general considerations about shock

1. Shock
BY DR. AHMED ABD EL-MABOUD ISMAIL
GENERAL SURGERY MASTER STUDY

2. Shock is a physiologic state characterized by a significant reduction
of systemic tissue perfusion, resulting in decreased oxygen delivery
to the tissues. This creates an imbalance between oxygen delivery
and oxygen consumption.
Prolonged oxygen deprivation leads to cellular hypoxia and
derangement of critical biochemical processes at the cellular level,
which can progress to the systemic level.

3. The effects of oxygen deprivation are initially reversible, but
rapidly become irreversible. The result is sequential cell death,
end-organ damage, multi-system organ failure, and death. This
highlights the importance of prompt recognition and reversal of
shock.

4. PHYSIOLOGY
Systemic tissue perfusion is determined by the cardiac output (CO)
and systemic vascular resistance (SVR):
CO is the product of heart rate and stroke volume. The stroke
volume is related to preload, myocardial contractility, and
afterload.
SVR is governed by the vessel length, blood viscosity, and vessel
diameter.

5. Decreased systemic tissue perfusion is a consequence of diminished
CO, SVR, or both. The CO or SVR may be elevated in shock if the
other is disproportionately low. As an example, SVR is decreased out
of proportion to the elevation of the CO in hyperdynamic shock.
In addition, complex interactions between humoral and
microcirculatory processes cause patchy regional blood flow and
reduced effective tissue perfusion. This results in derangement of
cellular metabolic processes.

6. STAGES OF SHOCK

7. COMPENSATED NONPROGRESSIVE
SHOCK (30 sec -48 hrs)
A. Decrease in BP leads to an increase in the sympathetic
responses.
1. Skin vasoconstriction.
2. Vasoconstriction to the kidneys: ↓ Urine Output.
3. Release of Epinepherine and NE.
4. Increases Heart Rate and the force of the contraction.

8. B. Release of Aldosterone to reabsorb Na+ and H2O follows Na+.
C. Release of ADH to reabsorb H2O.
D. Hypoxia leads to an increase of blood flow to the tissue but has
a harmful effect by increasing blood flow.

9. DECOMPENSATED PROGRESSIVE SHOCK
Loss of 15-20% of blood volume and the
deterioration of the cardiovascular system.

10. A. Decrease of BP below 60 mmHg leads to myocardial ischemia
and a weakened heart muscle and a decreased cardiac output and
a further decrease of BP setting up a positive feedback loop.
B. Decrease of BP below 50 mmHg leads to general vasodilatation
causing further loss of BP.

11. C. Increased Hypoxia leads to the increased permeability of the
capillaries due to loss of hydrostatic pressure causing the loss of
blood plasma into the tissue decreasing blood volume.
D. Intravascular Clotting : Decrease in blood volume leads to a ↓
in the velocity of the blood and an ↑ viscosity. This allows the
platelets to aggregate in the vessel leading to clot formation,
causing obstructions ( ↑ Viscosity = ↓Velocity)

12. E. Cellular Destruction is caused by the lysomosal rupture and ↓ in
the activity of the mitochondria, active transport and general
metabolism.
F. Build up of lactic acid lead to acidosis with pH dropping to
7.35- 6.80 or lower

13. IRREVERSIBLE SHOCK
Heart deteriorates until it can no longer pump and
death occurs.

14. TYPES OF SHOCK

15. Four types of shock are recognized
Hypovolemic
Cardiogenic
Obstructive shock
Distributive.

16. Hypovolemic Shock
Is a consequence of decreased preload due to intravascular
volume loss. During hypovolemic shock, the diminished preload
decreases the CO and the SVR increases in an effort to compensate
for the diminished CO and maintain perfusion to the vital organs.
The PCWP ( pulmonary capillary wedge pressure )is decreased.

17. Increased vascular capacitance
(venodilatation)
 Sepsis
 Anaphylaxis
 Toxins/drugs
Hemorrhagic:
 Trauma
 Gastrointestinal
 Retroperitoneal
Fluid depletion (non hemorrhagic):
 External fluid loss
Dehydration
Vomiting
Diarrhea Polyuria
 Interstitial fluid redistribution
Thermal injury Trauma
Anaphylaxis

18. Cardiogenic Shock
Is a consequence of cardiac pump failure. During cardiogenic
shock, the cardiac pump failure decreases the CO and the SVR
increases in an effort to compensate for the diminished CO and
maintain perfusion to the vital organs. The PCWP is increased.

