shock teaching for medical undergraduates

1. SHOCK
Dr.sugunakar

2. DEFINITION
Shock is simply
defined as perfusion
that is inadequate to
meet the body's
metabolic needs.

3. EFFECTIVE TISSUE
PERFUSION
 Cardiac Performance
 Vascular performance
 Cellular function
Oxygen unloading and diffusion
Energy generation

4. Encephalopathy
Respiratory failure Arrhythmias
ARDS Ischemia
Ischemic hepatitis
Cholestasis
DIC
Thrombocytopenia
Ileus
Erosive gastritis Hyperglycemia
Pancreatitis Hypoglycemia
Cholecystitis Electrolyte abnormalities
Transluminal bacterial
translocation
Cold extremities
Thready pulse

5. CLINICAL RECOGNITION
 Mean arterial pressure < 65 mm Hg (in
 previously normotensive individual

6. TYPES OF SHOCK
 Hypovolemic
 Cardiogenic
 Obstructive
 Distributive

7. CAUSES Hemorrhagic:
Don’t forget concealed
 Hemorrhagic bleeds:
Abdomen
Pelvis / Femoral
Retroperitoneal
Fluid depletion:
 Non-hemorrhagic Dehydration
(Fluid depletion) Vomiting
Diarrhea
Burns
Anaphylaxis
 Venodilation
Venodilation:
Sepsis
Anaphylaxis
Toxins / drugs
Common with
distributive shock

8.  small bowel obstruction, hypovolemic shock
can develop as a result of shift of fluid into
the bowel lumen.
 Patients with peritonitis after perforation of a
duodenal ulcer accumulate several liters of
inflammatory fluid in their peritoneal cavity,
 A reduction in intravascular volume is often
a contributing factor to hypotension in
patients with septic shock.

9.  Hemorrhagic shock can be categorized into three
grades of severity based on the magnitude of blood
loss:
 compensated shock,
 uncompensated shock,
 and lethal exsanguination

10. Patients with 20% to 40% of more than 40%
less than a 20% their blood of their blood
deficit in blood volume volume and
volume profound
cannot sustain hypotension
Can maintain mean aortic develops. With
pressure by severely
Or restore
blood vasoconstriction reduced blood
, have low flow to their
pressurewith iv
fluids cardiac output, brain, these
are subject to patients
anaerobic become
stress, and comatose within
have acidemia minutes and die
of cardiac
BLOOD arrest.

11.  Hypovolemia
! Preload
! Diastolic Filling
 ! Cardiac Output
 ! MAP
 Shock
 MODS

12. CARDIOGENIC
SHOCK

13. causes
Pump (CHF
Ischemia
1.infarction 1.bradycardia
1.Cardiomyopathy
2.tachycadia
2.Valve failure
3.Endocarditis
4.Acute massive pumonary emboli

14.  Hypovolemia Cardiogenic
 ! Preload ! Cardiac Output
 ! Diastolic Filling!  ! MAP
 Cardiac Output  Shock
 ! MAP  MODS
 Shock
 MODS

15. DISTRIBUTIVE
SHOCK

16. CAUSES
 Septic
 Toxic Shock Syndrome
 Anaphylactic /
 Anaphylactoid
 Neurogenic (Spinal
 Shock)
 Endocrinologic
 Adrenal Crisis
 Thyroid Storm
 Toxins

17.  Humans respond to invasive infection with an
immune response that involves multiple mediators.
These mediators enable the patient's inflammatory
processes to destroy the organisms at the site of
infection. These same mediators can damage the
individual's organs if they produce an exaggerated
systemic inflammatory response syndrome

18. PATHO PHYSIOLOGY OF SEPTIC
SHOCK
 Endo toxins
 Complement activation+macrophage
aaaaaaactivation
 Tnf, IL1, IL6
 NEUTROPHIL ACTIVATION+ENDOTHELIAL CELL
UPGRADATION
 BRADYKININ,COAGULATION CASCADE
ACTIVATION,ARACHIDONIC
ACIDMETABOLITES,NITRI ACID,O2 FREE
RADICALS
 CAPILLARY LEAKAGE,MICROTHROMBUS
FORMATION,VASODILATATION,TISSUE
DESTRUCTION
 ORGAN INJURY

19.  Distributive Shock
 ! Systemic Vascular
 Resistance
 Maldistribution of flow
 ! Cardiac Output
 ! MAP
 Shock
 MODS
 Myocardial Suppression

20. SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME
 36C < Fever > 38C
 Tachycardia > 90
 Hypocapnia (PaCO2 > 32 mm Hg) / RR >
20 or
 use of mechanical ventilation
 4000 < WBC > 12000 (or left shift)
 Sepsis
Same criteria as for SIRS but with a
clearly established focus of infection

21.  Severe sepsis - SIRS + Organ
dysfunction…Indicators of hypoperfusion:
▪ Systolic blood pressure <90 mm Hg ▪
>40 mm Hg fall from normal systolic blood pressure
▪ Lacticacidemia
▪ Oliguria
▪ Acute mental status changes
 Septic Shock - Severe sepsis + refractory
 hypotension despite adequate fluid &
resuscitation

