Shock is divided into four stages: initial, compensatory, progressive, and irreversible. In the compensatory stage, the body attempts to maintain blood pressure through mechanisms like vasoconstriction and increased heart rate. As shock worsens in the progressive stage, organ function begins to deteriorate. The irreversible stage occurs when damage is too severe to respond to treatment and organ failure leads to death.

2. To understand the physiologic responses and
subsequent clinical signs and symptoms is to
divide into separate stages:
initial stage of shock
compensatory,
progressive,
and irreversible.

3. identify an initial stage of shock, changes
attributed to this stage occur at the cellular level
and are generally not detectable clinically.
The earlier that medical management and nursing
interventions can be initiated along this, the
greater the patient’s chance of survival.

4.  In the compensatory stage of shock,
 the patient’s blood pressure remains within normal limits.
 Vasoconstriction,
 increased heart rate, and
 increased contractility of the heart
 contribute to maintaining adequate cardiac output.

5. This results from stimulation of the sympathetic
nervous system and subsequent release of
catecholamines (epinephrine and norepinephrine).

6. The body shunts blood from organs such as
the
skin,
kidneys, and
gastrointestinal tract
---to the brain and heart to ensure adequate
blood supply to these vital organs.

7. As a result,
the patient’s skin is cold and clammy,
bowel sounds are hypoactive,
and urine output decreases
in response to the release of aldosterone
and ADH.

8. normal blood pressure
inadequate organ perfusion--------anaerobic
metabolism--------lactic acid, --metabolic
acidosis
respiratory rate increases
raises the blood pH
confusion
arteriolar dilation.

9. identifying the cause of the shock,
correcting the underlying disorder
supporting those physiologic processes
compensation maintained

10. -measures such as
fluid replacement
 medication therapy must be initiated
to maintain an adequate blood pressure and
reestablish and maintain adequate tissue
perfusion.

11. Assess those patients at risk for shock
Early intervention along the continuum of
shock

12. In assessing tissue perfusion, the nurse
observes for changes in level of
consciousness,
vital signs (including pulse pressure), urinary
output, skin, and laboratory values.

13. In the compensatory stage of shock,
serum sodium and
blood glucose levels are elevated in
response
to the release of aldosterone and
catecholamines.

14. The role of the nurse at the
compensatory stage of shock is to
monitor the patient’s
hemodynamic status and promptly
report deviations to the physician.

15. assist in identifying and treating the
underlying disorder.
administer prescribed fluids and
medications, and promote patient safety.

16. Providing brief explanations about the
diagnostic and
treatment procedures,
supporting the patient during those procedures,

17. and providing information about their
outcomes are usually effective in reducing
stress and
anxiety and thus promoting the patient’s
physical and mental well-being.

18. monitoring potential threats to
the patient’s safety, because
a high anxiety level and
altered mental
status typically impair a person’s judgment.

19. may now disrupt
intravenous lines and
catheters and complicate
their condition.
Therefore, close monitoring is essential.

20. In the progressive stage of shock, the
mechanisms that
regulate
blood pressure can no longer compensate
and the MAP falls below normal limits,
with an average systolic blood pressure of
less than 90 mm Hg.

21. all organ systems suffer from hypoperfusion
at this
stage,
two events perpetuate the shock syndrome.
the overworked
heart becomes dysfunctional;

22. the body’s inability to meet increased
oxygen requirements produces
ischemia; and
 biochemical
mediators cause myocardial depression.

23. Second,
the autoregulatory function
of the microcirculation fails in response to
numerous biochemical mediators released by
the cells, resulting in increased
capillary permeability, with areas of
arteriolar and venous constriction.

24. further compromising cellular perfusion.
The relaxation of precapillary
sphincters causes fluid to leak from the
capillaries, creating interstitial
edema and return of less fluid to the heart.

25. Chances of survival depend on the patient’s
general health before
the shock state as well as the amount of
time it takes to restore tissue
perfusion.
As shock progresses, organ systems
decompensate.

26. The lungs, which become compromised early
in shock, are affected
at this stage.
Subsequent decompensation of the lungs
increases
the likelihood that mechanical ventilation
will be needed
if shock progresses.

