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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

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N. Barker et al.
ACS.Symptoms can include cardiogenic shock, chest pain, and pulmonary edema.
For free wall rupture, patients may also have cardiac arrest and develop cardiac
tamponade [4, 29]. Free wall rupture is managed through urgent surgical repair. Preand perioperative mechanical circulatory support may be needed to reduce left ventricular end diastolic pressure. Management of ventricular septal or papillary muscle
rupture involved a combination of pharmacotherapy to maintain blood pressure and
cardiac output (e.g., vasopressors and inotropes) as well as surgical repair, ideally
7days or more from the event [29, 35, 36]. Mechanical circulatory support may be
required for both complications. It is also recommended to incorporate palliative
care due to the nature and severity of the complications [29, 35].
Heart failure can also develop as a complication of acute coronary syndrome. HF
can be preexisting and can develop at the time of MI, during hospitalization, or following discharge. The risk factors for development of HF include female gender,
hypertension, diabetes, chronic kidney disease, atrial brillation, history of previous
MI, and age greater than 75years. Symptoms of excess uid and resting shortness
of breath are usually present in patients who present with MI and acute onset of
HF. Urgent concomitant management of both ACS and HF is essential to improve
patient outcomes. Intravenous diuretics (furosemide or bumetanide) are utilized for
uid management. Decreased cardiac output and symptoms of cardiogenic shock
are managed with the addition of inotropes (dobutamine and/or milrinone) and
vasopressors (norepinephrine or epinephrine). In some patients, temporary mechanical circulatory support (MCS) with or without respiratory and/or renal replacement
may be required. MCS can include intra-aortic balloon pump (IABP), heart pump,
or extracorporeal membrane oxygenation (ECMO). MCS has not consistently demonstrated consistent reduction in morbidity and mortality and, therefore, should be
evaluated on a case-by-case basis. Patients who have cardiogenic shock in the setting of MI should be managed at a PCI-capable hospital. Once patients who have
ACS and HF are stabilized, pharmacotherapy demonstrating the benet for patients
with HF should be initiated [4, 29, 37].
10.7 Long-Term Management
Long-term pharmacotherapy for stabilization of cardiac disease and prevention of
ACS recurrence and further morbidity and mortality includes DAPT, statins, betablockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor
blockers (ARBs), and mineralocorticoid receptor antagonists.
DAPT with aspirin and P2Y12 inhibitor post-acute coronary syndrome has demonstrated reduced rates of stent restenosis, myocardial infarction, death from cardiovascular causes, or stroke. DAPT-initiated post-acute coronary syndrome should
continue in ideal circumstances for 12 months. Premature discontinuation or

10 Acute Coronary Syndrome (ACS)
283
interruption of DAPT can increase the risk for stent thrombosis and mortality. Stent
thrombosis can result in mortality rates up to 45% [4, 29, 38, 39]. Aspirin should be
continued lifelong in all patients unless otherwise contraindicated.
Ticagrelor and prasugrel are recommended over clopidogrel as the P2Y12 of
choice in DAPT. In the results of the PLATO trial, patients receiving ticagrelor had
a signicant reduction in the combined primary efcacy end point evaluating the
occurrence of myocardial infarction, death from cardiovascular causes, or stroke
without experiencing increased fatal or TIMI major bleeding [40]. In the results of
the TRITON TIMI 38 study, patients undergoing PCI who received prasugrel in
comparison to clopidogrel demonstrated a signicant reduction in the rates of the
primary combined efcacy end point of myocardial infarction, death from cardiovascular causes, or stroke. However, patients receiving prasugrel also experienced
increased rates of fatal and nonfatal TIMI major hemorrhage. Patients demonstrating the greatest benet from prasugrel include patients with diabetes or who had
in-stent thrombosis. Subgroup analysis of TRITON TIMI 38 also dened three
patient groups that would not benet from prasugrel [41]. There is a risk for net
harm when prasugrel is used in patients with a history of stroke (ischemic or hemorrhagic). There is no net benet observed in patients who are 75years of age or
greater or who weigh less than 60kg [42]. Overall, in these three patient groups,
there is an increased risk of bleeding with prasugrel. The updated ESC guidelines
for ACS provide a class I recommendation for ticagrelor or prasugrel (when available and tolerated) over clopidogrel in patients undergoing PCI [4, 29, 38, 39].
