Cardiac arrhythmia in the peri operative period

Discuss the ethology and management of various cardiac arrhythmia occurring during anaesthesia ?

Arrhythmias are common during and after surgery  and the initiating factor for an arrhythmia after surgery is usually a transient insult such as hypoxemia, cardiac ischemia, catecholamine excess, or electrolyte abnormality.

Common intraoperative arrhythmias are

Sinus Bradycardia

Sinus bradycardia is diagnosed when 

  1. Heart rate: Slower than 60 beats/min. In patients maintained on chronic β-blocker therapy, it is defined as a heart rate of less than 50 beats/min.

  2. Rhythm: Regular

  3. P/QRS: Ratio of 1 : 1.

  4. QRS complex: Normal morphology.

  5. Significance:Treatment is recommended if hypotension, ventricular arrhythmias, or signs of poor peripheral perfusion are observed. 

  6. Treatment: Usually none is necessary. (1) atropine, 0.5 to 1.0 mg by intravenous bolus repeated every 3 to 5 minutes, up to 0.04 mg/kg or approximately a 3.0-mg total dose for the average 75-kg male patient; (2) ephedrine, 5 to 25 mg by intravenous bolus; (3) dopamine or dobutamine (if blood pressure is adequate), 5 to 20 µg/kg/min by intravenous infusion; (4) epinephrine, 2 to 10 µg/min by intravenous infusion; (5) isoproterenol, 2 to 10 µg/min by intravenous infusion. Temporary transcutaneous or transvenous pacing if drug refractory bradycardia persists.

Sinus Tachycardia

Sinus tachycardia is the most common arrhythmia in the perioperative period,Common causes include pain, inadequate anesthesia, hypovolemia, fever, hypoxia, hypercapnia, heart failure, and drug effects.

  1. Heart rate: Faster than 100 beats/min in adult patients and may be as high as 170 beats/min.

  2. Rhythm: Regular.

  3. P/QRS: Ratio of 1 : 1.

  4. QRS complex: Normal

  5. Significance: Prolonged tachycardia in patients with underlying heart disease can precipitate MI and congestive heart failure (CHF) 

  6. Treatment: Hypovolemia and light anesthesia are the most common causes. In patients with ischemic heart disease in whom tachycardia develops,  Hypovolemia or other causes should also be addressed in these patients.

Atrial Premature Beats

Helpful points in differentiating APBs with aberrant ventricular conduction from VPBs include (1) the presence of a preceding P wave, usually abnormally shaped; (2) an RBBB configuration of the QRS complex; (3) the presence of an rsR′ ventricular complex in V1; 

  1. Heart rate: Variable, depending on the frequency of the APBs.

  2. Rhythm: Irregular.

  3. P/QRS: Usually 1 : 1. The P waves have various shapes and may even be lost in the QRS or T waves. 

  4. QRS complex: Usually normal unless ventricular aberration is present.

  5. Significance: APBs represented around 10% of all intraoperative arrhythmias.

  6. Treatment: Rarely necessary.

Paroxysmal Supraventricular Tachycardia

        1.      Heart rate: 130 to 270 beats/min.

  2. Rhythm: Usually regular unless the impulse originates from multiple atrial foci.

  3. P/QRS: 1 : 1 relationship, although the P wave may often be hidden in the QRS complex or T wave.

  4. QRS complex: Generally normal,

  5. Significance:  During anesthesia, PSVT accounts for up to 2.5% of all arrhythmias,PSVT can be precipitated by changes in autonomic nervous system tone, by drug effects, or by intravascular volume shifts and can produce severe hemodynamic deterioration. 

Treatment: Even though this arrhythmia is not usually associated with hemodynamic deterioration, the following can be undertaken to treat it:

  a. Vagal maneuvers such as carotid sinus massage should be applied only to one side.

  b. Adenosine, which is the drug of choice, is given by 6-mg rapid (2 seconds) intravenous bolus, preferably through an antecubital or central vein. If no response is elicited, second and third doses of 12 to 18 mg of adenosine may be administered by rapid intravenous bolus.

  c. Verapamil (2.5 to 10 mg given intravenously) terminates AV nodal reentry successfully 

  d. Amiodarone (150-mg infusion over a 10-minute period for the loading dose) is a recent addition.

  e. Esmolol (1 mg/kg by bolus and 50 to 200 mg/kg/min by infusion) has been shown to be effective

  f. Edrophonium or neostigmine can be given by intravenous bolus.

  g. Phenylephrine (100 µg by intravenous bolus) is administered if the patient is hypotensive.

  h. Intravenous digitalization is performed with one of the short-acting digitalis preparations: ouabain (0.25 to 0.5 mg given intravenously) or digoxin (0.5 to 1.0 mg given intravenously).

  i. Rapid overdrive pacing may be done in an effort to capture the ectopic focus.

  j. Synchronized cardioversion may be performed with incremental doses of energy of 100, 200, 300, and 360 J, preferably after light sedative premedication.Electrode catheter ablation with radiofrequency energy has evolved as the definitive, long-term treatment of most persistent AV reentrant or focal atrial SVTs.

