seminar on shock

1

GOOD MORNING

AAFREEN SUMAIYA SP G STUDENTDEPT. OF PERIODONTICS

2

SHOCKDEFINITIONCLASSIFICATION ANDPATHOPHYSIOLOGY

3

DEFINITION: Shock is defined as “the state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then, if prolonged, to irreversible cellular injury.”

4

Classification of Shock

Shock

Hypovolaemic Cardiogenic Distributive

Neurogenic Anaphylactic Septic

5

Hypovolaemic shock

This type of shock is due to loss of intravascular volume

It is caused by hemorrhage, burns, vomiting, diarrhoea, dehydration etc. Pathophysiology:

Hemorrhage mostly occurs from systemic venules and small veins which usally contains about 50% of total blood volume .

6

loss of blood decrease filling of right heart

decrease filling of pulmonary vasculature decrease filling of left atrium and ventricle decrease left ventricular stroke volume this causes drop in arterial blood pressure

7

Blood Cardiac SystemicPressure = Output x Vascular

Resistance BP = CO x SVR

8

What happens if you get a drop in BP?

BP = CO x SVR

• We need to maintain homeostasis so need to increase BP.

• We can increase BP by increasing: - CO- SVR - CO & SVRto increase BP back up again.

9

Compensatory mechanisms: The compensatory mechanisms which occur after

haemorrhage include,

• Adrenergic discharge

• Hyperventilation • Release of vaso-active hormones

• Collapse

10

• Reabsorption of fluid from the interstitial tissue

• Reabsorption of fluid from the intracellular to the extracellular space

• Renal conservation of body water and electrolytes

11

1.Adrenergic discharge: starts within 60seconds after blood loss

It causes -constriction of venules and small veins -increase in heart rate -consticts the vascular sphincters in kidney,

splanchnic viscera and in skin• This selective vasoconstriction improves filling right

heart and increases cardiac output• Adrenergic discharge takes away a portion of blood flow

from the splanchnic viscera , kidneys, and skin and diverts it to the heart and brain.

12

2.Hyperventilation :It occurs within 1 minute of blood loss

• This occurs in response to metabolic acidaemia

• Spontaneous deep breathing sucks blood from extra thoracic sites to the heart and lungs

• This also increases the filling of left ventricle and also its stroke volume.

13

3.Release of vasoactive hormones:

Release of hormone renin from juxtaglomerular apparatus

Release of vaso-active hormones such as vasopressin and epinephrine

Release of vaso-active hormones usually takes place after 1 to 2 minutes of haemorrhage

14

THIRST

ANGIOTENSIN II

ADRENAL CORTEX

KIDNEYS increase Na+ reabsorption

from filtrate

BP

VASOCONSTRICTION

BLOOD PRESSURE

ALDOSTERONE

BLOOD VOLUME

ANGIOTENSIN CONVERTING ENZYME

JUXTAGLOMERULAR cells in the kidney

respond to a REDUCTION IN BLOOD VOLUME from EXCESS VOMITING, SWEATING, & HAEMORRHAGE etc.

RENIN released into blood

ANGIOTENSINOGEN ANGIOTENSIN I

17

Baroreceptors detect fall in BP

Sympathetic nervous system activated

1.Cardiac Effects

- increased force of contractions

- increased rate (tachycardia)

- increased cardiac output

18

2.Peripheral Effects

- arteriolar constriction

- increased peripheral resistance

- shunting of blood to main core organs (causing cold clammy skin)

19

3. Respiratory Effects

Tachypnoea is one of the first signs that reflects reduced blood flow and oxygen transport.

Cardiovascular and Respiratory systems work together-

• If blood flow around the body is compromised in any way, oxygen delivery to tissues is reduced.

• To compensate for this, ventilation will increase to attempt to increase oxygen uptake in the lungs. So how does this happen?

• The Baroreceptors not only stimulate the cardiovascular control centre but also the respiratory centre in the medulla, increasing the respiratory rate

20

4.Renal Effects

- decreased renal blood flow

- renin released from kidney

- initiation of RAAS results in peripheral vasoconstriction, reabsorption of Na+ and H2O

21

5.Hypothalamus Effects

- decreased blood flow to hypothalamus

- release of ADH from post pituitary results in retention of salt, water and peripheral vasoconstriction

22

6.Hormonal Effects

- Glucagon (contributes to hyperglycaemia)

- ACTH (stimulates cortisol release and glucose production)

23

4.Collapse:

Recumbent posture due to collapse automatically displaces blood from the lower part of the body to the heart and increases cardiac output.

