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C. V. Pollack, Jr. and V. G. Riese
Treatment of acute hypertensive heart failure. The left ventricular (LV) end diastolic pressurevolume relationships (compliance curves) in acute hypertensive heart failure (AHHF) before and after treatment with sodium nitroprusside are rep­resented schematically. In AHHF, the pressurevolume curve is shifted up and to the left, reecting an acute decrease in LV compliance caused by severe systemic hypertension. In this setting, a higher than normal LV enddiastolic pressure (LVEDP) is required to achieve any given level of LV enddiastolic volume (LVEDV). Normal LV systolic function (ejection fraction and cardiac output) is maintained but at the expense of a very high wedge pressure that results in acute pulmonary edema. Treatment with sodium nitroprusside causes a reduction in the elevated systemic vascular resistance, with a concomitant decrease in impedance to LV ejection. As a result, LV compliance improves. Pulmonary edema resolves owing to a reduction in LVEDP, despite the fact that LVEDV actually increases dur­ing treatment. Sodium nitroprusside is the preferred drug for treatment of AHHF. There is no absolute blood pressure goal. The infusion should be titrated until signs and symptoms of pulmonary edema resolve or the blood pressure decreases to hypotensive levels. Rarely is it necessary to lower the blood pressure to this extent, however, because reduction to levels still within the hypertensive range is usually associated with dramatic clinical improvement. Although hemodynamic monitoring is not always required, it is essential in patients in whom concomitant myocardial ischemia or compromised cardiac output is suspected. After the hyper­tensive crisis has been controlled and pulmonary edema has resolved, oral antihy­pertensive therapy can be substituted as the patient is weaned from the nitroprusside
32 Heart Failure
489
infusion. As in the treatment of hypertensive patients with chronic congestive heart failure symptoms owing to isolated diastolic dysfunction, agents such as β‐blockers, angiotensionconverting enzyme inhibitors, or calcium channel blockers may repre­sent logical rstline therapy. These agents directly improve diastolic function in addition to reducing systemic blood pressure. In patients with malignant hyperten­sion or resistant hypertension, however, adequate control of blood pressure may require therapy with more than one drug. Potent directacting vasodilators such as hydralazine or minoxidil may be used in conjunction with a β‐blocker to control reex tachycardia and a diuretic to prevent reex salt and water retention. [Nolan CR. Hypertensive Crises. In: Schrier RW, Wilcox CS. Atlas of Diseases of the Kidney, Volume 3: Hypertension and the Kidney. Philadelphia: Current Medicine Group; 1999. 182 p.] Caption from original
Goals of Treatment in Decompensated Heart Failure
Resolution of dyspnea and orthopnea Systolic blood pressure 80 mm Hg
Resolution of ascites and peripheral edema Right atrial pressure 8 mm Hg
Jugular venous pressure 8 cm H20
Control of hypertension
Minimize adverse effects of treatment, reduce duration and cost of stay
Initiate treatments that improve long-term outcome
Clinical goals Hemodynamic goals
Pulmonary capillary wedge pressure 16
mm Hg
Systemic vascular resistance ≤ 1200
dynes/s/cm-5
Goals of treatment in decompensated heart failure. Goals of in-patient therapy. The early goal of treatment is to improve symptoms while maintaining or improving the hemodynamic status. Progress may be tracked by following body weights and uid intake and output while monitoring vital signs, electrolytes, and renal function. Consideration also should be given to identifying precipitating factors and etiology, and patients who may benet from coronary revascularization. [Givertz MM, Colucci WS.Heart Failure. In: Libby P, editor. Essential Atlas of Cardiovascular Disease. 4th ed. Philadelphia: Current Medicine Group; 2009. 432 p.] Caption adapted from original
490
Drug Dosing Potential Advantage Potential Disadvantages
C. V. Pollack, Jr. and V. G. Riese
Nitroglycerin
Nitroprusside
Nesiritide
Sublingual: 1 tablet (or 1–2 sprays) three or four times at 5­minute intervals; IV:
0.4 μg/kg/min initially
(increase as needed)
IV: 0.1 μg/kg/min initially; increase as needed
0.005–0.01 μg/kg/min initially, ± bolus; increase as needed
Favorable effect on coronary vasculature and in myocardial ischemia/infarction; preload reduction > afterload
Relatively powerful preload and afterload reduction
Preload and afterload reduction; possible facilitative effect on diuresis
Tolerance during prolonged infusion; inadequate afterload reduction in catastrophic cardiovascular disorders (eg, acute valvular insufficiency, ventricular rupture)
Less favorable effects on coronary vasculature and myocardial ischemia; administration must be closely monitored to avoid marked hypotension; thiocyanate or cyanide toxicity during high-dose or prolonged infusions, particularly in patients with renal or hepatic dysfunction
Hypotension; meta-analysis of clinical trials suggests adverse effects on mortality and renal function
Principal preload and afterloadreducing drugs for acute or severe heart failure. Nesiritide, nitroglycerin, and nitroprusside are the primary vasodilators used to reduce excessive preload and afterload in acute or severe heart failure. Nitroglycerin is used most often, particularly in conditions caused by occlusive atherosclerotic coronary artery disease. Nitroprusside is the drug of choice when more aggressive afterload and preload reduction are needed; examples include catastrophic cardio­vascular events (eg, acute, severe mitral, or aortic regurgitation), hypertensive emer­gencies (eg, aortic dissection, pulmonary edema), and inadequate response to nesiritide or nitroglycerin. [Ooi H, Colucci WS.Management of the Hospitalized Patient. In: Colucci WS, editor. Atlas of heart failure, 5th ed. Philadelphia: Current Medicine Group; 2008. 344 p. ISBN: 1-57340-261-3] Caption adapted from
original