19. Myopathic
Myocardial infarction (hibernating
myocardium)
Left ventricle
Right ventricle
Myocardial contusion (trauma)
Myocarditis
Cardiomyopathy
Post-ischemic myocardial
stunning
Septic myocardial depression
Pharmacologic
Anthracycline cardiotoxicity
Calcium channel blockers
Mechanical
Valvular failure (stenotic or regurgitant)
Hypertropic cardiomyopathy
Ventricular septal defect
Arrhythmic
Bradycardia
Tachycardia

20. Extra-cardiac Obstructive Shock
Due to obstruction to flow in the cardiovascular circuit and
characterized by either impairment of diastolic filling or
excessive afterload

21. Impaired diastolic filling
(decreased ventricular preload)
Direct venous obstruction (vena cava)
• intrathoracic obstructive tumors
Increased intrathoracic pressure
• Tension pneumothorax
• Mechanical ventilation (with excessive
pressure or volume depletion)
• Asthma
Decreased cardiac compliance
• Constrictive pericarditis
• Cardiac tamponade
Impaired systolic contraction
(increased ventricular
afterload)
Right ventricle
• Pulmonary embolus (massive)
• Acute pulmonary hypertension
Left ventricle
• Saddle embolus
• Aortic dissection

22. Distributive (vasodilatory) Shock
Is a consequence of severely decreased SVR. The CO is typically
increased in an effort to compensate for the diminished SVR. The
PCWP may be low or normal.

23. Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
•Adrenal crisis
•Thyroid storm
Toxic (e.g., nitroprusside, bretylium)

24. Combined
The different types of shock can coexist. As an example, patients
with septic shock often have a hypovolemic component (due to
decreased oral intake, insensible losses, vomiting, diarrhea), a
cardiogenic component (due to sepsis-related myocardial
dysfunction), and a distributive component (due to the effects of
inflammatory and anti inflammatory cascades on vascular
permeability and vasodilation).

25. CLINICAL
PRESENTATION

26. The clinical presentation varies according to the type of shock, its
cause, and its stage of presentation. Several features are common
among all types of shock (Cardinal findings), while other features
may suggest a particular type of shock (Suggestive findings).

27. Cardinal findings
Cardinal features of shock include hypotension, oliguria, abnormal
mental status, metabolic acidosis, and, in some patients, cool and
clammy skin.

28. Hypotension occurs in the majority of shock patients. It may be
absolute hypotension (eg, systolic blood pressure <90 mmHg) or
relative hypotension (eg, a drop in systolic blood pressure >40
mmHg).
Relative hypotension explains, in part, why a patient may be in shock
despite having a high or normal blood pressure. Profound
hypotension may occur, with vasopressors necessary to maintain
adequate perfusion pressure as shock advances.

29. Oliguria may be due to shunting of renal blood flow to other vital
organs, intravascular volume depletion, or both.
When intravascular volume depletion is a cause, it may be
accompanied by orthostatic hypotension, poor skin turgor, absent
axillary sweat, or dry mucous membranes.

30. Change in mental status – The continuum of mental status changes frequently
encountered in shock begins with agitation, progresses to confusion or delirium,
and ends in Coma.
Cool, clammy skin – Potent vasoconstrictive mechanisms compensate for
decreased tissue perfusion by redirecting blood from the periphery to the vital
organs, thereby maintaining coronary, cerebral, and splanchnic perfusion. This
causes the cool and clammy skin that is typical of shock. Not all patients with
shock have cool and clammy skin, however. Patients with early distributive
shock or terminal shock may have flushed, hyperemic skin. The former occurs
prior to the onset of compensatory vasoconstriction, while the latter is due to
failure of compensatory vasoconstriction.

31. Metabolic acidosis develops as shock progresses, reflecting
decreased clearance of lactate by the liver, kidneys, and
skeletal muscle.
Lactate production may increase due to anaerobic
metabolism if shock progresses to circulatory failure and
tissue hypoxia, which can worsen the acidemia.

32. Suggestive findings
In addition to the cardinal symptoms and signs of shock, there may
be additional findings from the history, physical examination,
laboratory studies, or imaging that suggest a particular type of
shock. These findings are neither sensitive nor specific.