24

5.Reabsorption of fluid from the interstitial tissue:

• Due to adrenergic discharge the arterioles, pre capillary sphincters the venules and the small veins of the skin and splanchnic organs and skeletal muscles constricts• This leads to decrease of the capillary intravascular

hydrostatic pressure.• This leads to the influx of water, sodium and chloride from

the Interstitial tissue space into the capillaries

25

6.Reabsorption of fluid from the intracellular to the extracellular space

• Release of epinephrine, cortisol, glucagon and inhibition of insulin all lead to high extracellular glucose concentration .

• Products of anaerobic metabolism also accumulate in the extracellular space .

• Both these causes hyperosmolarity of the extracellular tissue which draws water out of the cells.

• Interstitial pressure increases ,which forces water, sodium and chloride across the capillary endothelium into the vascular space.

26

7.Renal conservation of body water and electrolytes:

• ACTH is released by any stress including shock.

• This hormone and angiotensin II stimulate the synthesis and release of hormone aldosterone from adrenal cortex.

• Aldosterone is concerned with reabsorption of sodium from the glomerular ultrafiltrate into the vascular space.

• Reabsorption of sodium and water by the kidneys help to maintain the vascular volume.

27

Compensatory shock• Presentation:

- Increased respiratory rate, restlessness, anxiety (earliest signs of shock)

- Tachycardia- Falling BP = late sign of shock- Possible delay in capillary refill- Pale, cool skin (Cardiogenic,

Hypovolaemic shock)

28

- Flushed skin (Anaphylactic, Septic, Neurogenic shock)- Nausea, vomiting, thirst- Decreased body temperature- Feels cold- Weakness

29

Progressive Shock

1.Cardiac Effects

- decreased RBC oxygenation- decreased coronary blood flow- myocardial ischaemia-decreased ventricular filling- decreased force of contraction

30

2. Peripheral Effects- peripheral pooling of blood- plasma leakage into interstitial

spaces- cold, grey waxy skin- restlessness, confusion, slow speech- tachycardia, weak thready pulse- decreased BP- decreased body temperature

31

3. Respiratory effects

• If oxygen delivery to tissues continues to be inadequate, cells must do anaerobic respiration to continue ATP production.

• Anaerobic respiration produces lactic acid as a waste product – this must be removed.

• Central chemoreceptors will detect a fall in pH and stimulate the respiratory centre to increase ventilation.

• This allows the excess acid to be ‘blown off’ in the form of CO2

.

32

Anaerobic respiration

Lactic acid

PCO2 and H+ in blood

expiration of PCO2

H+ in CSF

stimulation ofcentral

chemoreceptors

frequency of impulses to medullary rhythm generator

rate and depth of ventilation

Response to acidosis

34

Irreversible Shock• Loss of peripheral vascular resistance

• Confusion, slurred speech, unconscious

• Slow, irregular, thready pulse

• Falling BP (diastolic is zero)

35

• Cold, clammy cyanotic skin

• Slow, shallow, irregular respirations

• Dilated, sluggish pupils

• Severely decreased body temperature

36

Irreversible Shock leads to:

• Renal failure

• Hepatic failure

• Multiple organ systems failure

• Acute respiratory distress syndrome

• Death

37

Clinical features: Depend on the degree of loss of blood volume and on the duration of shock.

1. Mild shock: - loss of less than 20% blood volume is included in this

category- the feet become pale and cool. -sweat in forehead, hands and feet due to

adrenergic discharge. -urinary output, pulse rate and blood pressure at

this stage remains normal.

38

2. Moderate shock:- loss of blood volume from 20-40% causes this type of shock-oligouriaPulse rate is increased but usually less than 100 beats per

minute3. Severe shock:-loss of blood volume more than 40% usually causes severe

shock . At this stage there is- pallor -low urinary output-rapid pulse -low blood pressure

39

• Clinical monitoring:• Once shock is diagnosed, constant monitoring of patient

is required to asses the degree of blood loss and hemodynamic impairment.

