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CE Article: Diagnosis and Treatment of the Patient With Heart Failure

Objectives

  • List causes of both systolic heart failure and diastolic heart failure.
  • Describe the pathophysiology of left heart failure and right heart failure.
  • Identify the signs and symptoms of heart failure.
  • Explain the management of the patient in heart failure.

Heart failure (HF) is a common medical problem in the United States. It’s experienced by approximately 5.1 million persons, with more than 650,000 new cases diagnosed annually.13 The incidence of HF increases with age,2 and for Americans over 40 the lifetime risk of developing HF is 20%.4 It occurs most frequently among black men and least frequently in white women.5

HF is the primary diagnosis in more than a million annual U.S. hospital admissions.1 Patients admitted for HF are at risk for rehospitalization, with a one-month all-cause readmission rate of about 24% and a six-month rate greater than 50%.68

There were 60,341 deaths from heart failure in U.S. in 2012, the last year for which data is available.9 Considering that in 2012 cardiovascular disease (the leading cause of death in the U.S. that year) killed 782,985 persons, we can determine that 7.7% of all cardiovascular deaths in 2012 were from HF.9 While survival rates for persons with HF have improved, the absolute mortality rates for HF are approximately 50% within five years of diagnosis.3,10

This month’s EMS World CE article uses three case scenarios to explore the evaluation and prehospital treatment of the patient with HF. These cases explore the clinical context of all the elements of the history and clinical exam to form a “big picture” understanding of the event, and also discuss the appropriate management of the patient with chronic and acute HF in the prehospital setting.

Pathophysiology

Heart failure is the inability of the heart to produce adequate cardiac output to meet the perfusion and oxygenation requirements of the body’s tissues. It is a complex clinical syndrome that can arise from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood, resulting in decreased cardiac output.5 There are two mechanisms by which HF can occur:

  • Systolic dysfunction, the result of impaired cardiac contractile function; or
  • Diastolic dysfunction, the result of abnormal cardiac relaxation, stiffness or filling.

Systolic Heart Failure

In systolic heart failure (SHF), the heart has impaired contractile function, resulting in a decreased stroke volume (SV) and cardiac output (CO) and subsequent low blood pressure. Patients with SHF also have a decreased ejection fraction (EF). The EF is the percentage of blood pumped out of the ventricle with each heartbeat. A healthy adult would be expected to have an ejection fraction between 50%–75%. A patient with an EF less than or equal to 40% is said to have HF.5

A number of factors can lead to impaired myocardial contractile function. Acute myocardial infarction (AMI) can acutely lead to impaired contractility, as infarcted myocardium is significantly weaker than healthy myocardium. After an AMI the scarred, remodeled ventricular myocardium will have less contractile force than healthy myocardium. Dilated cardiomyopathy can result from many etiologies, including chronic hypertension.

Chronically increased blood pressure stretches and dilates the ventricular tissue, making it weaker. Valvular disease and ineffective heart valves can allow the retrograde movement of blood during systole, resulting in decreased SV. In addition, faulty heart valves (such as the aortic and pulmonary semilunar valves) can impede the forward movement of blood, resulting in decreased SV as well as increased intraventricular pressures, which can cause further problems such as cardiomyopathies.11

Diastolic Heart Failure

In diastolic heart failure (DHF), the ventricle wall cannot adequately relax, resulting in inadequate ventricular filling during diastole and a subsequent decrease in SV and CO. The inadequate ventricular filling occurs as a result of a stiffening of the ventricular wall that prevents the normal ventricular relaxation that occurs during diastole. Numerous etiologies can lead to ventricular wall stiffening. Chronic hypertension can result in ventricular hypertrophy as the ventricle is chronically pushing against an elevated systemic blood pressure and increased afterload. In amyloidosis, protein is deposited in the ventricular wall, causing it to stiffen. Patients with DHF do not suffer a marked decrease in their EF.5

EMS Perspectives

These mechanisms are typically not apparent to the prehospital provider managing a patient in the field. From an EMS perspective it makes more practical sense to approach heart failure via the concepts of right-sided HF versus left-sided HF, which are clinically distinctive and apparent to EMS.