33. Hypovolemic Shock
Depending upon the cause of the hypovolemic shock, patients may
report hematemesis, hematochezia, melena, vomiting, diarrhea, or
abdominal pain. There may be evidence of blunt or penetrating
trauma, or the patient may be postoperative.
Physical manifestations may include decreased skin turgor (in
younger patients), dry skin, dry axillae, dry tongue, or dry oral
mucosa. In addition, patients may have postural hypotension,
decreased jugular venous pressure, or diminished central venous
pressure. There may be anemia, or the amylase and lipase may be

34. Cardiogenic shock
Depending upon the cause of the cardiogenic shock, patients may
report dyspnea, chest pain, or palpitations. Many patients have a
history of cardiovascular disease. Lung examination may reveal
diffuse crackles and cardiac examination may reveal a new
murmur, gallops, or soft heart sounds. The jugular venous pressure
and central venous pressure may be increased, while the distal
arterial pulses may be diminished. There may be evidence of
pulmonary congestion or pulmonary edema on a chest radiograph,
as well as recent or current ischemia on an electrocardiogram.
Cardiac enzymes may be elevated. An echocardiogram may
demonstrate the etiology.

35. Distributive Shock
Depending upon the cause of the distributive shock, patients may
report dyspnea, productive cough, dysuria, hematuria, chills,
myalgias, rashes, fatigue, malaise, headache, photophobia, pain, or a
recent ingestion. There may be fever, tachypnea, tachycardia,
leukocytosis, an abnormal mental status, or flushing.

36. General Principles of
Shock Management

37. The overall goal of shock management is to improve oxygen
delivery or utilization in order to prevent cellular and organ
injury.
Effective therapy requires treatment of the underlying etiology.
Restoration of adequate perfusion, monitoring and comprehensive
supportive care
Interventions to restore perfusion center on achieving an adequate
B.P, increasing cardiac output and optimizing oxygen content of
the blood

38. In Summery
Management of Shock
1- Monitoring
2- Fluid Therapy
3- Vasoactive agents

39. Monitoring

40. Clinical Monitoring
Heart rate and respiratory rate.
Prephral perfusion (skin temperature, capillary refill time).
Arterial blood pressure.
Urine output.
Level of consciousness.
Arterial oxygen saturation by pulse oximeter

41. Laboratory Monitoring
Arterial blood gases
Serum electrolytes
Blood sugar
Hemoglobin and coagulation profile
Sepsis screen (C.B.C. – CRP – ESR – blood culture)
Renal function test.

42. Radiological and Imaging Monitoring
Chest X- ray
Echocardiography

43. Invasive Hemodynamic Monitoring
Measured values:
Central venous pressure (CVP).
Pulmonary arterial pressure (PAP).
Pulmonary capillary wedge pressure (PCWP).
Cardiac output (CO).
Derived values:
Cardiac Index (CI).
Systemic vascular resistance (SVR).

44. Summary of
cardiovascular
support in Shock state

45. 1- Oxygen Theraby
Give oxygen 100 % with a face mask.
Reduce concentration over the next few hours
2- Preload Augmentation
(Volume expansion)
Give ringer lactate or saline (20mg/kg, I.V. over 10-15
mins).
Consider albumin or plasma transfusion
Urgent chest X-ray and echocardiography if no response

46. Drug Trade name
Dose
(mcg/kg/min)
Effects
Dopamine
Intropin amp.
(200mg/5ml)
Low (0.5 - 4)
Medium (5 - 10)
High (11 - 20)
Renal vasodilator.
Inotropic.
Peripheral vasoconstrictor.
Dobutamine
Dobutrex vial
(250mg/10ml)
2 – 20
Inotropic.
Peripheral vasodilator
Pulmonary vasodilator
Adrenaline
Adrenaline amp
(1mg/ml)
0.05 – 1.0
Inotropic.
Peripheral vasoconstrictor.
Pulmonary vasoconstrictor.
Isoproterenol
Isuprel amp
(1mg/5ml)
0.05 – 2.0
Inotropic.
Peripheral vasodilator
Pulmonary vasodilator
3- Inotropic Drug Support in Cardiogenic Shock

47. 4- After Load Reduction
Drug Trade name
Dose
(mcg/kg/min)
Effects
Nitroglycerin
Tridil amp.
(50mg/10ml)
1– 20
Venous dilatation ( + + + )
Arterial dilatation ( + )
Nitroprusside
Nipride vial
(50mg/2ml)
0.5 – 10
Venous dilatation ( + )
Arterial dilatation ( + + + )
Amrinone
Inocor amp.
(100mg/20ml)
1 – 20
Vasodilator
Inotropic

48. 5- Treatment of Arrhythmias
Correct hypoxia, acidosis and electrolyte disturbance.
Give the appropriate antiarrhythmic drugs.

49. Thank you