Blood pressure: measurement of BP is very essential in shock.

The diastolic pressure is the main indication of degree of vasoconstriction .

The systolic pressure indicates vasoconstriction along with stroke volume and rigidity of main vessels.

40

Respiration : hyperventilation i.e. increase in rate and depth of respiration is an important indicator of shock.

Hyperventilation is a normal response of early shock.

Persistent hyperventilation is important sign and indicates improper treatment of shock.

Urine: urine output is a good indicator of severity of shock

Urine output is affected quite early even in moderate shock.

It is a good index of adequacy of replacement therapy

41

• CVP: Measurement of central venous pressure is important in assessing shock.

• In hypovolaemic shock the blood volume is decrease,so is the CVP

43

ECG: in severe shock electrocardiogram may show signs of myocardial ischemia with depression of ST-T segments

SWAN-GANZ Catheter: this catheter is used in sophisticated centers to get valuable information.

• flow in the cardiovascular system

• Samples of blood from the pulmonary artery

• Filling pressure of both right and left side of the heart can be measured

45

Treatment:

Resuscitation –it should begin immediately as the patient is admitted with hypovolaemic shock.

This starts with establishment of clear airway and maintaining adequate ventilation and oxygenation.

Lowering of head with support of jaw to prevent airway obstruction and administration of oxygen are usually needed.

50

Immediate control of bleeding:

• It is highly important in case of haemorrhagic shock

• This may be achieved by raising the foot end of bed and by compression bandage to tamponade external haemorrhage.

• Operation may be required to stop such bleeding .

51

Extracellular and fluid replacement:

A non-sugar, non-protein crystalloid solution with a sodium concentration approximately that of plasma is preferable.

That solution can be Ringer’s lactate, Ringer’s acetate or normal saline supplemented with 1 or 2 ampules of sodium bicarbonate.

This solution is run at a rapid speed i.e. 1000-2000ml in 45min intravenously

52

Drugs :

A few drugs are sometimes used in different types of shock.

1. Sedatives: these drugs are commonly used to alleviate pain in patients with shock.

Some amount of sedation is always required in any type of shock.

Morphine should be given intravenously.For children Barbiturates are preferred whereas in head

injuries Largactil is a better choice

53

2.Chronotropic agents:

They primarily increase the heart rate hence used in patients in shock who have slow heart rate

Atropine is the most widely used in this group, followed by isoproterenol.

3.Inotropic agents: These drugs improve the strength of cardiac muscle

contraction.Used in cardiogenic and severe septic shockThe most commonly used drugs in this group are Dopamine

and Dobutamine

54

4.Vasodilators : patients in severe septic, traumatic and in cardiogenic shock may require these drugs.

Most commonly used drugs in this group are nitroprusside and nitroglycerine.

5.Vasoconstrictors : these drugs are beneficial in neurogenic shock.

The main role of this drug is that they increases blood pressure and increases perfusion pressure for coronary circulation.

These drugs also increases myocardial contractility.Most commonly used drugs are Phenylephrine and

Metaraminol.

55

6.Beta-blockers:propranolol is most widely used drug in this group.

7.Diuretics: These drugs are sometimes used in treating patients with cardiogenic shock.

Diuretics should not be used in haemorrhagic and traumatic shock.

56

Traumatic shock

• This type of shock is caused by major fractures, crush injuries, extensive soft tissue injuries and intra abdominal injuries.

• There is hypovolaemia in this type of shock due to bleeding both externally and internally (intraperitoneal haemorrhage) from ruptured liver or spleen or from torn vessels of mesentary.

57

• Along with this there are toxic factors resulting from fragments of tissue entering the blood stream.

• This activates intravascular inflammatory response.

• The vascular permeability also increases resulting in further hypovolaemia.

58

Pathophysiology:1. The peculiarity of this type of shock is that traumatised tissue

activate the coagulation system and release microthrombi into the circulation.

2. These may occlude or constrict parts of pulmonary micro-vasculature to increase pulmonary vascular resistance.

3. This increases right ventricular diastolic and right atrial pressures

4. Humoral products of these microthrombi induce a generalised increase in capillary permeability.

5. This leads to the loss of plasma into the interstitial tissue throughout the body. This depletes the vascular volume to a great extent.

