328 SECTION IV Pediatric Critical Care Cardiovascular ventricular filling The Pms drives systemic venous return from the venous reservoirs to the central venous structures as in a normal circulation b[.]
328 S E C T I O N I V Pediatric Critical Care: Cardiovascular not be tolerated, as a decrease in preload and afterload leads to a decrease in ventricular operating volumes, exacerbating the obstruction.78 Restrictive cardiomyopathies invariably have severe abnormalities of ventricular diastolic dysfunction One would also expect these patients not to tolerate PPV owing to its impact on systemic venous return The impact of ITP on ventricular diastolic disease is exemplified in some patients following repair of tetralogy of Fallot, where varying degrees of RV diastolic dysfunction are common In a subgroup of these patients, the degree of impairment is severe and has been termed restrictive physiology In these patients, atrial systole causes RV diastolic pressure to rise above pulmonary arterial diastolic pressure, generating pulmonary arterial flow during ventricular diastole LV systolic function is, in most cases, normal; thus, the primary impact of changes in ITP is on the right heart Further, pulmonary venous pressure should not be elevated Therefore, PPV may be expected to increase the proportion of lung units with Ps (alveolar) Pi, increasing RV afterload, which may not be tolerated Shekerdemian and colleagues79 demonstrated a significant increase in CO when patients were converted from PPV to negative pressure ventilation using a cuirass Glenn and Fontan Procedures Hearts that cannot support two separate circulations after repair (univentricular hearts and hearts having one hypoplastic ventricle) are often palliated and then repaired by routing systemic venous return directly to the lung without an intervening subpulmonic pumping chamber (Glenn and Fontan procedures) In the Glenn circulation, pulmonary blood flow is derived from venous drainage from the upper extremities and brain by way of the superior vena cava and is sensitive to changes in ITP and its impact on the superior vena cava–pulmonary artery confluence, as well as lung volume and its impact on PVR One would expect pulmonary blood flow and oxygenation to improve during spontaneous respiration In the Glenn circulation, the inferior vena cava drains directly to the single ventricle While systemic venous return is adversely affected by increases in ITP, it is not impacted by the lack of a subpulmonic pumping chamber; thus, CO is generally well maintained following the Glenn procedure In the Fontan circulation, venous return from the lower body is diverted directly to the pulmonary arteries; thus, all systemic venous return must traverse the pulmonary circulation without a subpulmonic pumping chamber to maintain adequate ventricular filling The Pms drives systemic venous return from the venous reservoirs to the central venous structures as in a normal circulation but is also responsible for driving systemic venous return across the pulmonary circulation to the single ventricle.80 Decreases in the common atrial pressure during the cardiac cycle contribute to the pressure gradient driving pulmonary venous return.81 Because the pulmonary circulation and single ventricle reside entirely within the chest, changes in ITP not contribute to driving pulmonary blood flow other than by altering the pressure gradient for systemic venous return to the vena cava–pulmonary artery confluence, as well as by altering the effective compliance of the ventricle as in the normal circulation Shekerdemian and colleagues82 demonstrated the importance of ITP in the Fontan circulation Immediately following the Fontan procedure, negative-pressure ventilation using a cuirass significantly improved CO compared with PPV Williams and colleagues83 demonstrated the sensitivity of the Fontan circulation to PPV by exposing the inverse relationship between pulmonary vascular resistance and cardiac output with progressive increases in PEEP Key References Aubier M, Trippenbach T, Roussos C Respiratory muscle fatigue during cardiogenic shock Appl Physiol 1981;51:499-508 Funk DJ, Jacobsohn E, Kumar A The role of venous return in critical illness and shock—part I: physiology Crit Care Med 2013;41:255262 Gattinoni L, Chiumello D, Valenza C, F Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients Critical Care 2004;8:350-355 Gattinoni L, Marini JJ, Pesenti A, et al The “baby lung” became an adult Intensive Care Med 2016;42:663-673 Michard F, Chemla D, Richard C, et al Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP in patients with acute lung injury Am J Respir Crit Care Med 1999;159:935-939 Vieillard-Baron A, Loubieres Y, Schmitt J-M, et al Cyclic changes in right ventricular output impedance during mechanical ventilation J Appl Physiol 1999;87:1644-1650 Vieillard-Baron A, Matthay M, Teboul JL, et al Experts’ opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation Intensive Care Med 2016;42:739-749 The full reference list 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Fuhrman BP, Smith-Wright DL, Venkataraman S, Howland DF Pulmonary vascular resistance after cessation of positive end-expiratory pressure J Appl Physiol 1989;66:660-668 36 Venkataraman ST, Fuhrman BP, Howland DF PEEP-induced