Serum bicarbonate is usually low, and serum and blood lactate levels increase. As shock progresses, metabolic acidosis worsens, and blood pH decreases. It is caused by intrapulmonary shunting of blood resulting from airspace filling or Diffuse infiltrates may appear on the chest x-ray due to acute respiratory distress syndrome ARDS Acute hypoxemic respiratory failure is severe arterial hypoxemia that is refractory to supplemental oxygen.
BUN and creatinine usually increase progressively as a result of renal insufficiency. Bilirubin and transaminases may rise, although overt hepatic failure is uncommon in patients with normal baseline liver function. Many patients with severe sepsis develop relative adrenal insufficiency Secondary Adrenal Insufficiency Secondary adrenal insufficiency is adrenal hypofunction due to a lack of adrenocorticotropic hormone ACTH. Symptoms are the same as for Addison disease and include fatigue, weakness, weight However, in refractory septic shock, no cortisol testing is required before starting corticosteroid therapy.
Other monitoring Bedside echocardiography in the ICU is a practical and noninvasive alternative method of hemodynamic monitoring.
In septic shock, cardiac output is increased and peripheral vascular resistance is decreased, whereas in other forms of shock Etiology and Classification Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Neither CVP nor pulmonary artery occlusive pressure PAOP is likely to be abnormal in septic shock, unlike in hypovolemic, obstructive, or cardiogenic shock. Rapid ultrasonography for shock and hypotension RUSH includes echocardiographic methods and can be used to help determine the type of shock.
JAMA 8 —, Poor outcomes often follow failure to institute early aggressive therapy eg, within 6 hours of suspected diagnosis. Once severe lactic acidosis Lactic Acidosis Lactic acidosis is a high anion gap metabolic acidosis due to elevated blood lactate. Lactic acidosis results from overproduction of lactate, decreased metabolism of lactate, or both.
See also Mortality can be estimated with different scores, including the mortality in emergency department sepsis MEDS score.
The multiple organ dysfunction score MODS measures dysfunction of 6 organ systems and correlates strongly with risk of mortality. Patients with septic shock should be treated in an intensive care unit ICU. The following should be monitored frequently as often as hourly :. Arterial oxygen saturation should be measured continuously via pulse oximetry. Urine output, a good indicator of renal perfusion, should be measured in general, indwelling urinary catheters should be avoided unless they are essential.
The onset of oliguria eg, about 0. Following evidence-based guidelines and formal protocols for timely diagnosis and treatment of sepsis has been shown to decrease mortality and length of stay in the hospital 1 Treatment reference Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection.
IV fluids are the first method used to restore perfusion. Balanced isotonic crystalloid is preferred. Some clinicians add albumin to the initial fluid bolus in patients with severe sepsis or septic shock; albumin is more expensive than crystalloid but is generally a safe complement to crystalloid.
Starch-based fluids eg, hydroxyethyl starch are associated with increased mortality and should not be used. Initially, 1 L of crystalloid is given rapidly. However, the goal of therapy is not to administer a specific volume of fluid but to achieve tissue reperfusion without causing pulmonary edema due to fluid overload.
Estimates of successful reperfusion include ScvO2 and lactate clearance ie, percent change in serum lactate levels. Risk of pulmonary edema can be controlled by optimizing preload; fluids should be given until CVP reaches 8 mm Hg 10 cm water or PAOP reaches 12 to 15 mm Hg; however, patients on mechanical ventilation may require higher CVP levels.
The quantity of fluid required often far exceeds the normal blood volume and may reach 10 L over 4 to 12 hours. PAOP or echocardiography can identify limitations in left ventricular function and incipient pulmonary edema due to fluid overload. If a patient with septic shock remains hypotensive after CVP or PAOP has been raised to target levels, norepinephrine highly individualized dosing or vasopressin up to 0. Epinephrine may be added if a second drug is needed.
However, vasoconstriction caused by higher doses of these drugs may cause organ hypoperfusion and acidosis. Oxygen is given by mask or nasal prongs. Tracheal intubation and mechanical ventilation may be needed subsequently for respiratory failure see Mechanical ventilation in ARDS Mechanical ventilation in ARDS Acute hypoxemic respiratory failure is severe arterial hypoxemia that is refractory to supplemental oxygen.