For patients who underwent ischemia-guided therapy without intervention, the
aspirin can be combined with either clopidogrel or ticagrelor. TRITON-TIMI did not
include patients who received medical management for acute coronary syndrome
[39]. TRIOLOGY ACS evaluated patients receiving medical management with pra-
sugrel in comparison to clopidogrel in patients with unstable angina or NSTEMI.There
was not a statistically signicant difference in the occurrence of the primary end
point of myocardial infarction, death from cardiovascular causes, or nonfatal stroke
or the safety end point of major bleeding events in patients receiving prasugrel.
Therefore, prasugrel is not recommended as part of DAPT in patients with acute
coronary syndrome receiving medical/ischemia-guided management [4, 29, 38, 39].
DAPT may be stopped at 6months in patients who have stable ischemic heart
disease and elective PCI with stent placement. (Class I ACS) Shorter duration of
DAPT may also be considered in patients who have a lower ischemic risk, and the
risk of morbidity and bleeding with continuation exceeds the benets of therapy. In
patients who have an increased risk for bleeding, proton pump inhibitors can be
considered to reduce risk. While esomeprazole and omeprazole may decrease
response to clopidogrel, there is not enough evident to demonstrate increased risk of
ischemic events [4, 29, 38, 39]. Table10.5 provides details regarding DAPT deescalation following a minimum of 1month of DAPT therapy.

284
Table 10.5 DAPT de-escalation [4]. Adapted from ESC ACS guidelines 2023
Time (months) Abbreviated DAPT options DAPT de-escalation
0 HBR HBR and non-HBR patients Potent P2Y12 DAPT
1 1month 3months 6months P2Y12 inhibitor de-escalation
3
6
9 P2Y12 or ASA monotherapy
12
ASA+ticagrelor or prasugrel
Change to ASA+clopidogrel
N. Barker et al.
10.7.1 High Bleed Risk (HBR)
Pharmacists should counsel patients about the role and benet of taking DAPT and
the potential increased risk for stent thrombosis and mortality with noncompliance
or premature discontinuation.
10.7.2 Statins
Atherosclerotic coronary vascular disease is known to be related to circulating levels of cholesterol; in particular, the most atherogenic form is known to be lowdensity lipoprotein (LDL). High-density lipoprotein (HDL) cholesterol is not
atherogenic and may confer protective benets, and very-low-density lipoprotein
(VLDL) cholesterol is known to be both atherogenic and the primary transporter for
triglycerides. Apolipoprotein B, or apoB, is the main atherogenic component of
both LDL-C and VLDL-C and therefore may be a better measure of atherogenic risk
than cholesterol levels alone. High-intensity or maximally tolerated statin therapy is
recommended for secondary prevention in all patients who have ASCVD. Statins
inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is
the rate-limiting enzyme in cholesterol synthesis. This results in increased expression of LDL receptors on hepatic tissue and breakdown of LDL.Statin therapy is
usually well tolerated but does have a 5–20% occurrence of subjective statinassociated muscle symptoms (SAMSs), which can lead to noncompliance or avoidance of statin therapy. The guidelines recommend considering SAMS as a side
effect rather than an intolerance because patients will oftentimes be able to tolerate
therapy with an alternative statin or dose [4, 43–45].
