o Dopamine is the immediate precursor of endogenous norepinephrine. Dopamine’s hemodynamic effects are due to the release of norepinephrine from sympathetic nerves and the direct stimulation of alpha, beta, and dopaminergic receptors. Dopamine’s effect is less pronounced after endogenous norepinephrine stores have been depleted. At lower doses (2–5 μg/kg per minute), dopamine increases cardiac contractility and cardiac output without increasing heart rate, blood pressure, or systemic vascular resistance. Renal blood flow and urine output increase in response to doses of 0.5-2 μg/kg per minute as a result of selective stimulation of dopaminergic receptors. When doses reach 10 μg/kg per minute, dopamine has both a chronotropic and an inotropic effect. At infusion rates in excess of 10 μg/kg per minute, alpha-adrenergic stimulation occurs, along with an increase in systemic vascular resistance. The metabolic effects of dopamine administration include decreased aldosterone secretion, inhibition of thyroid-stimulating hormone and prolactin release, and inhibition of insulin secretion. Because it increases cardiac output, dopamine can increase pulmonary shunting by augmenting flow to poorly ventilated lung regions. After ensuring adequate fluid resuscitation, dopamine infusion is usually started at a dose of 5 μg/kg per minute and advanced until blood pressure increases. Used in low doses with norepinephrine, dopamine’s selective effect on the renal vasculature may continue to allow adequate urine production while norepinephrine supports the blood pressure by its vasoconstrictive effect.
o Dobutamine has predominantly β-adrenergic inotropic effects. It has a relatively minor chronotropic effect. It is the pressor of choice in patients with adequate blood pressure but depressed cardiac output. Onset of action is within 1–2 minutes, although the peak effect may not be reached until 10 minutes after administration. Dobutamine is a better choice for long-term infusion than dopamine because the latter depletes myocardial norepinephrine stores. Dosage typically ranges from 5–15 μg/kg per minute. Increased urine output also may be achieved after dobutamine administration because of increased renal perfusion from elevated cardiac output. Infusion is begun at a rate of 2–5 μg/kg per minute and titrated to the desired effect. Maximal benefit is usually achieved at levels between 10 and 15 μg/kg per minute
o Despite adequate volume resuscitation and improved cardiac output, blood pressure may remain depressed. Phenylephrine and norepinephrine are two agents commonly used to increase systemic vascular resistance. Norepinephrine is the biosynthetic precursor of epinephrine, and as such posses both α- and β-adrenergic activity. In low doses, its major effect is β-adrenergic. It increases cardiac contractility, conduction velocity, and heart rate. At higher doses, both α- and β-adrenergic effects occur, which include peripheral vasoconstriction, increased cardiac contractility, cardiac work, and stroke volume. Norepinephrine causes splanchnic vasoconstriction, which may lead to end-organ ischemia. The drug is cleared rapidly from the plasma with a half-life of approximately 2 minutes. Initial infusion rates are 0.5–1 μg/min. The usual maximum dose is 1 μg/kg per minute.
o Vasopressin (antidiuretic hormone) is normally released by the hypothalamus and produces vasoconstriction of vascular smooth muscle in addition to its antidiuretic effect on the renal collecting system. At low plasma concentrations it causes vasodilation of the coronary, cerebral, and pulmonary vessels. Vasopressin levels increase in early septic shock and later fall as sepsis worsens. When given in doses of 0.01–0.04 units/min, vasopressin infusion increases serum vasopressin levels and decreases the need for other vasopressors. At this dose, urinary output may increase, and pulmonary vascular resistance may decrease. Doses higher than 0.04 units/min can cause undesirable vasoconstrictive effects
o Because decreased vascular resistance is the primary cause of hypotension in septic shock, further pharmacologic vasodilation is contraindicated. Occasionally, severe myocardial depression is accompanied by an increase in systemic vascular resistance. This preterminal event puts further strain on the left ventricle and may cause complete hemodynamic collapse. Judicious use of vasodilators such as nitroprusside may be tried. Nitroglycerin is probably an inferior choice because it also reduces preload.
