1. SGD: Management of Shock
Dr. Sai Sailesh Kumar G
Associate Professor
Department of Physiology
RD Gardi Medical College
Ujjain, Madhya Pradesh
Email:dr.saisailesh@gmail.com
2. Learning objectives
1. Define shock
2. Describe physiological pathways operative in shock
3. List the causes of shock and briefly describe them
4. Discuss the principles of treatment of shock
3. Case-1
A 40 years old lady in anxiety was brought to the
Emergency Department with history of repeated
diarrhea and vomiting of one day duration. Her
main symptoms were severe exhaustion,
giddiness and decrease in urine output. On
examination her skin was cold and calmy, dry
mouth, pulse was 100 bpm and thready, BP 80/50
mmHg.
A. What is the most likely clinical diagnosis?
B. What is the basis of the signs and symptoms?
C. What is the physiological basis of the treatment?
D. What is the outcome if treatment fails?
4. Case-2
An individual was brought to hospital from the
Road accident site. He showed following signs
and symptoms. Restlessness, Extreme
Weakness, Pale Cold Clammy skin, Rapid &
thready pulse, Hypotension, oliguria.
A. What is your diagnosis?
B. How do you explain the signs and symptoms?
C. Explain Compensatory mechanism.
D. What immediate treatment do you suggest
5. Case-3
Can I treat a hypovolemic shock patient with
sympathomimetic drugs?
6. Management of shock
Replacement therapy
1. Blood and plasma transfusion: if a person is in shock
caused by hemorrhage, the best possible therapy is
transfusion of whole blood
2. If whole blood is not available, plasma transfusion can be
done to increase blood volume
3. Plasma can not increase hematocrit but human body can
usually stand a decrease in the hematocrit to half of normal
before serious consequences result
4. If plasma is not available use plasma substitutes like dextran
solution
7. Management of neurogenic and anaphylactic shock
Sympathomimetic drugs
1. A sympathomimetic drug is a drug that mimics
sympathetic stimulation
2. Nor-epinephrine and epinephrine
3. In two types of shock, these drugs have proved to
be especially beneficial
4. Sympathomimetic drugs have not proved to be very
valuable in hemorrhagic shock.
8. Management of neurogenic and anaphylactic shock
Sympathomimetic drugs
1. Sympathomimetic drugs have not proved to be very
valuable in hemorrhagic shock.
2. In hypovolemic shock, the sympathetic nervous system
is almost always maximally activated by the circulatory
reflexes already
3. So much of nor epinephrine and epinephrine already
circulating in the blood
4. Sympathomimetic drugs have not proved to be very
valuable in hemorrhagic shock.
9. Management of shock
Other therapies
1. Head down position: when the pressure falls too low
in most types of shock, especially in the hemorrhagic
and neurogenic shock, placing the patient with the head
at least 12 inches lower than the feet
2. Improves venous return
3. Increases cardiac output
4. First essential step in managing many types of shock
10. Management of shock
Other therapies
1. Oxygen therapy: major deleterious effect of most
types of shock is too little delivery of oxygen to the
tissues giving the patient oxygen to breathe can be
of benefit
2. However, in most of types of shock, is not due to
inadequate oxygenation but due to inadequate
transport of blood after it is oxygenated
11. Management of shock
Other therapies
1. Glucocorticoids: increases strength of the heart in
later stages of the shock
2. Stabilize lysozymes in tissue cells and prevents
release of lisosomal enzymes into the cytoplasm of
cells
3. Aid metabolism of glucose
12. Circulatory shock
Generalized inadequate blood flow through the body to
the extent that the body tissues are damaged,
especially because of too little oxygen and other
nutrients are delivered to the tissue cells.