27. Respirations are rapid and shallow. Crackles
are heard over the lung fields.
Decreased pulmonary blood flow
causes arterial oxygen levels to decrease
and carbon dioxide levels to increase.

28. Hypoxemia and biochemical mediators cause
an intense
inflammatory response and pulmonary
vasoconstriction,
perpetuating the pulmonary capillary
hypoperfusion and hypoxemia.

29. Pulmonary capillaries begin to leak their
contents, causing pulmonary edema, diffusion
abnormalities
(shunting), and additional alveolar collapse.
Interstitial inflammation
and fibrosis are common as the pulmonary damage
progresses.

30. This condition is
sometimes referred to as acute respiratory
distress syndrome
(ARDS), acute lung injury (ALI), shock lung,
or noncardiogenic
pulmonary edema..

31. A lack of adequate blood supply leads to
dysrhythmias and ischemia.
The patient has a rapid heart rate, sometimes
exceeding
150 bpm.
Cardiac enzyme levels (eg, lactate
dehydrogenase,
CPK-MB, and cTn-I) rise.

32. myocardial
depression and ventricular dilation may
further impair the heart’s
ability to pump enough blood to the tissues
to meet oxygen
requirements.

33. As blood flow to the brain becomes impaired, the
patient’s mental
status deteriorates. Changes in mental status
occur as a result
of decreased cerebral perfusion and hypoxia; the
patient
may initially exhibit confusion or a subtle change
in behavior.

34. Subsequently, lethargy increases and the patient
begins to lose
consciousness. The pupils dilate and are only
sluggishly reactive
to light.

35. When the MAP falls below 80 mm Hg the
glomerular filtration rate of the kidneys cannot be
maintained,
and drastic changes in renal function occur. Acute
renal
failure (ARF) can develop.

36. ARF is characterized by an increase in
blood urea nitrogen (BUN) and serum creatinine
levels, fluid and
electrolyte shifts, acid–base imbalances, and a
loss of the renalhormonal

37. regulation of blood pressure. Urinary output
usually
decreases to below 0.5/mL/kg per hour (or below
30 mL per
hour) but can be variable depending on the phase
of ARF.

38. Decreased blood flow to the liver impairs
the liver cells’ ability to
perform metabolic and phagocytic functions.
Consequently, the
patient is less able to metabolize
medications and metabolic waste
products, such as ammonia and lactic acid.

39. The patient becomes
more susceptible to infection as the liver
fails to filter bacteria
from the blood.

40. Liver enzymes
(aspartate aminotransferase [AST],
formerly serum glutamic-oxaloacetic transaminase
[SGOT];
alanine aminotransferase [ALT],
formerly serum glutamate pyruvate transaminase
[SGPT];
lactate dehydrogenase) and
bilirubin levels are elevated, and the patient appears
jaundiced.

41. Gastrointestinal ischemia can cause stress ulcers
in the stomach,
placing the patient at risk for gastrointestinal
bleeding. In the
small intestine, the mucosa can become necrotic
and slough off,
causing bloody diarrhea.

42. Beyond the local effects of impaired
perfusion,
gastrointestinal ischemia leads to bacterial
toxin translocation,
in which bacterial toxins enter the
bloodstream through
the lymph system.

43. In addition to causing infection, bacterial toxins
can cause cardiac depression, vasodilation,
increased capillary
permeability, and an intense inflammatory
response with activa- tion of additional
biochemical mediators. The net result is
interference
with healthy cells and their ability to metabolize
nutrients.

44. The combination of hypotension, sluggish blood
flow, metabolic
acidosis, and generalized hypoxemia can interfere
with normal
hemostatic mechanisms. Disseminated
intravascular coagulation
(DIC) can occur either as a cause or as a
complication of shock.

45. In this condition, widespread clotting and
bleeding occur simultaneously.
Bruises (ecchymoses) and bleeding
(petechiae) may appear
in the skin.

46. Coagulation times (prothrombin time, partial
thromboplastin time) are prolonged. Clotting
factors and
platelets are consumed and require
replacement therapy to
achieve hemostasis.

47. there are several differences
in medical management by type of shock,
some medical interventions
are common to all types.

