Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of substantial superiority of one vasopressor over another; however, using dopamine leads to an increased risk of arrythmia when compared with norepinephrine. 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 not to improve survival and is associated with a number of complications. Xigris was withdrawn from the market in 2011, and clinical trials were discontinued. The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes. If used at all it should only be considered if the pH is less than 7.0.

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 ml/kg in a child) which is usually instituted as the person is being further evaluated. 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 100 g/l.

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). 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.

Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply. This intervention can be life-saving.

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can; however, blood substitutes are being developed which can. Infusion of colloid or crystalloid IV fluids will also dilute clotting factors within the blood, increasing the risk of bleeding. It is current best practice to allow permissive hypotension in patients suffering from hypovolemic shock, both to ensure clotting factors are not overly diluted and also to stop blood pressure being artificially raised to a point where it "blows off" clots that have formed.

Fluid replacement is beneficial in hypovolemia of stage 2, and is necessary in stage 3 and 4. See also the discussion of shock and the importance of treating reversible shock while it can still be countered.

For a patient presenting with hypovolemic shock in hospital the following investigations would be carried out:

- Blood tests: U+Es/Chem7, full blood count, glucose, blood type and screen

- Central venous catheter or blood pressure

- Arterial line or arterial blood gases

- Urine output measurements (via urinary catheter)

- Blood pressure

- SpO2 Oxygen saturations

The following interventions would be carried out:

- IV access

- Oxygen as required

- Surgical repair at sites of hemorrhage

- Inotrope therapy (Dopamine, Noradrenaline) which increase the contractility of the heart muscle

- Fresh frozen plasma or whole blood

Vasopressors (like Norepinephrine, Dobutamine) should generally be avoided, as they may result in further tissue ischemia and don't correct the primary problem. Fluids are the preferred choice of therapy.

Medium-term (and less well-demonstrated) treatments of hypotension include:

- Blood sugar control (80–150 by one study)

- Early nutrition (by mouth or by tube to prevent ileus)

- Steroid support

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. A morning dose of caffeine can also be effective. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs increases venous return, thus making more blood available to critical organs in the chest and head. The Trendelenburg position, though used historically, is no longer recommended.

Hypotensive shock treatment always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed that hypotension is corrected. Still-debated methods are in parentheses, as are benchmarks for evaluating progress in correcting hypotension. A study on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. Water alone cannot be administered intravenously (because of osmolarity issue), but rather can be given with addition to dextrose or saline infusion solutions. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by a physician or other medical professional with experience in treatment of electrolyte imbalance, specific treatment like ACE inhibitors in heart failure and corticosteroids in nephropathy also can be used.

American and European guidelines come to different conclusions regarding the use of medications. In the United States they are recommended in those with SIADH, cirrhosis, or heart failure who fail limiting fluid intact. In Europe they are not generally recommended.

There is tentative evidence that vasopressin receptor antagonists (vaptans), such as conivaptan, may be slightly more effective than fluid restriction in those with high volume or normal volume hyponatremia. They should not be used in people with low volume. Their use in SIADH is unclear.

Demeclocycline, while sometimes used for SIADH, has significant side effects including potential kidney problems and sun sensitivity. In many people it has no benefit while in others it can result in overcorrection and high blood sodium levels.

Daily use of urea by mouth, while not commonly used due to the taste, has tentative evidence in SIADH. It, however, is not available in many areas of the world.

Options include:

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and/or symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- Severe hyponatremia or severe symptoms (confusion, convulsions, or coma): consider hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h. Hypertonic saline may lead to a rapid dilute diuresis and fall in the serum sodium. It should not be used in those with an expanded extracellular fluid volume.

The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase. The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly. A recent study of 59 acute episodes occurring in 37 hospitalized SCLS patients concluded that high-volume fluid therapy was independently associated with poorer clinical outcomes, and that the main complications of SCLS episodes were recovery-phase pulmonary edema (24%), cardiac arrhythmia (24%), compartment syndrome (20%), and acquired infections (19%).

