Anesthesiology and Intensive Care

◆ Cardiac contusion, or other trauma including surgery, ablation, pacing, etc. ◆ Congestive heart failure—acute and chronic. ◆ Aortic dissection. ◆ Aortic valve disease. ◆ Hypertrophic cardiomyopathy. ◆ Tachy- or bradyarrhythmias, or heart block. ◆ Apical ballooning syndrome (Takotsubo). ◆ Rhabdomyolysis with cardiac injury. ◆ Pulmonary embolism, severe pulmonary hypertension. ◆ Renal failure. ◆ Age (>70 years). ◆ Acute neurological disease, including stroke or subarachnoid haemorrhage. ◆ Infiltrative diseases, e.g. amyloidosis, haemochromatosis, sarcoidosis, and scleroderma. ◆ Inflammatory diseases, e.g. myocarditis or myocardial extension of endo- and pericarditis. ◆ Drug toxicity or toxins. ◆ Critically-ill patients, especially with respiratory failure or sepsis. ◆ Burns, especially if affecting >30% of body surface area. ◆ Extreme exertion .

TREATMENT ALGORITHM OF HYPERLACTATAEMIA click to zoom the image

Anaerobic causes ◆ Macrocirculatory shock. ◆ Microcirculatory shunting. ◆ Carbon monoxide poisoning (carboxyhaemoglobin). Aerobic causes ◆ Increased aerobic glycolysis:     • Catecholamine-stimulated increased Na+–K+-pump activity.     • Cytokine-mediated glucose uptake. ◆ Mitochondrial dysfunction. ◆ Pyruvate dehydrogenase dysfunction:     • Sepsis.     • Thiamine deficiency. ◆ Reduced clearance:     • Liver insufficiency/surgery.     • Sepsis. ◆ Alkalosis. ◆ Malignancy (Warburg effect). ◆ Epileptic seizure (grand mal). ◆ Congenital metabolic diseases. ◆ Drugs and intoxications:     • Nucleoside reverse transcriptase inhibitors.     • Epinephrine.     • Metformin.     • Propofol (propofol infusion syndrome).     • Corticosteroids.     • Cyanide.     • Ethylene glycol.     • Methanol.     • Carbon monoxide poisoning (inhibition of cytochrome       oxidase).

Click the link below to access PDF file Michigan checklist for central vascular access.

There are currently no licensed pharmacological therapies for ARDS, although there are a number of novel agents under development. Appropriate treatment of risk factors including pneumonia, non-pulmonary sepsis (e.g. peritonitis), aspiration of gastric contents, major trauma, transfusion, and acute pancreatitis. Protective mechanical ventilation using tidal volumes of 6 mL/kg predicted body weight (PBW), and a plateau pressure less than 30 cmH2O, confers a mortality benefit, and should be undertaken whenever possible Extracorporeal membrane oxygenation & extracorporeal carbon dioxide removal have not been proved to be of universal benefit in ARDS, although it is possible that there may be sub-populations of ARDS patients (e.g.H1N1 influenza patients and ECMO ) that derive benefit from these interventions. Fluid restriction , after patients are appropriately resuscitated, is probably of benefit. There is no evidence to support a specific feeding regimen in ARDS patients.

 Patient should be placed in the head-down position on the right side and should have also immediate tracheal suction to maintain a clear airway.  Correct hypoxia and support pulmonary function by assisted ventilation or positive-pressure oxygen.  Endotracheal intubation should be considered for patients who are unable to protect their airways.  The use of corticosteroids in the treatment of chemical pneumonitis is controversial . The administration of corticosteroids cannot be recommended in patients with ARDS. The prophylactic use of antibiotics is not recommended. Empirical antibiotic therapy is appropriate for patients who aspirate gastric contents and who have small-bowel obstruction or other conditions associated with colonization of the gastric contents. Antibiotic therapy should be considered for patients with aspiration pneumonitis that fails to resolve within 48 hours following aspiration.  Empirical therapy with broad-spectrum agents is recommended; antibiotic

Preload                   Full Afterload                Increased Contractility          Decreased, avoid inotropes Rate                        Normal Rhythm                  Sinus, atrial pacing if required ________________________________________________ Преднагрузка        Полная Постнагрузка        Увеличить Сократимость       Уменьшить, избегать инотропов ЧСС                         Поддерживать в норме Ритм                        Синусовый, стимуляция предсердий при                                                         необходимости

Antiemetics,  are known to prolong the QTc interval: butyrophenone neuroleptic drugs ( droperidol and haloperidol ) 5-HT 3 receptor antagonists (ondansetron, granisetron, and dolasetron ) phenothiazines ( chlorpromazine and promethazine ) metoclopramide However, the scopolamine patch has not been demonstrated to significantly increase the QTc interval.