Atrial Flutter

Atrial flutter most commonly represents a macro-reentrant arrhythmia that circulates in a specific manner in the right atrium  Because it is associated with very fast heart rates, it is generally accompanied by AV block. Classic sawtooth flutter waves (F waves) are usually present The characteristics of atrial flutter are as follows:

  1. Heart rate: The atrial heart rate is 250 to 350 beats/min with a ventricular rate of about 150 beats/min (2 : 1 or varying AV conduction block).

  2. Rhythm: The atrial rhythm is regular. The ventricular rhythm may be regular if a fixed AV block is present or irregular if a variable block exists.

  3. P/QRS: Usually there is a 2 : 1 block with an atrial rate of 300 beats/min and a ventricular rate of 150 beats/min, but it may vary between 2 : 1 and 8 : 1. F waves are best seen in leads V1 and II and the esophageal lead.

  4. QRS complex: Normal. T waves are lost in the f waves.

  5. Significance: Atrial flutter does not always indicate severe heart disease. It can be seen in patients with CAD, mitral valve disease, pulmonary embolism, hyperthyroidism, cardiac trauma, cancer of the heart, and myocarditis.

  6. Treatment: Pharmacologic or synchronized DC cardioversion, when indicated, should be performed only after careful consideration or evaluation of a possible thromboembolic event. Initial treatment should consist of control of the ventricular response rate with drugs that slow AV node conduction:

  a. β-Blockers such as esmolol (1 mg/kg by intravenous bolus) or propranolol.

  b. Calcium channel blockers such as verapamil (5 to 10 mg given intravenously) or diltiazem

If the ventricular response is excessively rapid or hemodynamic instability is present, or both, the following guidelines should be used:

  c. Synchronized DC cardioversion starting at a relatively high energy of 100 J and gradually increasing to 360 J is indicated.

  d. The class III antiarrhythmic agent ibutilide (Corvert, 1 mg in 10 mL saline or 5% dextrose in water [D5W] infused slowly intravenously over a 10-minute period) has been documented to convert atrial flutter to sinus rhythm in most patients with relatively new-onset atrial flutter. This may be repeated once, and although it is highly effective, life-threatening torsades de pointes ,may occur hours after ibutilide administration, thus making 4- to 8-hour monitoring after treatment highly desirable.

  e. Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no faster than 0.5 mg/kg/min)

  f. Amiodarone (150-mg intravenous loading dose infused over a 10-minute period, followed by 1 mg/min intravenously for 6 hours, a 0.5-mg/min intravenous infusion for 18 hours, and then a reduced intravenous dose or switching to an oral dose) has recently been shown to be effective.

Atrial Fibrillation

Atrial fibrillation is an excessively rapid and irregular atrial focus with no P waves appearing on the ECG; instead, fine fibrillatory activity is seen,most commonly encountered irregular rhythm. It is often described as irregularly irregular and may be associated with a pulse deficit. Its characteristics are as follows:

  1. Heart rate: The atrial rate is 350 to 500 beats/min, and the ventricular rate is 60 to 170 beats/min.

  2. Rhythm: Irregularly irregular.

  3. P:QRS: The P wave is absent and replaced by f waves or no obvious atrial activity at all.

  4. QRS complex: Normal.

  5. Significance:idiopathic, paroxysmal atrial fibrillation has become increasingly recognized.The loss of atrial “kick” from inefficient contraction of the atria may reduce ventricular filling and significantly compromise cardiac output.

may be associated with the development of atrial thrombi, possibly resulting in pulmonary or systemic embolization.

Atrial fibrillation is the most common postoperative arrhythmia,It is typically a transient, reversible phenomenon that may develop in patients who possess an electrophysiologic substrate for the arrhythmia that is present before or as a result of surgery. β-blockers are efficacious in the prevention of postoperative atrial fibrillation. Perioperative administration of amiodarone, sotalol, nondihydropyridine calcium channel blockers, and magnesium sulfate has also been associated with a reduction in the occurrence of atrial fibrillation

Treatment:

 Treatment of acute atrial fibrillation is by focussing on controlling the ventricular response, especially with the administration of diltiazem or esmolol intravenously. Ibut Synchronized DC cardioversion should be relied on in patients with pronounced hemodynamic instability. However, if fibrillation is present for longer than 48 hours, attempts to restore sinus rhythm may be associated with a heightened risk for thromboembolism. In a patient with a normal coagulation profile, adequate anticoagulation for 3 to 4 weeks should be considered before attempting to restore sinus rhythm. Alternatively, transesophageal echocardiographic examination to rule out atrial thrombi may be substituted. New developments in electrophysiologic techniques for ventricular defibrillation consisting of biphasic current shocks have shown superiority to the conventional monophasic

Junctional Rhythms

The AV node itself and sites just above and below it can act as pacemakers. It makes sense to consider this ectopic activity as arrhythmias of the AV junction. The resultant P wave is abnormal and, depending on the position of the ectopic pacemaker, may be very close to, buried in, or after the QRS complex. Depending on the rate of fire of the ectopic pacemaker, the resultant rhythm is nodal premature; nodal quadrigeminy, trigeminy, or bigeminy; nodal rhythm; or nodal tachycardia.