13. What happens to BP in Circulatory shock
1. Some cases in severe shock, person still have
almost normal BP due to powerful nervous reflexes
2. At other times, BP can fall to half normal, but the
person still has normal perfusion and is not in shock
3. In shock due to severe blood loss, BP decreases at
the same time cardiac output decreases. Although
usually not as much
14. Why cardiac depression in shock
1. Decrease in BP
2. Coronary blood flow decreases
3. Myocardium is not supplied with adequate nutrition
4. Weakens the heart muscle
5. Decreases cardiac output
6. Positive feedback cycle
15. Why cardiac depression in shock
1. Septic Shock- Endotoxins released from bodies of
dead gram negative bacteria in the intestines
2. Decreased blood flow in intestines often causes
enhanced formation and absorption of these
endotoxins
3. Circulating toxin increases cellular metabolism
despite inadequate nutrition of cells
4. Especially affect cardiac muscles causing cardiac
depression
16. Circulatory shock
1. Decrease in the Blood Pressure.
2. Perfusion of the organs falls.
3. Fall in cerebral perfusion pressure
4. Ischemia of neuronal cells
5. Brain death
17. Reversible and irreversible shock
1. To combat with damaging effects of shock, body
develops compensatory mechanisms
2. These mechanisms, up to a limit, can protect the
body from damages
3. As long as the compensatory mechanisms are
effective, the shock is called reversible shock
18. Reversible and Irreversible shock
1. If untreated shock, the compensatory mechanisms
breakdown
2. Some compensatory mechanisms become counter
productive (Positive feedback)
3. Now the shock is stated as irreversible shock
19. Reversible and Irreversible shock
1. If untreated shock, the compensatory mechanisms
breakdown
2. Some compensatory mechanisms become counter
productive (Positive feedback)
3. Now the shock is stated as irreversible shock
20. Reversible and Irreversible shock
1. Reversible and irreversible terms are old terms
2. In the past, patients with irreversible shock used to
die, but now not necessarily so
3. Hence, there terms can be dropped
4. Compensatory or early shock and
decompensated or advanced stage of shock
should be used
21. Counter productivity in shock
1. In early phase of shock, renal vasoconstriction
occurs
2. Lowers renal filtration
3. Lowers loss of fluid via urine
4. Conservation of body fluids
5. In advanced stage of shock, renal filtration stops
altogether
6. Anuria – renal acidosis – hyperkalemia - death
22. Counter productivity in shock
1. In early phase of shock, sympathetic stimulation
occurs
2. Splanchnic vasoconstriction
3. This blood is diverted for better perfusion of brain
4. In advanced stage of shock, prolonged
vasoconstriction of intestines
5. Sloughing of intestinal mucosa
6. Massive entry of gram negative bacteria
7. Septic Shock
23. Counter productivity in shock
1. In infection, various mediators (cytokines,
interleukins etc.) released by cells of body
2. These mediators help to battle with infection by
local vasodilation
3. In advanced stage of infection, severe vasodilation
4. Septicemic Shock
24. Counter productivity in shock
All these examples mean, in early stage of shock, the
shock must be effectively treated, otherwise there can
be grave consequences.
25. Consequences of shock
1. Decrease in the perfusion of vital organs
2. Brain – stroke ( particularly in old atherosclerotic
person)
3. Heart – Acute Myocardial Infarction (AMI)
4. Kidney – Acute Renal Failure (ARF)
5. Lungs – Mismatched V/P ratio – hypoxemia and
hypercapnia
26. Compensatory mechanisms of shock
1. Neural and endocrinal responses
2. Neural- As BP falls – Baro-receptor mechanism –
Vasomotor area activated – Sympathetic stimulation
– BP restored – perfusion restored
3. Endocrinal
A. Catecholamine
B. Renin- Angiotensin
C. ADH
D. ACTH responses
27. Catecholamine's
1. Nor adrenaline and adrenaline released from
adrenal gland in response to shock
2. These two hormones collectively called as
catecholamines
3. They cause vasospasm
4. Restoration of BP
28. Renin-angiotensin
1. In shock, kidney is under perfused
2. Formation of angiotensin II
3. Powerful vasoconstriction
4. Also stimulates aldosterone secretion
5. Aldosterone causes sodium retention which in turn
causes water retention
6. Increase in ECF volume ( blood volume) and
restoration of perfusion pressure
29. ADH
1. In shock, sharp fall of BP
2. ADH secretion from posterior pituitary
3. Reduce volume of urinary output
4. Increase in the volume of blood
5. In high doses it acts as vasoconstrictor
30. ACTH
1. In shock, high levels of stress
2. Heavy amount of ACTH secreted from anterior
pituitary
3. ACTH stimulates cortisol secretion
4. Cortisol facilitates vasoconstrictor action of
catecholamines
31. Role of fluid shift mechanism
1. In shock, sharp fall in BP
2. Decrease in hydrostatic pressure
3. Colloidal osmotic pressure remains same
4. In driving force is more than out driving force
5. Tissue fluid enters vascular compartment
6. Restoration of perfusion pressure
33. Hypovolemic shock
1. Occurs in conditions like hemorrhage, burns,