___________________________ Preload                          Increased ___________________________ Afterload                       Decreased ___________________________ Rate                               Increased ___________________________ Rhythm                         Controlled ___________________________

HEMODYNAMIC GOALS OF ACUTE MITRAL REGURGITATION Preload                            Increased -------------------------------------------- Afterload                         Decreased -------------------------------------------- Contractility                    Decreased ------------------------------------------- Rate                                 Increased ------------------------------------------- Rhythm                           Controlled

           INDICATIONS FOR ECMO Non-cardiogenic respiratory failure . Potentially reversible (Pneumothorax / large pleural effusion drained, trial of diuresis).                 IF : Optimal ventilation (including PEEP >10cmH2O)                  Consider PCV or CMV: VT < 8ml /kg (ideal body weight), prone ventilation, recruitment                    manouevre.               BUT : PaO2 / FiO2 < 80mmHg or pH < 7.25 for > 2 hours Cardiogenic shock of any aetiology . Potentially reversible OR candidate for destination therapy. Refractory to maximal medical Rx.   Fulminant myocarditis  requiring inotropes or IABP at any time( left heart failure + aseptic febrile illness < 2 weeks, marked troponin elevation, abnormal ECG and / or arrhythmia) ABSOLUTE CONTRAINDICATIONS TO ALL FORMS OF ECMO Significant pre-existing co-morbidity, such as irreversible neurological condition, Child-Pugh B or worse cirrrhosis (ascites, hepatic encephalopathy or recent

 MAC: prevents movement in response to surgical stimulationin 50% of patients  1.3 MAC: prevents movement in response to surgical stimulation in 95% of patients 0.3–0.4 MAC: associated with awakening from anesthesia  1.5–1.7 MAC: the concentration required to block autonomic reflexes to surgical stimulation

Bowel obstruction: Obstructed bowel is a closed space.  Emphysema: Blebs can accumulate N2O and burst. Air embolism: If suspected, turn off N2O immediately. Eye surgery when intraocular gases are used: Expansion of gas bubble can cause blindness. Middle ear surgery: Accumulation can dislodge a tympanic graft after tympanoplasty. Chest wall or head trauma: N2O can ↑ pneumothorax or ↑ ICP respectively _________________________________________________________________________________ Кишечная непроходимость: ущемленная кишка в закрытом пространстве Эмфизема: буллы могут накапливать N2O и разрываться Воздушная эмболия: при подозрении немедленно остановите подачу N2O  Глазная хирургия при использовании внутриглазных газов: расширение глазного яблока может привести к слепоте Хирургия среднего уха: накопление N2O может оттеснить тимпанический шунт после тимпанопластики Травма грудной стенки или головы: N2O может усугубить пневмоторакс или внутричерепное давление соответств

Higher  MAC indicates a lower potency of the volatile  anesthetic: Nitrous oxide            105 ______________________ Desfl urane                  6 ______________________ Sevofl urane                2 ______________________ Isofl urane                  1.2 ______________________ Enfl urane                  1.7 ______________________ Halothane                  0.75 ______________________ Methoxyfl urane       0.16

During induction of  general anesthesia  when a large volume of  nitrous oxide  is taken up from  alveoli  into pulmonary capillary blood, the concentration of gases remaining in the alveoli is increased. This results in effects known as the " concentration effect " and the "second gas effect". These effects occur because of the contraction of alveolar volume associated with the uptake of the nitrous oxide.      Second gas effect  occurs when the uptake of one gas enhances the rate of rise of alveolar partial pressure of another gas that is administered at the same time. The second gas effect causes an acute increase in the arterial partial pressure of oxygen by 10% when nitrous oxide is initially administered.This is called alveolar hyperoxygenation.

VOLATILE ANESTHETIC TOXICITIES • Carbon monoxide can accumulate due to desflurane degradation by dry CO 2 absorbent, especially barium hydroxide . Th is can also occur with sevoflurane and isoflurane . Avoid this by discarding desiccated CO 2 absorbent. • High-output renal failure can result from fluoride levels greater than 50 micromoles per liter produced by methoxyflurane metabolism. • Compound A accumulation results from sevoflurane degradation with soda lime or barium hydroxide lime. Ensure fresh gas fl ows greater than 2 L/min to avoid rebreathing of Compound A. • Macrocytic anemia can be caused by nitrous oxide exposure because it irreversibly oxidizes the cobalt atom in vitamin B12 and thus inhibits all vitamin B12-dependent enzymes. Nitrous oxide increases the risk of bone marrow suppression, macrocytic anemia, and peripheral neuropathies . • Fulminant hepatic necrosis and less severe hepatic dysfunction have been associated with halothane expos

UPTAKE AND DISTRIBUTION OF VOLATILE ANESTHETICS Vessel-rich organs: brain, heart, liver, kidneys, endocrine system; 10 % of the body weight; receive 75 % of the cardiac output ; small volume; moderate solubility; rapid saturation Muscle group : 50 % of body weight; receives 20 % of the cardiac output; continued uptake as a result of greater volume ; uptake can last for hours Fat group : 20 % of total body weight; receives 6 % of cardiac output; high solubility for anesthetic agent so can have sustained uptake for days Vessel-poor group : 20 % of body weight; minimal cardiac output; uptake is insignifi cant