calcium channel-mediated rise in PVR in neonatal lambs Crit Care Med 1993;21:1066-1076 37 Taylor RR, Covell JW, Sonnenblick EH, et al Dependence of ventricular distensibility on filling of the opposite ventricle Am J Physiol 1967;213:711-718 38 Mitchell JR, Whitelaw WA, Sas R RV filling modulates LV function by direct ventricular interaction during mechanical ventilation Am J Physiol Heart Circ Physiol 2005;289:H549-H557 39 Buda AJ, Pinsky MR, Ingels Jr NB, et al Effect of intrathoracic pressure on left ventricular performance N Engl J Med 1979;301: 453-459 40 Pinsky MR, Summer WR, Wise RA, et al Augmentation of cardiac function by elevation of intrathoracic pressure J Appl Physiol 1983; 54:950-955 41 Patten MT, Liebman PR, Hechtman HB Humorally mediated decreases in cardiac output associated with positive end expiratory pressure Microvasc Res 1997;13:137-139 42 Patten MT, Liebman PR, Manny J, et al Humorally mediated alterations in cardiac performance as a consequence of positive endexpiratory pressure Surgery 1978;84:201-205 43 Grindlinger GA, Manny J, Justice R, et al Presence of negative inotropic agents in canine plasma during positive end-expiratory pressure Circ Res 1979;45:460-467 44 Dunham BM, Grindlinger GA, Utsunomiya T, et al Role of prostaglandins in positive end-expiratory pressure-induced negative inotropism Am J Physiol 1981;241:783-788 45 Manny J, Grindlinger G, Mathe AA, et al Positive end-expiratory pressure, lung stretch and decreased myocardial contractility Surgery 1978;84:127-133 46 Glick G, Wechsler AS, Epstein SE Reflex cardiovascular depression produced by stimulation of pulmonary stretch receptors in the dog J Clin Invest 1969;48:467-473 47 Calvin JE, Driedger AA, Sibbald WJ Positive end-expiratory pressure (PEEP) does 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hemodynamics in ARDS patients: focus on the effects of mechanical ventilation Intensive Care Med 2016;42: 739-749 70 Enson Y, Giuntini C, Lewis ML, et al The influence of hydrogen ion concentration and hypoxia on the pulmonary circulation J Clin Invest 1964;43:1146-1162 71 Rudolph AM, Yuan S Response of the pulmonary vasculature to hypoxia and H1 ion concentration changes J Clin Invest 1966;45:339-411 72 Pepe PE, Lurie KG, Wigginton JG, et al Detrimental hemodynamic effects of assisted ventilation in hemorrhagic states Crit Care Med 2004;32(suppl):S414-S420 73 Aubier M, Trippenbach T, Roussos C Respiratory muscle fatigue during cardiogenic shock J Appl Physiol Respir Environ Exerc Physiol 1981;51:499-508 74 Hussain SNA, Roussos C Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs J Appl Physiol 1985;59:1802-1808 75 Viires N, Aubier SM, Rassidakis A, et al Regional blood flow distribution in dog during induced hypotension and low cardiac output J Clin Invest 1983;72:935-947 76 Pinsky MR Using ventilation-induced aortic pressure and flow variation to diagnose preload responsiveness Intensive Care Med 2004;30:1008-1010 77 Fifer MA, Vlahakes GJ Management of symptoms in hypertrophic cardiomyopathy Circulation 2008;117:429-439 78 Braunwald E, Oldham Jr H, Ross J, et al The circulatory response of patients with idiopathic hypertrophic subaortic stenosis to nitroglycerin and to the Valsalva maneuver Circulation 1964;29: 422-431 79 Shekerdemian LS, Bush A, Shore DF, et al Cardiorespiratory responses to negative pressure ventilation after tetralogy of Fallot repair: a hemodynamic tool for patients with a low-output state J Am Coll Cardiol 1999;33:549-555 80 Mace L, Dervanian P, Bourriez A, et al Changes in venous return parameters associated with univentricular Fontan circulations Am J Physiol Heart Circ Physiol 2000;279:H2335-H2343 81 Fogel MA, Weinberg PM, Hoydu A, et al The nature of flow in the systemic venous pathway measured by magnetic resonance blood tagging in patients having the Fontan operation J Thorac Cardiovasc Surg 1997;114:11032-11041 82 Shekerdemian LS, Bush A, Shore DF, et al Cardiopulmonary interactions after the Fontan operation Augmentation of cardiac output using negative pressure ventilation Circulation 1997;96:3934-3942 83 Williams DB, Kiernan PD, Metke MP, et al Hemodynamic response to positive end-expiratory pressure following right atriumpulmonary artery bypass (Fontan procedure) J Thorac Cardiovasc Surg 1984;87:856-861 e3 Abstract: Positive-pressure ventilation (PPV) alters ventricular loading conditions and compliance In patients who are hypovolemic, the effects of positive airway pressure on the right heart predominate, whereas in patients who have systemic ventricular systolic dysfunction, the effects of PPV on left ventricular afterload predominate Large changes in arterial pulse pressure over the respiratory cycle help to identify mechanically ventilated patients who may have a favorable response to the administration of fluid or who may not tolerate high levels of positive end-expiratory pressure without fluid administration PPV raises juxtacardiac pressure, thereby reducing left ventricular afterload Respiratory effort imposes critical loads on the heart, and respiratory muscle failure from inadequate oxygen delivery is a final common pathway to death from shock Key Words: positive-pressure ventilation, ventricular loading conditions, preload, afterload, juxtacardiac pressure 10 33 Chapter Title Disorders of