The prevention of episodes of SCLS has involved two approaches. The first has long been identified with the Mayo Clinic, and it recommended treatment with beta agonists such as terbutaline, phosphodiesterase-inhibitor theophylline, and leukotriene-receptor antagonists montelukast sodium.

The rationale for use of these drugs was their ability to increase intracellular cyclic AMP (adenosine monophosphate) levels, which might counteract inflammatory signaling pathways that induce endothelial permeability. It was the standard of care until the early 2000s, but was sidelined afterwards because patients frequently experienced renewed episodes of SCLS, and because these drugs were poorly tolerated due to their unpleasant side effects.

The second, more recent approach pioneered in France during the last decade (early 2000s) involves monthly intravenous infusions of immunoglobulins (IVIG), with an initial dose of 2 gr/kg/month of body weight, which has proven very successful as per abundant case-report evidence from around the world.

IVIG has long been used for the treatment of autoimmune and MGUS-associated syndromes, because of its potential immunomodulatory and anticytokine properties. The precise mechanism of action of IVIG in patients with SCLS is unknown, but it is likely that it neutralizes their proinflammatory cytokines that provoke endothelial dysfunction. A recent review of clinical experience with 69 mostly European SCLS patients found that preventive treatment with IVIG was the strongest factor associated with their survival, such that an IVIG therapy should be the first-line preventive agent for SCLS patients. According to a recent NIH survey of patient experience, IVIG prophylaxis is associated with a dramatic reduction in the occurrence of SCLS episodes in most patients, with minimal side effects, such that it may be considered as frontline therapy for those with a clear-cut diagnosis of SCLS and a history of recurrent episodes.

Cardiac resuscitation guidelines (ACLS/BCLS) advise that Cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole. There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse.

An intravenous or intraosseous line should be started to provide medications through. The mainstay of drug therapy for PEA is epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit. Epinephrine too has a limited evidence base, and it is recommended on the basis of its mechanism of action.

Sodium bicarbonate 1meq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).

All of these drugs should be administered along with appropriate CPR techniques. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.

POTS treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. For most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). 8–10 cups of water daily are recommended. Increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. Different physicians recommend different amounts of sodium to their patients. Salt intake is not appropriate for people with high blood pressure. Combining these techniques with gradual physical training enhances their effect. In some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention.

Large meals worsen symptoms for some people. These people may benefit from eating small meals frequently throughout the day instead. Alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. Exposure to extreme heat may also aggravate symptoms.

Prolonged physical inactivity can worsen the symptoms of POTS. Techniques that increase a person's capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. Aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. Exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. In these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing or swimming.

When changing to an upright posture, finishing a meal or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. Compression garments can also be of benefit by constricting blood pressures with external body pressure.

Excessive sodium and fluid intake:

- IV therapy containing sodium

- As a Transfusion reaction to a rapid blood transfusion.

- High intake of sodium

Sodium and water retention:

- Heart failure

- Liver cirrhosis

- Nephrotic syndrome

- Corticosteroid therapy

- Hyperaldosteronism

- Low protein intake

Fluid shift into the intravascular space:

- Fluid remobilization after burn treatment

- Administration of hypertonic fluids, e.g. mannitol or hypertonic saline solution

- Administration of plasma proteins, such as albumin

In those with high volume or hypervolemia:

- Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body) with restricted free water intake. This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic and free water is not available. There are several recorded cases of forced ingestion of concentrated salt solution in exorcism rituals leading to death.

- Mineralcorticoid excess due to a disease state such as Conn's syndrome usually does not lead to hypernatremia unless free water intake is restricted.

- Salt poisoning (this condition is most common in children). It has also been seen in a number of adults with mental health problems. Too much salt can also occur from drinking seawater or soy sauce.

