Shock diagnosis and treatment
In medical language, the word "shock" has a different meaning than in common language. Shock is a condition of severely reduced perfusion of the tissues of the body leading to their dysfunction. Pathophysiologic mechanisms leading to shock may involve decreased circulating blood volume, decreased cardiac output, and vasodilation. It is an emergency because without rapid and successful treatment it leads to multiple organ dysfunction (due to a diminished blood perfusion) which can lead to irreversible multiple organ damage and death.Hypotension is often, but not always present in patients with shock. Shock is not synonymous with hypotension. In some cases, the cardiac output and oxygen delivery to the tissues may be critically low, even though the blood pressure remains normal (due to peripheral vasoconstriction and increased systemic vascular resistance) and hypotension may follow at a more advanced stage.
Causes of circulatory shock
Oligemic (Hypovolemic) shock is caused by decreased volume of circulating blood. This can be the result of :Hemorrhage (internal or external,e.g. severe trauma, gastrointestinal hemorrhage)
Volume depletion (increased fluid losses e.g., vomiting, diarrhea, diuretic over-usage, diabetic ketoacidosis, thermal or chemical burns)
Internal sequestration, meaning redistribution of fluids in the body (pancreatitis, intestinal obstruction)
Cardiogenic shock is due to a severe impairment in cardiac function leading to a reduced cardiac output. This form of shock can be:
Myopathic, due to a dysfunction of the cardiac muscle (acute myocardial infarction, myocarditis, dilated cardiomyopathy)
Mechanical (acute mitral regurgitation, acute aortic regurgitation, severe aortic stenosis)
Arrhythmic (severe tachyarrhythmia or bradyarrhythmia resulting in a diminished cardiac output)
Obstructive shock, due to an impairment in ventricular filling with blood as a result of external compression of the cardiac chambers (pericardial tamponade, tension pneumothorax) or due to a mechanical obstruction to cardiac outflow (massive pulmonary embolism, severe aortic stenosis)
Distributive shock due to a profound decrease in systemic vascular tone leading to marked vasodilation resulting in a diminished arterial pressure:
Sepsis (septic shock, resulting from an infection)
Anaphylaxis (allergic shock)
Toxic (resulting from overdose of a drug or ingestion of a toxic substance)
Neurogenic (e.g., spinal cord injury)
Pathophysiology of shock
The fundamental disorder in shock is reduced perfusion of tissues resulting in a reduced delivery of oxygen (O2) to the cells which is inadequate for aerobic metabolism. Aerobic metabolism is the main source of energy for the cells. This causes the cells to shift to anaerobic metabolism resulting in an increased production of CO2 and accumulation of lactic acid. Cellular function declines, and if shock persists, irreversible cell damage will occur in many vital tissues and organs. In general, the diminished tissue perfusion results in tissue hypoxia, an inadequate supply of nutrients and the accumulation of waste products.Cardiac output plays an important role in tissue perfusion and in the physiology of shock. Cardiac output is the volume of blood being pumped by the heart, in particular by the left or right ventricle, per unit time. Cardiac output is the product of the heart rate (HR), which is the number of heart beats per minute, and the stroke volume (SV), which is the volume of blood ejected from a cardiac ventricle per beat. Thus, CO = SV × HR.
Hypovolemic shock results from a reduction of the blood volume by 15-20% or more. The low blood volume leads to a diminished venous return of blood to the heart and this results in a fall in cardiac output. Low volume of circulating blood can be the result of different situations, such as severe hemorrhage (whole blood is lost), severe vomiting and diarrhea (water and electrolytes are lost), extensive burns (serum is lost).
Cardiogenic shock occurs in acute severe heart disease which causes the inability of the heart to maintain an adequate cardiac output, e.g. in an acute myocardial infarction, with a resultant decrease in the contractile function of a large portion of the heart muscle.
Septic shock is caused by severe infections which cause the release of bacterial toxins into the circulation. The bacterial toxins (endotoxins) trigger a massive inflammatory and immune response,
leading to the release of inflammatory mediators. This causes profound vasodilation leading to hypotension and diminished tissue perfusion. A second mechanism is that these toxins can also cause depression of myocardial contractility.
Anaphylactic shock occurs in cases of severe anaphylaxis. Anaphylaxis is an acute allergic response, which can be triggered in sensitive individuals by substances, to which they are allergic (insect bites, foods, medications, latex exposure, etc). The onset is usually sudden. The allergic reaction induces a release of inflammatory mediators in the systemic circulation (e.g. histamine and bradykinin). This provokes vasodilation and venous pooling resulting in hypotension and reduction of tissue perfusion. Bronchoconstriction is also common leading to dyspnea and hypoxia.
