shock for nursing study

1. .

2. ‫‪shock‬‬
‫د / جيهان عبد الحكيم‬
‫مدرس التمريضيونس‬
‫الباطني والجراحي والحالت‬
‫الحرجة‬

3. Introduction
 Shock is a condition that leads to
inadequate tissue perfusion that results
in impaired cellular metabolism.
 To maintain an adequate blood flow to
the tissues, a balance exists between
the blood volume, myocardial
contractility and the peripheral
resistance.
 Disturbance in any of these three

4. Classification of shock
• Hypovolaemic shock is due to
diminished blood volume.
• Cardiogenic shock is due to inefficient
myocardial function.
• Neurogenic shock is due to peripheral
vasodilatation, reduced peripheral
resistance, and peripheral pooling of
blood.

5. 4.Anaphylactic shock is due to antigen
antibody reaction that leads to peripheral
pooling of blood.
5. Septic shock: chemical mediators are
released. These mediators affect the
microcirculation resulting in deficient
perfusion of the tissues.

6. Hypovolaemic Shock
 This type is due to diminished blood
volume.
 It is the most common types of shock.
Etiology
may occur secondary to loss of:
 Blood as in internal or external hemorrhage.
 Plasma as in burns, acute pancreatitis and
peritonitis.
 Sodium-containing fluids as in severe
vomiting, diarrhea, intestinal obstruction.

8. Pathophysiology of hypovolemic shock:
 Blood and/or fluids loss in the body, causing
a decreased amount of the blood vessels.
 Venous return is decreased because of the
lack of fluid in the vascular space, causing
decreased ventricular filling.
 The ventricles do not have enough blood to
pump out, so the stroke volume is
decreased.

9.  The heart rate will increase to compensate
for the diminished stroke volume and
resulting poor cardiac output and blood
pressure.
 If the fluid or blood loss continues, the heart
rate will not be able to compensate for the
decreased stroke volume. The end result of
hypovolemic shock is inadequate tissue
perfusion.

11. Clinical picture
 Weakness and fainting especially
when standing.
 The patient feels cold and thirsty.
 The patient look tired .
 Rapid, weak, thready pulse, tachypnea
and air hunger.
 Hypothermia.
 Skin become pale, cold (vasodilation)


12. Treatment of hypovoiaemic shock:
1) Fluid rsuscitation.
 Venous access. At least two large-gauge
catheters are inserted into appropriate
veins.
 At the same time, blood is drawn for
typing and cross matching.
 Lactated Ringer's solution is begun
immediately.

13.  The lactated Ringer's solution is run at a
rapid rate so that in a period of 45 minutes
between 1000 and 2000 ml of lactated
Ringer's solution are given intravenously.
 Blood should be given immediately after
typed and cross-matched.
 Colloid solutions: In the absence of
whole blood, many substances have
been given as human plasma, albumin
solution, dextran.

14.  Hypovoiaemic shock from other causes
other than bleeding, e.g., plasma loss in
major bums, or crystalloid loss in intestinal
obstruction does not need blood, and
infusion is by plasma or crystalloids
respectively.
 A modified Trendelenburg position is
recommended in hypovolemic shock.
 Elevating the legs promotes the return of
venous blood.

15. Dopamine and dobutamine
used to improve myocardial
contractility and increases renal
blood flow and urine output as
well.

16. 2) Pulmonary support:
 Oxygen mask for all shocked patients.
Oxygen at high concentration at first
through a face mask. Later adjustment
of rate and concentration depends on
arterial gas measurements.
 Endotracheal intubation and mechanical
ventilation may be used.

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18.  Measuring central venous pressure (CVP).
The normal pressure is 5-10 cm of water
Assuming that cardiac function is normal,
 a high centeral venous pressure indicates
over transfusion of blood , while a low
pressure indicates hypovolaemia.
 Repeated hematocrit and haemoglobin
assessment.

19. 4) Monitoring blood gases:
 PaO2 is normally between 80-100mmhg.
 PaCO2 is normally between 35-45 mm Hg.
5)Positioning:
 Elevating both legs with maintaining the
trunk and the remainder of the patient in
the supine position is the preferred
position in patients with hypovolaemic
shock.

20. 6) Pain relief:
 If analgesics are needed, the intravenous
route is used because of the poor
absorption from the subcutaneous tissues
or the muscles which are hypoperfused.