Parenteral antibiotics should be given as soon as possible after specimens of blood, body fluids, and wound sites have been taken for Gram stain and culture. Prompt empiric therapy, started immediately after suspecting sepsis, is essential and may be lifesaving.
Antibiotic selection requires an educated guess based on the suspected source eg, pneumonia, urinary tract infection , clinical setting, knowledge or suspicion of causative organisms and of sensitivity patterns common to that specific inpatient unit or institution, and previous culture results. Typically, broad-spectrum gram-positive and gram-negative bacterial coverage is used initially; immunocompromised patients should also receive an empiric antifungal drug.
There are many possible starting regimens; when available, institutional trends for infecting organisms and their antibiotic susceptibility patterns antibiograms should be used to select empiric treatment. In general, common antibiotics for empiric gram-positive coverage include vancomycin and linezolid.
Initial broad-spectrum coverage is narrowed based on culture and sensitivity data. Knowledge of institution- and care unit—specific trends in infecting organisms and their antimicrobial sensitivity is an important guide to empiric antibiotic selection. The source of infection should be controlled as early as possible. During diastole, ventricular filling and coronary artery perfusion takes place. Determinants of diastolic function include myocardial relaxation and passive properties of the ventricle such as stiffness and geometry.
Excitation—contraction E—C coupling is the process by which an action potential is converted to muscle contraction.
When a cardiac muscle action potential occurs, calcium enters the cell and this leads to the further release of calcium from the sarcoplasmic reticulum. This calcium-induced calcium release is mediated by the cardiac ryanodine receptor RyR2.
The calcium binds to troponin-C which then leads to conformational change and allows the binding of actin to myosin causing shortening of the myocyte and the onset of systole. A decrease in intracellular calcium concentration then occurs and prepares the myocardium for the next systolic event.
The clinical picture of early sepsis is a patient with a low systemic vascular resistance SVR and a normal or increased cardiac output, although the heart is compromised by poor contractility. Although the stroke volume may be maintained, there is an increase in left ventricular end-systolic volume LVESV and left ventricular end-diastolic volume LVEDV and very often a decrease in the ejection fraction EF , with cardiac output maintained by an increase in heart rate.
There is also diastolic dysfunction with decreased left ventricular compliance and a subsequent increase in left ventricular end-diastolic pressure LVEDP Figs 1—3. Pressure—volume curve for the normal LV. Phase A represents diastolic filling. B represents isovolumetric contraction. C represents ventricular ejection. D represents isovolumetric relaxation.
Point 1 represents opening of the mitral valve. Point 2 represents closure of the mitral valve. Point 3 represents opening of the aortic valve. Stroke volume SV is demonstrated. The slope of this line represents the contractility of the heart. Pressure—volume curve for the LV during sepsis. Stroke volume SV is maintained. The end-systolic pressure—volume relationship demonstrates decreased contractility.
Pressure—volume curve for the LV during severe sepsis. There is hypotension. In these circumstances, cardiac force is compromised by the resulting abnormalities of fibre length. Finally, NO decreases the sensitivity of the myocardium to endogenous adrenergic ligands by altering the response of second messenger systems. The protein kinase and cyclic GMP messenger systems are affected in this manner. Vasodilatation is the principal physiological abnormality in the cardiovascular response to sepsis.
This leads to a low SVR and hypotension. One of the physiological functions of NO is to provide an intrinsic response to alterations in peripheral blood flow myogenic control. When NO is formed in the endothelium, it diffuses into the vascular smooth muscle cells where it activates the enzyme guanylyl cyclase. This increases concentrations of cyclic GMP levels which lead to a reduction in intracellular calcium levels and activation of potassium channels.
This leads to vascular smooth muscle relaxation. Peripheral vascular dysfunction during sepsis is mediated by excessive production of NO by the enzyme iNOS. Increased NO concentration leads to hyperpolarization of potassium channels and persistent relaxation of smooth muscle. In addition to vasodilatation, there is a failure of the cardiovascular reflexes, which normally control arterial pressure.