Neurogenic shock is caused by spinal cord damage which interferes with normal nervous control of blood vessel diameter, leading to vasodilation, resulting in a fall in blood pressure and diminished tissue perfusion.
Compensatory mechanisms of the body in shock include:
-Stimulation of the sympathetic nervous system (through the baroreceptors, which detect hypotension). This leads to increased heart rate and contractility and peripheral vasoconstriction- Stimulation of the renin-angiotensin-aldosterone axis which leads to sodium and water retention by the kidneys and vasoconstriction
(The reduced blood flow to the kidneys stimulates the juxtaglomerular apparatus to secrete renin which leads to the production of angiotensin I which is converted by the angiotensin converting enzyme to angiotensin II. Angiotensin II has vasoconstrictor properties and also stimulates the adrenal cortex to release the mineralocorticoid hormone aldosterone which causes sodium and water retention)
-Stimulation of osmoreceptors in the hypothalamus which in turn stimulate the release of antidiuretic hormone (ADH) by the posterior pituitary gland. (ADH acts on the renal tubules to reduce water excretion and also has vasoconstrictor properties).
-Stimulation of the production of adrenocorticotropic hormone (ACTH) by the anterior pituitary gland which leads to the increased production of glucocorticoids by the adrenal cortex (among the actions of glucocorticoids is their effect to increase blood sugar to meet the increased metabolic needs of the body).
Clinical manifestations of shock
Manifestations are the result of inadequate tissue perfusion and compensatory activation of the sympathetic nervous system. Skin: cold, pale, clammy (due to sweating), peripheral cyanosis, slow capillary refill (these are manifestations of inadequate tissue perfusion). (The capillary refill time should be assessed in a room with normal temperature and it is the time needed for skin colour to return after the termination of pressure applied on the skin-e.g. on a finger- that caused blanching. Normal value is considered below 2-3 seconds and usually over 4 seconds is considered as abnormal, but it is not a very accurate test).
Exception: The appearance of the skin in septic shock is different than in the other types of shock. In septic shock, the skin is not pale, neither cold at the early stages, because of the vasodilation. So the skin is warm but it is often clammy due to sweating, as in the other types of shock.
Brain: Due to inadequate blood perfusion, manifestations may include irritability, confusion, drowsiness.
Kidneys: oliguria or anuria. Oliguria is a low urine output:in adults < 20ml/hour or < 400-500 ml/24 hours (but > 100 ml/24 hours). Anuria is defined as a urine output <100 ml/24 hours or no urine output. In children the definition of oliguria is as following:
In infants a urine output < 1 ml/kg/hour and in children < 0.5 ml/kg/hour Oliguria or anuria are not specific for shock. Apart from shock, oliguria or anuria can be due to other causes such as acute tubular necrosis (from prolonged ischemia, drugs, or toxins), primary glomerular diseases, severe heart failure leading to a reduced renal perfusion, post-renal causes such as bladder outlet obstruction or bilateral ureteral obstruction).
External hemorrhage is controlled with local pressure Nothing is given by mouth, and the patient’s head is turned to one side to avoid aspiration if vomiting occurs. Supplemental oxygen is provided via a face mask. Two large (14- to 16-gauge) venous catheters are placed in separate peripheral veins. When prompt placement of peripheral venous catheters is not successful, a central venous line or an intraosseous needle are alternative options.
-dobutamine 2-20 μg/kg/ minute which has positive inotropic properties but lacks vasoconstrictor activity, or
-only in severe refractory hypotension norepinephrine 0.5-30 μg/min (micrograms/minute). Norepinephrine is a potent vasoconstrictor with a moderate inotropic effect.
Combination therapy of an inotropic agent (eg, dopamine or dobutamine) with the aim to increase myocardial contractility with a vasodilator (nitroprusside or nitroglycerin) aiming to decrease cardiac workload and congestive symptoms by reducing systemic venous return (venodilation) and systemic vascular resistance (dilation of the arterial system) can be particularly useful. However, this treatment requires close ECG and hemodynamic monitoring and some patients may not tolerate the vasodilator (if they develop persistent hypotension) even in low doses, despite the concomitant administration of an inotropic agent. Then the vasodilator must be stopped and only the administration of the inotropic agent can be continued.