21. Cardiogenic Shock
o In cardiogenic shock, the left ventricle
has been injured leading to impaired
pumping.
o There is inadequate blood flow to vital
organs due to inadequate cardiac
output, despite a normal blood volume.

22. Etiology of cardiogenic shock:
 Acute myocardial infarction (commonest
cause).
 Severe arrhythmias.
 Massive pulmonary embolism.
 Cardiac tamponade due to penetrating
wounds of the chest.
 Myocarditis.
 High spinal anaesthesia, can cause
paralysis of the sympathetic supply of the
heart.

23. Pathophysiology of cardiogenic shock:
 Because the pumping is ineffective, less
blood is pushed out with each heartbeat,
leading to a decreased stroke volume.
 Theheart rate increases to compensate
for a low cardiac output and blood
pressure.

24.  The tissues begin to be inadequately perfused.
 The impaired pumping also leads to less blood
being pushed from the ventricle during systole.
 The left ventricle gradually fills with more and
more blood, causing an elevated pressure within
the LV and left atrium. This pressure "backs up"
into the pulmonary vasculature, causing an
increased pulmonary capillary pressure

26. Clinical picture:
 The systolic and diastolic pressures fail,
leading to compensatory peripheral
vasoconstriction.
 A cold sweaty skin.
 Inadequate tissue perfusion.
 Cardiogenic shock is characterized by
congested neck veins and a high CVP.

27. Treatment:
2. Oxygen should be administered,
3. Treatment of the cause:
 Myocardial infarction is treated by early
thrombolytic agent and potent analgesics.
 Relief of cardiac tamponade by emergency
insertion of a needle to drain blood in the
pericardium.

28. Neurogenic Shock
In neurogenic shock there is paralysis of the
vasomotor fibers leading to peripheral pooling
of blood and inadequate venous return.
.

29. Etiology:
2. Vasovagal attack due to hearing bad
news or watching an unpleasant event.
3. In severe painful stimuli.
4. Spinal cord injury
5. Anxiety
6. Spinal anaesthesia or deep general
anaesthesia

30. Pathophysiology:
 Neurogenic shock is caused by the loss of
sympathetic control (tone) of resistance
vessels, resulting in the massive dilatation of
arterioles and venules.
 There is an insult to the nervous system so
that impulses from the sympathetic nervous
system cannot maintain normal vascular
tone.
 This causes a small degree of arterial blood
pooling, which decreases the amount of
blood returning to the heart.

31.  On the arterial side, there is decreased
peripheral vascular resistance, which
actually helps the heart to pump with
less energy.
 Decreased peripheral pressure, there is
not the driving force to get blood,
oxygen, and nutrients to the cells.

32. • The lack of SNS stimulation causes a
massive venous and arterial
vasodilation.
• On the venous side, blood pools in the
distensible veins and does not return
to the larger veins. Because of this
pooling, there is a diminished amount
of blood that returns to the heart.
Stroke volume, cardiac output, and
blood pressure all fall.

34. Clinical picture:
 In neurogenic shock there is
hypotension,
 A normal pulse rate or bradycardia
 Warm dry skin.
Treatment:
– Positioning the patient by keeping him flat
and elevate the leg to increase the venous.
– I.V crystalloid solution as ringers lactate
– Vassopressors may be given.

35. Anaphylactic Shock
• This type of shock may follow administration
of antibiotics especially penicillin,
anaesthetics. The antigen unites with the
antibodies leading to the release of large
amounts of histamine. The patient develops
bronchospasm, laryngeal edema and
respiratory distress. Massive vasodilatation
occurs and there is hypotension.

36. Etiology:
2. Shock due to the severe allergic antigen
antibody reaction to substances such as
drugs, contrast media, blood products,
or insect.
3. Animal venom causes anaphylactic
shock.
4. Food products such as seafood, also
causes anaphylactic shock.

37. Pathophysiology:
 The individual is exposed to the substance
and develops antibodies against it.
 On subsequent exposure to the
substance (the antigen), these
antibodies will bind to the antigen,
forming an antigen-antibody complex.
 This complex causes the release of
chemicals that cause vasodilation.

