1. Shock
Prepared by Dr.Ahmed Abdul-Ameer Daffar ( Cardio-Thoracic & Vascular Surgeon )

2. Definition
It is a life thratening condition which is characterized by circulatory failure resulting in inadequate organ perfusion.
Types of Shock Hypovolemic shock Septic shock Cardiogenic shock Obstructive shock Neurogenic shock Anaphylactic shock Endocrine failure

3. 1-Hypovolemic Shock
Hypovolemic shock is a syndrome of reduced cardiac output caused by a reduction in blood volume.
Surgeons routinely encounter hypovolemic shock, with hemorrhage being the most frequent specific cause.
The severity of hemorrhagic shock can be defined in terms of the proportional deficit of blood volume.

4. Hemorrhagic Shock
There are three grades of severity based on the magnitude of blood loss : A-Compensated shock B-Uncompensated shock C-Lethal exsanguination

5. A-Compensated Shock Blood loss is less than 20% of the blood volume.
Patients in compensated shock maintain adequate perfusion of the brain and heart and normal mean arterial pressure because vasoconstriction mediated by neuroendocrine reflexes which decreases blood flow to the skin and skeletal muscle.
Patients in compensated shock can readily be resuscitated by IV infusion of balanced electrolyte solutions.

6. B- Uncompensated Shock
Blood loss is equivalent to 20% to 40% of blood volume
Patients in uncompensated shock can not sustain mean aortic pressure by vasoconstriction, have low cardiac output, are subject to anaerobic stress and metabolic acidosis.
Patients in uncompensated shock for hours are at risk for death. .
Patients in uncompensated shock would be susceptible to lethal anemia after full resuscitation by intravenous fluid , so these patients need to be transfused with blood to be fully resuscitated.

7. C-Lethal Exsanguination
Blood loss is more than 40% of blood volume and profound hypotension develops.
With severely reduced blood flow to the brain, patients become comatose within minutes and die of cardiac arrest.
Patients not only need immediate massive transfusion but also frequently require prompt performance of a surgical procedure to control the hemorrhage.

8. Clinical Diagnosis of Hemorrhagic Shock
Diagnosis must be established promptly.
Preventable deaths from hemorrhagic shock have occurred because surgeons have failed to recognize that a bleeding patient was in compensated shock.
Changes in vital signs are the principal clinical indication that a patient is in hemorrhagic shock.
Clinical Diagnosis of Hemorrhagic Shock

9. Clinical Features of Hemorrhagic Shock
Tachycardia
Hypotension(Systole)
Diaphoresis (excessive sweating)
Thirst
Skin pallor
Decreased urine output
An ominous indication that the patient is nearing death is the presence of symptoms of cerebral ischemia, including confusion, agitation and depressed level of consciousness.

10. Treatment of Hemorrhagic Shock
IV access is obtained & resuscitation is made with balanced electrolyte solutions.
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.
Surgical intervention may be indicated to control active hemorrhage.
Promptly performed hemostatic interventions are paramount.

11. After shock
After shock, patients are at risk for additional life-threatening problems. Organ system ( cardiac, renal, pulmonary, neurologic ) dysfunction and failure can develop after shock.
Reasons for this organ failure include : Delayed or in-complete resuscitation from shock A reperfusion injury that incites an exaggerated endogenous inflammatory response The development of invasive infection.
Thus, rapid resuscitation, timely hemostasis, and post-resuscitation support of organ function is mandatory.

12. Resuscitation
If large volumes of normal saline are used for resuscitation, hyperchloremic acidemia develops.
lactated Ringer's is the fluid of choice.
Coagulopathy may develop as a complication of massive transfusion, and selected blood components (i.e., coagulation factors, fresh frozen plasma, cryoprecipitate, and platelet concentrates) may be necessary to replenish coagulation factors, as well as restore blood volume.

13. Causes of hemorrhagic shock
Substantial hemorrhage can occur acutely in one of five locations: 1-Hemothorax). 2-Hemoperitoneum 3-Pelvic fracture 4-Long bone fractures 5-Out of the patient's body from wounds.