Cardiogenic shock-emedicine
Clinical manifestations of shock
Manifestations are the result of inadequate tissue perfusion and compensatory activation of the sympathetic nervous system. Skin: cold, pale, clammy (due to sweating), peripheral cyanosis, slow capillary refill (these are manifestations of inadequate tissue perfusion). (The capillary refill time should be assessed in a room with normal temperature and it is the time needed for skin colour to return after the termination of pressure applied on the skin-e.g. on a finger- that caused blanching. Normal value is considered below 2-3 seconds and usually over 4 seconds is considered as abnormal, but it is not a very accurate test).Exception: The appearance of the skin in septic shock is different than in the other types of shock. In septic shock, the skin is not pale, neither cold at the early stages, because of the vasodilation. So the skin is warm but it is often clammy due to sweating, as in the other types of shock.
Brain: Due to inadequate blood perfusion, manifestations may include irritability, confusion, drowsiness.
Kidneys: oliguria or anuria. Oliguria is a low urine output:in adults < 20ml/hour or < 400-500 ml/24 hours (but > 100 ml/24 hours). Anuria is defined as a urine output <100 ml/24 hours or no urine output. In children the definition of oliguria is as following:
In infants a urine output < 1 ml/kg/hour and in children < 0.5 ml/kg/hour Oliguria or anuria are not specific for shock. Apart from shock, oliguria or anuria can be due to other causes such as acute tubular necrosis (from prolonged ischemia, drugs, or toxins), primary glomerular diseases, severe heart failure leading to a reduced renal perfusion, post-renal causes such as bladder outlet obstruction or bilateral ureteral obstruction).
Circulatory system:
Tachycardia, narrowed pulse pressure, "weak" or "thready" pulse.
Hypotension <90 mmHg (Blood pressure can be normal at an early stage or in previously hypertensive patients).
Note that tachycardia and sweating, that are present in patients with shock, are typical manifestations of sympathetic nervous system activation. Sympathetic nervous system activation is a compensatory mechanism which also induces peripheral vasoconstriction).
Respiratory system: tachypnea (increased respiratory rate- normal respiratory rate in adults is 12-18 breaths/ minute). Tachypnea is indicated by a respiratory rate > 20 breaths per minute.Children (especially in the first 3 years) have higher resting ventilatory rates than adults- see the chapter on dyspnea and respiratory failure).
. In cardiogenic shock, the above signs of diminished perfusion and increased sympathetic tone are present, as they are also present in hypovolemic (oligemic) shock, but there is another difference between these two conditions. In cardiogenic shock, some or all the signs of heart failure are usually present, such as raised jugular venous pressure, gallop rhythm (the combination of a third heart sound and tachycardia), pulsus alternans, crackles at the lung bases or the clinical picture of pulmonary edema.
In obstructive shock (see the etiology above) the signs of low perfusion and sympathetic stimulation are present with the following additions:
An elevated jugular venous pressure
When cardiac tamponade is the underlying cause, pulsus paradoxus, jugular venous distention and muffled heart sounds are present. Pulsus paradoxus is a drop in systolic pressure during inspiration over 10 mmHg.
Hypotension <90 mmHg (Blood pressure can be normal at an early stage or in previously hypertensive patients).
Note that tachycardia and sweating, that are present in patients with shock, are typical manifestations of sympathetic nervous system activation. Sympathetic nervous system activation is a compensatory mechanism which also induces peripheral vasoconstriction).
Respiratory system: tachypnea (increased respiratory rate- normal respiratory rate in adults is 12-18 breaths/ minute). Tachypnea is indicated by a respiratory rate > 20 breaths per minute.Children (especially in the first 3 years) have higher resting ventilatory rates than adults- see the chapter on dyspnea and respiratory failure).
. In cardiogenic shock, the above signs of diminished perfusion and increased sympathetic tone are present, as they are also present in hypovolemic (oligemic) shock, but there is another difference between these two conditions. In cardiogenic shock, some or all the signs of heart failure are usually present, such as raised jugular venous pressure, gallop rhythm (the combination of a third heart sound and tachycardia), pulsus alternans, crackles at the lung bases or the clinical picture of pulmonary edema.
In obstructive shock (see the etiology above) the signs of low perfusion and sympathetic stimulation are present with the following additions:
An elevated jugular venous pressure
When cardiac tamponade is the underlying cause, pulsus paradoxus, jugular venous distention and muffled heart sounds are present. Pulsus paradoxus is a drop in systolic pressure during inspiration over 10 mmHg.