If nonpharmacological methods are ineffective, medication may be necessary. As of 2013, no medication has been approved by the U.S. Food and Drug Administration to treat POTS, but a variety are used off-label. Their efficacy has not yet been examined in long-term randomized controlled trials.

Fludrocortisone may be used to enhance sodium retention and blood volume which may be beneficial not only by augmenting sympathetically-mediated vasoconstriction but also because a large subset of POTS patients appear to have low absolute blood volume.

While POTS patients typically have normal or even elevated arterial blood pressure, the neuropathic form of POTS is presumed to constitute a selective sympathetic venous denervation. In these patients the selective Alpha-1 Adrenergic receptor agonist Midodrine may increase venous return, enhance stroke volume and improve symptoms. Midodrine should only be taken during the daylight hours as it may promote supine hypertension.

Ivabradine can successfully restrain heart rate in POTS without affecting blood pressure and approximately 60% of POTS patients treated in an open-label trial of ivabradine experienced symptom improvement.

Pyridostigmine has been reported to restrain heart rate and improve chronic symptoms in about half of patients.

The selective alpha 1 agonist phenylephrine has been used successfully to enhance venous return and stroke volume in some people with POTS. However, this medication may be hampered by poor oral bioavailability.

The initial stage is the capillary leak phase, lasting from 1 to 3 days, during which up to 70% of total plasma volume may invade cavities especially in the extremities. The most common clinical features are flu-like symptoms such as fatigue; runny nose; lightheadedness up to and including syncope (fainting); limb, abdominal or generalized pain; facial or other edema; dyspnea; and hypotension that results in circulatory shock and potentially in cardiopulmonary collapse and other organ distress or damage. Acute renal dysfunction or failure is a common risk due to acute tubular necrosis consequent to hypovolemia and rhabdomyolysis.

The loss of fluid out of the capillaries has similar effects on the circulation as dehydration, slowing both the flow of oxygen delivered to tissues and organs as well as the output of urine. Urgent medical attention in this phase consists of fluid resuscitation efforts, mainly the intravenous administration of saline solution plus hetastarch or albumin and colloids (to increase the remaining blood flow to vital organs like the kidneys), as well as glucocorticoids (steroids like methylprednisolone, to reduce or stop the capillary leak). However effective on blood pressure, the impact of fluid therapy is always transient and leads to increased extravascular fluid accumulation, engendering multiple complications especially compartment syndrome and thus limb-destructive rhabdomyolysis. Consequently, patients experiencing episodes of SCLS should be closely monitored in a hospital intensive-care setting, including for orthopedic complications requiring surgical decompression, and their fluid therapy should be minimized as much as possible.

How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes:

- Removing the underlying cause when possible.

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- For people with severe symptoms (severe confusion, convulsions, or coma) hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h should be given.

- Drugs

- Demeclocycline can be used in chronic situations when fluid restrictions are difficult to maintain; demeclocycline is the most potent inhibitor of Vasopressin (ADH/AVP) action. However, demeclocycline has a 2–3 day delay in onset with extensive side effect profile, including skin photosensitivity, and nephrotoxicity.

- Urea: oral daily ingestion has shown favorable long-term results with protective effects in myelinosis and brain damage. Limitations noted to be undesirable taste and is contraindicated in people with cirrhosis to avoid initiation or potentiation of hepatic encephalopathy.

- Conivaptan – an antagonist of both V and V vasopressin receptors.

- Tolvaptan – an antagonist of the V vasopressin receptor.

Raising the serum sodium concentration too rapidly may cause central pontine myelinolysis. Avoid correction by more than 12 mEq/L/day. Initial treatment with hypertonic saline may abruptly lead to a rapid dilute diuresis and fall in ADH.

Medications, while included in guidelines, have not been shown to improve survival to hospital discharge following out-of-hospital cardiac arrest. This includes the use of epinephrine, atropine, lidocaine, and amiodarone. Epinephrine is generally recommended every five minutes. Vasopressin overall does not improve or worsen outcomes compared to epinephrine.