14. The three phases after resuscitation from shock
-Phase 1 which starts at the time of the patient's arrival in the emergency department and ends when the operation or procedure needed to control the bleeding is complete. Patients are typically receiving fluid and blood to replace losses from hemorrhage, and there may be a contraction in the interstitial volume as fluids shift to compensate for shock Phase 2 starts at the end of surgery and is characterized as a period in which more fluid needs to be infused than is lost. Urine output is low, and patients gain weight due to fluid retention Phase 3 corresponds to recovery. Patients who were recovering from their injuries usually had diuresis in which the excess fluid gained during phase II was excreted as urine.

15. 2-Septic shock
Septic shock is the fourth level and the most severe category of SIRS (Systemic Inflammatory Response Syndrome). The organ dysfunction in patients in septic shock may progress to organ failure.
It is a vasodilatory shock secondary to circulating inflammatory mediators and cells.
Despite the hypotension, plasma catecholamine levels are elevated, and the renin-angiotensin system is activated.

16. Criteria for Four Categories of the SIRS
1-Systemic Inflammatory Response Syndrome (SIRS)
Two or more of the following:
Temperature (core) >38°C or <36°C.
Heart rate >90 beats/min.
Respiratory rate of >20 breaths/min for patients spontaneously ventilating or a Paco2 <32 mm Hg.
White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature (band) cells in the peripheral blood smear.
2-Sepsis
Same criteria as for SIRS but with a clearly established focus of infection.

17. Sepsis associated with organ dysfunction and hypoperfusion
3-Severe Sepsis
Sepsis associated with organ dysfunction and hypoperfusion
Indicators of hypoperfusion:
Systolic blood pressure <90 mm Hg
Lactic acidemia
Oliguria
Acute mental status changes
4-Septic Shock
Patients with severe sepsis who
Are not responsive to intravenous fluid infusion for resuscitation.
Require inotropic or vasopressor agents to maintain systolic blood pressure.

18. Treatment of septic shock
Intravenous infusion of fluids
Vasoactive agents: inotropic drugs and vasoconstrictors are used with monitoring of oxygen saturation and urine output
Antimicrobial agents.
Surgical intervention to control the focus of sepsis may be needed.
Intravenous steroid has a role in septic shock.
IV infusion of insulin to keep blood glucose levels tightly controlled improves survival.

19. Cardiogenic shock is failure of the cardiac ventricles to pump blood at a flow rate sufficient to maintain body perfusion pressure. The most common cause of cardiogenic shock is ischemia .
3-CARDIOGENIC SHOCK

20. Causes of Cardiogenic Shock
Acute myocardial infarction
Mechanical complications
Acute mitral regurgitation
Acute ventricular septal defect
Free wall rupture
Pericardial tamponade
Arrhythmia
End-stage cardiomyopathy
Myocarditis
Severe myocardial contusion

21. 4-Obstructive Shock Pericardial tamponade Pulmonary embolus
Obstructive shock can be caused by a number of different etiologies that result in mechanical obstruction of venous return to the heart. In trauma patients this is most commonly due to the presence of tension pneumothorax.
Causes of Obstructive Shock
Pericardial tamponade
Pulmonary embolus
Tension pneumothorax
IVC obstruction
Gravid uterus on IVC
Increased intrathoracic pressure
Excess positive end-expiratory pressure
Neoplasm

22. Shock from Massive Pulmonary Embolism
Clinical examination reveals distended neck veins and a tricuspid regurgitation murmur.
ECG findings S1Q3T3
Echocardiography reveals acute right heart distention and strain.
The infusion of inotropic agents to sustain cardiac output is necessary until definite treatment is applied.
The effectiveness of thrombolytic therapy has been established.
In patients with a substantial risk associated with thrombolytic therapy, embolectomy is a preferable alternative therapy.

23. 5-Neurogenic Shock
Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds.
Loss of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output.
Neurogenic shock is usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone.

24. Causes of Neurogenic Shock
Spinal cord trauma
Spinal cord neoplasm
Spinal/epidural anesthetic

25. Diagnosis The classic description of neurogenic shock consists of:
Decreased blood pressure.
Bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge)
Warm extremities (loss of peripheral vasoconstriction)
Motor and sensory deficits indicative of a spinal cord injury.
Radiographic evidence of a vertebral column fracture.

26. Treatment
After the airway is secured and ventilation is adequate, fluid resuscitation and restoration of intravascular volume often will improve perfusion in neurogenic shock.
If the patient's blood pressure has not responded to what is felt to be adequate volume resuscitation, dopamine or phenylephrine.

27. THANK YOU