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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Foreword
- •Contents of Volume I
- •Contents of Volume II
- •Contributors
- •1.1 Introduction
- •1.4.3 Acute Stroke
- •1.4.4 CNS Infection
- •1.4.1 Sepsis
- •1.4.2 Acute Encephalopathy
- •1.4.5 Severe Community-Acquired Pneumonia
- •1.4.6 Nosocomial Pneumonia
- •1.4.7 Pulmonary Edema
- •1.4.8 Fever
- •References
- •2.1 Introduction
- •2.4 ECG Nomenclature
- •2.4.1 P Wave
- •2.4.2 PR Interval
- •2.4.3 QRS Complex
- •2.4.4 J Point
- •2.4.5 ST Segment
- •2.4.6 T Wave
- •2.4.7 QT Interval
- •2.4.8 U Wave
- •2.4.9 RR Interval
- •2.5.1 P Wave
- •2.5.1.1 Atrial Arrhythmias
- •Atrial Fibrillation
- •Atrial Flutter
- •Atrial Tachycardia
- •Multifocal Atrial Tachycardia
- •2.5.1.2 Interatrial Blocks
- •Intermittent Interatrial Block (I-IAB)
- •Advanced Interatrial Block (A-IAB)
- •2.5.2 P-QRS Ratio
- •2.5.2.1 Shortened P-QRS Ratio
- •Wolff-Parkinson-White Syndrome (WPW)
- •Junctional Rhythm
- •Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
- •2.5.2.3 Prolonged P-QRS Ratio
- •2.5.3 PR Interval
- •2.5.3.1 Shortened PR Interval
- •2.5.3.2 Prolonged PR Interval
- •2.5.3.3 Second-Degree AV Block
- •Advanced AV Block
- •Third-Degree AV Block (Complete Heart Block)
- •2.5.4 PR Segment
- •2.5.4.1 PR-Segment Elevation
- •2.5.4.2 PR-Segment Depression
- •Acute Pericarditis
- •Acute Myocardial Ischemia
- •2.5.5 Q Waves
- •2.5.6 QRS Complex
- •2.5.6.1 Heart Rate
- •2.5.7 QT Interval
- •2.5.8 ST Segment
- •2.5.8.1 ST-Segment Depression
- •2.5.8.2 ST-Segment Elevation
- •2.5.9 T Waves
- •2.5.9.1 Inverted T Wave
- •2.5.9.2 Flattened T Wave
- •2.5.9.3 Peaked T Wave
- •References
- •Further Reading
- •3.1 Introduction
- •3.2.2 Nasogastric Tube
- •3.2.3 Central Venous Catheters
- •3.2.4 Cardiac Devices
- •3.2.5 Arterial Catheters
- •3.3 Cardiopulmonary Abnormalities
- •3.3.1 Pulmonary Edema
- •3.3.2 Acute Respiratory Distress Syndrome
- •3.3.3 Atelectasis
- •3.3.4 Aspiration
- •3.3.5 Pneumonia
- •References
- •4.1 Introduction
- •4.5 Modes of Mechanical Ventilation
- •4.5.1 Volume Control Ventilation
- •4.5.2 Pressure Control Ventilation
- •4.5.3 Pressure Support Ventilation
- •4.6 Patient-Ventilator Interactions
- •4.6.1 Trigger Dyssynchrony
- •4.6.2 Flow Dyssynchrony
- •4.6.3 Cycle Dyssynchrony
- •4.9.1 Acute Respiratory Distress Syndrome
- •4.9.2 Severe Asthma Exacerbation
- •4.11 Summary
- •5.10 Neuromuscular Blockade
- •References
- •5.1 Introduction
- •5.3 Pathobiology
- •5.4 ARDS Phenotypes
- •5.5 Lung-Protective Ventilation
- •5.6 Positive End-Expiratory Pressure
- •5.7 Conservative Fluid Management
- •5.8 Moderate-to-Severe ARDS
- •5.9 Prone Positioning
- •5.11 Corticosteroids
- •5.12 Inhaled Pulmonary Vasodilators
- •5.13 Veno-Venous Extracorporeal Membrane Oxygenation
- •5.14 Survivorship
- •References
- •6.1 Introduction/Epidemiology
- •6.2 Physiology
- •6.2.2 Physiology During COPD Exacerbation
- •6.4 Pharmacologic Treatment
- •6.4.1 Bronchodilators
- •6.4.1.1 Mechanism
- •6.4.2 Glucocorticoid Therapy
- •6.4.2.1 Mechanism
- •6.4.2.4 Duration
- •6.4.3 Antimicrobials
- •6.4.3.1 Antibiotic Patient Selection
- •6.4.4.1 Nonpharmacologic Interventions
- •6.4.4.2 Opioids
- •6.4.4.3 Benzodiazepines
- •6.4.4.4 Dexmedetomidine