High-intensity statin therapy includes atorvastatin 40 or 80mg daily or rosuvastatin 20 or 40mg daily. The denition of ASCVD includes patients who have experienced acute coronary syndrome, e.g., STEMI, NSTEMI, unstable or stable angina,
and coronary revascularization, as well as symptomatic peripheral arterial disease
or previous revascularization or amputation, stroke, and transient attack. Lowdensity lipoprotein (LDL) cholesterol is reduced 50% by high-intensity statin therapy. LDL and non-high-density lipoprotein (non-HDL) cholesterol treatment targets

10 Acute Coronary Syndrome (ACS)
Table 10.6 Statin dosing and intensity. Adapted from 2018 Cholesterol Guidelines [43]
Intensity LDL reduction (%) Statins Doses validated in RCT
High ≥50 Atorvastatin
Rosuvastatin
Moderate 30–49 Atorvastatin
Fluvastatin
Lovastatin
Pravastatin
Simvastatin
Rosuvastatin
Low <30 Lovastatin
Pravastatin
40 or 80mg daily
20 or 40mg daily
10mg daily
40mg twice daily
40mg daily
40mg daily
20 or 40mg daily
10mg daily
20mg daily
10 or 20mg daily
285
were removed in the 2013 ACC/AHA cholesterol guideline, as many patients with
ASCVD may still benet from reduction of LDL cholesterol levels by 50% or
greater than baseline levels even when already at prior target levels before therapy
[4, 43–45]. Table10.6 illustrates comparative statin potency and LDL reduction.
In the 2018 ACC/AHA multidisciplinary guideline for management of cholesterol, the addition of non-statin therapy with ezetimibe for LDL cholesterol reduction can be considered for patients who are considered to have a very-high-risk
ASCVD [43]. Very-high-risk ASCVD includes patients with multiple major
ASCVD events or ASCVD in combination with multiple high-risk conditions (e.g.,
diabetes, hypertension, current smoking, persistent LDL elevation of 70mg/dL or
greater despite high-intensity statin therapy) [43, 45]. Ezetimibe inhibits the absorption of cholesterol at the brush border of the small intestine [43–45]. Addition of
ezetimibe to statin therapy further improves cardiovascular outcomes and reduces
LDL cholesterol. Ezetimibe has a low risk for side effects and can lower LDL-C by
15–30% [4, 43–46]. Furthermore, proprotein convertase subtilisin/kexin type 9
(PCSK9) inhibitor therapy could be considered for very-high-risk ASCVD patients
who are already receiving statin therapy at the maximum tolerated dose in combination with ezetimibe and when LDL remains 70mg/dL or greater [4, 43–45]. PCSK9
binds to LDL receptors and promotes degradation within the liver. Circulating LDL
is primarily cleared when bound to the LDLR; therefore, lower levels of LDLR
result in increased levels of LDL-C.There are three agents available in the United
States that reduce PCSK9 activity, which include alirocumab, evolocumab, and
inclisiran. These agents have been observed to reduce LDL-C by 45–70%. Adverse
effects observed are typically mild and include injection-site reactions and nasopharyngitis. These are not usually therapies that are initiated during hospitalization
due to cost and require insurance review and approval to conrm that patients will
be able to obtain and afford them [4, 47].
Statin doses provided in the table were validated in the RCT and 2010 metaanalysis, which demonstrated reduced risk for major cardio
vascular events.
Although higher doses of simvastatin (80mg) were previously studied and demonstrated benet, due to the increased risk for myopathy and rhabdomyolysis, the
FDA does not recommend initiation or titration of simvastatin to 80mg dosing.

286
N. Barker et al.
10.7.3 Beta-Blockers
Long-term pharmacotherapy for acute coronary syndrome aims to decrease the risk
for stent thrombosis, mortality, chest pain, and recurrence of cardiac events. Data
supports the use of beta-blockers in patients who have chronic heart failure with
reduced ejection fraction (HFrEF, LVEF ≤40%); it reduces mortality as well as
cardiovascular events. The benecial effects of beta-blockers do not appear to be
dose dependent in this population. There is less data and experience regarding the
effects of beta-blockers in patients without previous heart failure or acute coronary
syndrome [4, 29, 48, 49]. Side effects associated with beta-blocker therapy are dose
related and include fatigue, bradycardia, and postural hypotension [4, 29, 48].
