Pediatric Critical Care Medicine Department of Pediatrics Penn State College of Medicine Penn State Hershey Children's Hospital Hershey, PA. We hope that the text will help the doctor to achieve success in the practice of pediatric intensive care medicine.
Contributors
Pediatric Critical Care Medicine, Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Golisano Children's Hospital, Rochester, NY, USA. Pediatric Nephrology, Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh UPMC, Pittsburgh, PA, USA VINAY M.
Fundamentals of Gas Exchange
LEARNING OBJECTIVES
CHAPTER OUTLINE
INTRODUCTION
THE PROCESS OF GAS EXCHANGE
Alveolar Ventilation and the Oxygen Cascade
Distribution of Alveolar Ventilation
Consequently, flow is a function of both pulmonary arterial and venous pressures, and because pulmonary arterial pressure is higher, blood flow decreases along this gradient.
Carbon Dioxide Elimination
Deoxygenated hemoglobin molecules bind hydrogen ions as well as carbon dioxide to form carbaminohemoglobin in order to buffer the pH and prevent substantial changes in pH
The result is an increase in the plasma HCO 3 - concentration by approximately 3.5-4 mEq/L for every 10 mm Hg increase in the PaCO 2 .
Assessing Adequacy of Gas Exchange
Assuming a PaCO 2 of 40 mm Hg, a normal diet and sea-level barometric pressure, P A O 2 is therefore approx. 100 mm Hg. P A O 2 is higher than the partial pressure of pulmonary artery and capillary blood, leading to diffusion of oxygen from the alveoli into the bloodstream.
In the Bloodstream
Conditions that cause a decrease in hemoglobin's affinity for oxygen result in a higher P 50 (higher PaO 2 at which hemoglobin is 50% saturated with oxygen). Increasing concentrations of H + and/or carbon dioxide will decrease the affinity of hemoglobin for oxygen.
To the Tissues
Conversely, conditions that cause a leftward shift of the curve due to an increase in hemoglobin's affinity for oxygen have a lower P50 (a lower PaO2 at which hemoglobin is 50% saturated with oxygen). Under these conditions, hemoglobin's affinity for oxygen is high, promoting the absorption of oxygen from the alveoli into the bloodstream and to the hemoglobin molecule in the red blood cell.
MECHANISMS OF HYPOXEMIA
Hypoventilation
Ventilation Perfusion Mismatch
The most extreme example is the patient in cardiac arrest who is being ventilated but is no longer perfusing the lung. Alveolar dead space consists of the alveoli not participating in gas exchange due to insufficient perfusion.
Shunting of Pulmonary Blood
Anatomical dead space consists of conductive airways (nasopharynx, trachea, subsegmental bronchi, terminal bronchioles), within which approximately 25% of each respiratory volume is lost. Physiological dead space is defined as a combination of anatomical and alveolar dead space.
Diffusion Limitation
When the V/Q ratio exceeds one, ventilation is wasted because it is not participating in gas exchange. The causes of increased dead space ventilation include: tachypnea (anatomical dead space is established, so rapid shallow breathing increases relative dead space), obstructive lung disease, pulmonary embolism, and increases in ventilator tube length beyond the separation ("Y") of the inspiratory and expiratory limbs in intubated patients.
OI has been used in a number of studies as a tool to quantify and compare the extent of lung injury. In contrast to OI, the P/F ratio does not require a mean airway pressure, and therefore, can be used to assess the degree of lung injury in non-intubated patients.
Pulse Oximetry
In connection with carboxyhemoglobinemia, blood gas analysis with co-oximetric detection of the other forms of hemoglobin is necessary to truly determine blood oxygen saturation. The pulse oximeter inappropriately interprets carboxyhemoglobin as oxyhemoglobin and therefore overestimates the true oxygen saturation of hemoglobin in the context of carbon monoxide poisoning.
Capnometry
The highest recorded value of carbon dioxide at the end of exhalation is recorded as. The highest recorded end-expiratory carbon dioxide value is recorded as end-tidal carbon dioxide.
Finally, capnography is also recommended in the setting of pediatric cardiopulmonary arrest to assess the adequacy of perfusion to the lungs. Although a specific value is not uniformly defined, providing cardiopulmonary resuscitation to maintain the end-tidal carbon dioxide level above a specified value for each patient will help ensure adequate pulmonary blood flow with compressions and reduce the chance of potentially harmful hyperventilation.
SUMMARY
Which of the following statements most accurately describes the body's response to hypercarbia? Although the pulse oximetry reading accurately reflects a well-oxygenated patient, 100% oxygen should be continued to treat possible carboxyhemoglobinemia.
REVIEW QUESTIONS
He is tachycardic and tachypneic on clinical exam with pulse oximetry readings of 85% and a good waveform that correlates with heart rate. It is difficult to determine whether the pulse oximetry value represents effective oxygenation because the pulse oximeter will inappropriately interpret carboxyhemoglobin to be oxyhemoglobin.
SUGGESTED READINGS
ANSWERS
Oxygen Delivery and Oxygen
The previous chapters describe the process by which molecular oxygen moves along a concentration gradient from the atmosphere to the blood, and from there to the cell and to the mitochondria. This chapter provides an overview of these biochemical processes, their changes in critical illness, and their relationship to the various methods for measuring oxygen supply and consumption.