  1. Heart rate: Variable, 40 to 180 beats/min (i.e., nodal bradycardia to junctional tachycardia).

  2. Rhythm: Regular.

  3. P/QRS: 1 : 1, but there are three varieties:

  a. High nodal rhythm: The impulse reaches the atrium before the ventricle; the P wave therefore precedes the QRS but has a shortened PR interval (0.1 second).

  b. Mid nodal rhythm: The impulse reaches the atrium and the ventricle at the same time. The P wave is lost in the QRS.

  c. Low nodal rhythm: The impulse reaches the ventricle first and then the atrium, so the P wave follows the QRS complex.

  4. QRS complex: Normal, unless altered by the P wave.

  5. Significance: Junctional rhythms are common in patients under anesthesia (about 20%), especially with halogenated anesthetic agents. Junctional rhythms frequently decrease blood pressure and cardiac output by about 15%, but they can decrease it up to 30% in patients with heart disease.

  6. Treatment: Usually, no treatment is required, and the rhythm reverts spontaneously. If hypotension and poor perfusion are associated with the rhythm, treatment is indicated. Atropine, ephedrine, or isoproterenol can be used in an effort to increase the activity of the SA node so that it will take over as the pacemaker. Dual-chamber electrical pacing at a rate faster than a slow nodal rhythm is another option.

Ventricular Premature Beats

VPBs result from ectopic pacemaker activity arising below the AV junction. The VPB originates in and spreads through the myocardium or ventricular conducting system, thereby resulting in a wide (>0.12-second), bizarre QRS complex. The ST segment usually slopes in the direction opposite the main deflection of the QRS complex. There is no P wave associated with a VPB, but retrograde depolarization of the atria or blocked sinus beats may obscure the diagnosis.

Although an APB normally reaches the SA node and resets the sinus rhythm, such an occurrence is rare when the ectopic pacemaker is in the ventricle. A VPB often blocks the next depolarization from the SA node, but the following sinus beat occurs on time. The result is a fully compensatory pause consisting of the interval from the VPB to the expected normal QRS, which is blocked at the AV node, plus a normal sinus interval.

VPBs are common during anesthesia, where they account for 15% of observed arrhythmias. They are much more common in anesthetized patients with preexisting cardiac disease. Other than heart disease, known etiologic factors include electrolyte and blood gas abnormalities, drug interactions, brainstem stimulation, and trauma to the heart.

  1. Heart rate: Depends on the underlying sinus rate and frequency of the VPBs.

  2. Rhythm: Irregular.

  3. P/QRS: No P wave with the VPB.

  4. QRS complex: Wide and bizarre, with a width of more than 0.12 second. If it is of an RBBB nature, prominent R forces are present in V1. If it is an LBBB in appearance, notching of the S wave and less acute downward sloping of the ST segment are common.

  5. Significance: The new onset of VPBs must be considered a potentially serious event because in certain clinical situations, the arrhythmia may progress to VT or ventricular fibrillation. Such situations include coronary artery insufficiency, MI, digitalis toxicity with hypokalemia, and hypoxemia. VPBs are more likely to precede ventricular fibrillation if they are multiple, multifocal, or bigeminal; occur near the vulnerable period of the preceding ventricular repolarization (i.e., R-on-T phenomenon)or appear in short-long-short coupling sequences. VPBs are markers, not the cause of more severe arrhythmias.

  6. Treatment: In most patients, VPBs (occurring as single, bigeminy, or trigeminy but excluding nonsustained VT) do not need to be treated, particularly if the patient does not have an acute coronary syndrome, and treatment is generally dictated by the presence of symptoms attributable to the VPBs. The first step in treatment is to correct any underlying abnormalities such as decreased serum potassium or low arterial oxygen tension. If the arrhythmia is of hemodynamic significance. lidocaine is the treatment of choice, with an initial bolus dose of 1.5 mg/kg. Recurrent VPBs can be treated with a lidocaine infusion at 1 to 4 mg/min; additional therapy includes esmolol, propranolol, procainamide, quinidine, disopyramide, atropine, verapamil, or overdrive pacing.

