Pathophysiology Of Heart Disease Pdf Download

More than 1 million cases of shock are estimated to present to U.S. hospital EDs each year. The presentation may be cryptic, as in the patient with compensated heart failure, or obvious as in the ultimate shock state of cardiac arrest. Despite aggressive treatment, mortality from shock remains high. Approximately 30 to 45 percent of patients in septic shock, and 60 to 90 percent for those with cardiogenic shock, die within 1 month of presentation. The definition and treatment of shock continues to evolve. With a contemporary understanding of the disease and new evolving technology, the emergency physician can recognize shock at an earlier stage and initiate expert, timely intervention. The general approach to a patient in the initial stages of shock follows similar principles regardless of the inciting factors or etiology. Keywords: Shock, peripheral circulatory failure, cardiogenic shock ,anaphylactic shock.

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Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Definition

Shock is defined as circulatory

insufficiency that creates an imbalance between

tissue oxygen supply and oxygen demand. The

result of shock is global tissue hypoperfusion and

is associated with a decreased venous oxygen

content and metabolic acidosis (lactic acidosis).(4)

Pathophysiology(4)

Shock is classified into four categories by

etiology:

(1) Hypovolemic (caused by inadequate

circulating volume),

(2) Cardiogenic (caused by inadequate

cardiac pump function),

Pathophysiology and management of

different types of shock

Monira Taha1 , Adel Elbaih 2 .

1, 2Assistant professor of Emergency Medicine, Faculty of Medicine, Suez Canal University, Egypt.

Corresponding author : Adel Elbaih, Email ID : elbaihzico@yahoo.com

ABSTRACT

More than 1 million cases of shock are estimated to present to U.S. hospital EDs each

year. (1) The presentation may be cryptic, as in the patient with compensated heart failure, or

obvious as in the ultimate shock state of cardiac arrest. Despite aggressive treatment, mortality

from shock remains high. Approximately 30 to 45 percent of patients in septic shock, and 60

to 90 percent for those with cardiogenic shock, die within 1 month of presentation. (2,3) The

definition and treatment of shock continues to evolve. With a contemporary understanding of

the disease and new evolving technology, the emergency physician can recognize shock at an

earlier stage and initiate expert, timely intervention. The general approach to a patient in the

initial stages of shock follows similar principles regardless of the inciting factors or etiology.

Keywords: Shock, peripheral circulatory failure, cardiogenic shock ,anaphylactic shock.

(3) Distributive (caused by peripheral

vasodilatation and mal distribution of

blood flow),

(4) Obstructive (caused by extra cardiac

obstruction to blood flow).

Clinically, shock may have a predominant

cause, but as the shock state persists or progresses

to irreversible end organ damage, other

pathophysiologic mechanisms become operative.

Knowledge of the principles of oxygen delivery

and consumptionis are important to the

understanding of shock. A maximum of four

molecules of oxygen is loaded onto each molecule

of hemoglobin as it passes through the lungs. If

all available oxygen sites are occupied(four per

molecule of hemoglobin), arterial oxygen

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

saturation (Sao2)is 100 percent . Arterial oxygen

content (Cao2) is the amount of oxygen bound to

hemoglobin plus the amount dissolved in plasma.

Oxygen is delivered to the tissues by the pumping

function (cardiac output) of the heart. Systemic

oxygen delivery (Do2) is the product of the Cao2

and cardiac output (CO). Systemic oxygen

consumption (Vo2) comprises a sensitive balance

between supply and demand.

Normally, the tissues consume

approximately 25 percent of the oxygen carried

on hemoglobin, and venous blood returning to

the right heart is approximately 75percent

saturated [mixed venous oxygen saturation

(pulmonary artery)(Smvo2)].

When oxygen supply is insufficient to

meet demand, the first compensatory mechanism

is an increase in CO. If the increase in CO is

inadequate, the amount of oxygen extracted from

hemoglobin by the tissues increases, which

decreases Smvo2.When compensatory

mechanisms fail to correct the imbalance between

tissue supply and demand, anaerobic metabolism

occurs, resulting in the formation of lactic acid.

Lactic acid is rapidly buffered, resulting in the

formation of measured lactate; normally between

0.5 and1.5 mM/L. An elevated lactate level is

associated with an Smvo2 <50percent. Most cases

of lactic acidosis are a result of inadequate oxygen

delivery, but lactic acidosis occasionally can

develop from an excessively high oxygen

demand, for example, in status epilepticus.

Figure (1) with insufficient oxygen supply,

pyruvate will be diverted to lactate, there by

assuring regeneration of NAD+ from NADH.

This will enable glycolysis, and the

accompanying ATP production to proceed.(5)

In other cases, lactic acidosis occurs

because of an impairment in tissue oxygen

utilization, as in septic shock and post

resuscitation from cardiac arrest; a normal Smvo2

with an elevated lactate indicates such an

impairment. Elevated lactate is a marker of

impaired oxygen delivery and/or utilization and

correlates with short-term prognosis of critically

ill patients in the ED.Smvo2 can also be used as

a measure of the balance between tissue oxygen

supply and demand. Smvo2 is obtained from the

pulmonary artery catheter, but similar information

can be obtained by central venous blood

cannulation (Scvo2). Scvo2 correlates well with

Smvo2and can be more easily obtained in the ED

setting.(6)

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Shock is usually, but not always, associated with

systemic arterial hypotension; i.e., systolic blood

pressure less than 90 mm Hg. Pressure is the

product of flow and resistance [mean arterial

pressure(MAP) = CO X systemic vascular

resistance (SVR)]. Blood pressure may not fall if

there is increase in peripheral vascular resistance

in the presence of decreased cardiac output,

resulting in inadequate flow to the tissue or global

tissue hypoperfusion. The insensitivity of blood

pressure to detect global tissue hypoperfusion has

been repeatedly confirmed. Thus, shock may

occur with a normal blood pressure, and

hypotension may occur without shock.

The onset of shock provokes a myriad of

autonomic responses, many of which serve to

maintain perfusion pressure to vital organs.

Stimulation of the carotid baroreceptor stretch

reflex activates the sympathetic nervous system

leading to

(1) Arteriolar vasoconstriction, resulting in

redistribution of blood flow from the skin,

skeletal muscle, kidneys, and splanchnic

viscera;

(2) an increase in heart rate and contractility

that increases cardiac output;

(3) constriction of venous capacitance

vessels, which augments venous return;

(4) release of the vasoactive hormones

epinephrine, norepinephrine, dopamine,

and cortisol to increase arteriolar and

venous tone; and

(5) release of antidiuretichormone and

activation of the renin-angiotensin axis to

enhance water and sodium conservation to

maintain intravascular volume. These

compensatory mechanisms attempt to

maintain Do2 to the most critical organs-

the coronary and cerebral circulation.

During this process, blood flow to other

organs such as the kidneys and

gastrointestinaltract may be compromised.

The cellular response to decreased Do2

is adenosine triphosphate depletion leading to ion-

pump dysfunction, influx of sodium, efflux of

potassium, and reduction in membrane resting

potential. Cellular edema occurs secondary to

increased intracellular sodium, while cellular

membrane receptors become poorly responsive

to the stress hormones insulin, glucagon, cortisol,

and catecholamines.

As shock progresses, lysosomal enzymes

are released into the cells with subsequent

hydrolysis of membranes, deoxyribonucleic acid,

ribonucleic acid, and phosphate esters. As the

cascade of shock continues, the loss of cellular

integrity and the breakdown in cellular

homeostasis result in cellular death. These

pathologic events give rise to the metabolic

features of hemoconcentration, hyperkalemia,

hyponatremia, prerenal azotemia, hyper- or

hypoglycemia, and lactic acidosis.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Effects of inadequate perfusion on cell function.