o Identification of the source of sepsis is imperative. If bacteremia is not treated, outcome will be adversely affected. Empirical broad-spectrum therapy should be instituted.
o Multiple factors contribute to hypergylcemia, including increased levels of stress hor-mones, peripheral insulin resistance, drugs, and exogenous dextrose infusion. Glucose control may be provided with either a glucose concentration dependent dose (“sliding scale”) or a constant infusion for higher serum glucose levels. Typically, glucose levels should remain below 130 mg/dL.
o More recent work has found that lower physiologic doses of corticosteroids for longer periods of time may be beneficial. Patients should undergo a Cortrosyn stimulation test. After obtaining blood for a baseline concentration of serum cortisol, 250 μg Cortrosyn is given intravenously, and blood for a repeat serum cortisol assay is collected 30–60 minutes later. If there is concern that the patients is hypoadrenal, 4 mg dexamethasone can be given prior because it does not interfere with the test. If the increase after Cortrosyn is less than 9 μg/dL, there is insufficient adrenal reserve, and 50 mg hydrocortisone should be given every 6 hours for 7 days. This should be supplemented with fludrocortisone 50 μg orally every day. It is likely that all patients should be started on replacement corticosteroid until the results of the stimulation study are known, at which time supplementation can be withdrawn from those who responded to the stimulation test.
o Proper prophylaxis against gastric stress ulceration should be provided. Additionally, renal function must be monitored closely, and appropriate support with either hemofiltration and/or dialysis should be provided. Adequate prophylaxis against deep venous thrombosis includes either unfractionated or low-molecular-weight heparin
o Anaphylactic shock and anaphylactoid reactions are due to the sudden release of preformed inflammatory mediators from mast cells and basophils. After exposure to the offending stimulus, initial symptoms may appear within seconds to minutes or may be delayed as long as 1 hour.Mast cells and basophils will release histamine and PAF into the circulation. These mediators result in vasodilation, bronchoconstriction, pruritus, bronchorrhea, platelet aggregation, and increased vascular permeability. The latter may lead to laryngeal edema that culminates in airway obstruction. Anaphylactoid reactions occur when the offending agent causes the direct release of these substances without mediation by IgE. An increased hematocrit is found commonly as a result of hemoconcentration from vascular permeability. Serum mast cell tryptase is usually elevated. Drug therapy should begin with epinephrine (1:1000), 0.3–0.5 mL subcutaneously. The dose of epinephrine may be repeated every 5–10 minutes as needed. If the patient does not respond to the initial dose or if severe laryngospasm or frank cardiovascular collapse is present → 5–10 mL of epinephrine (1:10,000) may be administered intravenously. Histamine antagonists should be administered as early as possible. Diphenhydramine (1 mg/kg intravenously) and ranitidine (50 mg intravenously over 5 minutes) are the preferred drugs. If hypotension persists after the repeated administration of epinephrine and histamine antagonists aggressive fluid resuscitation is required. If this fails, dopamine may be started. A second pressor be used if an adequate response has not yet been achieved. Biphasic anaphylaxis may occur in up to 25% of patients. Life-threatening reactions reappear after an asymptomatic interval of up to 8 hours following resuscitation. Hydrocortisone, 100–250 mg intravenously every 6 hours, may help to prevent the late manifestations of biphasic anaphylaxis. Steroids probably have no role in the immediate treatment of acute anaphylaxis. Patients who are receiving beta-blockers at the time of an anaphylactic reaction may be resistant to the effects of administered epinephrine. Atropine and glucagon may be useful adjuncts to reverse the cardiac manifestations of anaphylaxis in these patients
o Neurogenic shock is produced by loss of peripheral vasomotor tone as a result of spinal cord injury, regional anesthesia, or administration of autonomic blocking agents. Blood becomes pooled in the periphery, venous return is decreased, and cardiac output falls. If the level of interruption is below the midthorax, the remaining adrenergic system above the level of injury is activated, resulting in increased heart rate and contractility. If the cardiac sympathetic outflow is affected, bradycardia results. Blood pressure can decrease to extremely low levels as blood pools peripherally in the venous reservoir. All patients who have sustained spinal trauma should be assumed to have hypovolemic shock from associated injuries until proved otherwise.