- •6.4.4.5 Ketamine
- •6.4.5 Adjunctive Therapies
- •6.4.5.1 Magnesium
- •6.4.5.3 Vitamin D
- •6.4.5.4 Venous Thromboembolism Prophylaxis
- •6.4.5.5 Smoking Cessation
- •6.4.5.6 Bowel Regimen
- •6.4.5.7 Mucolytics
- •6.4.5.8 Nutrition
- •6.4.5.9 Post-Discharge Adjuncts
- •6.5 ICU-Level Interventions
- •6.5.1 Noninvasive Positive-Pressure Ventilation
- •6.5.2 High-Flow Nasal Canula
- •6.5.3 Invasive Mechanical Ventilation
- •6.6 Conclusion
- •References
- •7.1 Introduction
- •7.1.1 What Is Asthma?
- •7.2 Diagnosis
- •7.2.1 Physical Examination
- •7.2.2 Laboratory Data
- •7.2.3 Radiographic Findings
- •7.3.1 Standard-of-Care Therapy
- •7.3.3 Potential Adjunctive Therapies
- •7.3.3.1 Inhaled Corticosteroids (ICSs)
- •7.3.3.4 Intravenous (IV) Aminophylline
- •7.3.3.5 Intravenous (IV) Beta2-Agonists
- •7.3.3.6 Leukotriene Antagonists (LTRAs)
- •7.3.3.7 Intramuscular (IM) or IV Epinephrine
- •7.3.3.8 Inhaled Anesthetics
- •7.3.3.9 Inhaled Helium-Oxygen (Heliox)
- •7.3.3.10 Intravenous Ketamine
- •7.3.4.1 Subcutaneous (SC) Biologics
- •7.4.1 Noninvasive Ventilation (NIV)
- •7.4.2 Invasive Mechanical Ventilation (IMV)
- •7.6.1 Outpatient Follow-Up
- •7.7 Summary
- •References
- •8.1 Introduction
- •8.1.3.2 Anatomic Location
- •8.1.3.3 Chronicity
- •8.1.4 Clinical Presentation
- •8.1.4.1 Symptoms
- •8.1.4.2 Physician Examination
- •8.1.4.3 Cardiopulmonary Compromise
- •8.2.1.1 Clinical Pretest/Scores
- •8.2.1.2 D-Dimer-Level Interpretations
- •8.2.2 Computed Tomography Pulmonary Angiography (CTPA)
- •8.2.3 Mortality Risk Assessment
- •8.2.3.1 PE Severity Index Score
- •8.2.3.2 Prognostic Indicators
- •8.3.2 High-Risk PE
- •8.4 Systemic Thrombolytic Therapy
- •8.4.1.1 High-Risk PE
- •8.4.1.2 Intermediate-Risk PE
- •8.4.1.3 Cardiac Arrest
- •8.5.2 Percutaneous Mechanical Interventions
- •8.5.2.2 Catheter-Directed Thrombolysis
- •8.5.3 Surgical Embolectomy
- •8.5.4 Mechanical Circulatory Support
- •8.6.1 PE Response Team (PERT)
- •8.6.3.1 Renal Dysfunction
- •8.6.3.4 Cancer
- •8.6.3.5 Treatment Failure
- •8.7 Conclusion
- •References
- •9.1.2 ECMO Outcomes
- •9.2 ECMO During Cardiopulmonary Resuscitation (eCPR)
- •9.2.1 Extracorporeal Carbon Dioxide Removal
- •9.3 ECMO Management
- •9.3.3 Fluid Management
- •9.4.1 Coagulation Changes
- •9.4.2 Transfusion Thresholds
- •9.4.3.1 Heparin
- •9.4.3.2 Direct Thrombin Inhibitors
- •9.4.4 Monitoring Anticoagulation
- •9.6.2.1 Opioids
- •9.6.2.2 Ketamine
- •9.6.2.3 Propofol
- •9.6.2.4 Benzodiazepines
- •9.6.2.5 Dexmedetomidine
- •9.7.1 Aminoglycosides
- •9.7.2 Beta-Lactams
- •9.7.4 Antifungals
- •9.9 Other Complications
- •9.9.1 Bleeding
- •9.9.2 Thrombosis
- •9.9.3 Neurologic
- •9.10 Conclusion
- •References
- •10.1 Type 1–5 Myocardial Infarctions
- •10.2 Acute Coronary Syndrome (Type 1 MI)
- •10.3 Clinical Presentation/Evaluation
- •10.4 Non-pharmacologic Therapy
- •10.5 Pharmacologic Therapy
- •10.5.1 Fibrinolytics
- •10.5.2 Anticoagulants
- •10.5.2.1 Heparins
- •10.5.2.2 Direct Thrombin Inhibitors
- •10.5.3 Antiplatelets
- •10.5.3.1 Aspirin
- •10.5.3.2 P2Y12 Inhibitors
- •Clopidogrel
- •Prasugrel
- •Ticagrelor
- •10.5.3.3 Glycoprotein IIb/IIIa Receptor Inhibitors
- •10.5.3.4 Cangrelor
- •10.7 Long-Term Management
- •10.7.1 High Bleed Risk (HBR)
- •10.7.2 Statins
- •10.7.3 Beta-Blockers
- •10.7.5 Mineralocorticoid Receptor Antagonists
- •References
- •11.1 Introduction
- •11.2.2 What is Ejection Fraction?
- •11.4 Understanding Blood Pressure
- •11.5 Preload vs. Afterload
- •11.6 Acute Decompensated Heart Failure
- •11.6.2 Etiology
- •11.8 Treating Volume Overload
- •11.8.1 Loop Diuretics
- •11.9 Intravenous Vasodilators
- •11.10 Cardiogenic Shock
- •11.10.1 Inotrope Clinical Pearl
- •11.12 Digoxin
- •11.12.3 Loading Dose
- •11.12.4 Maintenance Dosing
- •11.12.5 Monitoring
- •11.12.7 Distribution
- •11.12.8 Drug-Drug Interactions
- •11.12.9 Digoxin Toxicity
- •11.13 ADHF Clinical Pearls
- •11.13.3 Avoid Phenylephrine
- •11.13.4 Use Mean Arterial Pressure (MAP)
- •11.14 Guideline-Directed Medical Therapy
- •11.15 Venous Thromboembolism (VTE) Prophylaxis
- •11.16 Conclusion
- •References
- •12.1 Introduction
- •12.3 Diagnostic Findings
- •12.4.1 Oxygen Therapy
- •12.4.2 Pharmacological Management
- •12.4.3 Mechanical Circulatory Support (MCS)
- •12.5 Pulmonary Hypertension
- •12.6 The Pharmacist’s Role
- •12.7 Conclusion
- •References
- •13.1 Introduction
- •13.2 Atrial Arrhythmias
- •13.2.2 Atrioventricular Blocks
- •13.2.3 Atrial Fibrillation
- •13.2.3.2 Anticoagulation
- •13.2.3.3 Rate vs. Rhythm Control
- •13.2.4 Atrial Flutter
- •13.2.5 Supraventricular Tachycardia (SVT)
- •13.3 Ventricular Arrhythmias
- •13.3.1 Premature Ventricular Complexes
- •13.3.2 Ventricular Tachycardia
- •13.3.2.1 Torsades de Pointes
- •13.3.3 Ventricular Fibrillation
- •13.3.4 Ventricular Arrhythmia Treatment Strategies
- •13.3.4.1 ICD Implantation
- •13.3.4.2 Pharmacologic Treatments
- •13.3.4.3 Catheter Ablation
- •13.4 Conclusion
- •References
- •14.1 Introduction
- •14.3.2 Laboratory Assessment
- •14.3.3 Imaging
- •14.3.4 Invasive Hemodynamic Monitoring
- •14.4.1 Distributive
- •14.4.2 Cardiogenic
- •14.4.3 Hypovolemic
- •14.4.4 Obstructive
- •14.5 Management
- •14.6 Conclusion
- •References
- •15.1 Background
- •15.2 Diagnosis
- •15.3 Management
- •References
- •16.1 Introduction
- •16.3 Hemodynamics
- •16.5 Pharmacological Management
- •16.5.1 Hyperosmolar Therapy
- •16.5.3 Barbiturate Coma
- •16.6 Nonpharmacological Treatments
- •16.6.2 Temperature Management
- •16.6.3 Prophylactic Hypothermia
- •16.7 Adjunct Therapies
- •16.7.2 Venous Thromboembolism (VTE) Prophylaxis
- •16.7.3 Antibiotic Prophylaxis
- •16.7.4 Stress Ulcer Prophylaxis (SUP)
- •16.7.5 Tranexamic Acid
- •16.7.6 Glucose Targets
- •16.7.7 Steroids
- •16.8 Complications
- •16.8.1 Paroxysmal Sympathetic Hyperactivity
- •16.8.3 Central Fever
- •16.8.4.1 Diabetes Insipidus
- •16.8.4.3 Cerebral Salt Wasting Syndrome
- •16.9 Conclusion
- •References
- •17.1 Introductory Case
- •17.2 Introduction
- •17.4 Pathophysiology
- •17.5 Acute Therapies
- •17.5.1 Thrombolytic Therapy
- •17.5.2 Thrombectomy
- •17.5.3 Blood Pressure Management
- •17.5.4 Acute Anticoagulation
- •17.5.5 Antiplatelet Therapy
- •17.6 Early Complications
- •17.6.1 Hemorrhagic Conversion
- •17.6.2 Angioedema
- •17.6.3 Malignant Cerebral Edema
- •17.7 Secondary Prevention
- •References
- •18.1 Introduction
- •18.4 Therapeutic Drug Monitoring
- •18.5 Adverse Drug Effects
- •18.7 Anti-seizure Medications
- •18.7.1 Available Parenteral Preparations
- •18.7.1.1 Benzodiazepines: GABAA Receptor Activation