Disease Course

• Prognosis depends on type and severity of failure.
• With aggressive medical therapy, ventricular assist devices, and even cardiac transplant, even severe heart disease is no longer a short-term mortality diagnosis.
• Patient compliance with management is an important predictor of both out­comes and quality of life.
32 Heart Failure
491

Related Evidence

Papers of particular interest have been highlighted as: ** Of key importance

Practice Guideline

Moe GW, Ezekowitz JA, O'Meara E, Lepage S, Howlett JG, Fremes S, Al-Hesayen
A, Heckman GA, Abrams H, Ducharme A, Estrella-Holder E, Grzeslo A, Harkness K, Koshman SL, McDonald M, McKelvie R, Rajda M, Rao V, Swiggum E, Virani S, Zieroth S, Arnold JM, Ashton T, D'Astous M, Chan M, De S, Dorian P, Giannetti N, Haddad H, Isaac DL, Kouz S, Leblanc MH, Liu P, Ross HJ, Sussex B, White M; Canadian Cardiovascular Society. The 2014 Canadian Cardiovascular Society Heart Failure Management Guidelines Focus Update: anemia, biomarkers, and recent therapeutic trial implications. Can J Cardiol. 2015 Jan;31(1):3-16. https://doi.org/10.1016/j.cjca.2014.10.022. PMID:
25532421. http://www.ncbi.nlm.nih.gov/pubmed/25532421 **
Dworzynski K, Roberts E, Ludman A, Mant J; Guideline Development Group of the
National Institute for Health and Care Excellence. Diagnosing and managing acute heart failure in adults: summary of NICE guidance. BMJ. 2014 Oct 8;349:g5695. https://doi.org/10.1136/bmj.g5695. PMID: 25296764. http://www.
ncbi.nlm.nih.gov/pubmed/25296764 **
National Clinical Guideline Centre (UK). Acute Heart Failure: Diagnosing and
Managing Acute Heart Failure in Adults. London: National Institute for Health and Care Excellence (UK); 2014 Oct. PMID: 25340219. http://www.ncbi.nlm.
nih.gov/pubmed/25340219 **
Page K, Marwick TH, Lee R, Grenfell R, Abhayaratna WP, Aggarwal A, Briffa TG,
Cameron J, Davidson PM, Driscoll A, Garton-Smith J, Gascard DJ, Hickey A, Korczyk D, Mitchell JA, Sanders R, Spicer D, Stewart S, Wade V; National Heart Foundation of Australia. A systematic approach to chronic heart failure care: a consensus statement. Med J Aust. 2014 Aug 4;201(3):146-50. PMID: 25128948.
http://www.ncbi.nlm.nih.gov/pubmed/25128948 **
Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, Fonarow GC,
Geraci SA, Horwich T, Januzzi JL, Johnson MR, Kasper EK, Levy WC, Masoudi FA, McBride PE, McMurray JJ, Mitchell JE, Peterson PN, Riegel B, Sam F, Stevenson LW, Tang WH, Tsai EJ, Wilkoff BL; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013 Oct 15;128(16):e240-327. https://
doi.org/10.1161/CIR.0b013e31829e8776. PMID: 23741058. http://www.ncbi. nlm.nih.gov/pubmed/23741058