48. These include use of
appropriate intravenous fluids and medications to
restore tissue
perfusion by (1) optimizing intravascular volume,
(2) supporting
the pumping action of the heart, and (3)
improving the competence
of the vascular system.

49. Other aspects of management may
include early enteral nutritional support and use
of antacids,
histamine-2 blockers, or antipeptic agents to
reduce the risk of
gastrointestinal ulceration and bleeding.

50. The patient in the
progressive stage of shock is often cared for in the
intensive care
setting to facilitate close monitoring
(hemodynamic monitoring,
electrocardiographic monitoring, arterial blood
gases, serum electrolyte
levels, physical and mental status changes),

51. rapid and frequent
administration of various prescribed medications
and
fluids, and possibly intervention with supportive
technologies,
such as mechanical ventilation, dialysis, and intra-
aortic balloon
pump.

52. Working closely with other members of the
health care team,
the nurse carefully documents treatments,
medications, and fluids
that are administered by members of the
team, recording the
time, dosage or volume, and the patient’s
response. Additionally,

53. the nurse coordinates both the scheduling of
diagnostic procedures
that may be carried out at the bedside and the
flow of health
care personnel involved in the patient’s care.


54. If supportive technologies are used, the
nurse helps reduce the
risk of related complications and monitors
the patient for early
signs of complications.


55. Monitoring includes evaluating blood levels
of medications, observing invasive vascular
lines for signs of
infection, and checking neurovascular status
if arterial lines are
inserted, especially in the lower extremities.

56. the
nurse promotes the patient’s safety and comfort
by ensuring that
all procedures, including invasive procedures

57.  and arterial and venous
 punctures, are carried out using correct aseptic
techniques
 and that venous and arterial puncture and infusion sites
are maintained
 with the goal of preventing infection.

58. Positioning and
repositioning the patient to promote
comfort, prevent pulmonary
complications, and maintain skin integrity
are integral to
caring for the patient in shock.

59. Efforts are made to minimize the cardiac
workload by reducing
the patient’s physical activity and fear or
anxiety. Promoting rest
and comfort is a priority in the patient’s
care.
SUPPORTING FAMILY MEMBERS

60. The irreversible (or refractory) stage of
shock represents the point
along the shock continuum at which organ
damage is so severe
that the patient does not respond to
treatment and cannot survive.

61. Despite treatment, blood pressure remains low.
Complete
renal and liver failure, compounded by the release
of necrotic
tissue toxins, creates an overwhelming metabolic
acidosis. Anaerobic
metabolism contributes to a worsening lactic
acidosis.

62. Reserves
of ATP are almost totally depleted, and
mechanisms for
storing new supplies of energy have been
destroyed.

63.  Multiple
 organ dysfunction progressing to complete organ failure
has occurred,
 and death is imminent. Multiple organ dysfunction can
 occur as a progression along the shock continuum or as a
syndrome
 unto itself.

64. Medical management during the irreversible stage
of shock is
usually the same as for the progressive stage.
Although the patient’s
condition may have progressed from the
progressive to the

65. irreversible stage, the judgment that the shock is
irreversible can
be made only retrospectively on the basis of the
patient’s failure
to respond to treatment.

66. Strategies that may be experimental
(ie, investigational medications, such as
antibiotic agents and
immunomodulation therapy) may be tried to
reduce or reverse
the severity of shock.

67. As in the progressive stage of shock, the nurse
focuses on carrying
out prescribed treatments, monitoring the
patient, preventing
complications, protecting the patient from injury,
and providing
comfort.

68.  family needs to be informed about the prognosis and likely
 outcomes. Opportunities should be provided, throughout the
patient’s



69.  care, for the family to see, touch, and talk to the patient.
 A close family friend or spiritual advisor may be of comfort to
the
 family in dealing with the inevitable death of the patient.

70.  Whenever
 possible and appropriate, the family should be approached
 regarding any living will, advance directive, or other written
or

71.  verbal wishes the patient may have shared in the event that
he or
 she cannot participate in end-of-life decisions. In some cases,
 ethics committees may assist the family and health care team
in
 making difficult decisions.