- •18.7.1.2 Other GABAergic Therapies
- •Barbiturates: GABAergic
- •Phenobarbital
- •Pentobarbital Infusion
- •Propofol Infusion: GABAergic
- •18.7.1.3 Second-Line Non-anesthetic ASMs
- •Levetiracetam: Synaptic Vesicle Protein 2A Binding

Right Ventricular Failure andPulmonary Hypertension intheICU
12
323
12.5.1 Classication ofPulmonary Hypertension
The World Health Organization (WHO) classies pulmonary hypertension under
ve different clinical subgroups (Table12.3) based on the underlying pathophysiology, clinical presentation, and hemodynamics. Understanding the different classications of PH is imperative as it will guide the course of treatment. Group 1 PH is
known as pulmonary arterial hypertension (PAH). PAH is the most aggressive form
of PH with the most targeted pharmacologic therapies to slow its progression. The
World Symposium on Pulmonary Hypertension proposed that the following medications and toxins have denitive association with PAH: anorexigens (e.g., aminorex, dexfenuramine, fenuramine), benuorex, dasatinib, methamphetamines,
Table 12.3 Clinical classication of pulmonary hypertension
Group Subclassications
1 Pulmonary arterial
hypertension (PAH)
2 PH associated with
left heart disease
3 PH associated with
lung diseases and/or
hypoxia
4 PH associated with
pulmonary artery
obstructions
5 PH with unclear and/
or multifactorial
mechanisms
• Idiopathic
• Heritable
• Associated with drugs and toxins
•
Associated with connecti
portal hypertension, congenital heart disease,
schistosomiasis
• PAH with features of venous/capillary (PVOD/PCH)
involvement
• Persistent PH of the newborn
• Heart failure with preserved ejection fraction
• Heart failure with reduced or mildly reduced ejection
fraction
• Valvular heart disease
•
Congenital/acquired cardio
postcapillary PH
• Obstructive lung disease or emphysema
• Restrictive lung disease
• Lung disease with mix
• Hypo
• Hypoxia without lung disease (e.g., high altitude)
• Developmental lung disorders
• Chronic thromboembolic PH
• Other pulmonary artery obstructions (sarcomas, malignant
•
•
• Metabolic disorders (glycogen storage disease, Gaucher
• Chronic renal f
• Pulmonary tumor thrombotic microangiopathy
• Fibrosing
ventilation syndromes
and nonmalignant tumors, arteritis without connective tissue
disease, congenital pulmonary arterial stenosis, hydatidosis)
Hematological disorders (inherited and acquired chronic
hemolytic anemia, chronic myeloproliferative disorders)
Systemic disorders (sarcoidosis, pulmonary Langerhans cell
histioc
ytosis, neurobromatosis)
disease)
ailure with or without hemodialysis
mediastinitis
ve tissue disease, HIV infection,
vascular conditions leading to
ed restrictive/obstructive pattern

324
A. S. Jutba
and toxic rapeseed oil. Certain genetic mutations may also predispose a patient to
develop PAH. Bone morphogenetic protein receptor 2 (BMPR2) mutations have
been identied in approximately 75% of patients with familial PAH. Other rare
mutations include activin-like receptor kinase 1 (ALK-1), endoglin (ENG), and
mothers against decapentaplegic homolog 9 (SMAD9). The pathophysiology of
PAH involves narrowing of the pulmonary arteries caused by an imbalance of prostacyclin, nitric oxide (NO), and endothelin 1 (ET1).