o Extremities are warm above the level of injury and cool below. Blood pressure may be extremely low, with a very rapid heart rate. Signs and symptoms of spinal cord injury and spinal shock will be present.
o Radiographs of the cervical, thoracic, and lumbosacral spine are important to determine whether fractures are present that may be unstable. CT and MRI may be useful to determine whether fragments within the spinal canal may be causing cord compression. When present, they may be amenable to neurosurgical decompression
o Isolated head injury does not cause shock. Rather, it may increase the blood pressure while slowing the heart rate (Cushing’s reflex).
o If volume infusion fails to restore the blood pressure, infusion of an alphaadrenergic agent is required to provide direct vasoconstriction. Either phenylephrine or norepinephrine may be used. These drugs are started in low doses and increased slowly until just sufficient to restore blood pressure to a mean between 60 and 80 mm Hg.
o If spinal cord transection is complete, the only role for surgery is stabilization of vertebral fractures to prevent further injury. If a foreign body is present, removal may promote return of function if the cord is intact.
o Cardiogenic shock occurs most commonly either after relentless progression of cardiac disease or after an acute event such as myocardial infarction or rupture of a cardiac valve or septum. A staging system has been developed for the classification of cardiogenic shock that develops on a chronic basis. Stage I (Compensated Hypotension)→The decreased cardiac output and resulting hypotension invoke compensatory mechanisms able to restore blood pressure and tissue blood flow to normal levels. These reflexes are mediated by the arterial baroreceptors, which increase the systemic vascular resistance Stage II (Decompensated Hypotension)→Cardiac output falls below that which enables the peripheral vasculature to maintain blood pressure by vasoconstriction. Blood pressure and tissue perfusion fall. Stage III (Irreversible Shock)→Profound reduction in flow activates ischemic mediators such as the complement cascade. Membrane injury develops that further aggravates the ischemic insult. Irreversible myocardial and peripheral tissue damage occur.
o Physical examination will reveal signs consistent with the underlying pathophysiologic mechanism of decreased cardiac output and absolute hypervolemia. Blood pressure is less than 90 mm Hg. The heart rate may be extremely high and exceed the maximum aerobic limit . When decompensation occurs, bradycardia usually develops. Neck veins are distended, and pulsations frequently can be observed more than 4 cm above the clavicle with the patient in the semierect position. Peripherally, the extremities are cool, reflecting inadequate perfusion. Abdominal examination may reveal a congested and dis-tended liver that is tender to palpation. Rales are detected on auscultation of the lungs in a patient who has a normal right ventricle. With biventricular failure or pulmonary hypertension, pulmonary auscultation may be normal. Cardiac examination typically reveals a third heart sound, and there may be a murmur characteristic of valvular disease. Require a pulmonary artery catheter for monitoring and evaluation of the response to therapy. The usual findings are elevation of central venous and pulmonary capillary wedge pressures and a cardiac index less than about 1.8 L/min/m2. If acute myocardial infarction is the precipitating cause, elevated cardiac bands of creatine kinase will be observed. A routine chemistry panel is required to evaluate K+ and HCO3–. Serum lactate may be elevated when shock has been prolonged. Hematocrit and hemoglobin should be determined to evaluate the need for transfusion. Intravenous nitroglycerin and beta-blockers are the main features of early treatment
o Although cardiogenic shock may occur in patients with whole body fluid overload, they may be effectively hypovolemic. If PCWP is less than 10–12 mm Hg, balanced salt solution should be administered in an attempt to increase filling pressures. Cardiac output should be measured after each change of 2–3 mm Hg in PCWP. Filling pressures near 20 mm Hg may be required before cardiac output increases.
o Cardiac compressive shock is a low-output state that occurs when the heart or great veins are compressed. Compression either impedes the return of blood to the heart or prevents effective pumping action of the heart itself. Pericardial tamponade, Distention of the abdomen with elevation of the diaphragm, PEEP used with mechanical ventilation increases the intrathoracic pressure, which both collapses the superior and inferior venae cavae and reduces the transmural pressure gradient, thereby decreasing cardiac filling. In similar fashion, tension pneumothorax increases the intrathoracic pressure and decreases venous return.
o The presence of distended neck veins is central to the diagnosis, although they may be absent if the patient is hypovolemic. When tension pneumothorax is the cause, hyperres-onance is noted on thoracic percussion, breath sounds are absent on the affected side, and the mediastinum is shifted away from the involved chest. Displacement of the trachea in association with distended neck veins is pathognomonic of tension pneumothorax. For patients who are breathing spontaneously, inspiration increases the degree of venous distention (Kussmaul’s sign). Paradoxic pulse also may occur with spontaneous breathing and consists of a decrease in systolic pressure of more than 10 mm Hg with inspiration. Central venous pressure is increased, as are pulmonary artery and pulmonary capillary wedge pressures. Equalization of central venous pressure, pulmonary artery, and pulmonary capillary wedge pressures strongly suggests pericardial tamponade. Central venous pressure cannot be used to guide such infusion because central venous pressure always will be elevated prior to the administration of fluid.
o Surgical decompression of the offending site is indicated. For tension pneumothorax, immediate insertion of a large-bore intravenous catheter into the affected hemithorax will rapidly release the increased pressure. After pulse and blood pressure return to normal, this small catheter can be replaced with a larger tube thoracostomy connected to a chest evacuation device. Placement of the smaller catheter never should be delayed pending procurement and placement of a more definitive thoracostomy tube. If cardiac compression is due to gastric distention, placement of a nasogastric tube may be helpful. When distention is due to other causes, surgical exploration is usually warranted. Pericardial decompression should be performed for pericardial tamponade. Reduction of ventilatory pressures and augmentation of the circulating blood volume, if possible, usually correct compression resulting from the use of PEEP
o Pulse pressure is the arithmetic difference between the systolic and diastolic pressures. Pulse pressures vary with stroke volume or vascular compliance. Pulse pressures less than 30 mm Hg are common with hypovolemia, tachycardia, aortic stenosis, constrictive pericarditis, pleural effusions, and ascites. Widened pulse pressures may be due to aortic regurgitation, thyrotoxicosis, patent ductus arteriosus, arteriovenous fistula, and coarctation of the aorta. Variability of pulse pressure and systolic pressure during the respiratory cycle has been correlated with response to intravascular fluid repletion.
o The arteries commonly used for invasive blood pressure monitoring, in order of usual preference, are the radial, ulnar, dorsalis pedis, posterior tibial, femoral, and axillary arteries. All patients should undergo an Allen test prior to catheter insertion.
o Central venous (CV) catheters are inserted via the subclavian, internal jugular, or a peripheral vein in the arm. Femoral venous catheters are not long enough to reach “central” veins but provide similar access for intravenous infusions. For monitoring purposes, CV catheters provide estimates of central venous pressure (CVP) and measure-ment of central venous oxygen saturation (ScvO2). A water manometer may be used to measure CVP. The normal range of CVP is between –4 and +10 mm Hg (–5.4 and +13.6 cm H2O).
o When positive end-expiratory pressure (PEEP) is applied, the positive pressure is transmitted through to the right atrium, causing a decrease in venous return and a rise in CVP.
o Mixed venous oxygen saturation (SvO2) reflects the relative delivery of O2 to the tissues compared with consumption. If lower than normal, concern should be raised about tissue hypoxia. True SvO2 must be measured in the pulmonary artery. Central venous O2 saturation (ScvO2) does not require a pulmonary artery catheter, but theoretically, the value will differ from SvO2. Generally, ScvO2 is about 5% higher than SvO2. Recent studies emphasizing early goal-directed therapy in sepsis have emphasized a target ScvO2 of greater than 70% by giving blood transfusion and cardiac inotropic drugs. ScvO2 can be obtained from a small sample of blood drawn back through the catheter or by using an oximeter-tipped CVP catheter.
