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G. J. Hu and C. O’Kane
cardiac ablation if they continue to have recurrent sustained monomorphic VT that is refractory to antiarrhythmic therapy, as epicardial ablations were found to be independent predictors for complete short-term success [44, 68]. However, long­term outcomes such as VT-free survival and recurrence were not as prevalent as compared to patients with ischemic cardiomyopathy. Although rare, complications associated with catheter ablation procedures include heart block, thrombosis, new­onset arrhythmias, and even death.

13.4 Conclusion

Early and/or urgent recognition and diagnosis of cardiac arrhythmias are crucial as these may have serious and fatal implications if not treated promptly. Depending on the type of arrhythmia that patients present with, treatments provided will vary. However, the overarching goal remains the same: correct the abnormal rhythm and address any reversible causes. Medication selection is often based on patient­specic factors and may sometimes require hospital admission for therapy initia­tion. A thorough evaluation of patients’ previous interventions can guide appropriate initiation of therapies if they present with persistent or refractory arrhythmias. There is an opportunity for pharmacists to have a signicant impact on arrhythmia man­agement for patients. Pharmacists can aid in obtaining prior medication histories, appropriately recommending and dosing medications, and assessing for drug inter­actions with other concurrent medication use. Especially in emergent situations, pharmacists can advocate for appropriate dosing and timing of medications as well as correct preparations of the medication product. These actions are of tremendous benet to the medical team and ultimately promote patient safety and efcacy.

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G. J. Hu and C. O’Kane
Chapter 14
Shock
LucasR.Goss, AnnetteEsper, andSeemaS.Tekwani