Right-Sided Heart Failure

Right-sided heart failure (RSHF) occurs when the right ventricle can no longer maintain adequate CO and effectively move blood forward. This can occur as a result of SHF or DHF mechanisms. As a result, blood and pressure back up into the vena cava. Increased pressures in the superior vena cava carry over to the jugular veins, leading to jugular venous distension (JVD). Increased pressures traveling down the inferior vena cava lead to clinical exam findings such as hepatomegaly, ascites and peripheral (pedal) edema.

Left-Sided Heart Failure

Left-sided heart failure (LSHF) occurs when the left ventricle can no longer maintain adequate CO and effectively move blood forward. As with RSHF, this can occur as a result of SHF or DHF mechanisms. Blood and pressure then back up into the pulmonary circulation, leading to increased capillary pressure, capillary dilation and congestion. Increased capillary pressures result in the leaking of fluid from the capillaries into the surrounding tissues, resulting in fluid buildup (edema). Left untreated, this will lead to pulmonary edema and congestive heart failure. Rales, or crackles, are the hallmark finding associated with LSHF. The pulmonary edema present in LSHF occurs for the same physiologic reasons as the ascites and peripheral edema of RSHF. Left unchecked, left heart failure will lead to right heart failure, as pressure backs up through the pulmonary vasculature and into the right ventricle.

Case #1

It’s 1152 hours. You and your partner are dispatched to a residential address in a retirement community for a patient complaining of weakness. A 66-year-old obese male presents conscious and alert to person, place, time and event; sitting upright on his couch, he complains of dyspnea, dizziness and weakness with exertion. He says he first noticed these symptoms about two weeks ago and that “it seems to be getting slowly worse every day.” Today the patient experienced “the worst weakness I’ve felt yet—I almost passed out” while walking home from a market around the corner. He says his symptoms are “not the same as my COPD when it gets bad,” so he doesn’t think it’s that.

While at rest on his couch, he denies any chest pain, pressure or discomfort. He also denies any difficulty breathing, weakness, dizziness, abdominal or back pain, headache, nausea or vomiting. “It all goes away as long as I’m resting,” he says. His wife, present on the scene, adds that the patient has been tired, which is not normal for him, and has been complaining of abdominal pain over the same period as his symptoms. Hearing this, the patient adds, “Oh, yeah, my belly’s been hurting and getting bigger—it’s been swelling. So have my legs and scrotum, but that’s not what’s bothering me now.”

The patient has a medical history significant for COPD and hypertension, and he is a 102-pack-year smoker. His medications include a Combivent (albuterol/ipratropium) MDI and lisinopril. He has no known drug allergies. Your clinical exam reveals jugular venous distension, bilateral lower 2+ extremity edema from the knees to feet, sacral edema and skin that is warm, pale and dry.

Auscultation of his lungs reveals slight expiratory wheezing in all fields, with good air movement. You note his abdomen is distended and his liver is palpable and large, and he reports pain with palpation. When you press on his liver, his JVD becomes more pronounced. His vital signs are: HR, 72/min. and regular; BP, 152/90 mmHg; RR, 22/min. with good tidal volume; SpO2, 90% on room air; EtCO2, 34 mmHg with a very slight “shark fin” waveform morphology. A 12-lead ECG reveals a sinus rhythm with dominant R-waves in V1 and V2, prominent S-waves in V5 and V6, and increased amplitude of the P-wave in lead II.

What is your best guess as to the etiology of the patient’s dyspnea, weakness and dizziness with exertion? What history and clinical exam findings help you narrow your differential diagnosis? How would you treat this patient?

Discussion

This patient shows the history and clinical exam findings characteristic of right-sided heart failure. It is most likely the result of his COPD, a condition termed cor pulmonale. COPD results in pulmonary hypertension, which causes a resistance to blood flow through the pulmonary capillaries. Pressure then backs up into the right ventricle, resulting in either ventricular hypertrophy or dilation. As the right ventricle becomes affected, pressure further backs up into and dilates the right atrium and eventually backs up into the venous system as well.

