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Therapeutic Applications of Beta Activation1 Heart Failure Heart failure is characterized by a reduction in the force of myocardial contraction advair diskus 250mcg discount, resulting in insufficient cardiac output cheap advair diskus 100 mcg. Because activation of beta1 receptors in the heart has a positive inotropic effect (i cheap advair diskus 500 mcg otc. Shock This condition is characterized by profound hypotension and greatly reduced tissue perfusion buy advair diskus 100mcg line. By increasing heart rate and force of contraction, beta stimulants can1 increase cardiac output and can thereby improve tissue perfusion. Cardiac Arrest By activating cardiac beta receptors, drugs have a role in initiating contraction1 in asystole or pulseless ventricular rhythms. Initial management focuses on cardiopulmonary resuscitation, external pacing, or defibrillation (whichever is applicable), and identification and treatment of the underlying cause (e. When a beta agonist 1 is indicated, epinephrine, administered intravenously, is the preferred drug. Adverse Effects of Beta Activation1 All of the adverse effects of beta activation result from activating beta receptors1 1 in the heart. Altered Heart Rate or Rhythm Overstimulation of cardiac beta receptors can produce 1 tachycardia (excessive heart rate) and dysrhythmias (irregular heartbeat). Angina Pectoris In some patients, drugs that activate beta receptors can precipitate an attack of1 angina pectoris, a condition characterized by substernal pain in the region of the heart. Anginal pain occurs when cardiac oxygen supply (blood flow) is insufficient to meet cardiac oxygen needs. The most common cause of angina is coronary atherosclerosis (accumulation of lipids and other substances in coronary arteries). Because beta agonists increase cardiac oxygen demand (by1 increasing heart rate and force of contraction), patients with compromised coronary circulation are at risk for an anginal attack. Clinical Consequences of Beta Activation 2 Applications of beta activation are limited to the 2 lungs and the uterus. Drugs used for their beta -activating ability include epinephrine, isoproterenol, and2 albuterol. Therapeutic Applications of Beta Activation2 Asthma Asthma is a chronic condition characterized by inflammation and bronchoconstriction occurring in response to a variety of stimuli. Because drugs that activate beta receptors in the lungs promote bronchodilation, these drugs can2 help relieve or prevent asthma attacks. For therapy of asthma, adrenergic agonists that are selective for beta2 receptors (e. This is especially true for patients who also suffer from angina pectoris or tachycardia because drugs that can activate beta receptors would1 aggravate these cardiac disorders. It should be noted, however, that inhalation does not guarantee safety: Serious systemic toxicity can result from overdosing with inhaled sympathomimetics, so patients must be warned against inhaling too much drug. Delay of Preterm Labor Activation of beta receptors in the uterus relaxes uterine smooth muscle. Adverse Effects of Beta Activation2 Hyperglycemia The most important adverse response to beta activation is hyperglycemia2 (elevation of blood glucose). The mechanism is activation of beta receptors in2 the liver and skeletal muscles, which promotes breakdown of glycogen into glucose. As a rule, beta agonists cause hyperglycemia only in patients with2 diabetes; in patients with normal pancreatic function, insulin release will maintain blood glucose at an appropriate level. If hyperglycemia develops in the patient with diabetes, medications used for glucose control will need to be adjusted. It occurs because2 activation of beta receptors in skeletal muscle enhances contraction. This effect2 can be confounding for patients with diabetes because tremor is a common symptom of hypoglycemia; however, when due to beta activation, it may be2 accompanied by hyperglycemia. Fortunately, the tremor generally fades over time and can be minimized by initiating therapy at low doses. Clinical Consequences of Dopamine Receptor Activation Activation of peripheral dopamine receptors causes dilation of the renal vasculature. This effect is employed in the treatment of shock: by dilating renal blood vessels, we can improve renal perfusion and can thereby reduce the risk for renal failure. It should be noted that, when dopamine is given to treat shock, the drug also enhances cardiac performance because it activates beta receptors in1 the heart. Multiple Receptor Activation: Treatment of Anaphylactic Shock Pathophysiology of Anaphylaxis Anaphylactic shock is a manifestation of severe allergy. The reaction is characterized by hypotension (from widespread vasodilation), bronchoconstriction, and edema of the glottis. Although histamine contributes to these responses, symptoms are due largely to release of other mediators (e. Anaphylaxis can be triggered by a variety of substances, including bee venom, wasp venom, latex rubber, certain foods (e. Treatment Epinephrine, injected intramuscularly or intravenously, is the treatment of choice for anaphylactic shock. Benefits derive from activating three types of adrenergic receptors: alpha, beta, and beta. By activating these receptors, epinephrine can1 1 2 reverse the most severe manifestations of the anaphylactic reaction. Activation of beta receptors increases cardiac output, helping elevate blood pressure. Blood1 pressure is also increased because epinephrine promotes alpha -mediated1 vasoconstriction. In addition to increasing blood pressure, vasoconstriction helps suppress glottal edema. Individuals who are prone to severe allergic responses should carry an epinephrine autoinjector (e. Antihistamines are not especially useful against anaphylaxis because histamine is only one of several contributors to the reaction. Properties of Representative Adrenergic Agonists Our aim in this section is to establish an overview of the adrenergic agonists. The information is presented in the form of “drug digests” that highlight characteristic features of representative sympathomimetic agents. Some of these drugs are used in specialty areas; however, the choices of representative drugs will increase understanding of adrenergic receptor activation. As noted, there are two keys to understanding individual adrenergic agonists: (1) knowledge of the receptors that the drug can activate and (2) knowledge of the therapeutic and adverse effects that receptor activation can elicit. By integrating these two types of information, you can easily predict the spectrum of effects that a particular drug can produce. Unfortunately, knowing the effects that a drug is capable of producing does not always indicate how that drug is actually used in a clinical setting. Similarly, although isoproterenol is capable of producing uterine relaxation through beta activation, it is no longer used for this purpose because2 safer drugs are available. Because receptor specificity is not always a predictor of the therapeutic applications of a particular adrenergic agonist, for each of the drugs discussed next, approved clinical applications are indicated. Epinephrine • Receptor specificity: alpha, alpha, beta, beta1 2 1 2 • Chemical classification: catecholamine Epinephrine [Adrenalin, others] was among the first adrenergic agonists employed clinically and can be considered the prototype of the sympathomimetic drugs. Therapeutic Uses Epinephrine can activate all four subtypes of adrenergic receptors. As a consequence, the drug can produce a broad spectrum of beneficial sympathomimetic effects: • Because it can cause alpha -mediated vasoconstriction,1 epinephrine is used to (1) delay absorption of local anesthetics, (2) control superficial bleeding, and (3) elevate blood pressure. Pharmacokinetics Absorption Epinephrine may be administered topically or by injection. After subcutaneous injection, absorption is slow owing to epinephrine-induced local vasoconstriction. Inactivation Epinephrine has a short half-life because of two processes: enzymatic inactivation and uptake into adrenergic nerves. Adverse Effects Because it can activate the four major adrenergic receptor subtypes, epinephrine can produce multiple adverse effects. Hypertensive Crisis Vasoconstriction secondary to excessive alpha activation can produce a1 dramatic increase in blood pressure.
If severe advair diskus 100mcg online, this can lead to: • Fighting against the ventilator • Increased use of sedatives • Prolonged duration of mechanical ventilation and increased frequency of tracheotomy trusted advair diskus 250mcg. These muscles already have to cope with increased elastic cheap advair diskus 250mcg fast delivery, resistive discount advair diskus 500 mcg without prescription, and threshold workload. This increased load can be overcome with ease in patients with well-preserved muscular force, but in difﬁcult-to-wean patients this force–load imbalance can signiﬁ- cantly hamper the process of weaning from mechanical ventilation. Poor patient– ventilator interaction during sleep can lead to sleep fragmentation, frequent arousals, and inadequate correction of nocturnal hypoventilation. It does not mean that asynchrony does not present a problem in patients with other diseases. Problem solving The ventilatory mode In approximately 70% of patients the most common assisted modes of ventilation do not cause major asynchronies. Pressure support may be primarily time cycled or time cycling may be set as a backup if ﬂow cycling fails. The characteristics of the ventilator Most available ventilators synchronize satisfactorily in most cases. There are several studies comparing the in vitro characteristics of the various ventilators, and the knowledge of these results may eventually drive the decision of the clinician to use a speciﬁc ventilator. Ventilator settings Alteration of the ventilator settings is the best available method to improve patient–ventilator interaction. Ventilator inspiration continues into patient (neural) expiration when the inspiratory muscles