BIOCHEMICAL BASIS
As such, simple measurements of blood lactate levels do not indicate the relative importance of the underlying processes, altered production and/or utilization. This fact must be understood when lactate is used as an indicator of insufficient oxygen supply, since it is not the main cause of the acidosis.
OXYGEN DELIVERY
With rapid infusion of sodium bicarbonate, there will be a significant increase in blood carbon dioxide, released from the dissociation of carbonic acid, which is formed when bicarbonate buffers extracellular hydrogen ions. Therefore, the use of sodium bicarbonate to correct the hypoxic acidosis may actually be harmful.
Arterial Oxygen Content
The decision about blood transfusions to improve oxygenation is not necessarily straightforward, except in cases of acute severe anemia. Some studies suggest that in critically ill adult cardiac patients, a "liberal" transfusion policy may improve outcomes, presumably by maintaining adequate oxygenation in the coronary circulation.
Cardiac Output
Heart Rate
Stroke Volume
The ejection fraction is another parameter that can be used to assess left ventricular function. Afterload can be defined as the force that opposes the contraction of left ventricular myocytes during systole.
INTERDEPENDENCE OF THE HEART, LUNGS AND BLOOD ON PERIPHERAL OXYGEN DELIVERY
This results in an increase in minute ventilation, a higher alveolar oxygen concentration (PAO 2 ) and ultimately an increase in arterial oxygen content due to the increase in oxygen saturation and PaO 2 . In the presence of acidosis, such as that likely to be present in the capillary circulation during hypoxia, its affinity for oxygen decreases, which facilitates the release of oxygen to the starved cells (Fig. 2-4.
OXYGEN CONSUMPTION
It has been suggested that this happens because the critical point of oxygen supply has been reset to a much higher point. Alternatively, it has been argued that this is the result of a reduced ability of the tissues to increase the extraction rate of oxygen.
Measurement Techniques
It requires determination of cardiac output, arterial oxygen content and mixed venous oxygen content. It requires determination of cardiac output, arterial oxygen content and mixed venous oxygen content.
Finally, a traditional criticism of the Fick equation has been that it provides an estimate of oxygen consumption at individual time points. Similarly, hypothermia globally reduces the metabolic needs of the body, including the brain, and may therefore be associated with reduced oxygen consumption.
OXYGEN EXTRACTION
In addition, increasing the work of breathing can significantly increase oxygen consumption; up to 40% of cardiac output may be required to support the work of breathing. In addition, given that the brain is one of the most demanding organs for metabolism, any condition that results in a significant reduction in brain activity will be accompanied by a dramatic decrease in oxygen consumption.
ASSESSMENT OF OXYGEN DELIVERY/OXYGEN CONSUMPTION
The normal oxygen extraction ratio (O 2 ER) is approximately 50% of the oxygen delivered to the tissues. The oxygen extraction ratio (O 2 ER) is determined by dividing the difference between the arterial and venous oxygen content by the cardiac output.
The cardiac cycle also influences the oxygen supply to the myocardium via the right and left coronary arteries originating from the aortic root. Restrictive disease affecting the pericardium or excess pericardial fluid can adversely affect cardiac filling and function during various parts of the cardiac cycle.
Myocardial Contraction – Cellular Components
The contraction continues until calcium levels are reduced, releasing TN-C from calcium with subsequent inhibition of actin-myosin interaction and relaxation of the myocardium (Fig. 3-3). At the cellular level, the 'excitation-contraction' coupling involves depolarization. from the heart to the cellular calcium current and the cellular contraction-relaxation sequence (Fig. 3-4.
Cardiac Pump Function
Plasma calcium concentrations have a direct influence on myocardial contractility; low levels of calcium which have a negative inotropic effect while increasing plasma calcium levels have a positive influence on contraction. It is important that clinicians correct low ionized calcium levels before or in conjunction with an attempt at pharmacological correction of acidosis.
Stroke Volume – Preload
Stroke Volume – Afterload
The effect of varying preload, afterload and contractility on the pressure-volume loop. a) When arterial pressure (afterload) and contractility are held constant, successive increases (lines in preload (measured in this case as end-diastolic volume (EDV)))) are associated with loops that have progressively higher stroke volumes but a constant end-systolic volume ( EVS. When the preload ( EDV ) and contractility are held constant, successive increases (points) in arterial pressure (afterload) are associated with loops that have progressively lower stroke volumes and higher end-systolic volumes.
Stroke Volume – Contractility
CARDIOPULMONARY INTERACTIONS
The extremely negative pleural pressures seen during airway obstruction and asthma exacerbations may also compromise cardiac outcome. In contrast, the use of PPV may improve cardiac outcome in patients with left ventricular dysfunction, whereas withdrawal from PPV may improve cardiac outcome in patients with right heart failure.
Neural Regulation of Cardiopulmonary Interactions
Respiratory sinus arrhythmia is a simple but physiologically important example of cardiorespiratory interactions that occur during spontaneous breathing. For example, apnea results in decreased heart rate and increased systemic vascular resistance due to vagal and sympathetic influences.
Intrathoracic Pressure Changes During Respiration
The transient increase in alveolar ventilation during inspiration is matched by an increase in venous return and pulmonary blood flow. This matching of ventilation and perfusion reduces dead space ventilation and intrapulmonary shunting, improving gas exchange.
The Effect of Respiration on Cardiac Function
Right Ventricular Preload/Systemic Venous Return
As P RA increases from A to B, the intercept on the venous return curve shifts and results in lower venous return. P RA decreases from A to C and the intercept on the venous return curve shifts to the left and increases venous return.
Right Ventricular Afterload
The relationship between lung volume and PVR is present during positive and negative pressure ventilation. The effect of increasing lung volume on the extra-alveolar vessels is shown in the inset and curve A.
Left Ventricular Preload/Pulmonary Venous Return
When respiration results in an increase in RV afterload, RV diastolic volume increases and LV filling decreases as a leftward shift of the intraventricular septum occurs. The use of PEEP greater than 15 cm H 2 O in patients with acute respiratory distress syndrome has been associated with a leftward shift of the intraventricular septum due to an increase in RV afterload.
Left Ventricular Afterload
An increase in venous return associated with negative intrathoracic pressure can also lead to leftward deviation of the intraventricular septum resulting in decreased LV compliance and diastolic volume. Understanding the complex cardiopulmonary dynamics during positive pressure ventilation has led to the appreciation of the clinical phenomenon of systolic pressure variation.
Effect of Respirations on Contractility
Clinically, an increase in SPV (>10 mm Hg) has been observed early in hypovolemia. An increased SPV can also be seen when the D up component is increased, rather than an excessive drop in the D down component.
Cardiac Effects on Respiratory Function
In children with congenital heart disease, changes in pulmonary blood flow and pulmonary artery pressure have been shown to affect lung mechanics. Increased pulmonary blood flow associated with increased pulmonary artery pressure results in decreased lung compliance and increased airway resistance.
SUMMARY OF CARDIOPULMONARY INTERACTIONS
Positive effect Systemic venous return. a ) Summary of the primary effects of spontaneous breathing on cardiac function. Liver compression transiently increased preload with a consequent increase in cardiac output (stroke volume) and slowing of heart rate.
BLOOD FLOW AND OXYGEN CONSUMPTION AT THE MAJOR TISSUE BEDS
MECHANISMS OF REGIONAL BLOOD FLOW REGULATION DURING STRESS AND
PATHOLOGIC CONDITIONS
When birth cannot meet the demand, the body's regulatory mechanisms ensure that the brain and heart receive sufficient blood flow to meet their metabolic demands. In various pathological conditions (cardiogenic or hypovolemic shock, hypertension, diabetes, sepsis, etc.) dysfunction of various regulatory mechanisms (eg endothelial dysfunction with reduced NO production and/or vasodilatory sensitivity) causes damage to the distribution of oxygen and blood flow. to the tissues.
CORONARY CIRCULATION
Oxygen supply, local and systemic mediators, and the autonomic nervous system regulate blood flow in different beds and move fractions of cardiac output to the organs that need more oxygen to sustain the stress endured. The analysis of circulatory regulation under pathological conditions is beyond the scope of this chapter.
Anatomy, Histology and Physiology
Two coronary arteries supply the myocardium with oxygen-enriched blood to meet the constant energy demands of the beating heart. Myocardial energy consumption is determined by the following factors: myocardial stress, heart rate and myocardial contractility (Table 4-1.
Local Regulation of Coronary Blood Flow
In order for the heart to meet its energy needs, the coronary blood flow must be able to adapt within a very short time. Coronary flow is dependent on the absolute pressure difference across the vascular bed and the coronary vascular resistance.
Specifi c Determinants of Coronary Blood Flow
As the tissue's metabolic needs increase, relaxation of the precapillary sphincter allows for a decrease in resistance and an increase in the density of the perfusing capillaries and blood flow per minute. 100 g of myocardial tissue. This pressure is called the Coronary Perfusion Pressure (CPP) and is calculated as the diastolic aortic pressure minus the right atrial diastolic pressure or the left ventricular end-diastolic pressure.
Transmural Distribution of Coronary Blood Flow
This is because the endocardial arterioles are maximally dilated and therefore flow is mainly pressure dependent. Reducing oxygen consumption with inhibition of adrenergic receptors reduces epicardial blood flow and increases perfusion pressure and blood flow to the ischemic myocardium by decreasing contractility.
Metabolic Regulation of Coronary Blood Flow
This flow redistribution from the endocardium to the epicardium is exaggerated during exercise, tachycardia, stress, and with the use of potent arteriolar vasodilators such as adenosine and dipyridamole. Pharmacological vasoconstriction of epicardial and large coronary vessels moves more blood to the endocardium.
Adrenergic Control of Coronary Blood Flow
All these changes lead to a greater demand for oxygen in the myocardium, which, through local metabolic mediators, causes vasodilation and increases coronary blood flow due to a drop in vascular resistance. The fact that coronary vessels have both alpha and beta adrenergic receptors further complicates the assessment of direct sympathetic activation of coronary blood flow.