There are three manifestations of volume overload in patients with HF: peripheral edema and elevated venous pressures in patients with RHF, and pulmonary congestion in patients with LHF. The patient in Case #1 exhibits these first two manifestations. His JVD and enlarged liver are the result of the elevated venous pressures present when the weakened right ventricle cannot move blood forward. He also exhibits a hepatojugular reflux, visible as a pulsatile wave in the jugular vein when the liver, engorged with blood and pressure, is palpated firmly. In addition, the patient described some upper right quadrant abdominal pain, common with hepatomegaly in RHF. The patient also exhibits peripheral edema. We would not expect to find sacral edema in this patient, as he is normally ambulatory and sacral edema is more common in patients who are bedridden.

The patient’s dyspnea, dizziness and weakness with exertion are characteristic of chronic and worsening RHF. This occurs as a direct result of the inability of the diseased right ventricle to increase cardiac output during periods of high demand. Everyday activities such as walking and working become difficult.

There are many risk factors for heart failure present in this patient’s medical and social history. He has been a heavy lifetime smoker and has COPD, putting him at risk for cor pulmonale. In addition, he is obese and has a history of hypertension.

The 12-lead ECG of a patient with cor pulmonale may exhibit findings suggestive of the disease. These include right bundle branch block, right axis deviation and signs of both right ventricular hypertrophy (RVH) and right atrial enlargement. ECG findings characteristic of RVH include a right axis deviation of 90-plus degrees, dominant R-wave in V1 and V2 (more than 7 mm tall), and prominent S-waves in V5 and V6 (more than 7 mm tall). Evidence of right atrial enlargement includes a greater than 2.5 mm increase in the amplitude of the P-wave in leads II, III and aVF.14,15 Other cardiac rhythms associated with cor pulmonale include wandering atrial pacemaker and multifocal atrial tachycardia.

The prehospital treatment of the patient with right heart failure and cor pulmonale centers on a number of goals:

  • Ensuring airway patency;
  • Ensuring adequate oxygenation and ventilation;
  • Assessing for STEMI and monitoring the cardiac rhythm;
  • Gaining intravenous access;
  • Reducing the pulmonary artery pressure (reducing right ventricular afterload);
  • Improving right ventricular contractility.

Assessment of the airway, supplemental oxygen administration and assisted ventilation via bag-valve mask or CPAP should be routine in all patients with HF when indicated. The 2010 Heart Failure Society of America guidelines state that routine administration of supplemental oxygen in the absence of hypoxia is not recommended.16 Supplemental oxygen administration is recommended if hypoxia is present. Administration of supplemental oxygen will result in a reduction in pulmonary artery pressure, as the correction of hypoxia will reverse any hypoxic vasoconstriction that has occurred.

For patients experiencing hypotension with RHF and cor pulmonale, right ventricular contractility can be increased with the administration of an inotropic agent such as dopamine or dobutamine. Dopamine, at intermediate doses (3–10 mcg/kg/min.), is a beta-1 adrenergic receptor agonist and promotes norepinephrine release. This results in increased cardiac contractility and chronotropy, increased CO and mild increases in systemic vascular resistance (SVR). At higher infusion rates (10–20 mcg/kg/min.), potent vasoconstriction occurs secondary to alpha-1 adrenergic receptor agonism. Dobutamine is a beta-1 and -2 adrenergic receptor agonist with very mild effects, offering the desired increases in inotrophy (alpha and beta effects) without the undesirable increases in SVR (alpha effects). Doses up to 15 mcg/kg/min. increase cardiac contractility without greatly affecting SVR.17

The patient in Case #1 does not require aggressive prehospital management. Arguably, with a history of COPD and SpO2 of 90% on room air, he should not be administered supplemental oxygen because of the dangers involved with giving that to chronic CO2 retainers. Likewise, with a blood pressure of 152/90, he does not require blood pressure support with an inotropic agent. This patient should be placed on the cardiac monitor and have a 12-lead ECG performed. Intravenous access should be obtained and no fluid administration provided. In addition, a breathing treatment with nebulized bronchodilators and/or anticholinergic can be considered, as he has a history of COPD, slight wheezing in all lung fields and presents with a slight “shark fin” waveform on capnography. He should be placed in a position of comfort and monitored en route to an emergency department for evaluation.