Epinephrine does appear to improve short-term outcomes such as return of spontaneous circulation. Some of the lack of long-term benefit may be related to delays in epinephrine use. While evidence does not support its use in children guidelines state its use is reasonable. Lidocaine and amiodarone are also deemed reasonable in children with cardiac arrest who have a shockable rhythm. The general use of sodium bicarbonate or calcium is not recommended.

The 2010 guidelines from the American Heart Association no longer contain the recommendation for using atropine in pulseless electrical activity and asystole due to the lack of evidence for its use. Neither lidocaine nor amiodarone, in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation, improves survival to hospital discharge but both equally improve survival to hospital admission.

Thrombolytics when used generally may cause harm but may be of benefit in those with a confirmed pulmonary embolism as the cause of arrest. Evidence for use of naloxone in those with cardiac arrest due to opioids is unclear but it may still be used. In those with cardiac arrest due to local anesthetic lipid emulsion may be used.

Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. Some teams have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.

Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.

Medical management of patients with CRS is often challenging as focus on treatment of one organ may have worsening outcome on the other. It is known that many of the medications used to treat HF may worsen kidney function. In addition, many trials on HF excluded patients with advanced kidney dysfunction. Therefore, our understanding of CRS management is still limited to this date.

Diuretics

ACEI, ARB, renin inhibitors, aldosterone inhibitors

Natriuretic peptides

Vasopressin antagonists

Adenosine antagonists

Ultrafiltration

Inotropes

Cooling adults after cardiac arrest who have a return of spontaneous circulation (ROSC) but no return of consciousness improves outcomes. This procedure is called targeted temperature management (previously known as therapeutic hypothermia). People are typically cooled for a 24-hour period, with a target temperature of . There are a number of methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body, or infusing cold saline. This is followed by gradual rewarming over the next 12 to 24 hrs.

Recent meta-analysis found that the use of therapeutic hypothermia after out-of-hospital cardiac arrest is associated with improved survival rates and better neurological outcomes.

Generally, the treatment for SIRS is directed towards the underlying problem or inciting cause (i.e. adequate fluid replacement for hypovolemia, IVF/NPO for pancreatitis, epinephrine/steroids/diphenhydramine for anaphylaxis).

Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving symptoms in clinical trials. Other antioxidants such as vitamin E may be helpful as well.

Septic treatment protocol and diagnostic tools have been created due to the potentially severe outcome septic shock. For example, the SIRS criteria were created as mentioned above to be extremely sensitive in suggesting which patients may have sepsis. However, these rules lack specificity, i.e. not a true diagnosis of the condition, but rather a suggestion to take necessary precautions. The SIRS criteria are guidelines set in place to ensure septic patients receive care as early as possible.

In cases caused by an implanted mesh, removal (explantation) of the polypropylene surgical mesh implant may be indicated.

Hypervolemia, or fluid overload, is the medical condition where there is too much fluid in the blood. The opposite condition is hypovolemia, which is too little fluid volume in the blood. Fluid volume excess in the intravascular compartment occurs due to an increase in total body sodium content and a consequent increase in extracellular body water. The mechanism usually stems from compromised regulatory mechanisms for sodium handling as seen in congestive heart failure (CHF), kidney failure, and liver failure. It may also be caused by excessive intake of sodium from foods, intravenous (IV) solutions and blood transfusions, medications, or diagnostic contrast dyes. Treatment typically includes administration of diuretics and limit the intake of water, fluids, sodium, and salt.

Initial management in hospital is by pericardiocentesis. This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. A left parasternal approach begins 3 to 5 cm left of the sternum to avoid the left internal mammary artery, in the 5th intercostal space. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.

In people following heart surgery the nurses monitor the amount of chest tube drainage. If the drainage volume drops off, and the blood pressure goes down, this can suggest tamponade due to chest tube clogging. In that case, the patient is taken back to the operating room for an emergency reoperation.

If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility.