Cardiac Failure Treatment Instant

Continue p-blockers, Dosage 0 if applicable Statins? Epiduralcatheter

Start p-blockers

Statins? Epiduralcatheter

Major surgery

Start p-bl ockers

No p-bt ockers

Start p-blocker-therapy or consult cardiologist

Perioperative arrhythmias are caused by physiologic and pathologic disturbances or by pharmacologic drug effects. Physiologic disturbances include hypoxemia, hypercapnia, acidosis, hypotension, hypovolemia, electrolyte imbalances, adrenergic stimulation (light anesthesia), vagal stimulation, and mechanical irritation (chest tube, pulmonary artery catheter). Pathologic cardiac disturbances include myocardial ischemia, infarction, acute heart failure, pulmonary embolism, and micro- or macrocirculatory shock. Therapy with proar-rhythmic drugs must also be considered when arrhythmias occur perioperatively.

The primary indications for antiarrhythmics are compromised hemodynamics due to critical tachycardias or bradycardias with impaired cardiac output. Another indication is the increased risk for cardiac death due to malignant or potentially malignant arrhythmias. Since all of the antiarrhythmic drugs also bear a proarrhythmic effect, treatment with antiarrhythmics may harm the patient, as was demonstrated in the Cardiac Arrhythmia Suppression Trial (CAST). Therefore, a thorough risk-benefit analysis is mandatory prior to long-term treatment with antiarrhythmics. Generally, the primary aim of antiarrhythmic therapy is to treat the underlying condition such as coronary heart disease or acute heart failure and not to cure symptoms.

In the perioperative setting, arrhythmias are observed quite commonly. Since in the operating room environment there are many reversible causes that predispose patients to arrhythmias, these conditions should be treated before considering pharmacological antiarrhythmic strategies. But in some patients perioperative arrhythmias pose the potential for rapidly developing life-threatening events necessitating immediate treatment.

3.1.2.1 Bradycardia

Bradycardia is defined as a heart rate below 60 beats per minute. In trained athlete patients as well as in patients with excessive beta-blocker therapy, the heart rate can drop below 40 beats per minute with no symptoms. When low cardiac output is associated with bradycardia, the following stepwise therapeutic approach is indicated, where continuously the next step should be taken on failure of the previous step:

• Start with the administration of a parasympatholytic drug such as atropine up to 3 mg intravenously. Then administer a beta-adrenergic drug, e.g., epinephrine in boluses of 10 |g i.v.

• Thereafter consider the application of a transient pacemaker, either as an external transthoracic stimulation with pads or via an esophageal stimulation probe.

When an external pacemaker is not available, a defibrillator with its stimulation mode maybe used in case of emergency. Alternatively, internal stimulation with a temporary transvenous-inserted sterile stimulation probe is the treatment of choice in severe heart block.

Supraventricular Tachyarrhythmias

Various adverse physiological phenomena can evoke supraventricular tachyarrhythmias in anesthetized or critically ill patients. For management of the surgical patient, a thorough but rapid consideration of potential causes is required, because correction of reversible conditions may prevent life-threatening conditions. Antiarrhythmic therapy should only be considered after these etiologies have been excluded or in cases of extreme hemodynamic instability.

The origin of supraventricular tachyarrhythmias lies in the area of the atria, the sinus node, or the atrio-ventricular node (AV node).

• Paroxysmal supraventricular tachyarrhythmia with preexcitation is caused (most commonly) by congenital short-circuit conductive fibers leading to a bypass of the regular excitation from the sinus node over the atria to the AV node.

Wolff-Parkinson-White syndrome (WPW) is the most common preexcitation syndrome with the so-called Kent fiber being the accessory conductive fiber. In type A WPW syndrome, ECG recordings show a positive delta wave in V1 and Q waves in II, III, and aVF. In type B WPW syndrome, a negative delta wave is recorded in V1 of the ECG. The delta wave is defined as a slow up-slope of the R in the widened QRS complex. The PQ interval is below 0.12 s. WPW syndrome is potentially life-threatening, because an atrial fibrillation with the fast conducting accessory Kent fiber may lead to ventricular tachycardia or ventricular fibrillation. For treatment, a short trial of vagal stimulation may be attempted initially by the Valsalva maneuver or massage of the carotid sinus. On failure, the antiarrhythmic ajmalin 50 mg is administered by slow intravenous injection under ECG monitoring. As an alternative, amiodarone, procainamide, or flecainide should be considered.

It should be noted that patients with accessory pathways may also develop atrial fibrillation. These patients are at increased risk for developing ventricular fibrillation when treated with classic AV-nodal blocking agents (digitalis, calcium channel blockers, beta-blockers, adenosine), because these agents reduce the accessory bundle refractory period.

• A type of paroxysmal supraventricular tachyarrhythmia (PSVT) without preexcitation is the AV

node reentry tachycardia. In two-thirds of patients, it is caused by a congenital defect of the cardiac conductive system, in one-third of patients, it is caused by a prolapse of the mitral valve, hyperthyroidosis, or other cardiac diseases. The ECG trace shows a heart rate of 180-200 beats/min, small QRS complexes, and a missing P wave. The symptomatic therapy consists of adenosine (6 mg bolus, after 3 min 12 mg bolus), verapamil (5 mg slow intravenous injection over 10 min), or overdrive pacing in circulatory stable patients. In unstable patients with a threat of cardiogenic shock, an electroconversion is indicated with initially 200 J, on failure with higher energy of 360 J. If the patient is conscious, a short-acting hypnotic such as etomidate or propofol should be used for sedation during the electroconversion. Causal therapy is high-frequency catheter ablation. • Atrial fibrillation (AF) is the most common type of supraventricular tachyarrhythmia. The prevalence is about 0.5% of the adult population, but at age greater than 60 years, the prevalence is 4%. The etiology is primary or idiopathic in patients without cardiac disease or secondary due to a cardiac disease such as mitral valve disease, coronary heart disease, or due to extracardial causes such as arterial hypertension or alcohol-toxic effects on the heart ("holiday-heart"). The irregular conduction in the AV node leads to a tachyarrhythmia of the ventricles with frequencies of 100 -150 beats/min. Treatment strategies include frequency control, conversion into sinus rhythm, and prophylaxis of recurrence. The frequency control is achieved by administering digitalis and verapamil (calcium channel blocker). ECG-triggered cardioversion is performed under short sedation with an initial energy of 100 J. It may be advisable to first establish a therapeutic level of an antiarrhythmic agent that maintains sinus rhythm (i.e., amiodarone, procainamide) in order to minimize the risk of SVT recurrence following electrical cardioversion. It is important to anti-coagulate the patient before the cardioversion, if the AF persists longer than 48 h because intracardi-ac thrombi may have been formed. Thrombi formation can be checked by TTE (transthoracic echocardiography) or by TEE (transesophageal echocardiography). As an alternative, a drug-induced chemical cardioversion maybe considered.

For intraoperative and postoperative patients developing new-onset AF who are stable and rate-controlled, pharmacological cardioversion of SVT is questionable. The 24-h rate of spontaneous conversion to sinus rhythm exceeds 50% and many patients who develop SVT under anesthesia will remit spontaneously before or during emergence. Moreover, the antiarrhythmic agents with long-term activity against atrial arrhyth mias have limited efficacy when used for rapid phar-macologic cardioversion. Improved rates have been seen with amiodarone, but further studies have to confirm this because of the potential for undesirable side effects. Finally, it should be kept in mind that in recent-onset perioperative SVT, reversible causes should be excluded or resolved before considering pharmacological antiarrhythmic therapies.

Ventricular Tachyarrhythmias

Morphology (monomorphic vs polymorphic) and duration (sustained vs nonsustained) characterizes ventricular arrhythmias. Nonsustained ventricular tachycardia (NSVT) is defined as three or more premature ventricular contractions that occur at a rate exceeding 100 beats/min and last 30 s or less without hemody-namic compromise. The origin of ventricular premature beats is below the bifurcation of the HIS fibers. Usually the sinus node is not stimulated backwards. This leads to a compensatory pause, which is felt by the patient as an extra beat of the heart. These arrhythmias are routinely seen in the absence of cardiac disease and may not require drug therapy in the perioperative period. In contrast, in patients with structural heart disease, these nonsustained rhythms do predict subsequent life-threatening ventricular arrhythmias. However, antiarrhythmic drug therapies in patients with structural heart disease may worsen survival. When nonsustained ventricular arrhythmias occur during or after major operations, early or late mortality of patients with preserved left ventricular function is not influenced. These patients usually do not require antiar-rhythmic drug therapy. However, as in SVT, these arrhythmias may signal reversible etiologies that should be treated. For example, potassium- and magnesiumserum levels should be checked and elevated digitalis levels should be excluded.

Sustained ventricular tachycardia (VT) presents as monomorphic or polymorphic. In monomorphic VT, the amplitude of the QRS complex remains constant, while in polymorphic ventricular tachycardia the QRS morphology continually changes.

Ventricular tachycardia is characterized as a regular tachycardia of 100-200 beats/min with bundle-branch-block-like deformed, widened ventricular complexes. The underlying etiology is idiopathic, severe organic cardiac disease, intoxication of digitalis or treatment with other antiarrhythmics, or the Brugada syndrome (congenital mutation of the sodium channel). The underlying mechanism for monomorphic VT is formation of a re-entry pathway, e.g., around scar tissue from a healed myocardial infarction.

This is a life-threatening condition and immediate action is required. Although lidocaine has traditionally been the primary drug therapy for all sustained ventricular arrhythmias, i.v. amiodarone is now also recommended for treatment of perioperative-occurring monomorphic VT.

Treatment strategies for sustained polymorphic ventricular tachycardia depend on the duration of the QT interval during a prior sinus rhythm. In the setting of a prolonged QT interval (torsades de points), emphasis is taken at reversal of QT prolongation. In addition to QT-prolonging antiarrhythmic drugs (class IA or III), a number of other medications used in the perioperative period may evoke QT prolongation and torsades de points. The management of torsades de points includes i.v. magnesium sulfate (2-4 g), repleting potassium, maneuvers increasing the heart rate (atropine, temporary atrial or ventricular pacing). Hemodynamic collapse requires asynchronous DC countershocks. When antiarrhythmic therapy is deemed necessary, i.v. amiodarone may be considered, because it bears the lowest risk of triggering torsades de points.

Unstable ventricular tachycardia and ventricular fibrillation are life-threatening arrhythmias in the operating room. The most important first maneuvers in patients who experience VF perioperatively are nonphar-macological: rapid defibrillation (360 J monophasic or 200 J biphasic), and correction of reversible etiologies. Amiodarone i.v. (300 mg) should be considered as pharmacological intervention in addition to other measures taken during resuscitation (Thompson and Balser 2004).

A new therapeutic option for the treatment of VT is the implantation of antitachycardic pacemakers. The implantable cardioverter defibrillator (ICD) is used in patients with increased risk of sudden cardiac death due to ventricular fibrillation in recurrent ventricular tachyarrhythmias or history of VF (ventricular fibrillation) with significantly impaired ventricular function. For supraventricular tachyarrhythmia, termination of the reentry mechanisms can be achieved by overdrive pacing with a stimulation frequency above the tachy-

cardic frequency, programmable electrostimulation to terminate circulating impulses through premature impulses, or atrial high-frequency stimulation for the conversion of atrial flutter (Herold et al. 2006).

For an overview of the antiarrhythmic therapy, please refer to Fig. 3.2.

Acute Heart Failure

The acute heart failure (AHF) is defined as the rapid onset of symptoms and signs secondary to abnormal cardiac function. It may occur with or without previous cardiac disease. The cardiac dysfunction can be related to systolic or diastolic dysfunction, abnormalities in cardiac rhythm, or preload and afterload mismatch. It is often life-threatening and requires urgent treatment.