Case #2

It’s 0530 hours. You and your partner are dispatched to a residential address for a patient with difficulty breathing. A 56-year-old female presents conscious, alert and oriented to person, place, time and event. She sits upright in a chair in obvious respiratory distress and says, “My breathing is really bad.” You note from the door that she is tripoding, using accessory muscles to breathe and has pale skin.

Her difficulty breathing started at around 1700 yesterday afternoon, and she also reports that she experienced “some pressure in the middle of my chest.” Last night she was unable to sleep lying flat and had to use pillows to prop herself up “so I didn’t feel like I was suffocating.” Eventually she gave up trying to sleep and moved to her living room chair. Her breathing got worse throughout the night and she was unable to get up to use the bathroom this morning, so she called 9-1-1. She tells you, “I can’t breathe when I try to get up and walk, and I feel like I am going to pass out.”

The patient denies any chest pain, dizziness, weakness, nausea or vomiting, syncope, abdominal or back pain. Her past medical history includes hypertension and a myocardial infarction three years ago with stent placement in her left coronary artery. Her medications include ASA, nitroglycerin as needed, Bumex, enalapril and verapamil. She has no known drug allergies. Your clinical exam reveals rales in the middle and upper lung fields, with no air movement to the lung bases bilaterally. Her skin is cool, pale and slightly diaphoretic. JVD is present, but there is no peripheral edema. Her vital signs are: HR, 102/min. and regular; BP, 230/110 mmHg; RR, 26/min. with good tidal volume; SpO2, 84% on room air; EtCO2, 56 mmHg with a normal waveform. A 12-lead ECG reveals sinus tachycardia with ST-segment elevation of 2–3 mm in leads V4, V5 and V6.

What is your best guess as to the etiology of the patient’s dyspnea, weakness and dizziness with exertion? What history and clinical exam findings help you narrow your differential diagnosis? How would you treat this patient?

Discussion

This patient is a classic example of left-sided heart failure secondary to AMI. As such, we can classify her as probably having systolic heart failure, though that will not change our management approach. Recall from Case #1 the three manifestations of volume overload in patients with HF: peripheral edema and elevated venous pressures in patients with RHF, and pulmonary congestion in patients with LHF. This patient exhibits the pulmonary edema characteristic of LVHF. This edema, or congestion, is what gives rise to the term congestive heart failure (CHF). CHF can result from LHF (pulmonary congestion) as well as RHF (hepatic congestion). Her left ventricle, already weakened from a previous MI and now weakened with an evolving AMI, cannot adequately pump blood forward in the cardiovascular system, resulting in a backup of blood and pressure through the left atrium and into the pulmonary circulation. Increased pulmonary capillary pressures force fluid out of the vasculature and into the interstitial spaces and alveoli of the lungs, resulting in pulmonary edema.

The patient exhibits many of the classic signs and symptoms of CHF, including orthopnea (difficulty breathing while lying supine), paroxysmal nocturnal dyspnea (difficulty breathing at night) and sitting in an upright position. Sitting upright allows gravity to pool and consolidate the edema at the bases of the lungs, allowing for optimal (considering the circumstances) ventilation of the alveoli and gas exchange. This patient also presented with JVD on clinical exam but no peripheral or sacral edema. JVD is not an uncommon assessment finding in patients with LHF and pulmonary edema, as the increased pulmonary capillary pressure leads to increased pressure on the right side of the heart as well. JVD occurs rapidly in patients with increased right-sided atrial and ventricular pressures. Pedal and sacral edema take longer to develop.

Note that she takes Bumex, a diuretic, and enalapril, an ACE inhibitor, both commonly prescribed to treat hypertension and heart failure.

The 12-lead ECG acquired in this case helps with understanding the mechanism of this patient’s CHF; acute myocardial infarction. The prehospital treatment of the patient with left heart failure centers on a number of goals:

  • Ensuring airway patency;
  • Ensuring adequate oxygenation and ventilation;
  • Sitting the patient upright;
  • Assessing for STEMI and monitoring the cardiac rhythm;
  • Gaining intravenous access;
  • Diuretic therapy;
  • Vasodilator therapy.