o Catheterization of the pulmonary artery is a useful addition to CVP monitoring. It provides information related to left heart filling pressures and allows sampling of pulmonary artery blood for determination of mixed venous oxygen saturation. Thermodilution cardiac output measurements are made using a thermistor-tipped catheter. The pulmonary capillary wedge (pulmonary capillary occlusion) pressure (PCWP) estimates left ventricular end-diastolic pressure and thus serves as an estimate of left ventricular preload.
o Pulse oximetry has widespread usefulness-in adjusting inspired oxygen, during weaning from mechanical ventilation, and in testing different levels of PEEP, inverse I:E ratio, or other mechanical ventilator adjustments. Other uses include monitoring during procedures such as bronchoscopy, gastrointestinal endoscopy, cardioversion, hemodialysis, and radiography. Pulse oximetry is particularly accurate in following O2 saturation in patients who have mild to moderate hypoxemia (O2 saturation >75%) but without severe hypoperfusion or hypotension
o Capnography is a continuous display or recording of CO2 concentration during each breath
o Transcutaneous PCO2 (PtcCO2) has been measured using a modified PCO2 electrode attached to the skin surface.
o Medical conditions requiring hospitalisation→Medical Management of Acute MI (Conservative Management Without Angiogram), Management Of Acute MI With Angiogram, Medical Management of Acute MI With Cardiogenic Shock, Medical Management of Acute MI Requiring IABP Pump, Medical Management of Refractory Cardiac Failure, Medical Management of Infective Endocarditis, Medical Management of Pulmonary Embolism, Medical Management of Complex Arrhythmias(carto guided), Ablation Therapy for Simple Arrythmias(focal ablation), Medical Management of Pericardial Effusion & Tamponade with Aspiration
o Surgical conditions & procedures requiring hospitalisation→ Coronary Balloon Angioplasty with stent, ASD Device Closure, VSD Device Closure, Patent Ductus Arterious – Stenting, Patent Ductus Arterious - Device Closure, Patent Ductus Arterious - Single Coil Closure, Patent Ductus Arterious - Multiple Coils Closure, Balloon Valvotomy, Balloon Atrial Septostomy, Permanent Pacemaker Implantation, Temporary Pacemaker Implantation, Coaractation of Aorta Repair With Stent + Aortoplasty, Coaractation of Aorta Repair Without Stent+ Aortoplasty, Renal Angioplasty, Peripheral Angioplasty, Vertebral Angioplasty, Perpheral Angioplasty - Additional Stent, Surgery for Cardiac injuries Without CPB, Surgery for Cardiac injuries With CPB, Peripheral Embolectomy Without Graft, Excision Of Arterio Venous Malformation – Large, Excision Of Arterio Venous Malformation – Small, Arterial Embolectomy, A V Fistula surgery (creation) at Wrist, A. V Fistula surgery (creation) At Elbow, DVT - Ivc Filter implantation, Surgical management of Vascular Tumors, Small Arterial Aneurysms – Repair, Medium Size Arterial Aneurysms – Repair, Medium Size Arterial Aneurysms - Repair With Synthetic Graft, Aorto Billiac - Bifemoral Bypass With Synthetic Graft, Axillo Bifemoral Bypass With Synthetic Graft, Femoro Distal Bypass With Vein Graft, Femoro Distal Bypass With Synthetic Graft, Axillo Brachial Bypass Using With Synthetic Graft, Brachio - Radial Bypass With Synthetic Graft, Excicion Of Carotid Body Tumor With Vascular Repair, Carotid Artery Bypass With Synthetic Graft, Coronary Bypass Surgery, CABG With IABP Pump, CABG With Aneurismal Repair, Mitral Valve Replacement (With Valve), Aortic Valve Replacement (With Valve), Replacement of Tricuspid valve, Double valve replacement (With Valve), Pericardiostomy, Pericardiectomy, Pericardiocentesis, Coarctation-Arota Repair With Graft, Coarctation-Arota Repair Without Graft, Aneurysm Resection & Grafting, Intrathoracic Aneurysm -Aneurysm Not Requiring Bypass, Intrathoracic Aneurysm -Requiring Bypass (With Graft), Surgical management of Dissecting Aneurysms, Surgical