Alpha-Adrenergic Coronary Vasoconstriction
Since the effects of local metabolic control have been described above, we will focus on neuron-mediated alpha and beta adrenoreceptor vasoactivity, which may be responsible for many of the immediate changes observed during exercise. In experimental models it is very difficult to isolate local metabolic effects from adrenergic effects.
Beta Adrenergic Coronary Vasodilation
When the sympathetic system is activated during exercise or under stress, it leads to an increase in contractility, heart rate and blood pressure that increases afterload.
Coronary Blood Flow During CPR
Recently, the effects of negative intrathoracic pressure on coronary perfusion pressure and myocardial blood flow during CPR have been investigated. Application of this concept has been shown in animal and human CPR trials to improve vital organ perfusion pressures, myocardial blood flow, and survival rates.
Effects of Acidosis, Hypocapnia, and Hypercapnia on Coronary Blood Flow
Coronary perfusion pressure below 15 mm Hg during CPR is a poor prognostic factor for a successful outcome. Also, with the direct transfer of negative intrathoracic pressure to the right atrium, right atrial pressure decreases and coronary perfusion pressure improves significantly.
When, during the decompression phase, the negative intrathoracic pressure is reinforced by inhibiting airflow to the chest (ie, with an inspiratory impedance threshold device), there is an increase in venous return, cardiac output, and mean aortic pressure.
Cerebral Circulation Autoregulation
The blood-brain barrier is thought to account for the blunted response of cerebral blood flow to systemic humoral stimuli. Systemic humoral stimuli can change the resistance of large vessels, but the autoregulatory function of the microcirculation prevents changes in blood flow.
Hypoxia and Carbon Dioxide Related Cerebral Autoregulation
Flow Mediated Regulation
Endothelium Derived Vasoactive Factors
Potassium Channels
Voltage-gated potassium channels or delayed rectifier potassium channels open when membrane depolarization occurs. The role of the inward rectifier potassium channels may be more important than initially thought, as they may play a significant role in neurovascular coupling.
PULMONARY CIRCULATION
Inhibition of calcium-dependent potassium channels causes contraction of large cerebral arteries, has no effect on arterioles, and plays an important role in regulating basal tone and blood flow. Activation of the same channels by NO and cGMP may play an important role in microcirculation.
Normal Pulmonary Pressures
The bronchial veins mostly drain into the systemic venous system, but some of them drain into the pulmonary veins, representing a normal physiologic (approximately 1%) right-to-left shunt. The bronchial arterial supply to the bronchioles forms anastomoses at the capillary level with the pulmonary circulation.
Pulmonary Vascular Resistance
About 70% of the total bronchial blood flow supplies the intrapulmonary bronchi and joins the pulmonary veins emptying into the left atrium. In addition, with exertion, pressure in the left atrium increases due to increased blood flow, leading to expansion of the pulmonary venous system with a further decrease in pulmonary resistance.
Hypoxic Pulmonary Vasoconstriction
This is possible only due to the recruitment of pulmonary arterial beds leading to a significant decrease in pulmonary vascular resistance. The larger the size of the hypoxic lung region, the less pronounced the flow deviation.
Pulmonary Vascular Tone and Clinical Implications
Hypoxic withdrawal of reactive oxygen species inhibits K + channels, thereby depolarizing pulmonary artery smooth muscle cells. For example, if an entire lung is hypoxic, the blood flow diversion will be 50%, but when only an area of 10% of the total lung is hypoxic, there is an 80% blood flow diversion.
Vasoconstrictors
Vasodilators
Vasomediators in the Pathogenesis of Pulmonary Hypertension
However, patients with pulmonary hypertension have increased levels of ANP and adrenomedullin suggesting that there is an intrinsic attempt to compensate with vasodilators and antiproliferative pathways. When the effects of the up-regulated pathways of these factors can no longer compensate, vasoconstrictive pathways dominate and severe pulmonary hypertension develops.
Autonomic Neural Regulation of Pulmonary Vascular Tone
Parasympathetic blockade does not alter resting vascular tone and therefore does not appear to play a crucial role in maintaining basal vasomotor tone. Increased vasoconstriction in the pulmonary and systemic microcirculation shifts blood volume in the chest and leads to capillary stress, failure, and development of pulmonary edema.
RENAL CIRCULATION
Intravenous administration of acetylcholine leads to constriction when vasomotor tone is low, but to vasodilatation when basal tone is elevated. These responses are blocked by atropine, indicating that the effect is secondary to muscarinic receptor activation.
Major Arteries
Renal Blood Flow and Autoregulation
Autoregulation of renal blood flow is extremely important for homeostasis, as glomerular filtration rate is highly dependent on blood flow. Inner medulla: vascular bundles disappear in the inner medulla and vasa recta become scattered with nephron segments.
Medullary Blood Flow
The different geometric and environmental characteristics of the medulla are also thought to account for the different response of medullary blood flow to sympathetic stimulation. Medullary blood flow is highest under the state of diuresis and minimal when fluid retention is desirable.
Cortical Blood Flow
Two mechanisms are thought to be responsible for this unique physiological property of the medulla: (i) the counterregulatory role of nitric oxide and (ii) paradoxical vasodilation in response to the effect of angiotensin II.