In the early phases of septic shock, these physiologic changes produce a clinical syndrome called

the systemic inflammatory response syndrome or SIRS, defined as the presence of two or more of the

following features:

(1) Temperature greater than 38°C (100.4°F) or less than 36°C (96.8°F);

(2) Heart rate faster than 90 beats/min;

(3) Respiratory rate faster than 20 breaths/min;

(4) White blood cell count greater than 12.0 X 109/L, less than 4.0 X 109/L, or with greater than 10

percent immature forms or bands.(7)

As SIRS progresses, shock ensues, followed by multi organ dysfunction syndrome (MODS)

manifested by myocardial depression, adult respiratory distress syndrome, disseminated intravascular

coagulation, hepatic failure, or renal failure.

Figure (2)Mechanism of organ dysfunction in sepsis

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

The fulminate progression from SIRS to

MODS is determined by the balance of anti-

inflammatory and pro inflammatory mediators

or cytokines that are released from endothelial

cell disruption Global tissue hypoperfusion alone

can independently activate the inflammatory

response and serve as a co morbid variable in the

pathogenesis of all forms of shock.(8) The failure

to diagnose and treat global tissue hypoperfusion

in a timely manner leads to an accumulation of

an oxygen debt, the magnitude of which correlates

with increased mortality.

There are four stages of shock

As it is a complex and continuous condition there

is no sudden transition from one stage to the

next.(9) At a cellular level, shock is the process

of oxygen demand becoming greater than oxygen

supply.(10)

Initial

During this stage, the state of hypoperfusion

causes hypoxia. Due to the lack of oxygen, the

cells perform lactic acid fermentation. Since

oxygen, the terminal electron acceptor in the

electron transport chain, is not abundant, this

slows down entry of pyruvate into the Krebs

cycle, resulting in its accumulation. Accumulating

pyruvate is converted to lactate by lactate

dehydrogenase and hence lactate accumulates

(causing lactic acidosis) figure (1).

Compensatory

This stage is characterised by the body employing

physiological mechanisms, including neural,

hormonal and bio-chemical mechanisms in an

attempt to reverse the condition. As a result of

the acidosis, the person will begin to

hyperventilate in order to rid the body of carbon

dioxide (CO2). CO2 indirectly acts to acidify the

blood and by removing it the body is attempting

to raise the pH of the blood. The baroreceptors in

the arteries detect the resulting hypotension, and

cause the release of epinephrine and

norepinephrine. Norepinephrine causes

predominately vasoconstriction with a mild

increase in heart rate, whereas epinephrine

predominately causes an increase in heart rate

with a small effect on the vascular tone; the

combined effect results in an increase in blood

pressure. The renin-angiotensin axis is activated,

and arginine vasopressin (Anti-diuretic hormone;

ADH) is released to conserve fluid via the

kidneys. These hormones cause the

vasoconstriction of the kidneys, gastrointestinal

tract, and other organs to divert blood to the heart,

lungs and brain. The lack of blood to the renal

system causes the characteristic low urine

production. However the effects of the renin-

angiotensin axis take time and are of little

importance to the immediate homeostatic

mediation of shock.

Progressive

Should the cause of the crisis not be successfully

treated, the shock will proceed to the progressive

stage and the compensatory mechanisms begin

to fail. Due to the decreased perfusion of the cells,

sodium ions build up within while potassium ions

leak out. As anaerobic metabolism continues,

increasing the body's metabolic acidosis, the

arteriolar smooth muscle and precapillary

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

sphincters relax such that blood remains in the

capillaries.(11) Due to this, the hydrostatic

pressure will increase and, combined with

histamine release, this will lead to leakage of fluid

and protein into the surrounding tissues. As this

fluid is lost, the blood concentration and viscosity

increase, causing sludging of the micro-

circulation. The prolonged vasoconstriction will

also cause the vital organs to be compromised

due to reduced perfusion.(11) If the bowel

becomes sufficiently ischemic, bacteria may enter

the blood stream, resulting in the increased

complication of endotoxic shock.(11,12)

Refractory

At this stage, the vital organs have failed and the

shock can no longer be reversed. Brain damage

and cell death are occurring, and death will occur

imminently. One of the primary reasons that shock

is irreversible at this point is that much cellular

ATP has been degraded into adenosine in the

absence of oxygen as an electron receptor in the

mitochondrial matrix. Adenosine easily perfuses

out of cellular membranes into extracellular fluid,

furthering capillary vasodilation, and then is

transformed into uric acid. Because cells can only

produce adenosine at a rate of about 2% of the

cell's total need per hour, even restoring oxygen

is futile at this point because there is no adenosine

to phosphorylate into ATP.(12)

Diagnosis

Signs and symptoms: The presentation of shock

is variable with some people having only minimal

symptoms such as confusion and weakness.(13)

While the general signs for all types of shock are

low blood pressure, decreased urine output, and

confusion these may not always be present.(14)

While a fast heart rate is common, those on ?-

blockers, those who are athletic and in 30% of

cases those with shock due to intra abdominal

bleeding may have a normal or slow heart rate.

Direct loss of effective circulating blood volume

leading to:

• A rapid, weak, thready pulse due to decreased

blood flow combined with tachycardia

• Cool, clammy skin due to vasoconstriction .

• Rapid and shallow breathing due to

sympathetic nervous system stimulation and

acidosis

• Hypothermia due to decreased perfusion and

evaporation of sweat

• Thirst and dry mouth, due to fluid depletion

• Cold and mottled skin , especially

extremities, due to insufficient perfusion of

the skin

The shock index (SI), defined as heart rate

divided by systolic blood pressure, is an accurate

diagnostic measure that is more useful than

hypotension and tachycardia in isolation.(15)

Under normal conditions, a number between 0.5

and 0.8 is typically seen. Should that number

increase, so does suspicion of an underlying state

of shock. Blood pressure alone may not be a

reliable sign for shock, as there are times when a

person is in circulatory shock but has a stable

blood pressure.(12)

Empirical criteria for diagnosis of circulatory

shock regardless of the cause ,four of these six

criteria should be met(16) :

1. Ill appearance or altered mental status.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

2. Heart rate> 100 beat/min .

3.Respiratory rate >20 cycle/min .or paco2< 32

mm/hg

4.serum lactate level > 4 mmol/L.

5.Arterial base deficit ? -4meq/L.

6.Arterial hypotension> 20 minutes duration .

The first changes seen in shock is an

increased cardiac output followed by a decrease

in mixed venous oxygen saturation (SmvO2) as

measured in the pulmonary artery via a pulmonary

artery catheter. Central venous oxygen saturation

(ScvO2) as measured via a central line correlates

well with SmvO2 and are easier to acquire. If

shock progresses anaerobic metabolism will begin

to occur with an increased blood lactic acid as

the result. While many laboratory tests are

typically performed there is no test that either

makes or excludes the diagnosis. A chest X-ray

or emergency department ultrasound may be

useful to determine volume state.

Differential diagnosis (17)

Shock is a common end point of many medical

conditions. It has been divided into four main

types based on the underlying cause:

hypovolemic, distributive, cardiogenic and

obstructive. A few additional classifications are

occasionally used including: endocrinologic

shock.

Hypovolemic: This is the most common type of

shock and is caused by insufficient circulating

volume. Its primary cause is hemorrhage (internal

and/or external), or loss of fluid from the

circulation. Vomiting and diarrhea are the most

common cause in children.. With other causes

including burns, environmental exposure and

excess urine loss due to diabetic ketoacidosis and

diabetes insipidus.

Table (I): Classes of hemorrhage.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Cardiogenic

This type of shock is caused by the failure of the

heart to pump effectively. This can be due to

damage to the heart muscle, most often from a

large myocardial infarction. Other causes of

cardiogenic shock include dysrhythmias,

cardiomyopathy/myocarditis, congestive heart

failure (CHF), or cardiac valve problems.