3.1.3.1 Etiology

In the perioperative setting, AHF poses a serious threat to the patient, because these patients have a very poor prognosis. The 60-day mortality rate was 9.6 % and the combined rate for mortality and rehospitalization was 35.2% in the largest randomized trial to date (Cleland et al. 2003). The most common cause of AHF in the elderly is coronary heart disease, whereas in the younger population it is caused by dilatative cardiomyopathy, arrhythmia, congenital or valvular heart disease, or myocarditis (see Table 3.2).

3.1.3.2 Diagnosis

The diagnosis of AHF is primarily based on clinical findings, electrocardiogram (ECG), laboratory tests, chest x-ray, and echocardiography.

An impaired right ventricular function may be suspected if prominent jugular veins are present. To a cer-

Pathway Svt
Fig. 3.2. Pathway for antiarrhythmic therapy. WPW Wolff-Parkison-White syndrome, AF atrial fibrillation, PSVT paroxysmal supra-ventricular tachycardia, VES ventricular extrasystole, VT ventricular tachycardia. Modified from Herold et al. (2006)

Table 3.2. Causes and precipitating factors in acute heart failure

Decompensation of preexisting chronic heart failure (e.g., cardiomyopathy) Acute coronary syndromes: myocardial infarction/unstable angina with large extent of ischemia and ischemic dysfunction; mechanical complication of acute myocardial infarction; right ventricular infarction Hypertensive crisis

Acute arrhythmia (ventricular tachycardia, ventricular fibrillation, atrial fibrillation or flutter, other supraventric-ular tachycardia) Valvular regurgitation/endocarditis/rupture of chordae ten-

dineae, worsening of preexisting valvular regurgitation Severe aortic valve stenosis Acute severe myocarditis Cardiac tamponade Aortic dissection Postpartum cardiomyopathy

Noncardiovascular precipitating factors: lack of compliance with medical treatment, volume overload, infections, particularly pneumonia or septicemia, severe brain insult, after major surgery, reduction in renal function, asthma, drug abuse, alcohol abuse, pheochromocytoma High output syndromes: septicemia, thyrotoxic crisis, anemia, shunt syndromes

Modified from Nieminen (2005)

tain extent, measurement of the central venous pressure (CVP) allows quantification of the amount of congestion. The normal range of the CVP is 4-12 cm H2O. Caution is necessary in the interpretation of high measured values of central venous pressure in AHF, as this maybe a reflection of decreased venous compliance together with decreased right ventricular (RV) compliance even in the presence of inadequate RV filling. If the left ventricular function is impaired, wet rales in the lung fields are present during chest auscultation.

A chest x-ray confirms the diagnosis of left ventricular failure and allows the differential diagnosis to inflammatory or infectious lung diseases. Additionally the chest x-ray is used for follow-up of improvement or unsatisfactory response to therapy.

The ECG usually shows pathologic signs in patients with AHF. It determines the etiology of the AHF and may indicate strain of the left or right ventricle or the atria, acute coronary syndromes, arrhythmias, peri-myocarditis, and preexisting conditions such as left or right ventricular hypertrophy or dilated cardiomyopa-thy.

The recommended laboratory test in AHF include arterial blood gas analysis (BGA), venous oxygen saturation, plasma B-type natriuretic peptide (BNP), and standard tests such as blood count, platelet count, urea, electrolytes, blood glucose, and creatinine phosphoki-nase. The arterial BGA allows assessment of oxygenation (paO2), adequacy of respiratory function (pCO2), and acid-base balance (pH). Venous oxygen saturation is determined by oxygen supply, oxygen consumption of the body and regional circulation. It is useful as an estimate of the total body oxygen supply-demand balance. Another useful laboratory test is the plasma BNP, which is released from the cardiac ventricles in response to increased wall stretch and volume overload. The decision cut-off point is proposed as 100 pg/ml.