Ventricular Tachycardia

The presence of three or more sequential VPBs defines VT. Diagnostic criteria include the presence of fusion beats, capture beats, and AV dissociation. The specific morphologic appearance of the QRS complex may also be helpful in distinguishing VT from other arrhythmias. VT is classified by its duration and morphology. In duration, nonsustained VT lasts three beats and up to 30 seconds, and sustained VT lasts 30 seconds or longer. With monomorphic morphology, all complexes have the same pattern, and with polymorphic morphology, complexes constantly change patterns. Polymorphic VT with a long QTc is also called “torsades de pointes.”

The characteristics of VT are as follows:

  1. Heart rate: 100 to 200 beats/min.

  2. Rhythm: Generally regular, but may be irregular if the VT is paroxysmal.

  3. P/QRS: Usually there is no fixed relationship 

  4. QRS complex: Wide, more than 0.12 second in width, with similar morphologic criteria in lead V1 as for VPB.

  5. Significance: Acute onset is life threatening and requires immediate treatment.

  6. Treatment: If the patient is hemodynamically stable, amiodarone administered as one or more intravenous doses of 150 mg in 100 mL saline or D5W over a period of 10 minutes, followed by an intravenous infusion of 1 mg/min for 6 hours and 0.5 mg/min thereafter, is the recommended current treatment (maximum intravenous dose, 2.2 g/24 hr). Although amiodarone is associated with substantially less hypotension than bretylium is, hypotension and bradycardia are its main side effects. Amiodarone's pharmacologic effects persist for more than 45 days. Lidocaine and procainamide have been used in the past with varying degrees of success to treat VT. Synchronized cardioversion is the indicated nonpharmacologic intervention in any wide-complex tachycardia, whether monomorphic VT or a wide-complex SVT. Polymorphic VT with a normal QT interval is treated with amiodarone and cardioversion. Metabolic abnormalities and drug toxicity must be considered and treated. Polymorphic VT with a prolonged QT interval is a more serious rhythm disturbance, and the recommended current treatment is an intravenous infusion of 1 g of magnesium administered over a 2- to 3-minute period. Precipitating metabolic or toxic causes should be treated. Overdrive pacing may also be helpful in this setting 

Ventricular Fibrillation

Ventricular fibrillation is an irregular rhythm that results from a rapid discharge of impulses from one or more ventricular foci or from multiple wandering reentrant circuits in the ventricles. The ventricular contractions are erratic and are represented on the ECG by bizarre patterns of various size and configuration. P waves are not seen. Important causes of ventricular fibrillation include myocardial ischemia, hypoxia, hypothermia, electric shock, electrolyte imbalance, and drug effects

Its characteristics are as follows:

  1. Heart rate: Rapid and grossly disorganized.

  2. Rhythm: Totally irregular.

  3. P/QRS: None seen.

  4. QRS complex: Not present.

  5. Significance: There is no effective cardiac output, and life must be sustained by artificial means, such as external cardiac massage.

  6. Treatment:

  a. Cardiopulmonary resuscitation must be initiated immediately, and then defibrillation must be performed as rapidly as possible. Asynchronous external defibrillation should be performed with a DC defibrillator using incremental energies in the range of 200 to 360 J. The introduction of biphasic (and rectilinear) transthoracic shocks has reduced the energy levels required and increased the efficacy of ventricular defibrillation. 120 J of biphasic current was superior to 200 J of monophasic current, especially in patients with increased chest wall impedance.

  b. Early administration of 1 g of magnesium sulfate may facilitate defibrillation. In some instances, epinephrine has been used for coarsening the fibrillation to facilitate defibrillation. Vasopressin has been added as a drug for the treatment of ventricular fibrillation. The vasopressin dose is a single 40-unit intravenous bolus. Subsequent administration of epinephrine should be delayed for at least 5 minutes after vasopressin. Supportive pharmacologic therapy may include lidocaine, amiodarone, bretylium, procainamide, phenytoin, or esmolol.

  c. Torsades de pointes, which may mimic ventricular fibrillation or VT, is a life-threatening arrhythmia that occurs in the presence of disturbed repolarization (hence its association with prolonged QT intervals)Discontinuation of drugs that predispose to prolongation of the QT interval and correction of electrolyte abnormalities are essential in the treatment of torsades de pointes. Acute therapy may include defibrillation, 1 to 2 g of intravenous magnesium sulfate, intravenous isoproterenol, and overdrive pacing.

Conduction Defects

Conduction defects are most often chronic, are present on the baseline preoperative ECG,However, conduction defects may be observed for the first time during surgery and anesthesia. They can occur as a result of simple manipulation, such as passage of a pulmonary artery catheter through the right ventricle, but they can also be a manifestation of myocardial ischemia. Because high-grade (second- and third-degree AV blocks) conduction defects often have deleterious effects on hemodynamic performance, intraoperative recognition is important.