38.  Both veins and arteries vasodilate,
leading to decreased blood returning
to the heart.
 The capillaries become permeable to
nearly everything, allowing fluids,
proteins, and sometimes blood to
pass through into the interstitial
space. This causes massive
interstitial edema.

39. Treatment:
2. Intravenous crystalloid infusion.
3. Antihistaminic.
4. Endotracheal intubation may be
needed if laryngeal edema and stridor
are developing.

41. Septic Shock
This is the most lethal type of shock
and is recognized as one of the
major killers in surgical practice.
Despite the availability of more
powerful antibiotics, the
incidences of septicemia and
septic shock are rising.

42.  Sepsis is the systemic response to
infection. Many types of organisms can
cause sepsis, including gram-negative
bacteria, gram-positive bacteria, and
fungi.
 The infections can occur anywhere in
the body; urinary tract infections are
the most common cause of sepsis.

43. Etiology:
 Developing reservoirs of resistant and
virulent organisms.
 Concentration of infected patients in
critical care units.
 More extensive operations in elderly
and poor-risk patients.
 Patients who are immunosuppressed by
organ transplantation, and by
chemotherapy.

44. Common sources of bacteria:
 Peritonitiscaused by perforated
viscus, gangrenous bowel, or leaking
anastomosis.
 Genitourinary infections.
 Infected central venous
catheter that
may be used for monitoring or for
nutrition.

45. Predisposing factors:
 All conditions which suppress the
immune mechanism predispose to
septic shock. These include:
 Old-age,
 Diabetes mellitus,
 Corticosteroids,
 Chemotherapy, malignancy,
 HIV / AIDS.

46. Pathophysiology:
• The immune and inflammatory response begins to
try to combat the organism that is causing an
infection.
• The body releases multiple chemicals into the blood
stream, including cytokines, vasodilators.
• In septic shock, this response is not adequate to
eliminate the infection and actually causes increased
damage.
• The organism itself also releases substances called
endotoxins or exotoxins, which further harm the
organs and tissues.

47. • The combination of these chemicals and toxins
cause: (1) peripheral vasodilation – interstitial edema
and decreased blood return to the heart, and (2)
decreased ability of the cells and tissues to take up
oxygen and nutrients.
• The heart tries harder and harder to get oxygen and
nutrients to the cells by increasing the heart rate and
contractility initially, sometimes driving the cardiac
output twice to three times its normal amount.
• However, the immune response and compensatory
mechanisms may not enough to combat the
infection and resulting cellular destruction. The
patient may develop multiorgan dysfunction.

48. Clinical features:
 Restlessness and confusion.
 Fever above 38°C and chills.
 Mild reduction in blood pressure.
 Tachypnoea.
 Tachycardia.
 Patient is flushed with warm dry extremities.
 Oliguria.
 The cardiac output is elevated at first then it
will decrease if this shock not treated
immediately.

49. Treatment:
1) Support of different systems:
(a) Cardiovascular support:
 The initial priority in managing septic shock is to
keep the patient alive.
 Fluid replacement. Prompt correction of fluid deficit
is essential. Most of these deficits are replaced with
a balanced salt solution such as Ringer's Lactate.
 Any deficiency in red blood cell as evidenced by low
hematocrit can be corrected by transfusion of
packed red blood cells.

50. • Huge quantities of fluids are often needed to
maintain an effective circulating volume. The amount
often exceeds 10L within a few hours.
• Give medications as vasopressors.
• If the patient remains hypotensive despite adequate
fluid replacement, as shown by a normal CVP
dopamine (or a combination of dopamine and
dobutarhine) drip is given to raise the blood
pressure.

51. (b) Respiratory support:
 Oxygen administration is essential for all
types of shock. Usually 100% oxygen is
administered as a start, and is later adjusted
according to the response.
 If the arterial oxygen is mildly reduced
oxygen by mask will be sufficient. Reduction
of its level below 60 mrpHg calls for
endotracheal intubation and mechanical
ventilation.

52. (c) Renal support:
• Adequate volume replacement and dopamine
administration improve renal blood flow.
• Haemodialysis is required in case of acute
renal failure, until the kidneys recover.

53. • 2) Fighting infection:
• Eradication of sepsis, e.g., drainage of
a huge abscess or peritonitis, or
resection of gangrenous bowel.
• Antibiotics is started immediately
without waiting for the results of
culture and sensitivity.