Obstructive

Obstructive shock is due to obstruction of blood

flow outside of the heart.(18)Several conditions

can result in this form of shock.

• Cardiac tamponade in which fluid in the

pericardium prevents inflow of blood into

the heart (venous return). Constrictive

pericarditis, in which the pericardium

shrinks and hardens, is similar in

presentation.

• Tension pneumothorax Through increased

intrathoracic pressure, blood flow to the

heart is prevented (venous return).

• Pulmonary embolism is the result of a

thromboembolic incident in the blood

vessels of the lungs and hinders the return

of blood to the heart.

• Aortic stenosis hinders circulation by

obstructing the ventricular outflow tract

Distributive

Distributive shock is due to impaired

utilization of oxygen and thus production of

energy by the cell. Examples of this form of shock

are:

• Septic shock is the most common cause of

distributive shock.(19) Caused by an

overwhelming systemic infection resulting

in vasodilation leading to hypotension.

Septic shock can be caused by Gram

negative bacteria such as (among others)

Escherichia coli, Proteus species, Klebsiella

pneumoniae which release an endotoxin

which produces adverse biochemical,

immunological and occasionally

neurological effects which are harmful to

the body, and other Gram-positive cocci,

such as pneumococci and streptococci, and

certain fungi as well as Gram-positive

bacterial toxins.

Septic shock also includes some elements

of cardiogenic shock. Septic shock can be defined

as "sepsis-induced hypotension (systolic blood

pressure <90 mm Hg or a reduction of 40 mm Hg

from baseline) despite adequate fluid resuscitation

along with the presence of perfusion

abnormalities that may include, but are not limited

to, lactic acidosis, oliguria, or an acute alteration

in mental status. Patients who are receiving

inotropic or vasopressor agents may have a

normalized blood pressure at the time that

perfusion abnormalities are identified.

Figure (1) petechial haemorrhage

in case of sepsis.

Early detection(20)

The qSOFA Score was introduced by the

Sepsis-3 group in February 2016 as a simplified

version of the SOFA Score as an initial way to

screen for sepsis.

The qSOFA Score is an easy to use and

apply score to help as an initial screening tool for

poor outcome in infection patients.

qSOFA, ie, alteration in mental status, systolic

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

blood pressure ?100 mm Hg, or respiratory rate

>22/min.

septic shock

• can be identified with a clinical construct

of sepsis with persisting hypotension

requiring vasopressors to maintain MAP

>65 mm Hg and having a serum lactate

level >2 mmol/L (18 mg/dL) despite

adequate volume resuscitation.

• With these criteria, hospital mortality is

in excess of 40%.

Figure (3) new definition of sepsis according to

The Third International Consensus Definitions

for Sepsis and Septic Shock (Sepsis-3).

• Anaphylactic shock (17,67) :

Anaphylaxis is a severe, life-threatening,

generalized or systemic hypersensitivity reaction.

Characterized by rapidly developing life-

threatening airway and or breathing and or

circulation problems usually associated with skin

and mucosal changes.

Figure (2,3) show skin and mucosal changes

with anaphylaxis

Caused by a severe anaphylactic reaction to an

allergen, antigen, drug or foreign protein causing

the release of histamine which causes widespread

vasodilation, leading to hypotension and

increased capillary permeability.

• Neurogenic shock: High spinal injuries

may cause neurogenic shock.(21) The classic

symptoms include a slow heart rate due to loss of

cardiac sympathetic tone and warm skin due to

dilation of the peripheral blood vessels. (This term

can be confused with spinal shock which is a

recoverable loss of function of the spinal cord

after injury and does not refer to the

haemodynamic instability per se.)

Cervical spine MRI of a patient with SCI: C4

fracture and dislocation, spinal cord

compression

Low blood pressure occurs due to

decreased systemic vascular resistance resulting

in pooling of blood within the extremities lacking

sympathetic tone. The slowed heart rate results

from unopposed vagal activity and has been found

to be exacerbated by hypoxia and endobronchial

suction.(22) Neurogenic shock can be a potentially

devastating complication, leading to organ

dysfunction and death if not promptly recognized

and treated. It is not to be confused with spinal

shock, which is not circulatory in nature.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Causes: Neurogenic shock can result

from severe central nervous system damage (brain

injury, cervical or high thoracic spinal cord). (23)

In more simple terms: the trauma causes a sudden

loss of background sympathetic stimulation to the

blood vessels. This causes them to relax

(vasodilation) (24) resulting in a sudden decrease

in blood pressure (secondary to a decrease in

peripheral vascular resistance).Neurogenic shock

results from damage to the spinal cord above the

level of the 6th thoracic vertebra. (25) It is found

in about half of people who suffer spinal cord

injury within the first 24 hours, and usually doesn't

go away for one to three weeks. (25)

Endocrine: Based on endocrine disturbances such

as: (26)

• Hypothyroidism (Can be considered a

form of Cardiogenic shock) in critically ill

patients, reduces cardiac output and can lead to

hypotension and respiratory insufficiency.

• Thyrotoxicosis (Cardiogenic shock)

• may induce a reversible

cardiomyopathy.

• Acute adrenal insufficiency (Distributive

shock) is frequently the result of discontinuing

corticosteroid treatment without tapering the

dosage. However, surgery and inter current

disease in patients on corticosteroid therapy

without adjusting the dosage to accommodate for

increased requirements may also result in this

condition.

• Relative adrenal insufficiency

(Distributive shock) in critically ill patients where

present hormone levels are insufficient to meet

the higher demands

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Initial Approach to the Patient in

Shock(27)

As any critically ill patient follow ABCDE

approach in our management (airway, breathing,

circulation, disability, and exposure). Early,

adequate hemodynamic support of patients in

shock is crucial to prevent worsening organ

dysfunction and failure. Resuscitation should be

started even while investigation of the cause is

ongoing. Once identified, the cause must be

corrected rapidly (e.g., control of bleeding,

percutaneous coronary intervention for coronary

syndromes, thrombolysis or embolectomy for

massive pulmonary embolism, and administration

of antibiotics and source control for septic shock).

Unless the condition is rapidly reversed, an

arterial catheter should be inserted for monitoring

of arterial blood pressure and blood sampling,

plus a central venous catheter for the infusion of

fluids and vasoactive agents and to guide fluid

therapy.

The initial management of shock is problem-

oriented, and the goals are therefore the same,

regardless of the cause, although the exact

treatments that are used to reach those goals may

differ. A useful mnemonic to describe the

important components of resuscitation is the VIP

rule(28) : ventilate (oxygen administration),

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

infuse (fluid resuscitation), and pump

(administration of vasoactive agents).

Ventilatory Support

The administration of oxygen should be started

immediately to increase oxygen delivery and

prevent pulmonary hypertension. Pulse oximetry

is often unreliable as a result of peripheral

vasoconstriction, and precise determination of

oxygen requirements will often require blood gas

monitoring. Mechanical ventilation by means of

a mask rather than endotracheal intubation has a

limited place in the treatment of shock because

technical failure can rapidly result in respiratory

and cardiac arrest. Hence, endotracheal intubation

should be performed to provide invasive

mechanical ventilation in nearly all patients with

severe dyspnea, hypoxemia, or persistent or

worsening acidemia (pH, <7.30).

Invasive mechanical ventilation has the

additional benefits of reducing the oxygen

demand of respiratory muscles and decreasing left

ventricular afterload by increasing trathoracic

pressure. An abrupt decrease in arterial pressure

after the initiation of invasive mechanical

ventilation strongly suggests hypovolemia and a

decrease in venous return.The use of sedative

agents should be kept to a minimum to avoid

further decreases in arterial pressure and cardiac

output.