Cardiovascular death or complications at 30days and 3-year follow-up were not
reduced in retrospective evaluation of 755,215 national registry patients 65years of
age or older with coronary artery disease undergoing elective PCI without a previous history of heart failure or acute coronary syndrome [49]. Reduction in mortality
and cardiovascular events was observed in patients undergoing CABG either with
or without a history of acute coronary syndrome [4, 29, 48–50]. The recommended
duration of beta-blocker therapy is still unclear [4, 50, 51]. There is questionable
benet for the use of beta-blocker therapy for greater than 1year in patients experiencing STEMI or NSTEMI [4, 52–54]. For patients who have left ventricular ejection fraction ≤40%, specic beta-blockers are recommended based upon data
demonstrating reduced mortality and improved cardiac function.
10.7.4 Angiotensin-Converting Enzyme Inhibitors/Angiotensin
Receptor Blockers
Outcomes in post-MI patients who have hypertension, LVEF ≤40%, chronic kidney
disease, or diabetes have also been improved by ACE inhibitors. In particular, initiation of ACE inhibitors post-MI has demonstrated a signicant reduction in mortality
at 30days and ventricular remodeling [4, 12]. Valsartan, losartan, and candesartan
are the ARBs determined to have benet in patients with HF or LVEF ≤40%,
whereas all ACE inhibitors provide similar benet. Although ACE inhibitor or ARB
transition to angiotensin receptor neprilysin inhibitor (ARNI, valsartan/sacubitril) is
recommended through guideline-directed medication therapy for heart failure
patients with LVEF ≤40%, trial data has not supported greater benet in post-MI
patients. A recent trial failed to demonstrate that valsartan/sacubitril reduced the
risk of death from cardiovascular causes or hospitalization due to symptomatic HF
compared to ACE inhibitors. No difference was observed in the ARNI vs. ACE
inhibitor group [55]. As a result, the guidelines recommend ACE inhibitor initiation
in patients post-MI who have LVAD ≤40% over ARNI [4, 29].

10
Acute Coronary Syndrome (ACS)
287
10.7.5 Mineralocorticoid Receptor Antagonists
Mineralocorticoid receptor antagonists (MRAs) block aldosterone binding to receptors in the distal renal tubules. As a result, sodium and water excretion is increased
without loss of potassium and hydrogen ions. In addition, effects on arterial smooth
muscle may also be blocked. Spironolactone administration in combination with
ACE inhibitor early post-myocardial infarction was found to reduce left ventricular
remodeling post-myocardial infarction [4, 12, 56]. There are two MRAs available,
spironolactone and eplerenone. Side effects associated with MRAs include hyperkalemia and impotence. Spironolactone is associated with a 10% risk of gynecomastia, whereas eplerenone is not. For patients who have experienced acute coronary
syndrome and LVEF ≤40%, MRAs reduce collagen formation and remodeling of
the ventricles of the heart [4, 12, 56, 57]. In patients who had experienced recent
ACS and had LVEF ≤40% with heart failure symptoms, eplerenone has demonstrated reduced all-cause and cardiovascular mortality or cardiovascular-related
hospitalizations [57]. Spironolactone or eplerenone is started at 25mg daily and
titrated up to 50mg daily, if tolerated. Eplerenone was further studied evaluating the
safety and efcacy of early treatment in patients with acute MI without previous
heart failure or reduced LVEF.The results demonstrated a reduction in the composite end point for rehospitalization, sustained ventricular arrhythmia, elevated natriuretic peptides, cardiovascular mortality, LVEF ≤40%, or extended hospitalization
due to heart failure diagnosis [58].