**
492
C. V. Pollack, Jr. and V. G. Riese
White RD, Patel MR, Abbara S, Bluemke DA, Herfkens RJ, Picard M, Shaw LJ,
Silver M, Stillman AE, Udelson J; American College of Radiology; American College of Cardiology Foundation. 2013 ACCF/ACR/ASE/ASNC/SCCT/SCMR appropriate utilization of cardiovascular imaging in heart failure: an executive summary: a joint report of the ACR Appropriateness Criteria ® Committee and the ACCF Appropriate Use Criteria Task Force. J Am Coll Radiol. 2013 Jul;10(7):493- 500.
https://doi.org/10.1016/j.jacr.2013.05.002. PMID: 23827001.
http://www.ncbi.nlm.nih.gov/pubmed/23827001 **

Review

Oktay AA, Shah SJ.Diagnosis and management of heart failure with preserved
ejection fraction: 10 key lessons. Curr Cardiol Rev. 2015;11(1):42-52. PMID:
24251461. http://www.ncbi.nlm.nih.gov/pubmed/24251461 **
Ferrero P, Iacovoni A, D'Elia E, Vaduganathan M, Gavazzi A, Senni M.Prognostic
scores in heart failure- Critical appraisal and practical use. Int J Cardiol. 2015 Mar 26;188:1-9. https://doi.org/10.1016/j.ijcard.2015.03.154. PMID: 25880571.
http://www.ncbi.nlm.nih.gov/pubmed/25880571 **
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy:
“Heart Failure”[Mesh] OR “Heart Failure”
Chapter 33
Hemoptysis
CharlesV.Pollack,Jr., RichardM.Cantor, andVictoriaG.Riese
Name andSynonyms
Hemoptysis

Incidence/Epidemiology

• Hemoptysis is the expectoration of blood from the respiratory tract with cough. Because coughing sometimes leads to vomiting (tussive emesis), it is important to distinguish between hemoptysis and hematemesis.
• Hemoptysis may range in severity from scant blood-streaked mucous that is self- limited to life-threatening airway obstruction from blood clots or dimin­ished gas exchange in blood-lled alveoli.
• Because there are so many varied causes of hemoptysis, epidemiologic data are not meaningful. Smokers and those with chronic lung or sinus disease are more likely to have hemoptysis.
C. V. Pollack,Jr. () Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA
R. M. Cantor Department of Emergency Medicine and Pediatrics, State University of NewYork Upstate Medical University, Syracuse, NY, USA
V. G. Riese Librarian Consultant, Eldersburg, MD, USA
C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_33
493© Springer Nature Switzerland AG 2019
494
C. V. Pollack, Jr. et al.
Denition of hemoptysis. [Bussières JS.Massive hemoptysis. In: Slinger P, editor. Principles and practice of anesthesia for thoracic surgery [Internet]. New York: Springer; 2011 [cited 2015 May 28]. p.485–96. Available from: http://link.springer.
com/10.1007/978-1-4419-0184-2_34] Caption from original