Group 2 PH is associated with left heart disease. Patients in this group typically
have concomitant heart failure with preserved or reduced ejection fraction.
Abnormalities on the left side of the heart increase PCWP to >15mmHg and cause
passive backow of lling pressures on the right side, thereby increasing
mPAP. Group 3 PH is associated with lung diseases and/or hypoxia. Lung diseases
associated with this group include COPD, interstitial lung diseases, and developmental lung diseases. Hypoxia releases molecules such as endothelin that lead to
smooth muscle cell vasospasm, proliferation, and vasoconstriction. Other pathophysiologic changes are arteriolar neo-muscularization, intimal thickening, and
adventitial collagen deposition. These changes will eventually obliterate the pulmonary vasculature.
Group 4 PH is associated with pulmonary artery obstructions. Pulmonary emboli
and prolonged obstruction of the pulmonary arteries will increase mPAP over time.
These patients may have underlying hematological disorders contributing to their
hypercoagulable state. Lastly, group 5 captures PH secondary to unclear causes or
multifactorial mechanisms. Sickle cell disease (SCD) in particular is a hallmark
disorder associated with group 5 PH. SCD patients have a component of group 2 PH
with left ventricular dysfunction but also characteristics of group 4 due to vasculopathy from intravascular hemolysis.
The severity of disease and its impact on a patient’s daily activities are classied
based on the WHO functional status, which was modeled after the NewYork Heart
Association functional class (Table12.4). WHO functional class is one of the strongest predictors of survival. A patient’s worsening functional status is an indicator of
disease progression [15].
12.6 The Pharmacist’s Role
Pharmacists are key healthcare team members in the ICU with pulmonary hypertension management. Pulmonary hypertension medications are highly specialized. The
pharmacist must be well versed in knowing which medications are indicated for a
specic WHO group and which have been studied as combination therapies.
Responsibilities of the pharmacist include regulatory compliance, medication safety,
medication reconciliation, transitions of care, and side effect management [20].
Endothelin receptor antagonists and soluble guanylate cyclase stimulators are
highly teratogenic. All prescribers and patients must be enrolled in a Risk Evaluation
and Mitigation Strategy (REMS) program to prescribe and receive the medication,

12 Right Ventricular Failure andPulmonary Hypertension intheICU
Table 12.4 WHO functional status classication
Class Description
I Patients with PH but without resulting limitation of physical activity. Ordinary physical
activity does not cause undue dyspnea or fatigue, chest pain, or near syncope
II Patients with PH resulting in slight limitation of physical activity. They are comfortable
at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near
syncope
III Patients with PH resulting in marked limitation of physical activity. They are comfortable
at rest. Less than ordinary activity causes undue dyspnea or fatigue, chest pain, or near
syncope
IV Patients with PH with an inability to carry out any physical activity without symptoms.
These patients manifest signs of right heart failure. Dyspnea and/or fatigue may even be
present at rest. Discomfort is increased by any physical activity
325
respectively. Female patients of childbearing potential are required to be on contraception and take monthly pregnancy tests. Bosentan carries a risk of hepatic impairment; therefore, liver function tests are required at baseline and monthly while a
patient is on therapy. Pharmacists are instrumental in ensuring safety and regulatory
compliance with the REMS programs when dispensing these medications.