The prevalence and consequences of ACS constitute the consideration of a medical emergency. Immediate medical attention is vital to survival and improved outcomes in many cases. While non-pharmacological therapies are the primary form of
management, concomitant pharmacological treatment is vital to preventing disease
progression and improving outcomes. A variety of complications can occur or be
exacerbated in relation to ACS.Management of these complications is often dynamic
depending on the severity of ischemia experienced and preexisting medical conditions. Long-term medication management with goal-directed therapy improves survival and cardiac outcomes. These therapies are often started in the intensive care unit
and should be considered early in management as tolerated by the patient. Timely
recognition, treatment, and secondary prevention are fundamental to patient outcomes.
References
1. Cardiovascular Diseases Fact Sheet. World Health Organization (WHO). June 2021. https://
www.who.int/news- room/fact- sheets/detail/cardiovascular- diseases- (cvds).
Heart
2.
3. Thygesen K, et al. Fourth universal denition of myocardial infarction. Circulation.
Disease and Stroke Statistics 2023 Update. American Heart Association (AHA).
January 2023. https://professional.heart.org/en/science- news/heart- disease- and- stroke- statistics-
2023-
update.
2018;38(20):e618–51.

288
4. Byrne RA, etal. ESC guidelines for the management of acute coronary syndromes. Eur Heart
J. 2023;2023(44):3720–826.
5. Gulati M, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the
evaluation and diagnosis of chest pain: a report of the American College of Cardiology/
American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation.
2021;144(22):e368–454.
6.
7.
8.
9.
10.
11. Kontos MC, Turlington JS.High-sensitivity troponins in cardiovascular disease. Curr Cardiol
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
val Y, etal. Type 1 and 2 myocardial infarction and myocardial injury: clinical transition
Sando
to high-sensitivity cardiac troponin I.Am J Med. 2017;130:1431–9.
farian D, et al. Heart disease and stroke statistics-2016 update: a report from the
Mozaf
American Heart Association. Circulation. 2016;133(4):e38–360.
olesova MV, Minor S.Silent myocardial infarction: a case report. Cureus. 2023;15(8):e43906.
K
Nathanson L
program for students and clinicians. http://ecg.bidmc.harvard.edu
Cai Q, et
tion guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa criteria ready for prime time? Am Heart J. 2013;166(3):409–13.
Rep. 2020;22(5):30.
vine G, et al. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary
Le
intervention for patients with ST-elevation myocardial infarction: an update of the 2011 ACCF/
AHA/SCAI guideline for percutaneous coronary intervention and the 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. JACC. 2016;67(10):1235–50.
Montalescot G, et
N Engl J Med. 2014;371:1016–27.
Meine
nary syndromes: results from the CRUSADE quality improvement initiative. Am Heart
J. 2005;149(6):1043–9.
Bonin M, et
cardial infarction. J Am Heart Assoc. 2018;7(4):e006833.
Jobs
coronary syndrome: a meta-analysis of randomised trials. Lancet. 2017;390:737–46.
Lawton JS, etal. 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: exec-
utive summary: a report of the American College of Cardiology/American Heart Association
Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(3):e4–e17.
Indications for brinolytic therap
tive overview of early mortality and major morbidity results from all randomised trials of
more than 1000 patients. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Lancet.
1994;343(8893):311–22.
vase [prescribing information]. South San Francisco, CA: Genentech, Inc.
Acti
TNKase [prescribing information]. South San Francisco, CA: Genentech, Inc.
Reta
Bivalirudin [prescribing information]. Princeton, NJ: Sandoz, Inc.
Argatroban [prescribing information]. Princeton, NJ: Sandoz, Inc.
Efent [prescribing information]. Indianapolis, IN: Eli Lilly & Compan
vix [prescribing information]. Bridgewater, NJ: Bristol-Meyers Squibb/Sano, Inc.
Pla
Partnership.
Brilinta [prescribing information].
Kangreal [prescribing information]. Cary, NC: Chiesi, Inc.
Sulli
JACC review topic of the week. JACC. 2021;78(15):1550–63.
Byrne RA, et
tary data. Eur Heart J. 2023;2023(00):1–52.