In distributive shock (septic and anaphylactic shock) vasodilation is a dominant feature and so the skin is usually warm and not pale (in contrast to all the other types of shock. Hypotension (due to vasodilation), tachycardia, sweating (due to sympathetic stimulation) and manifestations of reduced brain perfusion (see above) are present. Anaphylactic shock may be accompanied by some signs of an acute allergic (anaphylactic) reaction, such as urticaria, edema of the face, edema of the larynx (this causes coarseness of the voice and acute dyspnea with stridor), bronchoconstriction with shortness of breath and expiratory musical sounds (rhonci or wheezing).
In septic shock fever, chills, and focal signs of infection are often present, but in elderly or immunocompromised patients fever may be absent.
In septic shock fever, chills, and focal signs of infection are often present, but in elderly or immunocompromised patients fever may be absent.
Recognizing the cause of shock is very important because it enables the appropriate treatment. Often, the cause can be recognized quickly based on the history and physical examination, aided by simple testing but in some cases diagnosis of the cause can be difficult.
Usual testing of the patient with shock includes ECG, chest x-ray, complete blood count (CBC), arterial blood gases, serum electrolytes, BUN (blood urea nitrogen), creatinine, PT, aPTT, liver function tests, cRP (c-reactive protein), fibrinogen and fibrin split products.
If there are difficulties in determining the patient’s volume status, monitoring of central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) will be useful. When these pressures are low (CVP < 5 mm Hg or < 7 cm H2O/ or PCWP < 8 mm Hg) this is a strong indication of hypovolemia (reduced blood volume, e.g. due to hemorrhage or dehydration). On the contrary, in cardiogenic shock PCWP is>15 mmHg right ventricular end diastolic pressure is often >10mmHg and cardiac index (cardiac output divided by body surface area) is<2.2 liters/min/square meter. Rapid bedside echocardiography, done to assess adequacy of cardiac filling (by imaging the inferior vena cava and by measuring the end -diastolic dimension of the left ventricle) and left and right ventricular contractile function, is being increasingly used in the assessment of patients with shock.
If there are difficulties in determining the patient’s volume status, monitoring of central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) will be useful. When these pressures are low (CVP < 5 mm Hg or < 7 cm H2O/ or PCWP < 8 mm Hg) this is a strong indication of hypovolemia (reduced blood volume, e.g. due to hemorrhage or dehydration). On the contrary, in cardiogenic shock PCWP is>15 mmHg right ventricular end diastolic pressure is often >10mmHg and cardiac index (cardiac output divided by body surface area) is<2.2 liters/min/square meter. Rapid bedside echocardiography, done to assess adequacy of cardiac filling (by imaging the inferior vena cava and by measuring the end -diastolic dimension of the left ventricle) and left and right ventricular contractile function, is being increasingly used in the assessment of patients with shock.
Treatment of circulatory shock
Treatment begins simultaneously with evaluation. Airway and ventilation are checked, and respiratory assistance is given if necessary. The patient must lie down and should be kept warm (blankets).Treatment in shock aims to restore tissue perfusion and to achieve a systolic blood pressure at least 90-100 mmHg.External hemorrhage is controlled with local pressure Nothing is given by mouth, and the patient’s head is turned to one side to avoid aspiration if vomiting occurs. Supplemental oxygen is provided via a face mask. Two large (14- to 16-gauge) venous catheters are placed in separate peripheral veins. When prompt placement of peripheral venous catheters is not successful, a central venous line or an intraosseous needle are alternative options.
If shock is severe or if ventilation is inadequate (if PO2 <70 mmHg), endotracheal intubation is performed and the patient is started on mechanical ventilation.
A Foley catheter should also be inserted to monitor urine output.
An initial fluid challenge is administered, with the infusion of 0.9% saline (N/S 0.9%) 1 L (liter) in adults, or 20 ml/kg in children over 15 minutes. Ringer’s lactate is commonly used in hemorrhagic shock. If the clinical picture does not improve, the infusion is repeated. When hypotension persists despite adequate fluid administration consider the possibility of ongoing internal hemorrhage needing prompt diagnosis, blood transfusions and surgical treatment, the possibility that you have missed another cause needing specific treatment (e.g. pericardial tamponade, massive pulmonary embolism) or consider the administration of vasopressor drugs (norepinephrine is generally the preferred vasopressor agent in shock).