Furthermore, these medications are only available through certain outpatient specialty pharmacies to also maintain a limited dispensing process. In the inpatient
setting, it is crucial that the pharmacy department has outlined protocols for initiation and continuation of these therapies.
Parenteral prostacyclin analogs are recognized by the Institute for Safe Medication
Practices as a high-alert medication. There have been multiple documented medication errors surrounding these therapies. Examples of errors included unintentional
bolus administration from ushing the line, incorrect dose calculations, and pumprelated errors. Pharmacists can be instrumental in ensuring safe administration of
the prostacyclin analogs. First, pharmacists can contact the patient’s specialty pharmacy to conrm the patient’s dosing weight and dose. Next, pharmacists can double-check the calculations of IV bags and conrm the correct concentration.
Pharmacists can collaborate with the physician on dose titrations, which are dependent on the patient’s tolerability, and minimize adverse effects. The vasodilatory
effects of prostacyclin analogs may lead to ushing, headaches, nasal congestion,
nausea, and diarrhea [21]. Lastly, pharmacists can implement policies outlining the
entire medication distribution process within the hospital. They can create standardized order sets to prevent medication errors, restrict inpatient administration to units
with trained staff, and develop protocols for line exchanges and blood culture draws.
12.7 Conclusion
Acute RV failure is a multifaceted disease state that requires an in-depth understanding of the underlying pathophysiology and disease state for appropriate management. RV failure is commonly encountered in the critically ill population and is

326
A. S. Jutba
associated with poor prognosis if left untreated. Pulmonary hypertension is one of
many disease states that can progress to RV failure. Treatment of RV failure involves
preload optimization, afterload reduction, and cardiac contractility augmentation.
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Bulifon S, Montani D.Upfront triple combination therapy in pulmonary arterial hypertension:
a pilot study. Eur Respir J. 2014;43(6):1691–7.
19. Makdisi G, Wang IW.Extra corporeal membrane oxygenation (ECMO) review of a lifesaving
technology. J Thorac Dis. 2015;7(7):E166.
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hypertension and the pharmacist’s role. J Pharm Pract. 2016;29(1):67–76.
21.
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327

Chapter 13
Cardiac Arrhythmias
GwangYeeJ.Hu andCavanO’Kane
13.1 Introduction
Cardiac arrhythmias are dened as abnormal rhythms of the heart. The overall estimated prevalence is between 1.5% and 5% of the general population and is associated with signicant morbidity and mortality [1]. There are a wide range of
classications and presentations, but these arrhythmias are generally categorized
based on their origin (atrial vs. ventricular), conduction rate (tachycardia vs. bradycardia), and/or QRS complex width (narrow vs. wide). Diagnosis is determined and
conrmed by the readings on an electrocardiogram (ECG). In a normal conduction
pathway, an electrical impulse is rst triggered by the sinoatrial (SA) node and travels to the atrioventricular (AV) node, where it then passes through the bundle of His,
the left and right bundle branches of the heart, and nally the Purkinje bers. A
departure at any point of this electrical pathway is considered an arrhythmia and
may require medical or surgical treatment. This chapter is broken down into the
various atrial and ventricular arrhythmias and their respective management.
G. J. Hu (*)
Ernest Mario School of Pharmacy, Rutgers, the State University of New Jersey,
Piscataway, NJ, USA
Robert Wood Johnson University Somerset, Somerville, NJ, USA
e-mail: jessica.hu@pharmacy.rutgers.edu
C. O’Kane
Ernest Mario School of Pharmacy, Rutgers, the State University of New Jersey,
Piscataway, NJ, USA
Penn Medicine Princeton Medical Center, Plainsboro Township, NJ, USA
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_13
329© The Author(s), under exclusive license to Springer Nature

330
13.2 Atrial Arrhythmias
G. J. Hu and C. O’Kane
13.2.1
Sinus
Bradycardia
Sinus bradycardia is dened as sinus rhythm with a heart rate ≤50–60 beats per
minute (bpm) [2]. Sinus bradycardia may be a result of sinus node dysfunction
(SND), historically referred to as sick sinus syndrome. SND carries a prevalence of
403–666 per million individuals with an incidence of 63 per million per year requiring a permanent pacemaker [3]. One of the major causes of SND is idiopathic
degeneration associated with aging. In older adult patients ≥65years of age, SND
is present in 1 of every 600 individuals [4]. Other intrinsic and extrinsic risk factors
and etiologies for SND are listed in Table13.1 [2].