Vasoactive Mediators
Cyclooxygenase Inhibition
Adenosine and Renal Circulation
A1AR in afferent arterioles is selectively activated from the interstitial aspect of the vessel, away from the interface with the circulating blood volume. A2AR receptor-mediated vasodilation partially buffers adenosine-induced vasoconstriction in both pre- and postglomerular segments of the renal microvasculature.
SPLACHNIC CIRCULATION
Vascular Anatomy and Distribution
Baseline Vascular Tone Regulation
Postprandial Blood Flow Regulation
This observation implicates non-adrenergic and non-cholinergic neurons in the regulation of postprandial hyperemia. Adenosine levels in the portal circulation rise 3-10 minutes before increased mucosal oxygen uptake and blood flow.
Pathologic States
Hormones and peptides: Many vasoactive hormones and peptides have been identified in the gastrointestinal system (Gastrin, VIP, CCK, substance P, secretin, gastric inhibitory polypeptide, neurotensin, calcitonin gene-related peptide a (CGRP-a), glucagon, enkephalins, somatostatin and peptide YY) do not appear to have a role in whole-organ postprandial hyperemia at physiological levels. Local metabolic mediators: Active hyperemia is associated with increased oxygen consumption and villi debt.
CUTANEOUS CIRCULATION
This is only possible through neural and local mechanisms that directly affect the arterial tone and blood flow to the skin. In the rest of the skin (non-glabrous), blood flow is regulated by the balance between noradrenergic sympathetic nerves and cholinergic parasympathetic nerves in addition to the effects of local skin temperature.
Neural Control of the Skin Blood Flow
Arteries of bare skin areas (palms, lips, and soles) are innervated only by noradrenergic nerves, and the primary regulators of blood flow are vasoconstrictor nerves, which contribute to arterial tone and local effects of skin temperature. As Tc increases, neural regulation leads to increased blood flow to the skin to lose excess heat and return to normal core temperature.
Vasodilation
Cutaneous blood flow regulation is very powerful and can cause lack of blood flow during extreme cold and severe hypothermia. Increased blood flow due to active vasodilation (contributes 80% of increased blood flow) associated with sweating leads to heat dissipation and thermoregulation.
Vasoconstriction
Conversely, severe hyperemia with 60% of cardiac output can be directed at the skin during heat shock. During normothermia and resting conditions, the velars receive no nerve stimulation and the smooth muscles are considered to have their basal tone.
Local Temperature Control of Cutaneous Blood Flow
Contribution of vasodilatory prostanoids and nitric oxide to resting flow, metabolic vasodilation, and flow-mediated dilation in the human coronary circulation. Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.
LEARNING OBJECTIVES
Assessment of Cardiovascular Function
DETERMINANTS OF CARDIAC OUTPUT
ASSESSING CARDIOVASCULAR STATUS BY PHYSICAL EXAMINATION
Temperature
Capillary Refi ll
Urine Output
Blood Pressure
Systolic arterial pressure - Systolic pressure is primarily determined by the force and volume of the blood ejected from the left ventricle (LV) into the aorta. Diastolic arterial pressure - Diastolic pressure is primarily determined by the resistance to volume displacement in the arterial tree (arterial distensibility).
INVASIVE MEASURES OF CARDIOVASCULAR FUNCTION
Mean arterial pressure – The MAP is not halfway between the diastolic and systolic pressures because the duration of diastole is longer than that of systole. Physiologically, the MAP is determined by the force of blood ejected from the LV and the vascular tone of the arterial system (Fig. 5-3.
Arterial Waveform Analysis
Therefore, the contour of a peripheral arterial waveform is defined by both forward pulsations originating from LV ejection (stroke volume) and reflected pulsatile waves from distal vessel walls and bifurcation points. In the elderly, systolic hypertension is partly due to a loss of arterial distensibility, causing reflected waves to increase the systolic peak.
Arterial Waveform Technical Considerations
Wave Frequency and Resonance
If the natural frequency of the system is in the same range as the natural frequency of the arterial waveform, the amplitudes of the waves become additive or resonant. Therefore, resonance amplification can occur when the natural frequency of the system approaches the frequency of one of the component sine waves that make up the arterial pulse.
Damping
Clinically, resonant expansion of the arterial pressure wave causes an artificial increase in systolic pressure (also called pressure overshoot, ringing or resonance) and an artificial decrease in diastolic pressure. A system becomes overdamped when the oscillatory energy of the pressure wave is reduced by the physical forces of the system.
Fast Flush Test
Causes of excessive attenuation include multiple stopcocks, leaks, bubbles, clots, compliant tubing, or kinks in the cannula or tubing (Fig. 5-6.
Leveling and Zeroing
Variations in Arterial Waveforms
Pulsus Paradoxus
Pulsus paradoxus occurs when the normal drop in systolic pressure due to inspiration is exaggerated to > 10 mm Hg Appropriate attenuation. Panel B – Multiple resonance waves after rapid flushing indicating under-attenuation, increased resonance and artificial rise in systolic blood pressure.
Systolic Pressure Variation
Positive pressure increases the effects of reduced effective circulating volume and causes a greater drop in the D component down the SPV. During positive pressure inspiration, the D up component reflects a transient increase in left ventricular stroke volume with increased LV preload and decreased LV afterload.