22. TREATMENT

23.  Management of a patient in shock is focused on the
following:
 1. Identifying the presence of shock
 2. Searching for and treating immediately life-
threatening conditions
 3. Treating shock based on the underlying
pathophysiology

24. THINK ABOUT...
 2 large bore peripheral lines - iv fluids
 Central line - for CVP & vasopressors
 Arterial line - BP monitoring and repeated ABG
 Foley - urine output
 Nasogastric tube - maintain gut integrity

25. Hypovolemic Fluids---RINGER
LACTATE
BLOOD
HEMOSTASIS
Cardiogenic Cath Lab
Inotropes
IABP
Obstructive Remove obstruction
Distributive Antibiotics
Epinephrine

26.  A surgeon treating a patient in hypovolemic shock
faces two concurrent challenges. First, the surgeon
must restore intravascular volume to normal.
Second, the surgeon must identify the cause of the
patient's hypovolemic shock and decide whether
immediate surgical therapy is needed.

27. HEMORRHAGIC SHOCK
 Acidemia is used as a measure of the severity of
hemorrhagic shock
 bicarbonate excess …-10 mEq/L or less in a
hypovolemic patient is an indication that the patient
has uncompensated shock and is at risk for death if
resuscitation not done

28. HEMORRHAGIC SHOCK
 Adult patients who do not respond to 2 to 4 L of
balanced electrolyte solution (children are given 20
mL/kg) and remain hypotensive usually require
blood transfusions
 The surgeon must identify the potential sites of
active hemorrhage in an irreversibly hypotensive
patient and perform hemostatic interventions

29. HEMORRHAGIC SHOCK
 rapid resuscitation, timely hemostasis, and
postresuscitation support of organ function.

30. TRETMENT OF CADIOGENIC
SHOCK
 The most common cause of cardiogenic
shock is occlusion of a coronary artery in
which a plaque in the coronary artery
ruptures, combined with the formation of an
intraluminal thrombus
 The key to improving survival of patients in
cardiogenic shock is to promptly reestablish
blood flow at the site of the coronary artery
occlusion.[46]

aspirin and a β-blocker , fibrinolysis,
deployment of coronary artery stents, and
surgery

31. SHOCK CAUSED BY CARDIAC
CONTUSION
 dobutamine, epinephrine, or dopamine may
improve myocardial contraction in a patient with
cardiac contusion and profound pump dysfunction.
An intra-aortic balloon pump may provide
temporary support while the contused cardiac
muscle recovers

32. SHOCK CAUSED BY CARDIAC
TAMPONADE
 Acute cardiac tamponade is always suspected after
gunshot or stab wounds to the chest in the vicinity
of the sternum. Patients with acute cardiac
tamponade have hypotension, distended neck
veins pulsus paradoxus,
 pulsus paradoxus,
 immediate surgery to decompress the pericardium

33. SEPTIC SHOCK ….TREATMENT

34. SEPTIC SHOCK ….TREATMENT
 Culture relevant body fluids, including blood.
 Infuse a balanced electrolyte solution of 500
mL/15 min. Monitor the systolic blood
pressure response.
 Insert a central venous or pulmonary artery
catheter. ▪ If after a 500-mL bolus of
saline the patient remains hypotensive and
CVP is <8-12 mm Hg or PAWP is <8-12 mm
Hg, infuse another 500-mL bolus of fluid

35. SEPTIC SHOCK ….TREATMENT
 IfCVP is >15 or PAWP is 15-20 and the
patient remains hypotensive (<65 mm Hg),
start an infusion of the inotropedobutamine
or dopamine. The goal is a mean systemic
pressure >65 mm Hg and a pulse rate <120
beats/min. Determine the cardiac index and
systemic vascular resistance. ▪ If after
infusion of fluid and inotropes SVR is <600,
infuse avasopressor—either norepinephrine
or vasopressin—to increase SVR

36. SEPTIC SHOCK ….TREATMENT
 Monitor mixed venous oxygen saturation and urine
output as an indication that therapeutic
interventions have improved perfusion.
 CVP, central venous pressure; PAWP, pulmonary
artery wedge pressure; SVR, systemic vascular
resistance.

37. SEPTIC SHOCK ….TREATMENT
 As a final consideration in the treatment of any
patient in septic shock, resuscitation is often futile
without effective treatment of the source of the
sepsis. A patient's survival from an episode of
sepsis often hinges on prompt and effective
performance of a surgical procedure.

38. MONITORING & GOALS...
Hemodynamics Oxygen Organ
Dysfunction
1. MAP > 60 1. Hb > 10 1. Urine output
2. CVP > 12 2. Sa O2 > 92 2. Mental
3. CI > 2.2 L % Status
4.PCWP 3. Mechanical 3. Lactate
Ventilation levels
4.Serial blood 4. LFT
gases

39.  AVOID
 HYPOTHERMIA,
 HYPERGLYCEMIA
 ,HYPERCHLOREMIC ACIDOSIS,
 ACTIVATED PROTEIN C, LOW DOSE
STEROIDS IMPROVE SURVIVAL RATES.
 New therapeutic agents are still being
tested for sepsis in multicentre trials.

40. THANK YOU