Fluid Resuscitation

Fluid therapy to improve microvascular

bloodflow and increase cardiac output is an

essential part of the treatment of any form of

shock. Even patients with cardiogenic shock may

benefit from fluids, since acute edema can result

in a decrease in the effective intravascular volume.

However, fluid administration should be closely

monitored, since too much fluid carries the risk

of edema with its unwanted consequences.

Pragmatic end points for fluid resuscitation are

difficult to define. In general, the objective is for

cardiac output to become preload-

independent(i.e., on the plateau portion of the

Frank-Starling curve), but this is difficult to assess

clinically.

In patients receiving mechanical ventilation,

signs of fluid responsiveness may be identified

either directly from beat-by-beat stroke-volume

measurements with the use of cardiac-output

monitors or indirectly from observed variations

in pulse pressure on the arterial-pressure tracing

during the ventilator cycle. However, such

bedside inferences have some limitations(29)-

notably, that the patient must receive ventilation

with relatively large tidal volumes, have no

spontaneous breathing effort (which usually

requires the administration of sedatives or even

muscle relaxants),and be free of major arrhythmia

and right ventricular dysfunction. A passive leg-

raising test is an alternative method(30) but

requires a rapid response device, since the effect

is transient. Regardless of the test used, there

remains a gray zone in which it is difficult to

predict a patient's response to intravenous fluids.

A fluid-challenge technique should be used to

determine a patient's actual response to fluids,

while limiting the risks of adverse effects. A fluid

challenge incorporates four elements that should

be defined in advance. (31)

• First, the type of fluid must be selected.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Crystalloid solutions are the first choice, because

they are well tolerated and cheap. The use of

albumin to correct severe hypoalbuminemia may

be reasonable in some patients.(32)

• Second, the rate of fluid administration

must be defined. Fluids should be infused rapidly

to induce a quick response but not so fast that an

artificial stress response develops; typically, an

infusion of 300 to 500 ml of fluidis administered

during a period of 20 to 30 minutes. (33)

• Third, the objective of the fluid challenge

must be defined. In shock, the objective is usually

an increase in systemic arterial pressure, although

it could also be a decrease in heart rate or an

increase in urine output.

• Finally, the safety limits must be defined.

Pulmonary edema is the most serious

complication of fluid infusion. Although it is not

a perfect guideline, a limit in central venous

pressure of a few millimeters of mercury above

the baseline value is usually set to prevent fluid

overload. (34)

Stimulation of the patient and any other

change in therapy should be avoided during the

test. Fluid challenges can be repeated as required

but must be stopped rapidly in case of non-

response n order to avoid fluid overload.

Vasoactive Agents

Vasopressors

If hypotension is severe or if it persists

despite fluid administration, the use of

vasopressors is indicated. It is acceptable practice

to administer a vasopressor temporarily while

fluid resuscitation is ongoing, with the aim of

discontinuing it, if possible, after hypovolemia

has been corrected.

Adrenergic agonists are the first-line vasopressors

because of their rapid onset of action, high

potency, and short half-life, which allows easy

dose adjustment. Stimulation of each type of

adrenergic receptor has potentially beneficial and

harmful effects. For example, β -adrenergic

stimulation can increase blood flow but also

increases the risk of myocardial ischemia as a

result of increased heart rate and contractility.

Hence, the use of isoproterenol, a pure α -

adrenergic agent, is limited to the treatment of

patients with severe bradycardia.

At the other extreme, β -adrenergic

stimulation will increase vascular tone and blood

pressure but can also decrease cardiac output and

impair tissue blood flow, especially in the

hepatosplanchnic region. For this reason,

phenylephrine, an almost pure ?-adrenergic agent,

is rarely indicated.

We consider norepinephrine to be the

vasopressor of first choice; it has predominantly

β-adrenergic properties, but its modest α-

adrenergic effects help to maintain cardiac output.

Administration generally results in a clinically

significant increase in mean arterial pressure, with

little change in heart rate or cardiac output. The

usual dose is 0.1 to 2.0 μ g per kilogram of body

weight per minute.

Dopamine has predominantly β -

adrenergic effects at lower doses and α -adrenergic

effects at higher doses, but its effects are relatively

weak. Dopaminergic effects at very low doses (<3

μg per kilogram per minute, given intravenously)

may selectively dilate the hepatosplanchnic and

renal circulations, but controlled trials have not

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

shown a protective effect on renal function,(35)

and its routine use for this purpose is no longer

recommended.

Dopaminergic stimulation may also have

undesired endocrine effects on the hypothalamic-

pituitary system, resulting in immunosuppression,

primarily through a reduction in the release of

prolactin.

In a recent randomized, controlled, double

blind trial, dopamine had no advantage over

norepinephrine as the first-line vasopressor agent;

moreover, it induced more arrhythmias and was

associated with an increased 28-day rate of death

among patients with cardiogenic shock.(36)

Administration of dopamine, as compared with

norepinephrine, may also be associated with

higher rates of death among patients with

septicshock.(37)Hence, we no longer recommend

dopamine for the treatment of patients with shock.

Epinephrine, which is a stronger agent, has

predominantly β -adrenergic effects at low doses,

with α -adrenergic effects becoming more

clinically significant at higher doses. However,

epinephrine administration can be associated with

an increased rate of arrhythmia(38,39)and a

decrease in splanchnic blood flow(38)and can

increase blood lactate levels, probably by

increasing cellular metabolism.(38,40)

Prospective, randomized studies have not

shown any beneficial effects of epinephrine over

norepinephrine in septic shock.(39,40)We reserve

epinephrine as a second-line agent for severe

cases. (34)

The use of other strong vasopressor agents

as ontinuous infusions (e.g., angiotensin or

metaraminol)has largely been abandoned.

Non selective inhibition of nitric oxide has

not been shown to be beneficial in patients with

cardiogenic shock(41)and is detrimental in

patients with septic shock. (42)

Vasopressin deficiency can develop in

patients with very hyperkinetic forms of

distributive shock, and the administration of low-

dose vasopressin may result in substantial

increases in arterial pressure. In the Vasopressin

and SepticShock Trial (VASST), investigators

found that the addition of low-dose vasopressin

to norepinephrine in the treatment of patients with

septic shock was safe(43)and may have been

associated with a survival benefit for patients with

forms of shock that were not severe and for those

who also received glucocorticoids. (44)

Vasopressin should not be used at doses higher

than 0.04 U per minute and should be

administered only in patients with a high level of

cardiac output.

Terlipressin, an analogue of vasopressin,

has a duration of action of several hours, as

compared with minutes for vasopressin. For this

reason, we do not believe it offers an advantage

over vasopressin in the ICU. Vasopressin

derivatives with more selective V1-receptor

activity are currently being studied.

Inotropic Agents

We consider dobutamine to be the inotropic agent

of choice for increasing cardiac output, regardless

of whether norepinephrine is also being given.

With predominantly β -adrenergic properties

,dobutamine is less likely to induce tachycardia

than isoproterenol. An initial dose of just a few

micrograms per kilogram per minute may

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

substantially increase cardiac output. Intravenous

doses in excess of 20 μ g per kilogram per minute

usually provide little additional benefit.

Dobutamine has limited effects on arterial

pressure, although pressure may increase slightly

in patients with myocardial dysfunction as the

primary abnormality or may decrease slightly in

patients with underlying hypovolemia. Instead of

routine administration of a fixed dose of

dobutamine to increase oxygen delivery to

supranormal, predetermined levels, the dose

should be adjusted on an individual basis to

achieve adequate tissue perfusion. Dobutamine

may improve capillary perfusion in patients with

septic shock, independent of its systemic effects.

(45)Phosphodiesterase type III inhibitors, such as

milrinone and enoximone, combine inotropic and

vasodilating properties.

By decreasing the metabolism of cyclic

AMP, these agents may reinforce the effects of

dobutamine. They may also be useful when β-

adrenergic receptors are down regulated or in

patients recently treated with beta-blockers.

However, phosphodiesterase typeIII inhibitors

may have unacceptable adverse effects in patients

with hypotension, and the long half-lives of these

agents (4 to 6 hours) prevent minute-to-minute

adjustment. Hence, intermittent, short-term

infusions of small doses of phosphodiesterase III

inhibitors may be preferable to a continuous

infusion in shock states. Levosimendan, a more

expensive agent, acts primarily by binding to

cardiac troponin C and increasing the calcium

sensitivity of myocytes, but it also acts as a

vasodilator by opening ATP sensitive potassium

channels in vascular smoothmuscle. However,

this agent has a half-life of several days, which

limits the practicality of its use in acute shock

states.

Vasodilators

By reducing ventricular after load,

vasodilating agents may increase cardiac output

without increasing myocardial demand for

oxygen. The major limitation of these drugs is

the risk of decreasing arterial pressure to a level

that compromises tissue perfusion. Nevertheless,

in some patients, prudent use of nitrates and

possibly other vasodilators may improve

microvascular perfusion and cellular function.

(46)

Mechanical Support

Mechanical support with intraaortic

balloon counterpulsation (IABC) can reduce left

ventricular afterload and increase coronary blood

flow. However, a recent randomized, controlled

tria lshowed no beneficial effect of IABC in

patients with cardiogenic shock,(47)and its

routine use in cardiogenic shock is not currently

recommended.

Venoarterial extracorporeal membrane

oxygenation(ECMO) may be used as a temporary

lifesaving measure in patients with reversible

cardiogenicshock or as a bridge to heart

transplantation. (48)

Goals of Hemodynamic Support

Arterial Pressure

The primary goal of resuscitation should be not

only to restore blood pressure but also to provide

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

adequate cellular metabolism, for which the

correction of arterial hypotension is a prerequisite.

Restoring a mean systemic arterial pressure of65

to 70 mm Hg is a good initial goal, but the level

should be adjusted to restore tissue perfusion,

assessed on the basis of mental status, skin

appearance, and urine output, as described above.

In patients with oliguria, in particular, the effects

of a further increase in arterial pressure on urine

output should be assessed regularly, unless acute

renal failure is already established. Conversely, a

mean arterial pressure lower than 65 to 70 mm

Hg may be acceptable in a patient with acute

bleeding who has no major neurologic problems,

with the aim of limiting blood loss and associated

coagulopathy, until the bleeding is controlled.

Cardiac Output and Oxygen Delivery

Since circulatory shock represents an

imbalance between oxygen supply and oxygen

requirements, maintaining adequate oxygen

delivery to the tissues is essential, but all the

strategies to achieve this goal have limitations.

After correction of hypoxemia and severe anemia,

cardiac output is the principal determinant of

oxygen delivery, but the optimal cardiac output is

difficult to define. Cardiac output can be measured

by means of various techniques, each of which has

its own benefits and drawbacks(49).Absolute

measures of cardia coutput are less important than

monitoring trends in response to interventions such

as a fluid challenge.

The targeting of a predefined cardiac

output is not advisable, since the cardiac output

that is needed will vary among patients and in

the same patient over time. Measurements of

mixed venous oxygen saturation(SvO2) may be

helpful in assessing the adequacy of the balance

between oxygen demandand supply; SvO2

measurements are also very useful in the

interpretation of cardiac output.(50) SvO2 is

typically decreased in patients with low-flow

states or anemia but is normal or high in those

with distributive shock. Its surrogate,

central venous oxygen saturation (ScvO2), which

is measured in the superior vena cava by means

of a central venous catheter, reflects the oxygen

saturation of the venous blood from the upperhalf

of the body only. Under normal circumstances,

ScvO2 is slightly less than SvO2, but in critically

ill patients it is often greater. Rivers et al. (51)

found that in patients presenting to the emergency

department with septic shock, a treatment

algorithm targeting an ScvO2 of at least 70%

during the first 6 hours was associated with

decreased rates of death. The robustness of this

finding is currently being evaluated in three

multicenter trials. (ClinicalTrials.gov numbers,

NCT00975793and NCT00510835; and Current

Controlled Trials number, ISRCTN36307479).

Blood Lactate Level

An increase in the blood lactate level

reflects abnormal cellular function. In low-flow

states, theprimary mechanism of hyperlactatemia

is tissue hypoxia with development of anaerobic

metabolism, but in distributive shock, the

pathophysiology is more complex and may also

involve increased glycolysis and inhibition of

pyruvate dehydrogenase.

In all cases, alterations in clearance can

be due to impaired liver function.The value of

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

serial lactate measurements in the management

of shock has been recognized for 30 years. (52)

Although changes in lactate take place more

slowly than changes in systemic arterial pressure

or cardiac output, the blood lactate level should

decrease over a period of hours with effective

therapy. In patients with shock and a blood lactate

level of more than 3 mmol per liter, Jansen et al.

(46) found that targeting a decrease of at least

20% in the blood lactate level over a 2-hour period

seemed to be associated with reduced in-hospital

mortality.

Microcirculatory Variables

The development of hand held devices for

orthogonalpolarization spectral (OPS) imaging

and its successor, side stream dark-field (SDF)

imaging, is providing new means of directly

visualizing the microcirculation and evaluating

the effects of interventions on microcirculatory

flow in easily accessible surfaces, such as the

sublingual area. (53) Microcirculatory changes,

including decreased capillary density, a reduced

proportion of perfused capillaries, and increased

heterogeneity of blood flow, have been identified

in various types of circulatory shock , and the

persistence of these alterations is associated with

worse outcomes. (54)

Near-infrared spectroscopy is a technique

that uses near-infrared light to determine tissue

oxygen saturation from the fractions of

oxyhemoglobin and deoxyhemoglobin. Analysis

of the changes in tissue oxygen saturation during

a brief episode of forearm ischemia can be used

to quantify micro vascular dysfunction(55); such

alterations are associated with worse

outcomes.(56)

Various therapeutic interventions have

been shown to have an effect on these

microcirculatory variables, but whether therapy

that is guided by monitoring or targeting the micro

circulation can improve outcomes requires further

study and cannot be recommended at this time.

Therapeutic Priorities and Goals

There are essentially four phases in the

treatmentof shock, and therapeutic goals and

monitoringneed to be adapted to each phase .

• In thefirst (salvage) phase, the goal of

therapy is to achieve a minimum blood pressure

and cardiac output compatible with immediate

survival. Minimal monitoring is needed; in most

cases, invasive monitoring can be restricted to

arterial and central venous catheters. Lifesaving

procedures (e.g.,surgery for trauma, pericardial

drainage, revascularization for acute myocardial

infarction, and antibioticsfor sepsis) are needed

to treat the underlying cause.

• In the second (optimization) phase, the goal

is to increase cellular oxygen availability, and there

is a narrow window of opportunity for intervention

stargeting hemo dynamic status. (51) Adequate

hemodynamic resuscitation reduces inflammation,

mitochondrial dysfunction, and caspase activation.

(57,58) Measurements of SvO2 and lactate levels

may help guide therapy, and monitoring of cardiac

output should be considered.

• In the third(stabilization) phase, the goal

is to prevent organ dysfunction, even after

hemodynamic stability has been achieved.

Oxygen supply to the tissues is no longer the key

problem, and organ support becomes more

relevant.

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

• Finally, in the fourth (de escalation) phase,

the goal is to wean the patient from vasoactive

agents and promote spontaneous polyuria or

provoke fluid elimination through the use of

diuretics or ultra filtration to achieve a negative

fluid balance.

Treatment goals

The goal of treatment is to achieve a urine

output of greater than 0.5 ml/kg/h, a central

venous pressure of 8-12 mmHg and a mean

arterial pressure of 65-95 mmHg. In trauma the

goal is to stop the bleeding which in many cases

requires surgical interventions.