The sympathetic and neuroendocrine responses to shock cause vasoconstriction, which is mediated by G-proteins and second messenger systems, in turn activating intracellular pathways. These responses to sympathetic activity and angiotensin II are decreased due to the increased production of NO, which decreases the cellular activity of signal transduction mechanisms. The right ventricle RV differs embryologically, structurally, and functionally from the LV.
The principle function of the RV is to facilitate efficient gas exchange. It has a thin wall with a low muscle mass, ejecting into the pulmonary circulation, which has a low resistance and a high compliance. The pressures generated on the right side are low; mean pulmonary artery pressure is 15 mm Hg.
The RV depolarizes and then contracts in a longitudinal manner from the inflow tract to the outflow tract and produces a wave which is peristaltic in manner. This contrasts with the circumferential pressure generating contraction of the left side of the heart. Like the LV, the cardiac output of the RV is determined by changes in preload, afterload, and contractility. The changes in ventricular function in sepsis are similar to those on the left side. The function is compromised by changes in contractility and afterload.
The free wall of the RV has a low muscle mass and can respond to increases in preload by dilating, but it responds poorly to afterload because of its relative inefficiency as a muscle pump. The onset of sepsis leads to a change in contractility due to effects of circulating inflammatory mediators which are the same as those outlined above. There is a decrease in RVEF similar to that in the systemic circulation.
The stresses imposed by sepsis on the RV muscle mass and the changes in afterload can ultimately lead to right ventricular failure. The pulmonary circulation is a low-pressure system, which can respond to an increased cardiac output during exercise or after a physiological stress. The ability of the pulmonary circulation to respond to a large cardiac output without a major change in pressure ensures that effective gas exchange can take place.
It is important to consider the concept of blood flow in addition to generated pressure when considering the physiology of the pulmonary circulation. The right-sided circulation responds to changes in cardiac output by recruitment of pulmonary vessels which have low perfusion during stable conditions. In addition to recruitment, distension of these vessels allows an increase in blood flow which will support the need for improved gas exchange. These processes occur without vasomotor control.
The major stress imposed on the RV during sepsis is an increase in the afterload due to pulmonary hypertension. Hypoxic pulmonary vasoconstriction HPV is a response of the small arterioles of the pulmonary circulation to a decrease in alveolar or mixed venous oxygen content. The greater influence is from alveolar hypoxia.
The function of this response is to divert blood from the hypoxic areas of the lungs to those which are ventilated, thus attempting to maintain optimum ventilation and perfusion ratios and ensure efficient gas exchange.
It is a rapid response and occurs within seconds of induced hypoxia. The reflex occurs in the isolated lung and is independent of neural connections. The precise mechanism has not been proven, but NO is implicated. During sepsis, unregulated NO production in the systemic circulation leads to vasodilatation. In the presence of hypoxia, NO production decreases in the pulmonary circulation and local vasoconstriction occurs. It is also thought that local release of the potent vasoconstrictor endothelin occurs due to hypoxia.
There is evidence that the active control of the pulmonary circulation is influenced by ligands of systemic origin which lead to receptor activation. There are both cholinergic and adrenergic receptors in the pulmonary vascular tree, which allow changes in pulmonary vascular tone and resistance. The predominant response is vasoconstriction. Cholinergic parasympathetic nerves cause vasodilatation by stimulation of muscarinic M3 receptors, with NO acting as a mediator for cholinergic transmission.
Other circulating humoral factors can induce a local vasoconstrictor response, including endothelin, angiotensin, and histamine. Pulmonary hypertension is thus a multifactorial consequence of sepsis and is probably due to inhibition of NO production due to hypoxia and also an enhanced vasoconstriction due to acidosis, increased adrenergic stimulation, and local mediators such as endothelin Table 2.
The mediators involved in the active control of the pulmonary circulation 6. Ventricular interdependence is defined as the forces that are transmitted from one ventricle to the other ventricle through the myocardium and pericardium, independent of neural, humoral, or circulatory effects. Ventricular interdependence is a result of the close anatomical correlation of the ventricular cavities within the pericardium.