Three types of conduction system blocks are possible: SA block, AV heart block, and intraventricular conduction block.In an SA block, the block occurs at the sinus node. Because atrial excitation is not initiated, P waves are not found on the ECG. The next beat can be a normal sinus beat, a nodal escape beat, or a ventricular escape beat.

The second type of heart block is an AV heart block, or AV block, which may be incomplete or complete. First- and second-degree AV blocks are generally considered incomplete, whereas a third-degree AV block is considered to be a complete heart block. First-degree AV block is often found in healthy hearts, but it is also associated with CAD or digitalis administration. It is characterized by a PR interval longer than 0.21 second. All atrial impulses progress through the AV node to the Purkinje system. This form of heart block ordinarily requires no treatment. Second-degree AV block is associated with the conduction of some of the atrial impulses to the AV node and into the Purkinje system. It is further subdivided into two specific types. A Mobitz type I block, or a Wenckebach block, is characterized by progressive lengthening of the PR interval until an impulse is not conducted and the beat is dropped This form of block is relatively benign and often reversible, and it does not require a pacemaker. It may be caused by digitalis toxicity or MI and is usually transient. A Mobitz type I block reflects disease of the AV node.

Third-degree AV block, also called a complete heart block, occurs when all electrical activity from the atria fails to progress into the Purkinje system. The atrial and ventricular contractions are regular and irrespective to each other.The ventricular rate is approximately 40 beats/min. The QRS complex may be normal if the pacemaker site is in the AV node, but it is usually widened to longer than 0.12 second when the pacemaker site is located in the ventricle The heart rate is usually too slow to maintain adequate cardiac output, and syncope or Adams-Stokes syndrome may occur, as well as heart failure. These patients generally require insertion of a transvenous endocardial or epicardial pacemaker to increase their heart rate and cardiac output.

 

 

 

  

 

 

 

 

 

Physiological changes in geriatric population

What are the age related changes that occur in the nervous system,pulmonary and cardiovascular system of geriatric population and how does the renal changes affect the anesthetic management?

Nervous System

With aging memory decline occurs in greater than 40% of individuals older than age 60 years.

Cerebral atrophy occurs with aging with a decrease in the volume of gray and white matter.The decrease in gray matter volume is due to neuronal shrinkage but there is 15% loss of white matter with aging.Such loss results in gyral atrophy and increased ventricular size. Shrinkage in the subcortical white matter and the hippocampus may be accelerated by hypertension and vascular disease.

Significant regional reductions are seen in the neurotransmitters dopamine, acetylcholine, norepinephrine, and serotonin with aging. Levels of glutamate, the primary neurotransmitter in cortex, do not seem to be affected. Coupling of cerebral electric activity, cerebral metabolic rate, and cerebral blood flow remains intact in elderly individuals.

Decreases in brain reserve are manifested by decreases in functional ADL, increased sensitivity to anesthetic medications, increased risk for perioperative delirium, and increased risk for postoperative cognitive dysfunction.

Neuraxial changes include a reduction of the area of the epidural space, increased permeability of the dura, and decreased volume of cerebrospinal fluid. The diameter and number of myelinated fibers in the dorsal and ventral nerve roots are decreased in elderly individuals. In peripheral nerves, inter–Schwann cell distance is decreased, as is conduction.These changes tend to make elderly individuals more sensitive to neuraxial and peripheral nerve block.

Cardiovascular System

As the heart ages, changes occur in its morphilogy which results functionally, in decreased contractility, increased myocardial stiffness and ventricular filling pressures, and decreased β-adrenergic sensitivity.Vascular stiffness increases with advancing age related to breakdown of elastin and collagen.

Increased vascular stiffness causes increase in cardiac load.Alterations in left ventricular afterload can lead to left ventricular wall thickening, hypertrophy, and impaired diastolic filling.

Decreased ventricular compliance and increased afterload combine to cause a compensatory prolongation of myocardial contraction. This occurs at the expense of a decreased early diastolic filling time. Under these conditions, the contribution of atrial contraction to late ventricular filling becomes more important and explains why cardiac rhythm other than sinus is often poorly tolerated in elderly individuals.

Changes in the autonomic system with aging include a decrease in response to β-receptor stimulation and an increase in sympathetic nervous system activity,the attenuated β-receptor response in elderly individuals during exercise or stress is associated with decreased maximal heart rate and decreased peak ejection fraction. This response causes the increased peripheral flow demand to be met primarily by preload reserve, making the heart more susceptible to cardiac failure.

Some pathological conditions associated with aging heart are Impairment of diastolic relaxation leads to diastolic dysfunction in the aging heart. In its severest form, diastolic dysfunction may manifest as diastolic heart failure. Predisposing disease states for this condition include hypertension with left ventricular hypertrophy, ischemic heart disease, hypertrophic cardiomyopathies, and valvular heart disease.