Cardiac Rhythm CHAPTER FRANK A AUTHOR FISH AND PRINCE J KANNANKERIL PEARLS • • • • • To gain basicmay knowledge of the development ofask, the“What’s eye the Arrhythmias result from ongoing therapies; To develop essential understanding how abnormalities DEAL?” (drugs and drips, electrolytes, airway and acid-base,atlines) various stages of development can arrest or hamper normalarAppropriate diagnosis is key Always attempt to document formation the ocular structures and visual therapy pathways rhythmia inofmultiple leads before instituting For ventricular fibrillation or pulseless ventricular tachycardia, begin cardiopulmonary resuscitation and defibrillate immediately Involve a cardiologist before initiating (chronic) antiarrhythmic drug therapy Cardiac arrhythmias are frequently encountered in the intensive care unit (ICU) setting This chapter reviews diagnosis and management of arrhythmias representing a primary disease process and those that occur secondary to other conditions or therapies (Table 33.1).1,2 Prompt restoration of hemodynamic stability concurrent with appropriate identification of the arrhythmia mechanism and predisposing factors is emphasized while providing a broader overview of arrhythmia mechanisms and their associated presentations in pediatric patients Classification of Arrhythmias Arrhythmias can be classified according to rate, electrocardiographic features, and, when possible, the underlying electrophysiologic mechanisms Electrocardiographically, arrhythmias can be characterized as bradycardias, extrasystoles (ectopy), or tachycardias Bradycardias are further subdivided by the level of dysfunction (e.g., sinus node dysfunction vs atrioventricular [AV] block) and by the ensuing rhythm (sinus, atrial, junctional, or idioventricular) Extrasystoles and tachycardias are categorized as atrial, junctional, or ventricular in origin Tachycardias are initially characterized by the level of origin (supraventricular vs ventricular), by electrocardiographic pattern, and functional mechanism: reentry, automaticity, or triggered activity Whereas most treatment algorithms (e.g., Pediatric Advanced Life Support) assume a reentrant mechanism, abnormal triggering and automaticity may be particularly important in the ICU setting Although differentiating between these mechanisms is sometimes difficult, it may be essential in guiding appropriate therapy, especially when initial therapies prove ineffective • • • To acquire possible, adequateuse information anatomy of rate Whenever available about meansnormal to document atrial the eye and related structures and develop a strong foundation to discern correct ventricular-atrial relationship for the understanding of common ocular problems and their Supraventricular tachycardia is a nonspecific electrocardioconsequences graphic pattern Multiple types of supraventricular tachycardia exist; appropriate therapy depends on appropriate diagnosis Whenever possible, opt for therapies that maintain atrioventricular synchrony Bradycardias Appropriate Versus Normal Heart Rate Since normal heart rate ranges vary tremendously during childhood as a function of age and autonomic tone, “appropriate” heart rate is a more useful concept than “normal” heart rate Thus, any inappropriately fast or slow rate for a given clinical circumstance warrants evaluation for factors affecting the sinus rate, such as pain, agitation, respiratory insufficiency, oversedation, anemia, or acidosis, as well as the potential for other arrhythmias resembling sinus Sinus Bradycardia and Sinus Pauses Causes of sinus bradycardia include high vagal tone, hypothermia, acidosis, increased intracranial pressure, drug toxicities, or direct surgical trauma to the sinoatrial (SA) node Primary sinus node dysfunction in childhood is rare but has been described.3 Transiently profound sinus bradycardia or prolonged sinus pauses of several seconds’ duration may be caused by intense vagal episodes, such as those occurring during neurocardiogenic syncope, apnea, or endotracheal suctioning When clearly correlated with a vagal stimulus, pacing can usually be deferred However, the hemodynamically tenuous patient with persistent or recurring bradycardias may warrant vagolytic, sympathomimetic, or pacing therapies Atrial premature beats that fail to conduct over the AV node can be mistaken as sinus pauses (when isolated) or sinus bradycardia (when in a bigeminal pattern) The blocked P wave may be obscured when buried in the preceding T wave; searching for changes in T-wave morphology or for intermittently conducted P waves may reveal the diagnosis In cardiac patients, sinus node dysfunction may be the result of surgical injury or heterotaxy 329 ... Motley HL, Werko L, et al Physiologic studies of the effects of intermittent positive pressure breathing on cardiac output in man Am J Physiol 1948;152:162-174 Funk DJ, Jacobsohn E, Kumar A The... 2008;117:429-439 78 Braunwald E, Oldham Jr H, Ross J, et al The circulatory response of patients with idiopathic hypertrophic subaortic stenosis to nitroglycerin and to the Valsalva maneuver Circulation 1964;29:... therapy Cardiac arrhythmias are frequently encountered in the intensive care unit (ICU) setting This chapter reviews diagnosis and management of arrhythmias representing a primary disease process