The patient is in obvious moderate-to-severe respiratory distress but still ventilating adequately, making her a perfect candidate for CPAP. Ideally, CPAP could be administered with titrated oxygen at an FiO2 sufficient to correct hypoxia but not overoxygenate. CPAP decreases the need for intubation and improves respiratory parameters such as heart rate, dyspnea, hypercapnia and acidosis in patients with CHF.18 The increased airway pressure created by CPAP actually pushes free fluid from the alveolar and interstitial spaces back into the pulmonary vasculature, correcting pulmonary edema and improving ventilation. Patients in respiratory failure, as evidenced by inadequate respiratory rate or tidal volume, and patients in severe respiratory distress with contraindications to CPAP should be intubated and ventilated with a BVM or placed on mechanical ventilation if available. Positive end-expiratory pressure (PEEP) improves oxygenation and should be administered to all intubated patients.11

Patients with heart failure and fluid volume overload will benefit from the administration of a vasodilator such as nitroglycerin. Nitroglycerin added to diuretic therapy may lead to even more rapid improvement of pulmonary edema.5,16 IV nitrates such as nitroglycerin or nesiritide are preferred in the hospital environment but not typically available to prehospital care providers. Sublingual nitroglycerin, while not as fast-acting or easy to titrate as IV, is an effective means of achieving vasodilation. Vasodilation is a benefit to the patient in fluid volume overload, as it increases venous capacitance, reducing preload and decreasing net workload of the heart as well as allowing for a fluid shift from the alveoli and interstitial lung space into the vasculature, especially when combined with CPAP.

While there are no national guidelines for the SL administration of nitroglycerin in patients with CHF, we can consider the dosing guidelines for IV nitroglycerin and adapt them to the prehospital environment and SL administration. IV nitroglycerin is often administered at an initial dose of 5–10 mcg/min. and increased in increments of 5–10 mcg/min. every 3–5 minutes as required and tolerated, with a maximum dose of about 200 mcg/min. A typical 400 mcg (0.4 mg) dose of SL nitroglycerin used in the prehospital environment, administered every five minutes, would equal out to 80 mcg/min., well below the maximum dose considered for IV nitroglycerin. In addition, the bioavailability of SL nitroglycerin will be decreased secondary to first-pass metabolism.

Patients with systolic blood pressures greater than 150 can be administered 800 mcg (2 x 0.4 mg doses) of nitroglycerin every five minutes. Regardless of the dose administered, evaluate the patient’s blood pressure after each administration, as hypotension is a possible and undesirable side effect. In addition, question male patients about the use of erectile dysfunction medications within the previous 24 hours, as concomitant nitroglycerin use can result in profound hypotension.

Patients in LVHF are usually volume-overloaded and require reduction of that intravascular volume to reduce pulmonary edema. Current guidelines recommend that patients with acute decompensated heart failure with evidence of volume overload, regardless of etiology, be treated with intravenous diuretics as part of their initial management, level of evidence Class B (nitrates in this scenario are evidence Class A).5,16 Excluded from this treatment are patients with hypotension or cardiogenic shock. Loop diuretics are the most common medications administered in heart failure, and common starting doses include:11

  • Furosemide, 40 mg IV
  • Bumetanide, 1 mg IV
  • Torsemide, 10–20 mg IV

The use of diuretics in the treatment of heart failure is an ongoing debate in the academic literature, with many EMS medical directors opting to remove the practice from their prehospital protocols. One recent study found that in the prehospital setting, furosemide was frequently administered to patients in whom its use was considered inappropriate. In addition, it was “not uncommonly” administered to patients in clinical situations in which it was considered potentially harmful.12 As always, follow your local protocols.

Specific treatment for the patient in Case #2 would include oxygen administration and airway support with CPAP, as she is in moderate to severe distress and has no contraindications for the use of CPAP. Obtain IV access and administer 0.4 mg of nitroglycerin every 3–5 minutes while maintaining a blood pressure of at least 90–100 mmHg systolic. Nitroglycerin administration will not only help treat the patient’s pulmonary edema but will also treat the active STEMI that caused it. As such, give the patient 324 mg of aspirin and transport her to a STEMI center. An IV diuretic such as furosemide can also be administered to correct the fluid volume overload.