Pulsus Alternans
A decrease in LV preload and output leads to a smaller LV stroke volume and a brief decrease in arterial pressure that occurs later in positive pressure inspiration (D down). Therefore, a patient with congestive heart failure may actually have an increased SPV while using positive pressure ventilation.
Pulsus Parvus et Tardus
Stroke volume variation (SVV) is also a functional measurement taken during positive pressure breathing that provides valuable information about volume response. Using pulse contour analysis (see Emerging Techniques for Assessing Cardiac Output), distinct variations of left ventricular stroke volume during positive pressure breathing can be quantified.
Pulsus Bisferiens and Dicrotic Pulse
A reduced (parvus) and delayed (tardus) beat in the aortic and radial artery waveforms is seen in a patient with aortic valve stenosis (a. Reduced and delayed waveforms are seen in a second patient with aortic valve stenosis aortic valve as measured in the radial and femoral arteries (b.
Complications of Invasive Arterial Pressure Monitoring
Ischemic Injury
However, recent studies in adults and pediatrics have shown that brachial artery catheterization may not confer an increased risk of ischemic complications as previously believed. However, until larger studies are conducted on the safety of brachial artery catheterization, it should not be used as the primary site for intra-arterial pressure monitoring.
Infection
Central Venous Pressure Monitoring
The c wave, if present, occurs at the end of the QRS complex and the v wave occurs after the T wave of the ECG. To obtain a numerical value of the CVP, it is best to measure the average pressure of the wave.
Variations in CVP Waveform
Tamponade physiology causes elevation of CVP and equalization of diastolic filling pressure (CVP = LVEDP = PAEDP = PAWP).
Complications of Central Venous Catheters
The incidence of CRT is increased in children with malignancies and those at risk for hyperviscosity, such as children with diabetic ketoacidosis. Activated platelets arrive at the area of endothelial damage and act to spread the thrombus.
MEASUREMENT OF CARDIAC OUTPUT
Small vessel size relative to catheter size and venous stasis has been implicated as an increased risk of CRT in children. Tissue factor (thromboplastin) forms a complex with factor VIIa and activates factor IX, thereby initiating a procoagulant cascade that generates thrombin.
Conservation of Mass
Dye Dilution
Measurement of the dye in the distal artery is made problematic due to the recirculation phenomenon. The concentration of the dye will peak early and subsequently decrease as the slower particles arrive.
Fick Method
If the PA cannot be collected, blood from the superior part of the RA can be used. If an intracardiac shunt is present, the size of the shunt can be calculated as Q pul / Q syst.
Thermodilution
Measurement of cardiac output by the Fick method requires independent measurement of oxygen consumption (indirect calorimetry) or assumption of oxygen consumption using normal standards. Conversely, oxygen consumption can be estimated using the Fick equations, if cardiac volume is measured independently.
Pulmonary Artery Catheterization
The classic bedside approach used in many of the early studies of shock in critically ill children used a pulmonary artery catheter to measure cardiac output by thermodilution and CaO2-CmvO2 to calculate oxygen consumption. When used properly, pulmonary artery catheters can be clinically useful by allowing measurement of CO, detection of shunts, monitoring intracardiac pressure, and assessment of other important hemodynamic parameters.
Cardiac Output Determination Using Pulmonary Artery Catheterization
A pulmonary artery catheter should only be placed if a specific question about a patient's hemodynamic status cannot be satisfactorily answered using standard hemodynamic tools (examination, waveform analysis, echocardiography, biochemical markers) and if the answer can affect. therapy. According to the CO finding, due to the rapid mixing and rapid passage of the injection (cold water), a peak is reached earlier and the lower slope is sharper.
Intracardiac Pressures Obtained from Pulmonary Artery Catheterization
Pulmonary artery occlusion pressure is approximately equal to left atrial pressure, which reflects left ventricular end-diastolic pressure (LVEDP). If PAOP and pulmonary artery end-diastolic pressure correlate well, pulmonary artery end-diastolic pressure (PAEDP) can also be used as an indirect estimate of LVEDP.
Obtaining and Interpreting Pulmonary Artery Occlusion Pressures
The balloon is inflated and "floated" into a distal branch of the pulmonary artery where it becomes "wedge". With balloon inflation, flow in the distal segment of the pulmonary artery is occluded creating a continuous, uninterrupted column of blood from the tip of the pulmonary artery catheter into the left atrium.
Pulmonary Artery End Diastolic Pressure
During aortic regurgitation, the mitral valve closes prematurely as retrograde aortic flow continues to fill the LV and add to LVEDP. Atrial contraction against a stiff ventricle causes a rapid rise in LVEDP, which causes premature mitral valve closure.
Derived Hemodynamic Variables
Therefore, the LA and PAOP will be "protected" from the transmission of high LVEDP; however, a prominent wave would be appreciated as the LA contracts against a poorly compliant LV. In this setting, measuring the a-wave of the PAOP rather than the mean PAOP may be more reflective of LVEDP.