have stopped contraction. This leaves inadequate time for expiration and leads to ‘breath stacking’ and dynamic hyperinﬂation. The following inspiration starts at a high lung volume, when the pressure at the airway opening is still signiﬁcantly positive. Therefore, the inspiratory effort does not create a pressure gradient capable of being sensed by the ventilator. In the presence of severe expiratory ﬂow limitation, a more sensitive trigger (expiration staring at a higher percentage of peak ﬂow) may reduce the number of ineffective efforts. If using a helmet, increasing the ‘usual’ baseline inspiratory and expiratory pressures by 50%, and increasing the pressurization rate, reduces the number of asynchronies. However, pharmacological sedation should be used cautiously, since confusion and agitation may also be caused by hypoxia and hypercapnia. Opioids such as morphine and fentanyl are powerful analgesics, but even at therapeutic doses will cause respiratory depression. Other adverse effects include hypotension, bradycardia, ileus, delirium, and agitation. It is reasonable to administer small doses of opioids (fentanyl, morphine) where blunting of respiratory drive is desirable. It is indicated for younger patients, for chronic benzodiazepine users, and for patients with preserved lean mass and muscular force, where a mild muscle relaxant effect elicited by benzodiazepines can be desirable. Particularly in patients with airﬂow limitation it may cause increased dura- tion of mechanical ventilation and increased frequency of tracheostomy. The clinician should consider how best to correct this harmful interaction between the ‘two brains’ (i. Acute respiratory failure and forced ventilatory efforts can profoundly alter cardiovascular function, just as heart failure can alter ven- tilation and gas exchange. Many of these effects are predictable and can also be used to diagnose cardiovascular status. Heart–lung interactions involve four basic concepts: • Inspiration increases lung volume. Haemodynamic effects of changes in lung volume Lung inﬂation: • Alters the ﬂow characteristics of venous return • Affects pulmonary vascular resistance • Compresses the heart in the cardiac fossa—at high lung volumes this can limit cardiac volumes in a similar fashion to cardiac tamponade • Alters autonomic tone. Each of these processes may predominate in determining the ﬁnal cardio- vascular state. Venous return The major determinants of the hemodynamic response to increases in lung volume are mechanical in nature. Inspiration alters right atrial pressure and induces diaphragmatic descent, both of which alter venous return. Venous return is a function of: • The ratio of the pressure difference between the right atrium and the systemic venous reservoirs • The resistance to venous return. Increased intra-abdominal pressure (diaphragmatic descent) increases abdominal venous pressure and augments venous blood ﬂow. This increases hepatic outﬂow resistance, decreasing splanchnic venous reservoir ﬂow. Thus, increasing lung volume may increase, decrease, or not alter venous return depending on which of these factors are predominant. Usually: • Spontaneous inspiration increases venous return • Positive pressure inspiration decreases venous return in normo- and hypovolemic states and in patients with hepatic cirrhosis • Positive pressure inspiration increases venous return only in volume overloaded states. Hyperinﬂation therefore increases pulmonary vascular resistance and pulmonary artery pressure. Autonomic tone Small tidal volumes (<10mL/kg) increase heart rate by vagal withdrawal (respiratory sinus arrhythmia). Larger tidal volumes (>15mL/kg) decrease heart rate, arterial tone, and cardiac contractility by increased vagal tone and sympathetic withdrawal. These effects are probably only relevant in the diagnosis of dysautonomia and in the care of neonatal subjects where autonomic tone is high. Haemodynamic effects of changes in intrathoracic pressure The heart within the thorax is a pressure chamber within a pressure chamber. Venous return Variations in right atrial pressure represent the major factor determining the ﬂuctuation in pressure gradient for systemic venous return during ventilation. Ventilation as exercise Spontaneous ventilatory efforts are exercise and represent a metabolic load on the cardiovascular system. Cardiovascular insufﬁciency and failure to clear airway secretions are the two most common causes of failure to wean from mechanical ventilation. Volume responsiveness: • Ventricular volumes vary with positive pressure ventilation. Numerous studies have documented that quantifying this stroke volume or pulse pressure variation allows one to identify those subjects who are volume responsive. Thus, the clinical utility of stroke volume or pulse pressure variation to identify subjects who are volume responsive is only applicable during positive pressure breathing. Being volume responsive does not equate to the need for ﬂuid resuscitation, which is a clinical determination. Dealing effectively with