In patients with an acute myocardial infarction, a smaller quantity of N/S 0,9% can be given (250-500 ml), but a fluid challenge should not be given to patients with signs of pulmonary edema.
In patients with an acute myocardial infarction, a smaller quantity of N/S 0,9% can be given (250-500 ml), but a fluid challenge should not be given to patients with signs of pulmonary edema.
Further fluid administration depends on the underlying condition. A useful aid for the decisions regarding fluid administration or the administration of inotropic drugs is bedside echocardiography. Bedside echocardiography is used for the assessment of the contractile function of the ventricles, the inferior vena cava (its diameter provides information about the fluid status or the presence of venous congestion) and is also useful to detect other cardiac pathologic conditions. In many cases of severe shock, monitoring of central venous pressure (CVP) or pulmonary artery wedge pressure (PCWP) is necessary to guide fluid administration.
In hemorrhagic shock crystalloid solutions (such as Ringer's lactated or normal saline) and blood products (packed red blood cells and plasma) are used for volume replacement, but control of bleeding is the first priority. In cases of internal bleeding, control of bleeding is usually surgical. When there is an inadequate response to treatment consider insufficient volume administration or unrecognized ongoing hemorrhage.
Distributive shock
Cardiogenic shock: Inotropic agents can be given such asDistributive shock
In the resuscitation from hypoperfusion induced by septic shock at least 30 ml/kg of intravenous (IV) crystalloid fluid should be given within the first 3 hours. Septic shock with profound hypotension after initial fluid administration (0.9% saline) can be treated with the addition of inotropic or vasopressor drugs, such as norepinephrine or dopamine. Norepinephrine is preferred over dopamine because it is associated with lower mortality rates in septic and in cardiogenic shock. Broad-spectrum intravenous antibiotics are also administered in cases of septic shock. In septic shock, guidelines recommend the administration of intravenous antimicrobials to be initiated as soon as possible after recognition (within 1 hour for both sepsis and septic shock).
When using dopamine, one must know that the kind of pharmacologic action depends on the dose range as following
Dopamine in a low dose of 1-2 μg/kg/min mainly facilitates diuresis. In doses 2-10 μg/kg/minute it has positive inotropic effects (increases ventricular contractile function in the heart) and positive chronotropic effects (increases heart rate).
In higher doses, 10-20 μg/kg/ min dopamine in addition to its positive inotropic and chronotropic effects, also causes generalized vasoconstriction, which can be helpful to elevate blood pressure. Norepinephrine is preferred in refractory hypotension [dose range 0.5-30 μg/min (micrograms per minute)]
Patients with anaphylactic shock are treated with epinephrine (adrenaline) 0.05 to 0.1 mg intravenously, followed by epinephrine infusion of a solution of 5 mg epinephrine in 500 ml 5% D/W with a rate of 10 mL/h or 0.02 mcg/kg/minute (μg/kg/min). Corticosteroids are also administered intravenously to patients with anaphylaxis.When using dopamine, one must know that the kind of pharmacologic action depends on the dose range as following
Dopamine in a low dose of 1-2 μg/kg/min mainly facilitates diuresis. In doses 2-10 μg/kg/minute it has positive inotropic effects (increases ventricular contractile function in the heart) and positive chronotropic effects (increases heart rate).
In higher doses, 10-20 μg/kg/ min dopamine in addition to its positive inotropic and chronotropic effects, also causes generalized vasoconstriction, which can be helpful to elevate blood pressure. Norepinephrine is preferred in refractory hypotension [dose range 0.5-30 μg/min (micrograms per minute)]
-dobutamine 2-20 μg/kg/ minute which has positive inotropic properties but lacks vasoconstrictor activity, or
-only in severe refractory hypotension norepinephrine 0.5-30 μg/min (micrograms/minute). Norepinephrine is a potent vasoconstrictor with a moderate inotropic effect.
In patients with shock in the context of an acute myocardial infarction, the definitive treatment is myocardial reperfusion, usually by percutaneous coronary intervention - PCI. In an acute ST elevation myocardial infarction (STEMI) PCI or intravenous thrombolysis are the main treatment options, with PCI being preferred when it can be performed promptly in an experienced center. If the time-delay for the transfer of the patient to a PCI-capable hospital is not acceptable, then thrombolysis is administered to achieve early myocardial reperfusion, provided that there is no absolute contraindication to thrombolysis. (See this link to a chapter of my cardiology free book Coronary artery disease: Stable angina, unstable angina, and myocardial infarction ). In case of a non- ST elevation myocardial infarction (NSTEMI), thrombolysis is not indicated. Note that an acute myocardial infarction is the most common cause of cardiogenic shock.