The ventricles can be considered in series. Stroke volume of systolic contraction of one cavity creates the preload of the next Fig. This is an oblique transverse section of the heart taken through the mid-cavity. It demonstrates the thick walled LV and the thinner wall of the RV. It demonstrates the crescentic shape of the RV in comparison with the round ventricular cavity on the left.
The septum is noted. The failing RV can impede left-sided performance by decreasing LV preload. This severe RV diastolic dysfunction can be seen in sepsis Fig. In modern scanners, the x-ray detector usually MRI does not use x-rays and is usually very safe Other tests are done to look for signs of organ malfunction and other complications of sepsis. They may include the following:. Blood tests to measure levels of lactic acid and other metabolic waste products, which may be high, and the number of platelets cells that help the blood clot , which may be low.
Blood tests or a sensor placed on a finger pulse oximetry to measure oxygen levels in the blood and thus evaluate how well the lungs and blood vessels are functioning.
This record, the electrocardiogram also known as an ECG Without treatment, most people with septic shock die. Even with treatment, there is a significant risk of death. However, the risk of death varies greatly depending on many factors, including how quickly people are treated, the type of bacteria involved particularly whether the bacteria are resistant to antibiotics Antibiotic Resistance Antibiotics are drugs used to treat bacterial infections.
They are ineffective against viral infections and most other infections. Antibiotics either kill microorganisms or stop them from reproducing Doctors immediately treat sepsis and septic shock with antibiotics. Doctors do not wait until test results confirm the diagnosis because a delay in antibiotic treatment greatly decreases the chances of survival. Treatment occurs in a hospital.
People with septic shock or who are severely ill are immediately admitted to an intensive care unit for treatment. When choosing the initial antibiotics, doctors consider which bacteria are most likely to be present, which depends on where the infection started, for example the bacteria that cause urinary tract infection are typically different from the bacteria that cause skin infection.
Also, doctors consider what bacteria are most common in infections in the person's community and in their particular hospital. Often, two or three antibiotics are given together to increase the chances of killing the bacteria, particularly when the source of the bacteria is unknown.
Later, when the test results are available, doctors can substitute the antibiotic that is most effective against the specific bacteria causing the infection. People with septic shock are also given large amounts of fluid by vein intravenously to increase the amount of fluid in the bloodstream and thus increase blood pressure.
Giving too little fluid is not effective but giving too much fluid can cause severe lung congestion. Oxygen is given through a mask, through nasal prongs, or through a breathing endotracheal tube if one has been inserted.
If needed, a mechanical ventilator Mechanical Ventilation Mechanical ventilation is use of a machine to aid the movement of air into and out of the lungs. Some people with respiratory failure need a mechanical ventilator a machine that helps air get If present, abscesses are drained. Catheters, tubes, or other medical devices that may have started the infection are removed or changed.
Surgery may be done to remove infected or dead tissue. If intravenous fluids do not increase blood pressure, doctors sometimes give drugs, such as vasopressin or norepinephrine which cause blood vessels to narrow , to raise blood pressure and increase blood flow to the brain, heart, and other organs. However, because these drugs may narrow blood vessels within organs, they sometimes decrease the amount of blood flow through the organs.
Sometimes people who have septic shock develop a high blood sugar glucose level. Because high blood sugar impairs how the immune system responds to an infection, doctors give insulin by vein to people to lower the level of glucose in the blood.
Corticosteroids such as hydrocortisone may be given by vein to people whose blood pressure remains low despite having received adequate fluids and drugs to increase blood pressure and despite having the source of their infection treated.
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Common Health Topics. Risk Factors. Antibiotics Intravenous fluids Oxygen Removal of the source of infection Other treatments. Bacteremia, Sepsis, and Septic Shock. Test your knowledge. Dengue is a viral infection that causes fever, aches throughout the body, and, in severe cases, bleeding in multiple areas. How is the dengue virus transmitted? More Content. Click here for the Professional Version. Usually, sepsis results from certain bacterial infections, often acquired in a hospital.
Rapid heart rate. They can cause the blood vessels to widen dilate , decreasing blood pressure. The decreased blood pressure and small clots lead to a series of harmful complications:.
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