For those with haemorrhagic shock the

current evidence supports limiting the use of

fluids for penetrating thorax and abdominal

injuries allowing mild hypotension to persist

(known as permissive hypotension).(59)Targets

include a mean arterial pressure of 60 mmHg, a

systolic blood pressure of 70-90 mmHg.(60) or

until their adequate mentation and peripheral

pulses.(60)

Specific treatment for different type of shock

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Management Hypovolemic shock:

Management may include securing the

airway via intubation to decrease the work of

breathing, oxygen supplementation, intravenous

fluids and blood transfusions. It is important to

keep the person warm as well as adequately

manage pain and anxiety as these can increase

oxygen consumption.

Fluids Aggressive intravenous fluids are

recommended in most types of shock (e.g. 1-2

liter normal saline bolus over 10 minutes or 20ml/

kg in a child) which is usually instituted as the

person is being further evaluated(61) Which

intravenous fluid is superior, colloids or

crystalloids, remains undetermined. Thus as

crystalloids are less expensive they are

recommended.

If the person remains in shock after initial

resuscitation packed red blood cells should be

administered to keep the hemoglobin greater than

10gms/l. For those with hemorrhagic shock the

current evidence supports limiting the use of

fluids for penetrating thorax and abdominal

injuries allowing mild hypotension to persist

(known as permissive hypotension). (62) Targets

include a mean arterial pressure of 60 mmHg, a

systolic blood pressure of 70-90 mmHg, or until

their adequate mentation and peripheral pulses.

Medications Vasopressors may be

used if blood pressure does not improve with

fluids. There is no evidence of superiority of one

vasopressor over another. (63) Vasopressors have

not been found to improve outcomes when used

for hemorrhagic shock from trauma, but may be

of use in neurogenic shock. Activated protein C

(Xigris) while once aggressively promoted for the

management of septic shock has been found to

improve survival ,thus recommended. (64) The

use of sodium bicarbonate is controversial as it

has not been shown to improve outcomes. (65)

If used at all it should only be considered if the

pH is less than 7.0.

Figure (3) show The main pathophysiological

mechanisms involved in acute traumatic

coagulopathy and transfusion strategy. SAP,

systolic arterial pressure; RBC, red blood cells;

FFP, fresh-frozen plasma(66).

Septic shock:(20) The leadership of the

Surviving Sepsis Campaign (SSC) has believed

since its inception that both the SSC Guidelines

and the SSC performance improvement indicators

will evolve as new evidence that improves our

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

understanding of how best to care for patients with septic shock the SSC Executive Committee has

revised the improvement bundles as follows:

Anaphylaxis(67)

Narayana Medical Journal Volume-6 | Issue-1 | January-June 2017

Cardiogenic shock

Cardiogenic shock is defined by sustained

low blood pressure with tissue hypo perfusion

despite adequate left ventricular filling pressure.

Signs of tissue hypoperfusion include low urine

production (<30 mL/hour), cool extremities, and

altered level of consciousness.

Treatment of cardiogenic shock depends

on the cause. If cardiogenic shock is due to a heart

attack, attempts to open the heart's arteries may

help. An intra-aortic balloon pump or left

ventricular assist device may improve matters

until this can be done. Medications that improve

the heart's ability to contract (positive inotropes)

may help; however, it is unclear which is best.

Norepinephrine may be better if the blood

pressure is very low whereas dopamine or

dobutamine may be more useful if only slightly

low.(68)

Treatment of Neurogenic shock

• Dopamine (Intropin) is often used either

alone or in combination with other inotropic

agents.

• Vasopressin (antidiuretic hormone

[ADH])(69)

• Certain vasopressors (ephedrine,

norepinephrine). Phenylephrine may be used as

a first line treatment, or secondarily in people who

do not respond adequately to dopamine.

• Atropine is administered for slowed heart

rate.(70)

Conclusions

Circulatory shock is associated with high

morbidity and mortality. Prompt identification is

essential so that aggressive management can be

started. Appropriate treatment is based on a good

understanding of the underlying

pathophysiological mechanisms. Treatment

should include correction of the cause of shock

and hemodynamic stabilization, primarily through

fluid infusion and administration of vasoactive

agents. The patient's response can be monitored

by means of careful clinical evaluation and blood

lactate measurements;

microvascular evaluation may be feasible in the

future.

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List of Abbreviations

(a-v)CO2 Arterial-central venous carbon dioxide

difference

Cao2 Arterial oxygen content

Cmvo2 Mixed venous oxygen content

CI Cardiac index (cardiac output/body surface

area)

CO Cardiac output

CPP Coronary perfusion pressure

CVP Central venous pressure

Do2 Systemic oxygen delivery

DBP Diastolic blood pressure

Hb Hemoglobin

MAP Mean arterial pressure

MODS Multi organ dysfunction syndrome

OER Oxygen extraction ratio

Paco2 Arterial carbon dioxide pressure

Pao2 Arterial oxygen pressure

PAOP Pulmonary artery occlusion (wedge)

pressure

Sao2 Arterial oxygen saturation

Scvo2 Central venous oxygen saturation

Smvo2 Mixed venous oxygen saturation

(pulmonary artery)

Srvo2 Retinal venous oxygen saturation

SIRS Systemic inflammatory response syndrome

SVR Systemic vascular resistance

Vo2 Systemic oxygen consumption

... Th e main challenge lies in the diagnosis of the disease, diff erent treatment protocols, multiple risk factors, etiology, and outcomes. In this connection, the question arises regarding an integrated approach to the study of this condition and the development of recommendations for the management of patients of this kind, which served as the purpose of this manuscript [4]. ...

... It includes deaths that occur due to complications of the pregnancy (direct deaths), and those resulting from worsening of other disease processes due to the pregnancy (indirect deaths). Deaths that occur from causes completely unrelated to pregnancy or birth are termed incidental deaths, and are not included in calculation of the MMR [4]. ...

... Additionally, postpartum infections can be treated using antibiotics. In fact, the use of broad-spectrum antibiotics both for the prevention and treatment of maternal infection is common in low-income countries [5,4]. Maternal death due to eclampsia can also be prevented through the use of medications such as magnesium sulfate. ...

Adel Hamed Elbaih
Adnan Um Al-Nasser

Background: Maternal collapse occurs any time during pregnancy, up to 42 days following delivery and is an acute event involving cardiorespiratory systems and/or brain, resulting in impaired consciousness or death. Therefore, we aim to look into the common pitfalls that both medical students and new physicians face in the recognition, diagnosis, and management of these conditions. Targeted Population: Maternal collapse patients who are requiring urgent management in the ED, with Emergency Physicians for teaching approach protocol. Aim of the study: Appropriate for identifi cation of women at risk and review of maternal collapse with neonatal outcomes by training protocol to Emergency Physicians. Based on patients' causes of maternal collapse pregnant women. Methods: Collection of all possible available data about the Pregnancy in Maternal Collapse in the Emergency department. By many research questions to achieve these aims so a midline literature search was performed with the keywords "critical care", "emergency medicine", "principals of ACLS therapy in Pregnancy ", "ACLS and Maternal Collapse". Literature search included an overview of recent defi nition, causes and recent therapeutic strategies. Results: All studies introduced that the initial diagnosis of Pregnancy in Maternal Collapse and their therapy is a serious condition that face patients of the emergency and critical care departments. Conclusion: Emergency obstetric care to address the major causes of maternal death, Postnatal care which is the six weeks following delivery and Public health approach to decrease with addressing maternal mortality. Keywords: Maternal collapse; Pregnant women; Emergency physicians; Skill approach.