14.1 Introduction

Shock is a life-threatening condition that requires prompt recognition and treat­ment, as it is often the nal common pathway for which illnesses lead to death. Shock is a state in which the supply of oxygen is inadequate to meet the demand for oxygen by the body’s tissues. This results in cellular hypoxia, which subsequently results in cell membrane dysfunction, intracellular edema, leakage of intracellular contents into the extracellular space, and inadequate regulation of intracellular pH.If left untreated, this will result in cell death, organ dysfunction, lactic acidosis, inammatory cascades, and potentially death. Although shock may be reversible, the longer the shock is present, the more the tissue hypoxia and organ dysfunction occur. This may potentially result in irreversible organ dysfunction and ultimately death [14]. This is why identication of shock as well as diagnosing and treating the underlying cause is crucial.
14.2 Pathophysiology ofShock
Shock is a state of global tissue hypoperfusion, leading to an imbalance between oxygen supply to the tissue and its demand. Oxygen delivery depends on the arterial oxygen content of the blood and the cardiac output (Table14.1). The arterial oxygen content is the sum of the oxygen bound to hemoglobin (product of hemoglobin concentration (Hb) and the percentage of hemoglobin saturated with oxygen (sO2)
L. R. Goss · A. Esper · S. S. Tekwani (*) Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Emory University School of Medicine, Atlanta, GA, USA e-mail: seema.tekwani@emory.edu
Switzerland AG 2025 Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_14
359© The Author(s), under exclusive license to Springer Nature
360
Table 14.1 Relevant equations in shock physiology
Delivery of oxygen DO2=CO×{(1.39×Hb×sO2)+(PaO2×0.003)} Fick CO=VO Cardiac output CO=HR×SV MAP CO×SVR
DO
delivery of oxygen, CO cardiac output , Hb hemoglobin, sO2 arterial oxygen saturation, PaO2
2
arterial partial pressure of oxygen; VO tion, CVO cular resistance, MAP mean arterial pressure
central venous oxygen saturation; HR heart rate, SV stroke volume, SVR systemic vas-
2
/1.34(Hb) (10) (CA O2%CV O2%)
2
oxygen consumption, CAO2 central arterial oxygen satura-
2
L. R. Goss et al.
and the amount of dissolved oxygen in the blood (PaO2). Cardiac output is deter­mined by the product of stroke volume (SV) and heart rate (HR). Stroke volume is the amount pumped by the heart with each contraction, which further depends on preload/end-diastolic volume, contractility of the heart, and afterload.
The abnormalities in each of these determinants of oxygen delivery can lead to
several types of shock (Flowchart 14.1).
Irrespective of the etiology of shock, when the delivery of oxygen (DO2) decreases, more oxygen is extracted from the hemoglobin to a point of critical DO2, beyond which the tissue starts producing energy by anaerobic metabolism. In sep­sis, the cells may be unable to utilize oxygen despite normal to supranormal oxygen delivery, thus leading to dysoxia and an anaerobic pathway for adenosine triphos­phate (ATP) production.
When oxygen extraction is increased, this is seen as a drop in the oxygen satura­tion of the venous blood. This is often measured in the blood collected from the superior vena cava via a central venous line and reported as central venous oxygen saturation (ScVO2). Normal ScVO2 is 70–75%, and values <70% are indicative of impaired oxygen delivery and increased extraction. In cases of dysoxia with impaired tissue oxygen utilization, ScVO2 may be >80% and may indicate cell death [5].
When anaerobic metabolism ensues, lactate is produced, leading to lactic acido­sis. However, high lactate is nonspecic, and high lactate may also be seen in cases of ischemia due to vascular causes like gut ischemia and gangrenous limb and in cases of liver and kidney failure and many other causes like seizures, drug overdose, cyanide poisoning, and thiamine deciency [6].
14 Sho ck
361
Heart Rate
output
Cardiac
Stroke
Volume
Determinants of oxygen delivery
blood
oxygen in
Dissolved
Afterload
Contractility
Decreased
Brady
/Tachy
arrhythmias
afterload
Decreased
Decreased
contractility
filling of
the heart
shock
Cardiogenic
shock
Neurogenic
shock
Distributive
Sepsis
Anaphylaxis
shock
Cardiogenic
shock
Obstructive
Arterial
Oxygen
content
O2
Arterial
Saturation
Hemoglobin
Preload
preload
Decreased
shock
Hemorrhagic
body fluid
Hypovolemic
shock / Loss of
Flowchart 14.1 Determinants of oxygen delivery and its abnormalities leading to several types of shock
362
L. R. Goss et al.
14.3 Diagnosis andEvaluation
Shock is a clinical diagnosis, made by incorporating history, physical examination, and laboratory ndings. It is important to note that although these tools are used to diagnose shock, shock is not dened by any single vital sign, physical examination nding, or laboratory value. This understanding is crucial, as if misunderstood, it may result in either more or less aggressive treatment than necessary. As an exam­ple, consider a patient who presents with symptoms of acute decompensated heart failure, blood pressure of 90/70, heart rate of 112, elevated lactic acid, and cool extremities. Although the mean arterial pressure (MAP) is above 65, it would be a mistake to not diagnose this patient with cardiogenic shock, as it may result in delayed, less aggressive, or inappropriate care. So, although shock is not dened by any single vital sign, physical examination nding, or laboratory value, there are common ndings seen in patients with shock.
14.3.1 Vital Signs andPhysical Exam
Vital sign abnormalities are common in patients with shock. Most patients have hypo­tension, tachycardia, and tachypnea. Blood pressure, however, may be normal or rarely elevated, due to sympathetic stimulation. Normotension in a patient that typically has hypertension may be another clinical indication or shock. Tachycardia is commonly present; however, patients on AV nodal blocking medications may not develop tachy­cardia. The metabolic derangements associated with shock as well as bradyarrhyth­mias that are the primary source of shock may cause bradycardia. Patients may have tachypnea related to poor diaphragmatic perfusion, acidosis, pulmonary edema, pneu­monia, or ARDS.As shock progresses and diaphragmatic weakness worsens, patients may have a normal respiratory rate, bradypnea, or frank respiratory failure [7, 8].
Abnormal physical exam ndings in patients with shock are related to inade­quate organ perfusion, cause of shock, and sympathetic stimulation. The occurrence of these ndings is variable, and not all patients may have them. Table14.2 sum­marizes potential physical exam ndings one may see in patients with shock. These ndings may support the diagnosis of shock and help to determine the shock’s cause, but the lack of certain ndings does not rule out shock. It is worth noting that decreased urine output is one of the rst signs of impaired organ perfusion in shock.
Urine output and capillary rell time are used at the bedside as surrogates for organ perfusion. Decreased urine output reects renal hypoperfusion and is used as a nonspecic marker of shock and is used to guide uid resuscitation in the absence of advanced hemodynamic monitoring.
Capillary rell time (CRT) has been used as a sensitive marker of hypovolemia in children and has been recently shown to be useful in adult shock as a prognostic marker and as a guide to resuscitation [9]. Normal CRT is less than 3s, and more than 5s is suggestive of impaired perfusion.
14 Sho ck
Table 14.2 Common physical exam ndings in patients with shock
General Ill appearing
Neuro Altered mental status
Cardiovascular Tachycardia
Respiratory Tachypnea
Renal Oliguria or low urine output
Skin Cool skin and extremities
Pale Weak Restlessness
Agitation Somnolence
Bradycardia Arrhythmias Weak pulse Jugular venous distension
Hypoxemia Poor O
saturation waveform
2
Bradypnea
Anuria or no urine output Dark urine
Warm skin and extremities Diaphoresis Delayed capillary rell
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14.3.2 Laboratory Assessment

Lactic acid is commonly used to evaluate patients for shock and trend for therapy response. The pathophysiology of lactic acidosis in shock is complex and occurs through multiple mechanisms as described above. This includes a shift towards anaerobic metabolism due to ischemia, catecholamine production, and decreased clearance [10]. Unlike in other causes of shock, lactic acidosis in sepsis is mostly due to catecholamine response, impaired cellular metabolism, and microcirculatory dysfunction as opposed to tissue hypoxia [11, 12]. It is also important to note that organ dysfunction in shock is related to elevated lactate due to impaired clearance. This is because lactate clearance is primarily performed by the liver and kidney, which are commonly affected in shock. Lactic acid may be used to aid in diagnosing shock and evaluating response to treatment, particularly in cardiogenic and hemor­rhagic shock [13, 14]. Elevated lactic acid has also been associated with increased mortality in many causes of shock [1517].
Central venous oxygen saturation (ScVO2) is another test used to aid in deter­mining the cause of shock and monitoring response to therapy. Its pathophysiology is described above and is based on the principles of delivery of oxygen (DO2) equa­tion and Fick equation. By measuring a central venous oxygen saturation, one can calculate the cardiac output; however, one may also presume that cardiac output is low if the central venous oxygen saturation is low (<65%). Typically, a low ScVO2