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مدرس التمريض الباطني والجراحي مدرس التمريض الباطني والجراحي

والحاالت الحرجةوالحاالت الحرجة

– جامعة طنطا – جامعة طنطاكلية التمريضكلية التمريض

shockshock

د / جيهان عبد الحكيم يونس

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 components

can lead to shock.

Introduction

1.Hypovolaemic shock is due to diminished

blood volume.

2.Cardiogenic shock is due to inefficient

myocardial function.

3.Neurogenic shock is due to peripheral

vasodilatation, reduced peripheral

resistance, and peripheral pooling of blood.

Classification of shock

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.

This type is due to diminished blood volume.

It is the most common types of shock.

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.

Hypovolaemic Shock

Etiology

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.

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.

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)

Oliguria due to diminished renal perfusion.

Clinical picture

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.

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.

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.

Dopamine and

dobutamine used to

improve myocardial

contractility and

increases renal blood

flow and urine output as

well.

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.

3) Monitoring: A frequnt monitoring of patient with

hypovolaemic shock to check the

adequacy of volume replacement.

Monitoring clinical parameters as

the pulse, blood pressure.

A Foley catheter is introduced to

check urine output every hour,

optimum output is 0.5-1 ml/kg/hour.

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.

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.

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.

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.

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.

Etiology of cardiogenic shock:

Pathophysiology of cardiogenic shock:

Because the pumping is ineffective, less

blood is pushed out with each heartbeat,

leading to a decreased stroke volume.

The heart rate increases to compensate

for a low cardiac output and blood

pressure.

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

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.

Treatment:

1.Oxygen should be administered,

2.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.

In neurogenic shock there is paralysis of the

vasomotor fibers leading to peripheral pooling

of blood and inadequate venous return.

.

Neurogenic Shock

Etiology:

1. Vasovagal attack due to hearing bad news or

watching an unpleasant event.

2. In severe painful stimuli.

3. Spinal cord injury

4. Anxiety

5. Spinal anaesthesia or deep general anaesthesia

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.

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.

• 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.

Clinical picture:

In neurogenic shock there is

hypotension,

A normal pulse rate or bradycardia

Warm dry skin.

Treatment:

1. Positioning the patient by keeping him flat

and elevate the leg to increase the venous.

2. I.V crystalloid solution as ringers lactate

3. Vassopressors may be given.

• 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.

Anaphylactic Shock

Etiology:1.Shock due to the severe allergic antigen

antibody reaction to substances such as drugs,

contrast media, blood products, or insect.

2.Animal venom causes anaphylactic shock.

3.Food products such as seafood, also causes

anaphylactic shock.

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.

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.

Treatment:

1. Intravenous crystalloid infusion.

2. Antihistaminic.

3. Endotracheal intubation may be

needed if laryngeal edema and stridor

are developing.

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.

Septic Shock

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.

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.

Common sources of bacteria:

Peritonitis caused by perforated viscus,

gangrenous bowel, or leaking

anastomosis.

Genitourinary infections.

Infected central venous catheter that may

be used for monitoring or for nutrition.

Predisposing factors:

All conditions which suppress the immune

mechanism predispose to septic shock. These

include:

Old-age,

Diabetes mellitus,

Corticosteroids,

Chemotherapy, malignancy,

HIV / AIDS.

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.

• 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.

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.

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.

• 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.

(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.

(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.

• 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.