Diastolic dysfunction or failure is often related to systemic blood pressure and does not imply volume overload. Echocardiography is the diagnostic modality of choice,Classically, echocardiography shows preserved or hyperdynamic left ventricular systolic function and characteristic changes of flow velocity at the mitral valve.

Respiratory System.

Structural changes in the lung with aging include the loss of recoil which combined with altered surfactant production leads to an increase in lung compliance. Increased compliance leads to limited maximal expiratory flow and a decreased ventilatory response to exercise.Loss of elastic elements within the lung is associated with enlargement of the respiratory bronchioles and alveolar ducts, and a tendency for early collapse of the small airways on exhalation causes increased anatomic dead space, decreased diffusing capacity, and increased closing capacity all leading to impaired gas exchange.

Loss of height and calcification of the vertebral column and rib cage lead to a typical barrel chest appearance with diaphragmatic flattening so the chest wall becomes less compliant, and work of breathing is increased.

alterations in lung volumes with aging are residual volume increases by 5% to 10% per decade. Vital capacity decreases. Closing capacity increases with age. Change in the relationship between functional residual capacity and closing capacity cause an increased ventilation-perfusion mismatch and represent the most important mechanism for the increase in alveolar-arterial gradient for oxygen observed in aging In younger individuals, closing capacity is below functional residual capacity. At 44 years of age, closing capacity equals functional residual capacity in the supine position, and at 66 years of age, closing capacity equals functional residual capacity in the upright position.When closing capacity encroaches on tidal breathing, ventilation-perfusion mismatch occurs. When functional residual capacity is below closing capacity, shunt increases, and arterial oxygenation decreases. This results in impairment of preoxygenation. Increased closing capacity in concert with depletion of muscle mass causes a progressive decrease in forced expiratory volume in 1 second by 6% to 8% per decade.

Increases in pulmonary vascular resistance and pulmonary arterial pressure occur with age and may be secondary to decreases in cross-sectional area of the pulmonary capillary bed.Hypoxic pulmonary vasoconstriction is blunted in elderly individuals and may cause difficulty with one-lung ventilation.

Renal changes that affect the anesthetic management 

Renal cortical mass also decreases by 20 to 25% with age, but the most prominent effect of aging is the loss of up to half of the glomeruli by age 80.The decrease in the glomerular filtration rate of approximately 1 mL/min/yr after age 40 typically reduces renal excretion of drugs to a level where drug dosage adjustment becomes a progressively important consideration beginning at approximately age 60. Nevertheless, the degree of decline in glomerular filtration rate is highly variable and is likely to be much less than predicted in many individuals, especially those who avoid excessive dietary protein.

The aged kidney does not eliminate excess sodium or retain sodium when necessary as effectively as that of a young adult.Part of the failure to conserve sodium when appropriate may be because of reduced aldosterone secretion. Similarly, the aged kidney does not retain or eliminate free water as rapidly as young kidneys when challenged by water deprivation or free water excess. Lastly, the sensation of thirst declines with age. Fluid and electrolyte homeostasis is more vulnerable in the older patient.Renal blood flow seems to decrease about 10% per decade. There is a progressive decline in creatinine clearance with age, yet with normal aging, serum creatinine remains relatively unchanged. This occurs because muscle mass also decreases with aging. Serum creatinine is a poor predictor of renal function in elderly patients. This concept is important in proper dosage adjustment for medications that are excreted by the kidneys.

Post operative Hypoxemia

What are factors which affect arterial hypoxemia in the post operative care unit and what are the differential diagnosis?

Anesthetic considerations in obesity

Preoperative Evaluation

The preoperative assessment  include consideration of comorbid conditions like hypertension, diabetes, heart failure, and obesity-hypoventilation syndrome. 

 The history of previous surgeries, their anesthetic challenges, need for ICU admission, surgical outcomes, and the weight of the patient at that time are noted.

 Recommended preoperative laboratory evaluations include fasting blood glucose, lipid profile, serum chemistries (to evaluate renal and hepatic function), complete blood count, ferritin, vitamin B₁₂, thyrotropin, and 25-hydroxyvitamin D. OSA by means of overnight oximetry or polysomnography, or both, if appropriate. If identified with OSA and CPAP is recommended, patients are encouraged to initiate therapy at home, and it should be continued throughout the perioperative period. AHI score greater than 30, implying severe sleep apnea, is a warning sign and a predictor for rapid and severe desaturation at induction. CPAP score greater than 30, implying severe sleep apnea, is a warning sign and a predictor for rapid and severe desaturation at induction.

Intraoperative Care

Obese patients present special challenges for the anesthesiologist in airway management, positioning, monitoring, choice of anesthetic technique and anesthetic agents, pain control, and fluid management. .