... Conventionally, there's four shock categories: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic shock happens when intravascular volume is decreasing to the extent of cardiovascular failure [7,8]. The hypovolemic shock may result from extreme dehydration by a variety of mechanisms or from lack of blood. ...

... ICP is normally ≤ 15 mmHg in adults, and pathologic ICH is present at pressures ≥ 20 mm Hg. Homeostatic mechanisms stabilize ICP, with occasional transient elevations associated with physiologic events, including sneezing, coughing, or Valsalva maneuvers [5,8] (Table 1). ...

... Multiple causes have been identified that disturb the electrical function of the heart and cause sudden cardiac arrest, and they can be divided into two branches cardiac and non-cardiac causes. Cardiac causes can be further divided into non-structural and structural, with structural causes having two categories, ischemic and non-ischemic [9]. ...

Adel Hamed Elbaih

Background: Sudden Cardiac Arrest (SCA) in pregnancy is a particularly challenging clinical condition. Although management and resuscitation of these patients are quite similar to other adult patients except for few modifications because of the changes of pregnancy, but the uniqueness of this situation lays in the fact that here you are dealing with two patients instead of one. Targeted Population: All Pregnancy patients who are requiring urgent management in the ED, with Emergency Physicians for teaching protocol. Aim of the Study: Appropriate knowledge and training for pregnancy patients by teaching protocol to Emergency Physicians. Methods: Collection of all possible available data about the pregnancy with cardiac arrest in the Emergency Department. By many research questions to achieve these aims so a midline literature search was performed with the keywords "critical care", "emergency medicine", "principals of resuscitation in pregnancy", "Maternal Collapse". Literature search included an overview of recent definition, causes and recent therapeutic strategies. Results: All studies introduced that the initial diagnosis of pregnancy with cardiac arrest and their therapy is a serious condition that face patients of the emergency and critical care departments. Conclusion: Appropriate knowledge and training for pregnancy patients by teaching protocol to Emergency Physicians are extremely important for a better outcome, since a poor resuscitation techniques and knowledge deficit are strongly linked to poorer outcomes. Keywords: Cardiac arrest in pregnancy; Emergency physicians; Protocol; SCA; SCD

Adel Hamed Elbaih
Emad Amjad Abou

Background: Trauma continues to be the leading cause of death; responsible for more than 5 million deaths worldwide each year. Uncontrolled hemorrhage is the leading cause of preventable death in such cases, attributing about 50% of trauma-related deaths within 24 h of injury. Deaths from haemorrhage represents a substantial global problem, with more than 60,000 deaths per year in the United States and an estimated 1.9 million deaths per year worldwide, 1.5 million of which result from physical trauma. Therefore, we aim to look into the common pitfalls that both medical students and new physicians face in the recognition, diagnosis, and Emergency Traumatic Haemorrhagic Shock Resuscitations. Targeted population: Haemorrhagic Shock patients who are requiring urgent management in the ED, with Emergency Physicians for teaching approach protocol. Aim of the study: Appropriate for assessment and priorities for Haemorrhagic Shock Patients Resuscitations by training protocol to Emergency Physicians. Based on Resuscitations guidelines by applying the ATLS protocol in traumatic Haemorrhagic shock. Methods: Collection of all possible available data about the haemorrhagic patients' therapy in the Emergency department. By many research questions to achieve these aims so a midline literature search was performed with the keywords "critical care", "emergency medicine", "principals of urgent therapy in haemorrhage", "Resuscitations and ATLS". All studies introduced that the initial diagnosis of hypovolemia is a serious condition that face patients of the emergency and critical care departments. Literature search included an overview of recent definition, causes and recent therapeutic strategies. Conclusion: Haemorrhage is the cause of shock in most trauma patients and Treatment of these patients requires immediate haemorrhage control and fluid or blood replacement. Initial assessment of a shocked patient involves careful physical examination, finding signs of life-threatening problems and other causes of shock. In case of, Shock does not respond to initial crystalloid fluid bolus. Think about an internal bleeding or a non-Haemorrhagic source of shock. Keywords: Haemorrhagic shock, Emergency physicians; Skill approach; Management

... • Costochondritis: An inflammation of the cartilage between the ribs. Pain is typically located in the mid-chest, with intermittently dull and sharp pain that may be increased with deep breaths, movement, and deep touch [38]. ...

Introduction: The hospital ED is one of the most important components of the health care system. There is an increase in numbers of chest pain patients visiting EDs leading to overcrowding, long waiting time, missed diagnostic cases and negative impact on patient satisfaction. Chest pain is one of the most common reasons people call for emergency medical help. Fortunately, chest pain was not always a signal for a heart attack. Often chest pain is unrelated to any heart problem. However, even if the chest pain the patient experience has nothing to do with his cardiovascular system, the problem may still be important and worth the time spent in an emergency room for evaluation. So, we aimed to update knowledge and review researches in the field of chest pain and reduction in waiting time, missed diagnostic cases and Overcome Crowdness Patients in emergency department. Methods: Collection of all possible available data about the chest pain patients in the Emergency department. By many research questions to achieve these aims so, a midline literature search was performed with the keywords "critical care", "emergency medicine", "acute chest pain", "myocardial ischemia". All studies introduced that the myocardial ischemia is a serious pathology that face patients of the emergency and critical care departments. Literature search included an overview of recent definition, causes, pathophysiology, prophylactic and recent therapeutic strategies. Results: Myocardial Ischemia means narrowing of Coronaries whatever it was transient or permanent, partial or complete, painful or silent, recurrent or firstly experienced, recordable or not. This, although chambers are full of blood, makes heart muscle blood supply decreases and if it continued, it may result in myocardium permanent damage (Myocardial infarction). Conclusion: "Prevention is better than cure" Decline in death rates could be achieved by adopting a healthier lifestyle. That is why it is important for healthcare professionals to implement primary and secondary prevention. And there are many types emergency department of chest pain risk stratifications so any one of them should be applied e.g. TIMI or HEART score in daily emergency work. Keywords: Emergency Department; Myocardial Ischemia; Management

... In Egypt, it estimated that the mortality rate as result of cardiovascular diseases (5.6%) and by 2018, over millions people would suffer serious CA. Unfortunately, of all who suffer CA only less than 8% survive (3). ...

Aim: Determination of the effect of training CPR program on the nurses working practice and knowledge in Emergency department (ED). Nearly 20% survive rate in adult of hospital cardiac arrest (CA). Cardiopulmonary Resuscitation (CPR) is increase the survival rate into double number but CA without treatment is falling 10-15% per minute of survival rate; however, the performed proper CPR likely shifts this curve towards a higher probability of survival. Material and Methods: The study is Interventional included 65 nurses. They fill questionnaire sheet used and constructed via the Research Committee in Murcia's Hospital based on the "American Heart Association (AHA) 2010 Guidelines of CPR". To assess nurses' knowledge about sudden cardiac arrest and CPR but we used Pre and post questionnaire knowledge that applied in three phases: Assessment phase, Implementation phase, and Evaluation phase. Results:The study revealed 73% of nurses do not have previous training. Twenty-seven percentage nurses not have any information about CPR and 22.5% of them the main source of the information gained through training program more than one year ago. While the 94.6% of them willing to attend CPR training program and report they need to perform high quality CPR respectively. Conclusion: The study give a clear view of the current knowledge and practice of CPR among nursing staff in our institution and can help in developing it. It also gives detailed information about the exact weak points, which would improve, in next workshops.

... The major cause of unstability in polytrauma patients diagnosed by RUSH is hypovolemic shock (64%), followed by obstructive 13 , whose second and third causes are respectively cardiogenic shock and obstructive shock. Anyway hypovolemic shock is still the dominant cause. ...