59

Clinical features:

The two differentiating features are:

• Presence of peripheral and pulmonary oedema

• Infusion of large volumes of fluid which may be adequate for pure hypovolaemic shock, is usually inadequate for traumatic shock.

60

Treatment :1.Resuscitation : In this type of shock mechanical ventilatory support is more needed.

2.Local treatment of trauma and control of bleeding: this is similar to hypovolaemic shock .• Surgical debridment of ishchaemic and dead tissues . • Immobilisation of fractures is required

.

61

3.Fluid replacement: more fluids should be required to bring back the patient to normalcy than hypovolaemic shock.

4.Anticoagulation therapy: one intravenous dose of 10,000units of heparin seems to be effective.

62

Cardiogenic shock

This type of shock is usually caused by injury to the heart, myocardial infarction, cardiac arrhythmias or congestive cardiac failure.

In this condition the heart fails to pump the blood.

63

Pathophysiology:• It is usually due to primary dysfunction of one ventricle or other.

• In cardiogenic shock caused by dysfunction of right ventricle, the right heart is unable to pump blood in adequate amount to the lungs.

• Filling of the left heart decreases .

• So left ventricular output decreases.

• In cardiogenic shock caused by dysfunction of left ventricle, the left ventricle unable to maintain an adequate stroke volume.

64

• Left ventricular output and systemic arterial blood pressure decrease.

• There is engorgement of the pulmonary vasculature due to normal right ventricular output, but failure of the left heart.

• Cardiac compressive shock arises when the heart is compressed enough from outside to decrease cardiac output.

• The important causes are tension pneumothorax, pericardial tamponade and diaphragmatic rupture with herniation of the bowel into the chest.

65

Clinical features:In the beginning the skin is pale and cool and the urine output is low.

Gradually the pulse becomes rapid and the arterial blood pressure becomes low.

In case of right ventricular dysfunction the neck veins become distended and the liver may also be enlarged.

In left ventricular dysfunction the patient has broncheal rales and a third heart sound is heard.

Gradually the heart becomes enlarged and when right ventricle also fails distended neck veins will be visible.

66

Treatment:

• Airway must be clear with adequate oxygenation.

• In case of right sided failure caused by massive pulmonary embolus should be treated with large doses of heparin intravenously.

• If pain is complained in case of left sided failure eg: morphine should be prescribed.

• Fulminant pulmonary edema should be treated with a diuretic.

67

Neurogenic shock

•This is caused by paraplegia, quadriplegia, trauma to the spinal cord or spinal anaesthesia.

•Such shock is primarily due to blockade of sympathetic nervous system resulting in loss of arterial and venous tone.

•With pooling of blood in the dilated peripheral venous system.

68

Pathophysiology• In this type of shock there is dilatation of systemic vasculature

which lowers the systemic arterial pressure.

• Blood pools in the systemic venules and small veins.

• The right heart filling and stroke volume decreases.

• This decreases pulmonary blood volume and left heart filling so that left ventricular output decreases.

• Discharge of adrenergic nervous system to the innervated parts of the body and release of angiotensin and vasopressin are the compensatory mechanisms which of course fails to restore cardiac output to normal, though systemic arterial pressure response in part.

69

Clinical features:

The peculiar features are that the skin remains warm, pink and well perfused in contradistinction to the hypovolaemic shock.

Urine output may be normal.

But the heart rate is rapid and the blood pressure is low.

70

Treatment:• Elevation of the legs is effective in treating patients with

neurogenic shock .

• Trendelenburg position displaces blood from the systemic venules and small veins into the right heart and increases cardiac output .

• Administering fluid is important though not so as in hypovolaemic shock.

• This increases filling of right heart which in its turn increases the cardiac output.

• Use of vasoconstrictor drug.

71

Septic shockThis type of shock is due to gram negative septicaemia.

Such a type of shock may occur in cases of severe septicaemia, cholangitis, peritonitis , meningitis.

72

Pathophysiology

•The most frequent causative organisms are gram-positive and gram-negative bacteria.