Signs and symptoms of sinus bradycardia vary from asymptomatic to symptomatic. Symptomatic presentations often include hypotension, fatigue, weakness, dizziness, lightheadedness, syncope, and exercise intolerance [2]. ECG ndings usually
consist of a regular rhythm, rate ≤50bpm, normal QRS duration, and PR interval,
and P-wave is usually visible before each QRS complex (Fig.13.1).
Treatment is only necessary if the patient is symptomatic, as many patients have
a heart rate of less than 60bpm under normal physiological conditions. The patient
should be assessed for any reversible causes of sinus bradycardia, such as drugs.
For patients who recently had a myocardial infarction (MI) or heart failure with
reduced ejection fraction (HFrEF), β-blockers may need to be continued despite
sinus bradycardia for their mortality-lowering effects. For most patients, you can
monitor and observe the patient without intervention. However, if the patient is
Table 13.1 Select intrinsic and extrinsic causes of SND
Intrinsic causes
Idiopathic degenerative disease associated with aging (most common cause)
Myocardial ischemia
Inltrative diseases (e.g., sarcoidosis, amyloidosis)
Collagen vascular diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis,
scleroderma)
Infection (e.g., infecti
Surgical trauma (e.g., valve replacement, heart transplantation)
Extrinsic causes
Drug induced
Examples: β-blocker, non-dihydropyridine calcium channel blockers, amiodarone,
dronedarone, propafenone, ecainide, ivabradine, clonidine, dexmedetomidine, propofol,
cisplatin, uorouracil, paclitaxel, donepezil, citalopram
Neurologic disorders
Autonomic syndromes
Hypothyroidism
Electrolyte abnormalities (e.g., hyper/hypokalemia, hypomagnesemia)
Hypothermia
Hypoxia
Metabolic acidosis
ve endocarditis, Lyme disease, Chagas disease, toxoplasmosis)

13
Cardiac Arrhythmias
Fig. 13.1 Sinus bradycardia
331
persistently bradycardic with hypotension, altered mentation, evidence of shock,
ischemic chest discomfort, and/or acute heart failure, atropine 1mg intravenously
may be considered [2]. Repeat dosing every 3–5min may be performed up to a
maximum dose of 3mg. Atropine is a parasympatholytic drug that enhances AV
nodal conduction and automaticity [5]. The efcacy of atropine for sinus bradycardia is supported by small nonrandomized studies with small populations [5–7].
Atropine was shown to increase heart rate above 60 bpm for most individuals
included in these studies. One study reported that approximately 47% of patients
had a complete or partial response to atropine treatment to achieve a heart rate
≥60bpm and systolic blood pressure ≥90 mmHg [5]. Of note, atropine will not
improve AV block at the bundle of His, and some reports suggest worsened AV
conduction and hemodynamic compromise [2]. Adverse effects of atropine include
dry mouth, blurred vision, urinary retention, and altered mentation. If bradycardia
is unresponsive to atropine, then transcutaneous pacing may be initiated and/or
dopamine 2–10 mcg/kg/min or epinephrine 2–10 mcg/min continuous infusions
titrated to response [2]. In refractory cases, transvenous pacing may be considered.
Goals of therapy include correcting heart rate and preventing further hemodynamic
instability. Monitor heart rate, blood pressure, electrocardiogram, symptoms, and
adverse effects of interventional medications.
13.2.2 Atrioventricular Blocks
The prevalence of atrioventricular blocks is not well characterized. First-degree AV
blocks appear to be more common than second-degree or third-degree AV blocks
[2]. For rst-degree AV block, prevalence has been reported in African American
patients compared with Caucasian patients in most age groups [8]. The etiologies of
AV block are similar to those described for SND (see Table13.1). AV block may be
classied by the degree of blockage (i.e., rst-degree, second-degree, and thirddegree) or anatomically by the site of block (i.e., AV node, within the bundle of His,
or below the bundle of His) [2]. Anatomic determination of block is usually determined by invasive electrophysiology studies but may be clinically important to
guide interventions. For example, AV nodal blocks are typically more responsive to
autonomic manipulation, and blocks occurring within or below the bundle of His
are less likely to respond to atropine therapy [2]. Conduction delays in the AV node

332
Fig. 13.2 First-degree AV block
Fig. 13.3 Second-degree AV block, Mobitz I
G. J. Hu and C. O’Kane
Fig. 13.4 Second-degree AV block, Mobitz II
may be present in all degrees of blocks, while conduction delays within or below the
bundle of His may occur in second-degree and third-degree blocks.