Case #3

You’re dispatched to a residential address for an unconscious person. Upon arrival you find a 72-year-old male slumped in a chair, unresponsive and in respiratory failure. The patient’s wife says he got up out of bed last night at about 2300 “because he was not feeling well and his breathing was bothering him.” She awoke this morning about 10 minutes ago, found him as described and promptly called 9-1-1. She says he complained only of difficulty breathing. He has a history of two myocardial infarctions with three stent placements, CHF, atrial fibrillation, hypertension and type I diabetes. His medications include ASA, nitroglycerin as needed, Lasix, diltiazem, dofetilide, Coumadin and insulin. He has no known drug allergies.

Your clinical exam reveals peripheral and sacral edema, JVD, rales in all lung fields with little air movement bilaterally and cold, diaphoretic, cyanotic skin. His vital signs are: HR, 96/min. and irregular; BP, 70/palp.; RR, 8/min. and shallow; SpO2, 68% on room air. A 12-lead ECG reveals atrial fibrillation with a left bundle branch block and concordant ST-segment depression in lead V3.

Discussion

The patient in Case #3 is presenting in decompensated cardiogenic shock with pulmonary edema and requires immediate intervention. The prehospital treatment of the patient with cardiogenic shock and pulmonary edema centers on the following goals:

  • Ensuring airway patency;
  • Ensuring adequate oxygenation and ventilation;
  • Assessing for STEMI and monitoring the cardiac rhythm;
  • Gaining intravenous access, administering fluid volume;
  • Correcting hypotension with inotropic or vasopressor medications.

He is clearly in respiratory failure, and that and his unconsciousness are contraindications for the use of CPAP. This patient requires immediate BLS airway maneuvers, the insertion of a BLS airway adjunct and BVM ventilation with 100% oxygen at 15 lpm in preparation for endotracheal intubation. The positive pressure generated via BVM ventilation, with a PEEP valve attached, has the same effect as CPAP with regard to driving fluid from the alveoli and interstitial lung space back into the pulmonary vasculature.

The administration of nitroglycerin is not an option in this patient because of his profound hypotension. This patient is having a pump problem and so should be administered IV fluid and an inotropic or vasopressor agent used to increase the blood pressure and improve end-organ perfusion and mental status.

Dobutamine is frequently used to treat severe and refractory HF and cardiogenic shock,13 though it’s not always available in the prehospital environment. Norepinephrine (Levophed) is a potent vasopressor with some inotropic properties and if available can be considered in patients with severe cardiogenic shock. Dopamine, arguably the most common inotropic or vasopressor utilized in the prehospital environment, can also be used. Dopamine, however, is not necessarily “better” than dobutamine or norepinepherine. While the efficacy of dopamine over norepinephrine is unclear, some evidence suggests that outcomes may be better with norepinephrine.14

Regardless of the vasopressor or inotropic agent used, titrate it to achieve a blood pressure that both ensures end-organ perfusion and creates a blood pressure reserve. The emphasis in patients in cardiogenic shock, from the EMS perspective, is ensuring adequate ventilation and oxygenation, administering vasopressors to ensure end-organ perfusion, and rapid transport to a hospital for more definitive care.

Table 1: Risk Factors for Heart Failure

  • Hypertension
  • Metabolic syndrome
  • Cigarette smoking
  • Valvular heart disease
  • Diabetes mellitus
  • Coronary artery disease/Atherosclerosis
  • Obesity

Table 2: Classes of Diuretics Used to Treat Heart Failure

Loop Diuretics
Furosemide (Lasix)
Bumetanide (Bumex, Burinex)
Etacrynic acid (ethacrynic acid, Edecrin)
Torasemide (torsemide)

Thiazides
Hydrochorothiazide (HCTZ)

Potassium-Sparing Diuretics
Spironolactone (Aldactone)
Amiloride (Midamor)
Trimterene ((Dyrenium)

Conclusion

Patients in heart failure can present on a wide clinical and hemodynamic spectrum from seemingly minor complaints and stable vital signs to decompensated cariogenic shock. Recognition of the signs and symptoms that accompany right- versus left-sided HF can aid in the understanding of the underlying problem and treatment required. Regardless of the mechanism of HF, the treatment goals are similar for all patients:

  • Ensuring airway patency;
  • Ensuring adequate oxygenation and ventilation;
  • Assessing for STEMI and monitoring the cardiac rhythm;
  • Gaining intravenous access;
  • Correcting hypotension with inotropic or vasopressor medications.