severe diarrhea
2. Pallor – paleness of skin due to cutaneous
vasoconstriction
3. Air hunger – due to hypoxemia and hypercapnia
4. Oliguria – due to renal vasoconstriction
34. Hypovolemic shock – plasma loss
1. Loss of plasma without loss of RBC reduce total
blood volume and cause hypovolemic shock
2. Severe burns cause loss of plasma through the
denuded skin areas so that plasma volume
decreases markedly
35. Hypovolemic shock – Trauma
1. Most common cause of circulatory shock is trauma
to the body
2. Shock results from hemorrhage caused by trauma
3. Hypovolemia
36. Management of hypovolemic shock
1. Removal of cause – stopping the bleeding
2. Restoration of fluid – transfusion of
saline/blood/plasma, etc.,
3. Oxygen inhalation
4. Correction of acidosis if any due to renal failure
5. ORS is given in case of diarrhea instead of fluid
transfusion
37. Cardiogenic shock
1. Occurs in conditions like AMI (Acute Myocardial
Infarction) resulting in heart failure
2. Pulmonary edema –Accumulation of blood due to
failure of left ventricle + hypervolemia of blood
3. Air hunger - due to pulmonary edema
4. Cold, pale skin due to reflex vasoconstriction due to
low BP
38. Management of cardiogenic shock
1. Oxygen inhalation
2. Veno-dilators (e.g. Nitrates) to relieve pulmonary
edema
3. Dobutamine (cardiac stimulant) is often used
39. Anaphylactic shock
1. This is an allergic condition in which the cardiac
output and arterial pressure decreases drastically
2. It primarily results from antigen – antibody reaction
that rapidly occurs after an antigen to which the
person is sensitive enters the circulation
3. Histamine is releases from basophils in the blood
and mast cells in the peripheral tissues
4. Intravenous injection of large amount of histamine
causes histamine shock
40. Anaphylactic shock
1. Occurs in conditions like after injection of drug like
penicillin to a patient who is sensitive to that drug
(penicillin in this example)
2. In anaphylactic shock, after the injection to the
sensitized person, massive amounts of histamine
and some other chemicals are liberated
3. Histamine relaxes vascular smooth muscle but
causes bronchospasm
4. Sharp fall in BP and asthma
41. Management of anaphylactic shock
1. Adrenaline injection (vasoconstrictor and
bronchodilator)
2. Antihistamines
3. Corticosteroids are also given but their effects begin
only some times after
4. If not treated immediately, anaphylactic shock can
kill the patient
42.
43.
44.
45.
46. Septic shock
1. Occurs in conditions like severe bacteremia,
particularly due to gram negative bacteria
2. Gram negative bacteria causes release of
mediators like cytokines, TNF and interleukins
3. These mediators causes vasodilation and
hypotension
4. Also causes cardiac insuficiency, hypoxemia,
edema
47. Septic shock
1. Formerly known as blood poisoning
2. Most cases of septic shock is by gram positive
bacteria followed by endotoxin- producing gram
negative bacteria
3. Septic shock is extremely important to clinician
because other than cardiogenic shock, septic shock
is most frequent cause of shock related death in the
modern hospital.
48. Typical causes of Septic shock
1. Peritonitis caused by spread of infection spread
from uterus and fallopian tubes
2. Generalized body infection resulting from spread of
a skin infection such as streptococcal and
staphylococcal infection
3. Generalized gas gangrene infection by gas
gangrene bacilli
4. Infection spreading into the blood from kidney
caused by colon bacilli
49. Septic shock
1. In later stages, renal failure, and multiple oran
failure may occurs
2. Management:
3. Proper antibiotic therapy
4. Oxygen inhalation ( Oxygen therapy)
5. Nor adrenaline injection to increase BP
6. Treatment of organ failure- use of corticosteroids
50. Neurogenic shock
1. No loss of blood volume
2. Vascular capacity increases so much that even the
normal amount of blood is incapable of filling the
circulatory system adequately
3. Sudden loss of vasomotor tone through out the body
4. Severe vasodilatation of veins – neurogenic shock
5. Deep general anesthesia depress the vasomotor center
6. Brain damage causes paralysis of vasomotor center
51. Case-1
A 40 years old lady in anxiety was brought to the
Emergency Department with history of repeated
diarrhea and vomiting of one day duration. Her
main symptoms were severe exhaustion,
giddiness and decrease in urine output. On
examination her skin was cold and calmy, dry
mouth, pulse was 100 bpm and thready, BP 80/50
mmHg.
A. What is the most likely clinical diagnosis?
B. What is the basis of the signs and symptoms?
C. What is the physiological basis of the treatment?
D. What is the outcome if treatment fails?
52. Case-2
An individual was brought to hospital from the
Road accident site. He showed following signs
and symptoms. Restlessness, Extreme
Weakness, Pale Cold Clammy skin, Rapid &
thready pulse, Hypotension, oliguria.
A. What is your diagnosis?
B. How do you explain the signs and symptoms?
C. Explain Compensatory mechanism.
D. What immediate treatment do you suggest
53. Case-3
Can I treat a hypovolemic shock patient with
sympathomimetic drugs?