Intra-aortic balloon counterpulsation is valuable for temporarily reversing shock in patients with acute myocardial infarction. This procedure is used as a bridge to permit coronary angiography and reperfusion with percutaneous coronary intervention (PCI) with stent placement. PCI is the usual life-saving treatment in acute myocardial infarction (especially if it is a STEMI or in a NSTEMI with high-risk features of decompensation, such as shock, signs of congestive heart failure, recurrent ischemia, or a sustained ventricular tachyarrhythmia).
Intra-aortic balloon counterpulsation is also used before coronary angiography and surgical intervention in patients with acute myocardial infarction (MI) complicated by ventricular septal rupture or severe acute mitral regurgitation, especially if they require vasopressor support for >30 minutes. Mechanical complications of an acute MI, such as ventricular septal rupture, or acute mitral regurgitation due to rupture of a papillary muscle head, need prompt emergency cardiac surgery which combines correction of the mechanical complication with coronary artery by-pass grafting (CABG).
Obstructive shock needs specific treatment:
Non-traumatic cardiac tamponade requires immediate needle-pericardiocentesis, which can be performed at the bedside. Trauma-related cardiac tamponade is managed with emergency cardiac surgery (surgical decompression and repair).
Tension pneumothorax requires immediate decompression with a large venous catheter inserted into the 2nd intercostal space at the midclavicular line. This will save the patient until the insertion of a chest tube follows.
A massive pulmonary embolism resulting in shock is treated with anticoagulation and thrombolysis (which is the usual and effective treatment), or surgical embolectomy, in selected cases.
(Note: A pulmonary embolism without hypotension does not have an indication for thrombolysis and is treated only with anticoagulation. Anticoagulation is initiated with unfractionated or low molecular weight heparin in therapeutic doses, followed, after some days, by oral anticoagulation, usually for 6 months, or indefinitely only in cases with no reversible predisposing factor for venous thrombosis).
GO BACK TO THE TABLE OF CONTENTS
LINK: Emergency medicine book-Table of contents
Bibliography and links
GO BACK TO THE TABLE OF CONTENTS
LINK: Emergency medicine book-Table of contents
Bibliography and links
Shock diagnosis and treatment-The Merck Manual Professional Edition
Richards JB, Wilcox SR. Diagnosis and management of shock in the emergency department. Emergency medicine |Practice 2014;16:1-23
LINK: file:///C:/Users/admin/Downloads/0314%20Shock.pdf
Patestos Dimitrios, DOCTORS OF THE WORLD GREECE The MDM DIAGNOSIS AND TREATMENT MANUAL
LINK:
DOCTORS OF THE WORLD The MDM DIAGNOSIS AND TREATMENT MANUAL
Gotts JE, Matthay MA. Sepsis: pathophysiology and clinical management.
BMJ. 2016 23;353:i1585. doi: 10.1136/bm
Vincent J-L, Ince C, Bakker J. Clinical review: Circulatory shock - an update: a tribute to Professor Max Harry Weil. Critical Care. 2012;16(6):239. doi:10.1186/cc11510.
LINK https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3672555/
Richards JB, Wilcox SR. Diagnosis and management of shock in the emergency department. Emergency medicine |Practice 2014;16:1-23
LINK: file:///C:/Users/admin/Downloads/0314%20Shock.pdf
Patestos Dimitrios, DOCTORS OF THE WORLD GREECE The MDM DIAGNOSIS AND TREATMENT MANUAL
LINK:
DOCTORS OF THE WORLD The MDM DIAGNOSIS AND TREATMENT MANUAL
Gotts JE, Matthay MA. Sepsis: pathophysiology and clinical management.
BMJ. 2016 23;353:i1585. doi: 10.1136/bm
Vincent J-L, Ince C, Bakker J. Clinical review: Circulatory shock - an update: a tribute to Professor Max Harry Weil. Critical Care. 2012;16(6):239. doi:10.1186/cc11510.
LINK https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3672555/
A power point presentation: Shock (by Dr Khalid)
LINK https://www.slideshare.net/aljonaieh/shock-3217657
LINK https://www.slideshare.net/aljonaieh/shock-3217657
Critical Care Medicine: March 2017 - Volume 45 - Issue 3 - p 486–552
doi: 10.1097/CCM.0000000000002255Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016
doi: 10.1097/CCM.0000000000002255Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016
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