled bleeding disorder
• Severe bilateral peripheral vascular disease
• Bilateral femoral popliteal bypass grafts for severe
peripheral vascular disease.

28. Complications of IABP
• Cholesterol Embolization
• CVA
• Sepsis
• Balloon rupture
• Thrombocytopenia
• Hemolysis
• Groin Infection
• Peripheral Neuropathy

29. The special case of right ventricular infarction
1. Pathogenesis:
a. Usually right coronary artery occlusion
b. More frequent inferior infarctions
2. Exam may reveal:
a. Hypotension
b. Clear lungs
c. Elevated jugular venous pressure
d. Kussmaul’s sign (jugular venous distension with
inspiration

30. 3. Hemodynamics:
a. Right atrial pressure>10 mm
4. Frequent EKG findings:
a. RBBB
b. Complete heart block
c. 1 mm ST elevation in lead V4R (very
specific)

31. 5. Treatment:
a. IV volume loading with saline
b. Avoid nitrates, morphine, and diuretics
c. Correct arrythmias
d. Dobutamine if shock persists
e. IABP
f. Consider angioplasty (or thrombolysis if
angioplasty not immediately available)

32. Management of Extracardiac
Obstructive shock
A. Pulmonary Embolus
1. Thrombolytics
B. Pericardial Tamponade
1. Intravenous fluids
2. Pericardiocentesis
C. Pneumothorax
1. Chest tube
D. Pulmonary hypertension
1. Vasodilators

33. OLIGEMIC SHOCK
• In a 70kg adult male
• Class1: 500-750ml(10-15%)BV loss; no cinical
features
• Class2: 750-1500ml(15-30%)BV loss; postural
hypotension
• Class3: 1500-2000ml(30-40%)BV loss;
hypotesion,tachycardia
• Class4: >2000ml(40%)BV loss;severe shock

34. Managementof oligemic shock
• Operative control of blood loss is the major
consideration in patients with continuing
hemorrhage
• Passive leg raising to increase central blood
volume during resucitation

35. Management of oligemic shock
Protect/ensure patent airway and provide
ventilation if necessary
A. Establish Adequate Venous Access
 optimally, place 2 wide bore peripheral IVs

36. Volume replacement
1. Solutions:
a. Saline
b. Lactated Ringer’s solution
c. Albumin
d. Dextran
e. Hydorxyethyl starch
f. Packed red blood cell
2. Volume expansion equivalents:
a. 6 liters D5W = 2 liters saline/Ringer’s =1 liter albumin =
1 unit PRBCs

37. SEPSIS
• Clinical syndrome with infection along with
two criteria of systemic inflammatory
response :
changes in
temperature(>38 ̊c<36̊c),tachycardia(>90
per minute) , tachypnea (>20 per minute)
changes in wbc count in peripheral bld
(<4000or>12000cells per µL ,or immature
forms of granulocytes

38. SEPTIC SHOCK
• Severe sepsis is diagnosed by presence of
tissue hypoperfusion (elevated lactate or
altered mental status), arterial hypotension
or other organ dysfunction due to systemic
manifestations of infection.
• Once BP remains low, despite adequate
fluid resucitation, progression of sepsis to
shock

39. • Diagnosis
– Appropriate cultures at least two blood cultures
with at least one drawn percutaneously and one
drawn through each vascular access device,
unless the device was recently (<48 hrs)
inserted. Cultures before antibiotic therapy .

40. • Initial Resuscitation
– as soon as the syndrome is recognized
• Central venous pressure: 8-12 mm Hg
• Mean arterial pressure >65 mm Hg
• Urine output >0.5 mL/kg/hr
• Central venous (superior vena cava) or mixed venous oxygen
saturation >70%

41. • Antibiotic Therapy
– within the first hour of recognition of severe sepsis.
The choice of drugs- susceptibility patterns of
microorganisms in the community and in the hospital.
– reassessed after 48-72 hrs on the basis of
microbiological

42. • Vasopressors
– When an appropriate fluid challenge fails to restore
adequate blood pressure and organ perfusion.
– Either norepinephrine or dopamine first-choice
– All patients requiring vasopressors should have an
arterial catheter placed as soon as practical.
– Vasopressin use may be considered at infusion rates
of 0.01- 0.04 units/min.

43. • Inotropic Therapy
– In patients with low cardiac output despite adequate
fluid resuscitation, dobutamine to increase cardiac
output. If used in the presence of low blood pressure,
it should be combined with vasopressor therapy.

44. • Steroids
– IVcorticosteroids (hydrocortisone 200-300 mg/day, for 7
days in three or four divided doses or by continuous
infusion) who, despite adequate fluid replacement,
require vasopressor therapy to maintain adequate blood
pressure.
• Some experts consider tapering the dose of corticosteroids at the
end of therapy.

45. – In the absence of shock, corticosteroids should
not be administered for the treatment of sepsis.

46. – Unless contraindicated, mechanically
ventilated patients should be maintained
semirecumbent, with the head of the bed
raised to 45 degrees to prevent the
development of ventilator-associated
pneumonia.

47. • Deep Vein Thrombosis Prophylaxis:
• A low-dose unfractionated heparin or low-molecular weight heparin.
Mechanical prophylactic device (graduated compression
stockings or intermittent compression device) contraindication for
heparin use (i.e., thrombocytopenia, severe coagulopathy, active
bleeding, recent intracerebral hemorrhage), the use of a peripheral
vascular disease). In very high-risk patients such as those who
have severe sepsis and history of deep vein thrombosis, a
combination of both.
• Stress Ulcer Prophylaxis

48. Anaphylactic shock
Initial Therapy
1. Maintain Adequate Ventilation
a) Oxygen
b) Establish an airway if needed
2. Stop absorption
3. Epinephrine
a) This remains the most important pharmacological management of
anaphylaxis
b) 0.3 – 0.5 mg IV or SC
a) Use 0.3 – 0.5 ml of 1:1,000 dilution SC
b) Use 3 – 5 ml of 1:10,000 dilution IV
4. Inhaled beta-agonists
5. Establish Adequate Venous Access

49. Secondary Therapy
1. Antihistamines (H1 & H2 blockers)
a) 25-50mg hydroxyzine or diphenhydramine Q6 hours
b) Cimetidine 300mg every 8-12 hours
2. Corticosteroids (may shorten protracted reactions but do not
provide immediate benefit)
a) 250 mg hydrocortisone Q6 hours IV
3. Aminophylline (probably not as useful as inhaled b-agonists)
a) Load with 6 mg/kg/hr IV
b) Maintain with 0.3 – 0.6 mg/kg/hr IV
4. Observation in the hospital for at least 24 hours (for relapse)
5. Glucagon (1 mg IV) can be useful in patients which
anaphylactic shock on beta-blockers as these patients may be
resistent to epinephrine

50. Thank you