this common problem requires the clinician to understand the potential interactions between the treatment instituted and the underlying pathophysiological process. It should be read in conjunction with b Respiratory physiology and pathophysiology, p. Increase FiO2 • Increasing FiO2 quickly corrects hypoxaemia due to hypoventilation. As shunt fraction increases above 20%, increases in FiO2 have less effect on PaO2. An increase in FiO2 will still improve blood oxygen content to some extent by increasing dissolved oxygen in those capillaries exposed to ventilation. Increase airway pressure Traditionally, increasing mean airway pressure is associated with improved oxygenation, but it can also result in haemodynamic instability, ﬂuid retention, and barotrauma (Table 5. Principles Increases in airway pressure are designed to open (or recruit) collapsed alveoli. The lung volume response to airway pressure is described by the static pressure–volume curve. Lung hysteresis is a complex phenomenon related to the properties of surfactant, the viscosity of the alveolar lining, the law of Laplace (P = 2T/r), and the disordered sequence of alveolar reopening. It affects the relationship between mPaw and oxygenation as well as inﬂuencing the relationship between mPaw and haemodynamic effects. It is easier to keep open a lung unit that has been opened than it is to open a lung unit that has been allowed to close. In an injured lung there are pressures above which all recruitable units will open given sufﬁcient time, and pressures below which all collapsible lung units will close. More interestingly, there is a conditional area between these values where lung unit opening will depend on the pre-existing state of the lung: if there are lots of closed lung units before airway pressure reaches the conditional zone, most will remain closed until they reach the threshold ‘opening pressure’. If there are many lung units open before airway pressure drops into the conditional zone, most will remain open until they reach the threshold ‘closing’ pressure. However, it is conceptually useful to explain the different gas exchange responses produced by different approaches to raising mPaw (see examples below).
The first goal of potassium replacement is to eliminate or treat the condition underlying a transcellular shift 500mcg advair diskus otc. Assuch generic 100mcg advair diskus, magnesium also must bereplaced to a normal level when replacing serum potassium buy advair diskus 500 mcg mastercard. However buy 500mcg advair diskus otc, hyperkalemia can often be spurious due to traumatic venipuncture and subsequent potassium release, or specimen hemolysis. Thus, unexpected hyperkalemia should be validated with repeat blood draw if possible. The causes of hyperkalemia can also be categorized as transcellular shifts ver sus impaired renal excretion. Impaired renal excretion in critical care patients is mostly due to renal insuficiency. Furthermore, many drugs, such as sulfamethoxazole (Bactrim), subcutaneous heparin, and pentamidine can cause hyperkalemia by inhibiting the renin-angiotensin-aldosterone system. Lastly, blood transfsions can contribute to hyperkalemia, as the potassium in stored eryth rocytes leaks out slowly. The accumulation of extracellular potassium in stored blood is usually cleared renally in patients receiving transfsions, but this may become a problem in patients with acute renal failure or hemodynamic shock. First, to inhibit the arrhythmo genic nature of hyperkalemia, calcium infusions are used to stabilize the myocar dium. These infsions are temporary, lasting 20 to 30 minutes, and will temporize the condition until the efects of definitive measures take place. Note, however, that bicarbonate actually has little clini cal value because it binds to calcium in theplasma, whichwould render our calcium infsion inefective if given together. Third, more definitive measures should be undertaken to remove excess potassium from the body. These include sodium polystyrene (Kayexalate), a cation exchange resin, frosemide, a loop diuretic that enhances urinary potassium excretion, and dialysis, the most efective method in patients with acute renal failure. Mag nesium is also responsible for regulating calcium movement into smooth muscle cells. As such, it is essential in helping the body maintain cardiac contractility and peripheral vascular tone. These functions make it important for magnesium levels in the plasma to be maintained at normal values. Diuretics can cause hypo magnesemia, as inhibition of sodium reabsorption interferes with magnesium reab sorption. Similar to potassium, deficiencies in plasma magnesium are largely asymptom atic. Phosphorus Phosphorus is an important electrolyte because of its participation in aerobic energy production. The presentation of phosphorus abnormalities is usually subclinical, though impaired cellular energy production may develop secondary to hypophos phatemia and can be detrimental to systemic oxygen delivery. Decreased energy production in the heart can cause decreased