management of Annulus Aortic Ectasia With Valved Conduits, Aorto-Aorto Bypass With Graft, Aorto-Aorto Bypass Without Graft, Femoro- Poplitial Bypass With Graft, Femoro- Poplitial Bypass Without Graft, Femoro- Ileal Bypass With Graft, Femoro- Ileal Bypass Without Graft, Femoro-Femoral Bypass With Graft, Femoro-Femoral Bypass Without Graft, TGA - Arterial Switch, TGA - Sennings Procedure, TGA - Carotid Embolectomy, Surgery For Intracardiac Tumors, surgical management of Ruptured Sinus Of Valsalva, surgical management (Correction) of TAPVC, Systemic Pulmonary Shunts With Graft TOF, Systemic Pulmonary Shunts Without Graft TOF, Total Correction of Tetralogy of Fallot, Intra Cardiac Repair Of ASD, Intracardiac Repair Of VSD, Surgery for-PDA, Ross procedure - Intracardiac repair of complex congenital heart diseases with Special Conduits, Ross procedure - Intracardiac repair of complex congenital heart diseases without Special Conduits, Valve repair with Prosthetic Ring, Valve repair without Prosthetic Ring, Open Pulmonary Valvotomy, Closed Mitral Valvotomy, Mitral valvotomy (Open), Surgery for Arterial Injuries, Venous Injuries Without Graft, Surgical Management of Vascular Injury In Upper Limbs - Axillary,Branchial,Radial And Ulnar -With Vein Graft, Major Vascular Injury -In Lower Limbs-Repair, Surgical Management of Minor Vascular Injury - Tibial Vessels In Leg, Surgical Management of Minor Vascular Injury -Vessels In Foot, Surgical Management of Vascular injuries with vein graft, Surgical Management of Vascular Injury With Prosthetic Graft, Surgical Management of Neck Vascular Injury - Carotid Vessels, Surgical Management of Abdominal Vascular Injuries - Aorta, Illac Arteries, Ivc, Iliac Veins, Surgical Management of Thoracic Vascular Injuries.
3’o clock: Lungs, Respiration
o Status asthmaticus is very severe asthma that is unremitting and poorly responsive to usual therapy. Airway obstruction is the major feature of this disorder, and asthma is both an acute reversible obstructive disease and a chronic pulmonary disease leading to permanent airway obstruction. Failure to control asthma symptoms is associated with a more rapidly progressive decline in lung function and loss of reversibility. This is the basis for consensus recommendations for chronic asthma management, which can be summarized as follows: (1) There is a key role for anti-inflammatory therapy (eg, corticosteroids), (2) regular β-adrenergic agonist use as the sole therapy for asthma is ineffective and potentially harmful, and (3) the goal of asthma treatment is to keep the patient completely symptom-free at all times. Airway obstruction in asthma results from three mechanisms: enhanced bronchial smooth muscle contraction (increased tone and response to stimuli), bronchial mucosal inflammation and edema, and plugging of the bronchi by secretions and inflammatory debris. Because airway obstruction in asthmatics is intrathoracic, airway narrowing is more marked during the expiratory.
o The physical examination is helpful for identifying signs of severe airway obstruction (eg, absence of wheezing, use of accessory muscles of respiration, intercostal retractions, and pulsus paradoxus) or signs of impending respiratory muscle fatigue (eg, paradoxical abdominal wall movement), but these signs are insensitive or unreliable when used by themselves to assess severity.Laboratory findings→ hypoxemia of mild to moderate degree. Most asthmatics (80%) presenting with an acute episode have mild respiratory alkalosis, Only a small proportion have normal or elevated PCO2, and there is an association between severe airway obstruction and hypercapnia in asthma. Metabolic acidosis owing to an increase in blood lactate in patients presenting with acute asthma, especially in association with hypoxemia, may be seen. Although pulse oximetry gives an estimate of arterial oxygenation, an arterial blood gas determination of pH and PCO2 is mandatory