Patient Positioning

 Even in the supine position, rhabdomyolysis from pressure on the gluteal muscles leading to renal failure and death has been reported. For obese patients placed in the prone position, cushioning gel pads or other weight-bearing rolls may have excessive weight placed on them. Pressure points must be checked carefully,

Airway management of obese patients: Patients should be readily intubated by direct laryngoscopy if placed carefully in the ramped position. Obese patients must be examined for the common objective signs of potential difficult intubation, which include small mouth opening, large protuberant teeth, limited neck mobility, and retrognathia. Alternative airway management techniques such as awake, topicalized direct laryngoscopy with modest sedation can be used to assess the laryngoscopic view when deciding whether to proceed with induction of general anesthesia or awake, sedated fiberoptic intubation. Of course, the equipment for emergency airway management, including laryngeal masks and a fiberoptic bronchoscope, should be immediately available.

 Pulmonary physiology Obese patient's pulmonary physiology is especially important to appreciate techniques to maintain oxygenation and lung volume when caring for an obese patients as they  have multiple pulmonary abnormalities, including decreased vital capacity, inspiratory capacity, expiratory reserve volume, and functional residual capacity.A variety of intraoperative maneuvers to maintain lung volume and oxygenation are use of PEEP,the application of noninvasive modes of ventilation, including pressure support and bilevel support delivered by mask for preoxygenation, induction, and maintenance of anesthesia to maintain oxygenation and ventilatory mechanics in obese patients,to continue CPAP if already  exposed and right position of mild reverse trendelenburg position .

Thermal management in the operating room is best accomplished with forced-air warmers. Armboards may need extra padding to keep the patient from having the arm and shoulder out of an anatomic position. If the arms are to be tucked by the side of the patient, a wide, well-padded sled may be useful.

Fluid requirements may be greater than predicted, and in even a relatively short, 2- to 3-hour case, 4 to 5 L of crystalloid fluid may be needed to prevent acute tubular necrosis in the kidneys. Hypovolemia, which can cause a protracted prerenal state, can be prevented by appropriate hydration. 

Anesthetic Drugs and Dosing

Commonly used anesthetic drugs can be dosed according to total-body weight (TBW) or IBW based on lipid solubility. Lean body mass is a good weight approximation to use when dosing hydrophilic medications. The volume of distribution is changed in obese patients with regard to lipophilic drugs like benzodiazepines and barbiturates, among the commonly used anesthetic drugs. Three exceptions to this rule are digoxin, procainamide, and remifentanil, which even though highly lipophilic, have no relationship between properties of the drug and their volume of distribution_. Consequently, dosing of commonly used anesthetic drugs such as propofol, vecuronium, rocuronium, and remifentanil is based on IBW. In contrast, thiopental, midazolam, succinylcholine, atracurium, cisatracurium, fentanyl, and sufentanil should be dosed on the basis of TBW. Another caveat to this recommendation is that maintenance doses of propofol should be based on TBW and, conversely, on IBW for sufentanil. This implies that one can use, based on patient weight, larger amounts of benzodiazepines, fentanyl, or sufentanil, although these drugs are best titrated to the desired clinical effect. Conversely, based on real body weight, smaller amounts of propofol are needed to anesthetize the patient.The choice of volatile agents is based on the physical characteristics of tissue solubility, expressed as blood-gas partition coefficients and fat-blood partition coefficients. Some evidence suggests that desflurane may be the anesthetic of choice because of a more consistent and rapid recovery profile than is seen with sevoflurane and propofol.

Even though nitrous oxide provides some analgesic effect and is eliminated rapidly, we prefer to avoid it because of the high oxygen demand in the obese. 

Induction of Anesthesia

 Obesity itself does not increase the risk for aspiration,however, acid aspiration prophylaxis, including H₂ receptor agonists or proton pump inhibitors, must be considered in patients with identifiable risk for aspiration. Awake fiberoptic intubation may also be considered in such patients

Regional anesthesia, especially epidural and spinal, is safe and feasible in patients with large body habitus but technically more difficult because of the physical challenge of placing the catheters and the tendency of these catheters to migrate out of the epidural space. Special equipment, in terms of longer needles or special ultrasound probes, may be needed for correct placement of catheters in these patients. Care should be exercised in dosing these catheters because of the increased cephalad spread of the drug and the block as a result of a smaller epidural space than in normal-weight patients.

Indications for invasive monitoring depends on the comorbid conditions like  obesity-hypoventilation syndrome with pulmonary hypertension and cor pulmonale may require a pulmonary artery catheter or intraoperative use of transesophageal echocardiography,central venous access is useful if  peripheral access is difficult. Similarly, difficulty in noninvasive blood pressure measurements because of body habitus–related difficulty in appropriate cuff placement may be an indication for placement of an arterial catheter. Arterial blood gas analysis may help guide intraoperative ventilation and extubation.