References

1. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circ, 2013; 128(16): 1,810.

2. Djousse L, Driver JA, Gaziano JM. Relation between modifiable lifestyle factors and lifetime risk of heart failure. JAMA, 2009; 302: 394–400.

3. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics–2013 update: a report from the American Heart Association. Circ, 2013; 127: e6–245.

4. Curtis LH, Whellan DJ, Hammill BG, et al. Incidence and prevalence of heart failure in elderly persons, 1994–2003. Arch Intern Med, 2008; 168: 418–24.

5. Roger VL, Weston SA, Redfield MM, et al. Trends in heart failure incidence and survival in a community-based population. JAMA, 2004; 292: 344–50.

6. Deaths: Final Data for 2012. Natl Vital Stat Rep, 63(9).

7. Levy D, Kenchaiah S, Larson MG, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med, 2002; 347: 1,397–402.

8. Krumholz HM, Merrill AR, et al. Patterns of hospital performance in acute myocardial infarction and heart failure 30-day mortality and readmission. Circ Cardiovasc Qual Outcomes, 2009; 2: 407–13.

9. Joynt KE, Jha AK. Who has higher readmission rates for heart failure, and why? Implications for efforts to improve care using financial incentives. Circ Cardiovasc Qual Outcomes, 2011; 4: 53–9.

10. Chun S, Tu JV, Wijeysundera HC, Austin PC, Wang X, Levy D, Lee DS. Lifetime analysis of hospitalizations and survival of patients newly-admitted with heart failure. Circ Heart Fail, 2012; 5(4): 414–21.

11. Zile MR, Weller L, Gaash WH. Pathophysiology of diastolic heart failure. www.uptodate.com/contents/pathophysiology-of-diastolic-heart-failure.

12. He J, Ogden LG, et al. Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study. Arch Intern Med. 2001;161(7):996.

13. Colucci WS. Evaluation of the patient with heart failure or cardiomyopathy. Up to Date, www.uptodate.com/contents/evaluation-of-the-patient-with-heart-failure-or-cardiomyopathy.

14. Klings ES. Cor Pulmonale. Up to Date, www.uptodate.com/contents/cor-pulmonale.

15. Burns E. Right ventricular hypertrophy. Life in the Fast Lane, http://lifeinthefastlane.com/ecg-library/basics/right-ventricular-hypertrophy/.

16. Overgaaerd CB. Džavik V. Inotropes and vasopressors. Review of physiology and clinical use in cardiovascular disease. Circ, 2008; 118: 1,047–56.

17. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail, 2010; 16(6): e1.

18. Bauman KA, Hyzy RC. Noninvasive positive pressure ventilation in acute respiratory failure in adults. Up to Date, www.uptodate.com/contents/noninvasive-positive-pressure-ventilation-in-acute-respiratory-failure-in-adults.

19. 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.

20. Manaker S. Use of vasopressors and inotropes. Up to Date, www.uptodate.com/contents/use-of-vasopressors-and-inotropes.

21. De Backer D, Biston P, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med, 2010; 362(9): 779.

Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. He is also a paramedic with AMR: Sonoma Life Support in Santa Rosa, CA. E-mail scottrsnyder@me.com.

Sean M. Kivlehan, MD, MPH, NREMT-P, is the emergency medicine chief resident at the University of California San Francisco and a former New York City paramedic for 10 years. Contact him at sean.kivlehan@gmail.com.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also the performance improvement coordinator for AirLink/VitaLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at kcollopy@colgatealumni.org.

 

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