inotropy and cardiac output. Hypo phosphatemia is also associated with reduced deformability of red blood cells, lead ing to hemolytic anemia. The use of phosphate binders, such as sucralfate, can iatrogenically lower the phosphate level in the serum. The reintro duction of nutrition in patients with prolonged periods of nonfeeding can cause low phosphate levels via the refeeding syndrome. On evaluation of the patient, you find her vital signs to be the following: temperature 37. Yesterday, her nasogastric tube was removed and she was started on a clear liquid diet. Laboratory testing reveals a serum sodium con centration of 122 mmol/L and serum osmolarity of 240 mOsm/kg water. She most likely presents with altered mental status due to hyponatremia second ary to cerebral salt wasting syndrome. As such, this woman should be fluid bolused with an isotonic solution, such as normal saline. If the patient still remains symptomatic at that time, considerations should then be made for correction with hypertonic saline. Using the equation from Adrogue et al, infsion of a liter of 3% saline will change the serum concentration by 12. The evaluation and treatment of hyperkalemia involves all of the afore mentioned answers except for fuid boluses. More definitive treatment includes giving polystyrene (Kayexalate), frosemide, orundergoing hemodialysis if the patient is in acute renal failure. Disturbances in sodium in critically ill adult neurologic patients: a clinical review. The neurosurgeon determined that these injuries do not warrant surgical treatment at this time. These measures include the use of mannitol, vasopressors, brief hyperventilation, elevation of the head of bed (if possible), and maintaining the head in midline position. To learn the optimal supportive strategies (ventilation, fluid/electrolyte, and hemodynamic strategies) for patients with severe brain injuries and intracranial hypertension. The ability to minimize swelling and maintain adequate perfsion to the brain is of the utmost importance, as secondary injury to the brain significantly worsens the outcome. Special attention needs to be paid to ensure that there are no episodes of hypotension or hypoxia. A ventriculostomy is helpful in the diagnosis and treatment of traumatic brain injury. The injury can consist of skull fractures, intracranial bleeding (subdural, epidural, intraparenchymal), and difuse axonal injury. Within the skull, there is brain tissue, cerebrospinal fuid, and intracranial blood. Under normal cir cumstances, the cerebral blood flow remains constant over a wide range of cerebral perfsion pressure. Acute disease processes can alter the range of the zone of autoregulation, leading to increased risk of cerebral damage. In the United States, brain injury was only recently surpassed by gunshot wounds as the number 1 cause of death in trauma patients. Identifing those factors which tend toward a worse prognosis is not as clear, how ever. The inclusion of other clinical information such as secondary insults (hypotension and hypoxia), and laboratory parameters (glucose and hemoglobin) appears to strengthen the prognostic indication. For example, a patient who is a new paraplegic, but can follow commands with their arms is given a score of 6 on the motor scale (not a 1 because he does not move his legs). The pupillary examination is an essential component of the initial examination for all trauma patients. Detection of a pupil asymmetry, dilation or loss of light reflex in an unconscious patient is concerning for ipsilateral intracranial pressure increase. The mass efect of intracranial injuries increases the intracranial pressure and this is refected by compression of the cranial nerves and pupillary changes. Direct lacerations of epidural arteries produce epidural hematomas, while it is the disruption ofbridging subdural veins that causes subdural hematomas. Intracerebral contusions are most likely the result of tissue disruption from the direct force of the injury. Conversely, an epidural hematoma was associated with a better outcome, possibly due to the ability to emergently evacuate the hematoma. The brain damage caused by an epidural hematoma is secondary to compression, instead of intrinsic brain injury. There are several difer ent therapies and maneuvers that can be utilized to achieve these goals. Cerebro spinal fluid drainage, controlled hyperventilation, mannitol, and barbiturates are among the most commonly used therapies to alleviate intracranial hypertension. Maneuvers directed at improving cerebral perfsion require that patients have appropriate continuous monitoring with intracranial pressure monitors, central venous catheters, and arterial lines. Patients with increased intracranial pressures should be positioned to optimize venous drainage from the brain, and this can be accomplished with elevation of the head of the bed and positioning the head in a neutral, midline position. Maintaining adequate blood flow to the brain is important treatment therapy, but it is not as easy as it would seem.