Novel Techniques for CO Assessment
Transpulmonary Thermodilution
Both measurements may be particularly useful in guiding fluid resuscitation, as GEDV has been shown to be more reliable than CVP as an indicator of preload in adult patients. TPTd may be a safer and less invasive method to measure CO than the traditional pulmonary artery catheter.
Pulse Contour Waveform Analysis
Other systems (Flow Trac, Vigileo) do not use another method of CO determination for calibration. Currently, both the calibrated and non-calibrated systems are undergoing validation studies of their ability to estimate CO compared to the traditional pulmonary artery catheter under various clinical conditions.
Transesophageal Doppler Echocardiography
Unlike PiCCO and LiDCO, these systems use the patient's demographic and physical characteristics (age, height, gender, and weight) to estimate predicted SV.
MIXED VENOUS SATURATION, CENTRAL VENOUS SATURATION, LACTATE AND BRAIN NATRIURETIC
Mixed Venous and Central Venous Saturation
Due to the low oxygen tension, pyruvate can no longer undergo aerobic metabolism in the mitochondria and is diverted towards lactate production. Serum lactate increases during low oxygen conditions as pyruvate can no longer undergo aerobic metabolism in the mitochondria and is diverted to lactate production.
Brain Natriuretic Peptide
When evaluating a normal central venous pressure (CVP) waveform (figure), the a wave represents which of the following. When evaluating a normal central venous pressure (CVP) waveform (figure), the c wave represents which of the following.
Articles
The utility of left ventricular stroke volume variation in assessing fluid responsiveness in patients with impaired cardiac function. Systolic pressure variation as a guide to fluid management in patients with sepsis-induced hypotension.
Overview, Structure and Function of the Nephron
Urine is formed as an ultrafiltrate in the glomeruli, which are located in the cortex. Growth, usually assessed by ultrasound, is rapid in the first two years and then slows until an adult size of about 12 cm is reached in adolescence.
STRUCTURE OF THE NEPHRON
In the next segment of the nephron (Fig. 6-3), the loop of Henle, sodium is reabsorbed in excess of water, generating a hypotonic urine and a hypertonic interstitium, which is necessary for urine concentration. In the loop of Henle, 15-25% of the filtered sodium chloride is reabsorbed, and active calcium and magnesium regulation takes place.
REGULATION OF RENAL BLOOD FLOW
Regulation of Renal Blood Flow, Determinants of Glomerular Filtration Rate
An increase in tone on either side of the glomerular capillaries will increase vascular resistance and decrease renal plasma flow. Autoregulation refers to the ability of the kidney to maintain RPF and GFR over a wide range of blood pressure.
DETERMINATION OF GFR
The net result of autoregulation is the ability to maintain GFR and RPF within a narrow range as long as mean arterial pressure is greater than 70 mm Hg in the adult. RPF and GFR will fall with any further reduction in systemic pressure, and if MAP falls below 40–50 mm Hg in the adult, no ultrafi ltrate is formed.
Changes in GFR with Age
This contributes to autoregulation as it results in an increase in pressure within the glomerular capillary, maintaining GFR even in the face of decreased perfusion pressure. This may be compounded by the fact that newborn kidneys have higher urinary sodium levels, with a higher fractional forced sodium excretion (FENA).
Exogenous GFR Markers
Creatinine Clearance
This violates the steady-state assumption underlying the GFR calculation, leading to inaccurate GFR estimates. A final factor limiting the utility of creatinine clearance for estimating GFR is the difficulty in performing urine collection in children.
Serum Creatinine
For example, a change in serum creatinine from 1 to 2 mg/dl may represent a decrease in GFR from 120 to 60 ml/min. As a result, in pathological states, serum creatinine may remain within the normal range until there is significant destruction of the renal parenchyma.
Urea
Additionally, these equations were developed and intended to be used when there is a steady state in terms of creatinine production and clearance. In situations such as acute renal failure, a sudden drop in GFR leads to an increase in serum creatinine until a new steady state is reached.
WATER AND SALT BALANCE – OVERVIEW
In addition, 45–50% of filtered urea is usually reabsorbed in the tubules by a passive process associated with sodium and water reabsorption. During states of hypovolemia, severe sodium and water retention occurs, resulting in passive reabsorption of urea.
Maintenance of Effective Circulating Volume
Effects of Renin/Angiotensin II
In the kidney, AII causes arteriolar vasoconstriction, efferent more than afferent, leading to increased glomerular capillary pressure, which contributes to autoregulation. However, to prevent compromise of renal blood flow by excessive vasoconstriction of the renal vessels, AII causes prostaglandin release in the glomerulus, leading to protective vasodilation.
Aldosterone
Other effects of AII include a direct effect on the cells of the proximal tubule to stimulate sodium reabsorption, contraction of the glomerular mesangium to reduce the surface area available for filtration, and increased sensitivity to tubuloglomerular feedback.
Renal Sodium Handling
Pressure natriuresis, the mechanism of which is not fully understood, occurs when small changes in systemic blood pressure cause a significant decrease in sodium and water reabsorption in the proximal tubule and loop of Henle. It has multiple effects on the kidney that lead to natriuresis, including inhibition of sodium reabsorption in the medullary collecting duct, direct increase in GFR, lower basal renin release, and inhibition of aldosterone secretion, which in turn decreases the action of ADH in the collecting duct and inhibits the increase in sodium reabsorption in the proximal tubule , caused by AII.