First-degree AV block is dened as sinus rhythm with a PR interval >200milliseconds (ms) (Fig.13.2). First-degree AV block is not a true block but rather delayed
electrical conduction through the AV node [1]. Second-degree AV block is further
classied into Mobitz I (Wenckebach conduction) and Mobitz II [9]. In both classications, the ECG will show group beating as a result of dropped QRS complexes.
Mobitz I block occurs after gradual PR prolongation and Mobitz II does not. The PR
interval lengthens between successive beats due to increasing delayed conduction
through the AV junction until a beat is dropped. At that point, the cycle starts again.
The QRS duration is usually narrow unless there is a preexisting bundle branch
disease (Fig.13.3). In Mobitz II, the impulse either passes through the AV junction
normally or is blocked completely. Beats are intermittently not conducted and QRS
complexes dropped, usually in a repeating cycle of every third (3:1 block) or fourth
(4:1 block) P wave [1]. Additionally, Mobitz II AV blocks are commonly located in
the bundle of His, which results in widening QRS intervals (Fig.13.4).
There are some exceptions when a second-degree AV block cannot be classied
as Mobitz I or Mobitz II.In the event that the ECG demonstrated second-degree AV
block with 2:1 conduction (i.e., two P waves for every QRS complex), then you may

13
Cardiac Arrhythmias
Fig. 13.5 Third AV block
333
have to concede that further categorization is indeterminate since it is impossible to
differentiate between the two classications based on the P:QRS ratio or the lengthening PR intervals. Additionally, in second-degree high-grade AV blocks, ≥2 consecutive P waves at a normal rate are not conducted without complete loss of AV
conduction. High-grade AV block is generally considered to be a block at the level
of the bundle of His and typically treated with pacing. It may be difcult to distinguish between high-grade second-degree AV blocks and third-degree AV blocks.
Third-degree AV block (commonly referred to as “complete heart block”) is
complete AV dissociation (Fig.13.5). Third-degree AV block implies no conduction
at all from atria to ventricles, may be paroxysmal or persistent, and is usually associated with either a junctional or a ventricular escape mechanism. A narrow QRS
rhythm suggests a junctional escape focus usually in the AV node. A wide QRS
rhythm suggests a ventricular escape focus. The location of the block may be in the
AV junction or bilaterally in the bundle of His.
Signs and symptoms of AV blocks vary and depend on the degree of AV block,
the ventricular rate, and the frequency of its occurrence. Symptoms may include
hypotension, fatigue, weakness, dizziness, lightheadedness, syncope, heart failureassociated symptoms, and exercise intolerances [2]. Patients with rst-degree and
second-degree AV blocks may be asymptomatic or symptomatic. Patients with
third-degree AV blocks are almost always symptomatic.
Treatment of AV blocks is similar to sinus bradycardia described previously. In
patients persistently bradycardic with hypotension, altered mentation, evidence of
shock, ischemic chest discomfort, and/or acute heart failure, atropine 1mg intravenously may be considered [2]. Repeat dosing every 3–5min may be performed up
to a maximum dose of 3mg. For patients with second-degree and third-degree AV
blocks with widening QRS intervals, atropine may be avoided as the block is likely
below the level of the AV node, which may hinder the efcacy or increase the risk
for adverse outcomes as described above. β-Agonists such as isoproterenol, dopamine, dobutamine, and epinephrine may be considered in select patients with
second- degree and third-degree AV blocks who carry a low risk for coronary ischemia [2]. β-Agonists exert direct effects to enhance AV node conduction and HisPurkinje conduction. These drugs may also enhance automaticity of secondary
junctional and ventricular pacemakers in third-degree AV block. Adverse effects of
β-agonist therapy include increased risk for ventricular arrhythmias and induction
of coronary ischemia. Isoproterenol may exacerbate hypotension due to its vasodilatory effects [10]. Lastly, aminophylline may be considered for select patients with
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