A, McClennen S, Safran C, Goldberger AL.ECG wave-maven: self-assessment
al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarc-
al. Prehospital ticagrelor in ST-segment elevation myocardial infarction.
TJ, et al. Association of intravenous morphine use and outcomes in acute coro-
al. Effect and safety of morphine use in acute anterior ST-segment elevation myo-
A, etal. Optimal timing of an invasive strategy in patients with non-ST-elevation acute
y in suspected acute myocardial infarction: collabora-
vase [prescribing information]. Cary, NC: Chiesi, Inc.
Wilmington, DE: AstraZeneca Pharmaceuticals LP.
van AE, et al. Bridging antiplatelet therapy after percutaneous coronary intervention:
al. ESC guidelines for the management of acute coronary syndromes supplemen-
N. Barker et al.

Acute Coronary Syndrome (ACS)
10
30. Rodevic G, etal. Acute pericarditis after percutaneous coronary intervention: a case report.
Medicina. 2021;57:490.
31. Imazio M, etal. Incidence and prognostic signicance of new onset atrial brillation/utter in
acute pericarditis. Heart. 2015;101:1463–7.
32.
Frampton J, et
2023;96:83–94.
33.
Thomsen
tricular systolic dysfunction according to mode of revascularization: a cardiac arrhythmias and
risk stratication after myocardial infarction (CARSIMA) study. Europace. 2021;23:616–23.
34.
Echt DS, et al. Mortality and morbidity in patients recei
The Cardiac Arrhythmia Suppression Trial. NEJM. 1991;324(12):781-8.
35.
Damluji
2021;144:e16–35.
36.
Mahtta D, Ibrahim M, Elgendy IY
myocardial infarction mechanical complications. Ann Cardiothorac Surg. 2022;11(3):322–4.
37.
Jenca D, et
Fail. 2021;8:222–37.
38.
Smith SC, et
coronary and other atherosclerotic vascular disease: 2011 update. JACC. 2011;58(23):2432–46.
39. Virani SS, etal. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA guideline for the management of
patients with chronic coronary disease: a report of the American Heart Association/American
College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation.
2023;148:e9–e119.
40. Wallentin L, etal. Ticagrelor versus clopidogrel in patients with acute coronary syndromes.
N Engl J Med. 2009;361(11):1045–57.
41. Wiviott SD, etal. Prasugrel versus clopidogrel in patients with acute coronary syndromes.
N Engl J Med. 2007;357(20):2001–15.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
Windecker S, etal. Antithrombotic therapy in patients with atrial brillation and acute coro-
, etal. Prasugrel versus clopidogrel for acute coronary syndromes without revascular-
Roe MT
ization. N Engl J Med. 2012;367:1297–309.
Grundy SM, et
PCNA guideline on the management of blood cholesterol. Circulation. 2019;139:e1082–143.
Stone NJ.
2017;69(22):2707–9.
Smith SC Jr
Pokhrel B,
[Internet]. Treasure Island, FL: StatPearls Publishing; 2024. https://www.ncbi.nlm.nih.gov/
books/NBK448100/.
Cannon CP
Med. 2015;372(25):2387–97.
Collete JP
patients presenting without persistent ST-segment elevation: supplementary data. Eur Heart
J. 2020;00:1–35.
Li C, et
patients with acute coronary syndrome undergoing percutaneous coronary intervention. J Am
Heart Assoc. 2016;5:E004190.
Gibson CM, et
N Engl J Med. 2016;375:2423–34.
nary syndrome treated medically or with percutaneous coronary intervention or undergoing
elective percutaneous coronary intervention: insights from the AUGUSTUS trial. Circulation.
2019;140:1921–32.
al. Arrhythmias after acute myocardial infarction. Yale J Biol Med.
AF, etal. Risk of arrhythmias after myocardial infarction in patients with left ven-
ving encainide, ecainide, or placebo.
AA, et al. Mechanical complications of acute myocardial infarction. Circulation.