Adel Hamed Elbaih
Ahmed M Housseini
Mohamed E.M. Khalifa

Purpose "Polytrauma" patients are of a higher risk of complications and death than the summation of expected mortality and morbidity of their individual injuries. The ideal goal in trauma resuscitation care is to identify and treat all injuries. With clinical and technological advanced imaging available for diagnosis and treatment of traumatic patients, point of care---rapid ultrasound in shock and hypotension (RUSH) significantly affects modern trauma services and patient outcomes. This study aims to evaluate the accuracy of RUSH and patients outcomes by early detection of the causes of unstable polytrauma. Methods This cross-sectional, prospective study included 100 unstable polytrauma patients admitted in Suez Canal University Hospital. Clinical exam, RUSH and pan-computed tomography (pan-CT) were conducted. The result of CT was taken as the standard. Patients were managed according to the advanced trauma life support (ATLS) guidelines and treated of life threatening conditions if present. Patients were followed up for 28 days for a short outcome. Results The most diagnostic causes of unstability in polytrauma patients by RUSH are hypovolemic shock (64%), followed by obstructive shock (14%), distributive shock (12%) and cardiogenic shock (10%) respectively. RUSH had 94.2% sensitivity in the diagnosis of unstable polytrauma patients; the accuracy of RUSH in shock patients was 95.2%. Conclusion RUSH is accurate in the diagnosis of unstable polytrauma patients; and 4% of patients were diagnosed during follow-up after admission by RUSH and pan-CT.

Eric Kagunza

A Case study of a 25 year old male motorcyclist (Alex) who was brought into the emergency department of Jaramogi Oginga Odinga Teaching and Referral Hospital by an ambulance following an accident. The patient vital signs were :blood pressure 80/42 mmhg, heart rate 130 b/m, minimal urinary output. Provide a detailed explanation of why Alex's blood pressure dropped, pulse increased and how his body system will respond to bring his blood pressure within normal range.

Background: IN 2010, Institute of Medicine in USA report that medical errors are estimated to result in about between 44,000 and 98,000 preventable deaths and 1,000,000 excess injuries each year in U.S. hospitals. The annual cost of treating medical injuries in USA has been estimated to be $9 billion. The objective of this study was to follow up guidelines in treatment of Traumatic hypovolemic shocked patients. Methods: The design of this study is a cross sectional descriptive study was conducted on traumatic patients who presented to the emergency department between the periods from October 2012 to October 2013. This study was conducted at the emergency department Suez Canal University Hospital, Ismailia, Egypt. On 100 patients with traumatic hypovolemic shock male or female within the age ranges from 18 years till 65 years old. Patients admitted to the hospital with other types of shock with trauma, non-traumatic hypovolemic shock, pregnant females, advanced malignancy, patients below 18 years old or patients more than 65 years old should excluded from the study. Questionnaire was filled by the researcher during resuscitation of the patient diagnosed as traumatic hypovolemic shock by the medical team in details; medical error was identified by comparing the actual management plan to the standard plan according to the guidelines from "The Washington manual of critical care". Results: This study was conducted on 100 patients who presented to the Emergency Department, Seuz Canal University Hospital, Ismailia, Egypt. Between the period from October 2012 to October 2013 in order to detect medical errors in treatment of Traumatic hypovolemic shocked patients and to reach the optimal scheme of management. 1-More than half of the patients were in age group (≥30-45). And most of them were males about 70% of the studied patients and females were 30%. 2- Most of the patients were delayed in hospital arrival as we found that 50% reached in more than 40 min. 3-The initial medical help in the pre-hospital period was given to almost all of the patients (94%). 4- Incomplete exposure of patients is a very frequent medical error occurs during hospital assessment in about 22% of patients. Conclusions: Failure in oxygen saturation monitoring and forgetting complete exposure of the patient has statistically significant relation with mortality during in hospital assessment of the patient. Delayed insertion of 2 large cannula or central line, Fluid given not warmed and blood received not at the proper time all of them show statistically significant Relation with mortality during in hospital resuscitation of the patient with traumatic hypovolemic shock. Keywords: Unwarmed fluids, Incomplete exposure, Temperature monitoring

R Bellomo
Marianne J Chapman
S. Finfer
D Williams

Background Low-dose dopamine is commonly administered to critically ill patients in the belief that it reduces the risk of renal failure by increasing renal blood flow. However, these effects have not been established in a large randomised controlled trial, and use of dopamine remains controversial. We have done a multicentre, randomised, double-blind, placebo-controlled study of low-dose dopamine in patients with at least two criteria for the systemic inflammatory response syndrome and clinical evidence of early renal dysfunction (oliguria or increase in serum creatinine concentration). Methods 328 patients admitted to 23 participating intensive-care units (ICUs) were randomly assigned a continuous intravenous infusion of tow-dose dopamine (2 mug kg(-1) min(-1)) or placebo administered through a central venous catheter while in the ICU. The primary endpoint was the peak serum creatinine concentration during the infusion. Analyses excluded four patients with major protocol violations. Findings The groups assigned dopamine (n=161) and placebo (n=163) were similar in terms of baseline characteristics, renal function, and duration of trial infusion. There was no difference between the dopamine and placebo groups in peak serum creatinine concentration during treatment (245 [SD 144] vs 249 [147] mu mol/L; p=0 . 93), in the increase from baseline to highest value during treatment (62 [107] vs 66 [108] mu mol/L; p=0 . 82), or in the numbers of patients whose serum creatinine concentration exceeded 300 mu mol/L (56 vs 56; p=0 . 92) or who required renal replacement therapy (35 vs 40; p=0 . 55). Durations of ICU stay (13 [14] vs 14 [15] days; p=0 . 67) and of hospital stay (29 [27] vs 33 [39] days; p=0 . 29) were also similar. There were 69 deaths in the dopamine group and 66 in the placebo group. Interpretation Administration of low-dose dopamine by continuous intravenous infusion to critically ill patients at risk of renal failure does not confer clinically significant protection from renal dysfunction.

Joe Kanter
Peter DeBlieux

To effectively treat an aging and increasingly complex patient population, emergency physicians and other acute-care providers must be comfortable with the use of vasopressors, inotropes, and chronotropes. These medicines are used to augment the cardiovascular function of critically ill patients. Each class of medication produces a different hemodynamic effect. Some agents produce only one of these actions, whereas others have multiple effects. For the emergency physician, these agents are used with the explicit goal of preserving vital organ perfusion during acute and severe illness. This article reviews the physiologic receptors targeted by such drugs, common agents used, and specific clinical indications for their use. Copyright © 2014 Elsevier Inc. All rights reserved.

Early diagnosis of haemorrhagic shock (HS) might be difficult because of compensatory mechanisms. Clinical scoring systems aimed at predicting transfusion needs might assist in early identification of patients with HS. The Shock Index (SI) – defined as heart rate divided by systolic BP – has been proposed as a simple tool to identify patients with HS. This systematic review discusses the SI's utility post-trauma in predicting critical bleeding (CB). We searched the databases MEDLINE, Embase, CINAHL, Cochrane Library, Scopus and PubMed from their commencement to 1 September 2013. Studies that described an association with SI and CB, defined as at least 4 units of packed red blood cells (pRBC) or whole blood within 24 h, were included. Of the 351 located articles identified by the initial search strategy, five met inclusion criteria. One study pertained to the pre-hospital setting, one to the military, two to the in-hospital setting, and one included analysis of both pre-hospital and in-hospital values. The majority of papers assessed predictive properties of the SI in ≥10 units pRBC in the first 24 h. The most frequently suggested optimal SI cut-off was ≥0.9. An association between higher SI and bleeding was demonstrated in all studies. The SI is a readily available tool and may be useful in predicting CB on arrival to hospital. The evaluation of improved utility of the SI by performing and recording at earlier time-points, including the pre-hospital phase, is indicated.

Source: https://www.researchgate.net/publication/317577007_Pathophysiology_and_management_of_different_types_of_shock

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