Water Balance
In the presence of maximum ADH, a urine concentration as high as mOsm/kg can be achieved. In the case of SIADH, ADH secretion occurs independently of serum osmolality and intravascular volume status.
Role of Renal Prostaglandins
In healthy individuals, the physiological significance of this is not known, but this effect may be used therapeutically in the treatment of some bleeding disorders. The retention of water leads to activation of volume receptors, leading to urinary sodium excretion with the net result of hyponatremia without significant edema.
POTASSIUM REGULATION
DIURETICS
Oral/IV inhibits carbonic anhydrase Metabolic acidosis Hypokalemia Nephrolithiasis Osmotic Proximal tubule Thin ascending limb of Henle. There are two additional types of diuretics that act via alternative mechanisms in the proximal tubule: osmotic agents and carbonic anhydrase inhibitors.
ENERGY REQUIREMENT OF THE NORMAL KIDNEY
They also increase medullary blood flow, decreasing medullary tonicity and impairing countercurrent concentrating mechanisms, further reducing sodium reabsorption in the loop of Henle. Similarly, the distal part of the proximal tubule (segment S3), located in the outer medulla, has high metabolic activity with low oxygen under normal conditions.
ACID BASE
In the adhesive part of the hairpin, the partial pressure of oxygen in the tissue can be as low as 8 mm Hg. The proximal tubule is impermeable to the charged molecule, and thus, NH 4 + is trapped in the lumen.
Regulation of Renal Hydrogen Excretion
In most conditions, the main adaptive mechanism in response to acid stress is the production and excretion of ammonium, which can result in the excretion of up to 300 mEq H + /day in the case of acidosis. Chloride also has sodium-independent direct effects on renal acid-base transport that may contribute to further alkalosis in the setting of hypochloremia.
Defects in Acidifi cation
A close examination of the urine can provide additional information useful in the assessment of RTA. Urine electrolytes can be used to calculate the net charge of the urine, which provides an estimate of urinary ammonium excretion.
Treatment of RTA
A simple assessment of glomerular filtration rate in full-term infants during the first year of life. Use of plasma creatinine concentration to estimate glomerular filtration rate in infants, children and adolescents.
Physiology of Skeletal Muscle
NEUROMUSCULAR JUNCTION
The Presynaptic Nerve Terminal
Opening of voltage-gated and Ca 2+ -activated K + channels likely limits the duration of nerve terminal depolarization. Acetylcholine molecules are first hydrolyzed to choline and acetylmonocholine, and finally, to choline and acetate.
The Acetylcholine Receptor
Acetylcholine molecules that do not bind to post-synaptic receptors, and those that diffuse away, are rapidly hydrolyzed by acetylcholinesterase.
Muscle Action Potential and Electromechanical Coupling
NEUROMUSCULAR FUNCTION IN THE NEWBORN
In addition, they also exhibit variable responses to muscle relaxants due to differences between the child and adult in terms of neuromuscular junction, volume of drug distribution, and fiber type distribution.
INHIBITION AT THE NEUROMUSCULAR JUNCTION
Non-depolarizing Neuromuscular Blockers
Depolarizing Neuromuscular Blockers
Other Non-competitive Inhibition of the Neuromuscular Junction
In the closed position, drugs block the opening of the channel and prevent the flow of ions, so that these do not reach the end plate and depolarization does not occur. In both forms, the normal flow of ions through the receptor channel is impeded, endplate depolarization is prevented, and neuromuscular transmission is blunted or blocked.
SENSITIVITY TO NEUROMUSCULAR BLOCKADE
These conformational changes may be due to binding of moieties or a change in the environment of the receptor. This inhibition of ion current may occur at the level of the acetylcholine receptor when doses of these drugs are used clinically.
NEUROMUSCULAR MONITORING USING PERIPHERAL NERVE STIMULATION
The set of four ratio refers to the amplitude of the fourth twitch (T4) compared to the amplitude of the first twitch (T1). The subjective determination of the ratio of the set of four is unreliable and requires objective measurement using techniques such as e.g.
ABNORMALITIES OF SKELETAL MUSCLE AND THE NEUROMUSCULAR JUNCTION
Which of the following series of four responses is most indicative of a patient without residual neuromuscular blockade. A decrease in muscle contraction that is only observed at the height of the fourth response (T4).
EXAMINATION
Consciousness
The scoring system was derived for adult patients with traumatic brain injury and has some population-based prognostic value for that group. Recent evidence suggests that the motor component of the GCS is as reliable a predictor of outcome as the full GCS score.
B rainstem
Drowsiness: The patient is drowsy but awakens to an alert state and sensorium is intact. Although the GCS is easily defined and widely understood in describing patients with traumatic coma, it does not have validated prognostic implications for non-traumatic coma.
Cranial Nerve Exam
GCS was first described in adult patients but has been modified for use in infants and children. Patients with head injury who have a GCS of 8 or less are categorized as having a severe brain injury and have a worse prognosis than those with a GCS of 9–13 (moderate head injury).