. Overview of prevalence, trends, and outcomes of post
al. Heart failure after myocardial infarction: incidence and predictors. ESC Heart
al. AHA/ACCF secondary prevention and risk reduction therapy for patients with
al. AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/
Statins in secondary prevention, intensity matters. J Am Coll Cardiol.
, etal. AHA/ACCF secondary prevention: 2011 update. JACC. 2011;23:2432–46.
Yuet WC, Levine SN.PCSK9 inhibitors. [Updated 2022 May 13]. In: StatPearls
, etal. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J
, etal. 2020 ESC guidelines for the management of acute coronary syndromes in
al. Relationship between b-blocker therapy at discharge and clinical outcomes in
al. Prevention of bleeding in patients with atrial brillation undergoing PCI.
289

290
52. Steg PG, etal. Low-dose vs standard-dose unfractionated heparin for percutaneous coronary
intervention in acute coronary syndromes treated with fondaparinux: the FUTURA/OASIS-8
randomized trial. JAMA. 2010;304:1339–49.
53.
Lopes RD, et
lation. N Engl J Med. 2019;380:1509–24.
54. Dewilde WJ, etal. Uninterrupted oral anticoagulation versus bridging in patients with longterm oral anticoagulation during percutaneous coronary interv
the WOEST trial. EuroIntervention. 2015;11:381–90.
55.
fer MA, etal. Angiotensin receptor-neprilysin inhibition in acute myocardial infarction.
Pfef
N Engl J Med. 2007;357(20):1845–55.
56.
Hayashi M, et
ronolactone prevents post-infarct left ventricular remodeling associated with suppression of a
marker of myocardial collagen synthesis in patients with rst anterior acute myocardial infarction. Circulation. 2003;107:2559–65.
57.
Pitt B, et
function after myocardial infarction. N Eng J Med. 2003;348(14):1309–21. EPHESUS.
58. Montalescot G, etal. Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: the randomized double-blind reminder study. Eur Heart
J. 2014;35:2295–302. REMINDER.
al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial bril-
ention: subgroup analysis from
al. Immediate administration of mineralocorticoid receptor antagonist spi-
al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dys-
N. Barker et al.

Chapter 11
Acute Decompensated Heart Failure
CaitlinE.Kulig
11.1 Introduction
Heart failure (HF) is an extremely common disease state with an overall poor prognosis, despite advancements in guideline-directed medical therapy (GDMT). With
an aging population, the incidence of heart failure continues to grow in the United
States and worldwide. An estimated 6.5million Americans over the age of 20 have
heart failure, with an estimated 960,000 new heart failure cases per year. Heart failure is a progressive disease and, by some estimates, contributes to roughly 36% of
all cardiovascular deaths, with some studies citing that heart failure is mentioned in
one in every eight death certicates [1]. Heart failure hospitalization, due to acute
decompensated heart failure (ADHF), is a sentinel event associated with a worse
prognosis and a negative disease trajectory and remains a huge burden on both
patients and the healthcare system [2]. Heart failure hospitalizations remain the
number one cause of hospitalizations in Medicare patients and the most common
cause of hospitalization in the United States for patients greater than 65years of age
[3]. Heart failure hospitalization has the highest 30-day rehospitalization rate among
all medical and surgical conditions, accounting for up to 26.9% of total readmission
rates. HF costs the US healthcare system nearly 31billion dollars per year, and the
costs are projected to increase by 50billion by 2030 [4].
The landscape of heart failure therapy has changed drastically in the past
30years, with a number of medication classes now found to decrease the incidence
of mortality and morbidity in these patients. However, heart failure hospitalizations
are still extremely common, and the practitioner must be prepared and familiar with
the nuances of management of this specialized patient.
C. E. Kulig (*)
Ernest Mario School of Pharmacy, Rutgers the State University of New Jersey, Piscataway
New Jersey and St. Joseph’s University Medical Center, Paterson, NJ, USA
e-mail: Caitlin.kulig@pharmacy.rutgers.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_11
291© The Author(s), under exclusive license to Springer Nature
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