•Any agents capable of producing infection (including viruses, parasites and fungi) may cause septic shock.

•The common organisms which are concerned with septic shock are – 1.E.Coli 2.Klebsiella aerobacter 3.Proteus 4.Pseudomonas 5.Bacteroids

73

Pathogenesis of Shock

Infectious or noninfectious triggers

Cytokine and inflammatory mediator cascade

Cardiac dysfunction and microvascular injury

Hypotension and shock

74

EFFECTS OF EXCESS CYTOKINE RELEAS

Primary mediators (IL-1, TNFα)

Endothelial/Leukocyte molecular activation

Secondary mediators (NO,PAF)

Vasodilation, capillary leak, endothelial damage

Shock ,MODS,DEATH

75

General signs and symptoms:– fever, chills– general malaise, irritability, lethargy• Tachycardia and hypotension• Hyperventilation• Site of infection may or may not beevident

76

Cardiovascular signs:• Systemic vasodilation and hypotension (Psys <

90mmHg)• Tachycardia (>100 beats/min)• Increased cardiac output (hyperdynamic),

although contractility is depressed; hypodynamic in late shock

• Ventricular dilation; decreased ejection fraction• Loss of sympathetic responsiveness

77

• Hypovolemia due to vascular leakage; centralvenous pressure may be decreased orincreased depending upon fluid resuscitation

• Compromised nutrient blood flow to organs;decreased organ oxygen extraction

78

• Hyperventilation with respiratory alkalosis• Pulmonary hypertension and edema• Hypoxemia (arterial pO2 < 50 mmHg)• Reduced pulmonary compliance; increased work• Respiratory muscle failure• Renal hypoperfusion; oliguria• Acute tubular necrosis and renal failure

79

Disseminated intravascular coagulation (DIC)• Blood dyscrasias– leukopenia– thrombocytopenia– polycythemia• Central and peripheral nervous dysfunction• Increased lactate occurs early

80

Treatment of Septic Shock• Antibiotics (early administration)• Hemodynamic support– (fluid resuscitation)• Restore tissue perfusion• Normalize cellular metabolism– Vasopressor agents• Dopamine, norepinephrine, dobutamine

81

• Source control– Surgical debridement of infected, devitalized tissue– Catheter replacement• Supplemental oxygen (treatment of acuterespiratory distress syndrome,ARDS)• Nutritional support

82

Controversial Current Therapies for Septic Shock

• Anti-inflammatory agents– Cortocosteroids– Ibuprofen– Prostaglandin E1– Pentoxifylline• Oxygen Scavengers– N-acetylcysteine– selenium

83

• Drugs modifying coagulation– Anti-thrombin III• Drugs enhancing host defenses– Intravenous immunoglobulin (IVIG)– Interferon-gamma– immuno-nutrition

84

Other drugs– Growth hormone, antibiotics, fresh frozen plasma,

anesthetic sedative and analgesic agents, catecholamines Hemofiltration, plasma filtration, plasma exchange

85

Experimental Therapies of Septic Shock

• Anti-endotoxin therapies– IVIG• Anti-TNF-alpha, soluble TNFR• PLA2 inhibitors, PAF inhibitors• Anti-coagulants

86

Miscellaenous types:This include , Anaphylactic shock, insulin shock etc.

Anaphylactic shock is commonly seen after administration of penicillin, serum, dextrose, anaesthetics etc.

Such type of shock is due to increased released of histamine and slow release substance(SRS) of anaphylaxis by combination of antigen with IgE on the mast cells and basophils.

87

This histamine and SRS are concerned to cause bronchospasm, laryngeal edema and respiratory distress which totally lead to hypoxia.

This is aggravated by massive vasodilatation which causes hypotension and ultimately shock.

88

REFERENCES

• Bailey & Love’s SHORT PRACTICE OF SURGERY , 23rd Edition.• Critical Care Cardiovascular Disease , Anand Kumar and Joseph E.

Parrillo• Manipal Manual of Surgery.• Kumar Cotran Robbins, BASIC PATHOLOGY 6th edition.• Stanley F Malamed,Medical Emergencies In Dental Office 6th

edition• Das , Somen A TEXT BOOK OF SURGERY 3RD EDITION

seminar on shock

Health & Medicine