Echocardiography is used in AHF to evaluate the functional and structural changes of the heart and to assess acute coronary syndromes. Additional information is gathered by echo-Doppler studies, which can estimate pulmonary artery pressures (from the tricuspid regurgitation jet) and left ventricular preload.

Additional diagnostic procedures such as angiogra-phy, CT scan, or scintigraphy may be indicated according to the etiology of the AHF.

3.1.3.3 Therapy

If the diagnosis of AHF is verified, the patient must be treated in specialized wards such as emergency units, chest pain units, or intensive care units. The physicians should be trained and should follow guidelines.

If immediate resuscitation is necessary, basic and advanced life support (BLS/ALS) is applied according to the applicable guidelines.

The patient in distress or pain requires treatment with a sedative or analgesic agent. In this context, morphine is recommended in the early stage of the treatment, when a patient is admitted with severe AHF presenting with the signs of restlessness and shortness of breath (dyspnea). Additional effects of morphine include venodilation, mild arterial dilation, and reduction of the heart rate. Intravenous boluses of 3 mg (2-5 mg) are recommended and may be repeated as needed.

To achieve adequate tissue oxygenation, an arterial oxygen saturation of greater than 95 % is favorable. It is important to realize that increased concentrations of oxygen to patients without evidence of hypoxemia may cause harm, because hyperoxemia can be associated with reduced coronary blood flow, reduced cardiac output, increased blood pressure, and increased systemic vascular resistance. When arterial oxygen saturation is too low, oxygen supply via a face mask with reservoir bag is effective to increase inspiratory oxygen concentration. In case of failure, ventilatory support without endotracheal intubation is supplied as noninvasive ventilation: continuous positive airway pressure (CPAP) or biphasic positive airway pressure (BiPAP). If acute respiratory failure by AHF-induced respiratory muscle fatigue does not respond to vasodilators, oxygen therapy and noninvasive ventilation, the trachea has to be intubated and mechanical ventilation of the lungs commenced.

During bradycardia-induced AHF, external or internal pacing restores an adequate heart rhythm. Cardiac arrhythmias or tachycardia can cause AHF. Since antiarrhythmic drugs and beta-blocking agents such as metoprolol have negative inotropic properties, they should be used with extreme caution in AHF. However, in patients with acute myocardial infarction, who stabilize after having developed AHF, beta-blockers should be initiated early.

In patients with AHF and absence of hypotension (mean blood pressure above 70 mmHg) vasodilators are indicated. The primary pharmacologic treatment options include nitrates such as glyceryl trinitrate or isosorbide dinitrate, sodium nitroprusside, and the new agent nesiritide (atrial natriuretic peptide). The nitrates relieve pulmonary congestion without compromising stroke volume or increasing myocardial oxygen demand in acute left heart failure, particularly in patients with acute coronary syndrome. Their effect is limited to 16 - 24 h primarily due to development of tolerance. Sodium nitroprusside is indicated in patients with severe heart failure and in patients with predominantly increased afterload such as hypertensive heart failure or acute mitral regurgitation due to ruptured papillary muscle as a complication of severe myocardial infarction. The substance should be used cautiously, invasive monitoring of blood pressure is usually required, and toxicity of the cyanide metabolites should be taken into account. The new drug nesiritide is a recombinant human brain peptide, which is identical to the endogenous hormone produced by the ventricle (see description above). Nesiritide has venous, arterial, and coronary vasodilatory properties, reducing preload and af-terload and thereby increasing cardiac output without direct inotropic effects. Calcium antagonists are con-traindicated in AHF; ACE inhibitors are not indicated in the early stabilization phase of patients with AHF.

If the patients show symptoms of AHF secondary to fluid retention, diuretics are indicated. Usually loop diuretics such as furosemide or torasemide are administered. Hydrochlorothiazide (HCT) or spironolactone is added to loop diuretics in patients that are refractory to loop diuretics alone; a concomitant alkalosis is treated with acetazolamide. In refractory renal failure, hemo-dialysis or hemofiltration is initiated.