In preparation for emergence from anesthesia, the neuromuscular blockade must be fully reversed before the patient is extubated.Pressure-support ventilation mode on many newer models of anesthesia machines,can be used to  maintained on pressure support during emergence as soon as spontaneous ventilation has resumed. When adequate muscle strength has returned, as demonstrated by sustained tetanus with the nerve stimulator and performance of a 5-second head lift, an awake patient who is following commands can be safely extubated. Pressure support or CPAP can be delivered immediately by mask applied to the face as is done during preoxygenation before induction of anesthesia. 

Postoperative pain management include  intravenous analgesia via patient-controlled analgesia (PCA) or thoracic epidural analgesia. 

Opioid-based PCA with local anesthetic infiltration of the wound and adjunctive non-narcotic medication is a reasonable approach for most patients. Injection of local anesthetic into the incision site before making the incision may result in preemptive analgesia. Adjunctive analgesia with non-narcotic medications, unless contraindicated, will decrease opioid requirements and thereby opioid-induced side effects as well.

ASA Classifiaction

This topic has come as a question recently and though we always classify our patients as ASA but in exam writing the same topic as answer is very difficult

Intraoperative Bronchospasm

this topic was given recently as 'what are the differential diagnosis of intraoperative Bronchospasm and what is its management?"

Smoking and anesthesia

This topic can come as what are the pulmonary complications in a patient who is a chronic smoker?
Or smoking and the anaesthetist

anaphylaxis in anesthesia

Clinical manifestations and management of anaphylactic reaction in anaesthesia practice?

positioning in anesthesia

Topic for the day is "what are the different positions given in anesthesia and what are the adverse effects of each?"

Acid-base balance

Biochemistry was one subject which scared me a lot ,all those molecular level breakdown of carbohydrates,fats and protein with ultrastructure of DNA went above my head but i made my own peace with the subject in due course of time  so today i am taking a topic which reminds me of biochemistry and that is Acid-base balance,the question is , Define Base excess?How do kidneys compensate for acid-base balance?

Neuromuscular blockade

In the physiology practicals we did pithing of the frogs and connect their gastrocnemius muscle to graphic display which showed muscle twitch pattern with electrical stimulation,at that point the most important concern for me was  how to hold the frog as I felt it very slimy,much later during my PG times when I struggled with neuromuscular monitoring in operative cases that I used to remember these old times,so lets go on today with a staple question"What are the factors affecting neuromuscular blockage?Discuss various methods to monitor neuromascular blockage?
Potentiation by inhalational agents
 Volatile anaesthetics decrease the requirement of neuromascular blocking drugs by at least 15%,the actual degree of this post synaptic augmentation depends upon both the inhalational drug and the muscle relaxant(desflurane>sevoflurane>isoflurane and enflurane>halothane>N2O/O2/narcotic) and (pancuronium>vecuronium and atracurium)
Temperature
 Hypothermia prolongs the blockade by decreasing the metabolism(mivacurium,atracurium and cisatracurium) and by delaying the excretion (pancuronium and vecuronium ) of the muscle relaxants.
Acid base balance
 Respiratory acidosis potentiates the blockade of most nondepolarising muscle relaxants and antagonises its reversal.
Electrolyte abnormalities
Hypokalaemia and hypocalcemia augment the nondepolarising block while hypermagnesemia potentiates the peripheral nerve blocks.
Age

 Neonates have an increased sensitivity to nondepolarising relaxants because of immature
neuromascular junctions but it does not need dose to be decreased as they have greater volume of

distribution .
Drug interaction
Drugs like dantrolene ,quinidine calcium channel blockers,streptomycin,aminoglycosides,kanamycin,
Neomycin,polymixin,clindamycin are known to potentiate the nondepolarising muscle relaxants.
Concurrent diseases
 Cirrhotic liver disease and chronic renal failur often result in greater volume of distribution and a lower plasma concentration for the given water soluble muscle relaxant drug hence in these patients the initial dose is increased but due to prolonged excretion time the maintenance doses are lowered.

Continuation of adjuncts in anesthesia

In continuation with the topic "adjuncts in anesthesia " today we shall go with antacid
And anti emetics .These drugs attain special significance in emergency surgeries or in
patients with delayed gastric emptying time,yesterday I had a emergency LSCS and I had to administer these drugs before shifting the patient to OT.

Physiology of thermoregulation

First with the foot

Anesthesia thought for the day

Regional anesthesia

Advantages of a subarachnoid block

• Improved analgesia,greater and quicker mobility.
• Decrease stress response
• Decreased thromboembolic complications
• Decrease blood loss and transfusion requirements
• No aspiration pneumonia
• Decreased opiate requirements and its side effects
• No airway manipulation
• Minimal or no effects on foetal and maternal physiology
• Earlier establishment of breast feeding and GI function

The last two are true for obstetric patients,so when studying we have to read as 9 points because that is how it will be asked in exams,keep it simple and to the point.