Differential Diagnosis

• The important rst differential issue to address is whether the bleeding is a result of a respiratory or gastrointestinal (GI) cause. The possibility of epi­staxis as a cause should also be evaluated. Beyond that, the differential con­cerns regard the cause of hemoptysis, which generally may be divided into these categories:
• Infectious
• Vascular
• Iatrogenic
• Coagulopathic
• Traumatic
• Neoplastic
• Pulmonary miscellaneous
33 Hemoptysis
495
Causes of hemoptysis. [Subramanian S, Kate AH, Chhajed PN.Role of bronchos­copy in hemoptysis. In: Mehta A, Jain P, editors. Interventional bronchoscopy [Internet]. Totowa, NJ: Humana Press; 2013 [cited 2015 May 28]. p. 245–56. Available from: http://link.springer.com/10.1007/978-1-62703-395-4_14] Caption
from original
Pathophysiology andEtiology
• Hemoptysis may result from several different processes.
• The two most common causes are bronchitis and other lung infections and endobronchial carcinoma with erosion into a bronchial vessel.
• Many patients may never have a denitive cause identied.
• Hemoptysis may result from inammation/infection or from physical injury to a bronchial vessel.
496
• Hemoptysis may also result from the high pulmonary venous pressure that results from severe mitral valve stenosis
• The mnemonic “BATTLE CAMP” may be helpful in remembering common etiologies of hemoptysis:
Causes of hemoptysis—“Battlecamp.” [Hogan MJ.Bronchial artery interventions in children. In: Temple M, Marshalleck FE, editors. Pediatric interventional radiol­ogy [Internet]. NewYork: Springer; 2014 [cited 2015 May 28]. p.71–83. Available from: http://link.springer.com/10.1007/978-1-4419-5856-3_6] Caption from original
C. V. Pollack, Jr. et al.

Presentation

Typical/“Classic”

• Patients who present “coughing up blood” usually are hemodynamically stable (massive hemoptysis that causes shock is a medical emergency).
• Patients may not be able to distinguish among cough with expectoration of blood caused by pulmonary sources, posterior epistaxis, and GI bleeding with hematemesis.
• The amount of blood loss should be quickly assessed, and that will drive the pace of evaluation and management.

Atypical

• “Rusty”-colored sputum may not be recognized as hemoptysis.
33 Hemoptysis

Primary Differential Considerations

• Primary differential considerations for hemoptysis are limited to:
• Epistaxis
• Hematemesis
• To help differentiate, remember that blood from the GI tract likely has
been exposed to the acidic pH of the stomach and will be darker, whereas blood from the respiratory tract tends to be a brighter red, although chronic infection/tumor may result in expectoration of “older” blood that is darker in color.
• Airway foreign bodies
History andPhysical Exam
• Expectoration of even small amounts of blood may provoke signicant anxiety in patients, and their quantication of the amount of blood loss may be exaggerated.
• The rst historical factors to be established include:
497
• Timeframe—how long has hemoptysis been occurring?
• Course—is it getting worse or better?
• Character of hemoptysis—is it blood-streaked sputum or is it frank blood?
• Associated issues—fever and chills? Night sweats? Weight loss? Using an
anticoagulant or antiplatelet drug? Any chronic lung disease?
• Is there pleuritic chest pain with or without dyspnea, suggesting a pulmo-
nary embolism? Are there any signs of deep venous thrombosis?
• Is the patient a smoker?
• On physical examination, the lungs should be auscultated for evidence of bronchospasm, consolidation, or pleural friction.
• Check the heart sounds for a murmur of mitral stenosis.
Mitral stenosis murmur. [Mitral stenosis (diastolic murmur); Easy Auscultation;
www.easyauscultation.com; copyright 2015, MedEdu LLC]
http://www.easyauscultation.com/cases?coursecaseorder=14&courseid=31