If the preload is low, a fluid challenge is indicated, but should be administered with extreme caution.

After executing all of the therapeutic steps mentioned above, the adequacy of cardiac output is assessed by reversal of metabolic acidosis, venous oxygen saturation, and clinical signs of adequate organ perfusion. The application of catecholamines or phosphodi-

Fluid Chart For Dialysis Patients

Fig. 3.3. Flow chart for immediate goals in treatment of the patients with acute heart failure. In coronary artery disease, the patient's mean blood pressure (mBP) should be higher to ensure coronary perfusion, mBP> 70, or systolic > 90 mm Hg. BLS basic life support, ALS advanced life support, CPAP continuous positive airway pressure, NIPPV noninvasivepositivepressureventila-tion. From Nieminen et al. (2005)

Fig. 3.3. Flow chart for immediate goals in treatment of the patients with acute heart failure. In coronary artery disease, the patient's mean blood pressure (mBP) should be higher to ensure coronary perfusion, mBP> 70, or systolic > 90 mm Hg. BLS basic life support, ALS advanced life support, CPAP continuous positive airway pressure, NIPPV noninvasivepositivepressureventila-tion. From Nieminen et al. (2005)

3.2 Deep Vein Thrombosis and Pulmonary Embolism

esterase inhibitors as inotropic agents is indicated in persistent heart failure, if tissue hypoperfusion does not suspend under the therapy described previously; but one must pay particular attention to these patients as catecholamines increase the oxygen consumption of the heart.

Dopamine incorporates dose-dependent properties of action on the receptors: it stimulates dopamine receptors at low doses (<2 |g/kg/min), beta-adrenergic receptors at medium doses (2-5 |g/kg/min), and alpha receptors at high doses (>5 |g/kg/min). Dopamine maybe used as an inotropic (> 2 |g/kg/min i.v.) in AHF with hypotension. Infusion of low doses of dopamine (<2-3 |g/kg/min i.v.) may be used to improve renal blood flow and diuresis in decompensated heart failure with hypotension and low urine output. However, if no response is seen, the therapy should be terminated, because no controlled trials regarding its long-term effects on renal function and survival have been conducted and concerns regarding its potential untoward effects on pituitary function, T cell responsiveness, gastrointestinal perfusion, chemoreceptor sensitivity, and ventilation have been raised.

Dobutamine stimulates betal receptors and beta2 receptors in a 3: 1 ratio. The effect is a positive inotropic and chronotropic action as well as peripheral vasodila-tion. To increase cardiac output, dobutamine is initiated with an infusion rate of 2 - 3 |g/kg/min, which can be increased up to 20 |g/kg/min. After 24-48 h, beta-receptor tolerance decreases the effect of dobutamine. The indication for dobutamine is evidence of peripheral hypoperfusion (hypotension, decreased renal function) with or without congestion or pulmonary edema refractory to volume replacement, diuretics, and vasodilators at optimal doses.

Phosphodiesterase inhibitors such as enoximone and milrinone have a site of action distal of the beta receptors, which results in persistent inotropic, lusitro-pic, and peripheral vasodilatory effects even in the presence of beta-blockers. Therefore, they are preferred to dobutamine in patients with concomitant beta-blocker therapy. In severe heart failure, a combination of phosphodiesterase inhibitors with epinephrine or norepinephrine is indicated in order to provide sufficient cardiac output with adequate perfusion pressure.

The new substance levosimendan (calcium sensitizer) has two main mechanisms of action: calcium sensitization of the contractile proteins, responsible for positive inotropic action, and smooth muscle potassium channel opening, responsible for peripheral vasodilatation. It is indicated in patients with symptomatic low cardiac output heart failure secondary to cardiac systolic dysfunction without severe hypotension.

If the combined administration of inotropic substances and a fluid challenge fail to relieve the symp toms of AHF, a potent vasopressor such as epinephrine is indicated. Norepinephrine may be considered in right heart failure or in combination with phosphodiesterase inhibitors (Fig. 3.3) (Nieminen et al. 2005).

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