CC
A 65-year-old male presents to the emergency department after a witnessed mechanical fall complaining of “a bad bite and shortness of breath.”
HPI
The patient had been unloading his groceries when he tripped on the sidewalk and fell forward, hitting his chin. There was no reported loss of consciousness, and no other traumatic bodily injuries were sustained. Upon arrival, he was noted to be in moderate respiratory distress with oxygen saturation of 92%. Head-of-bed elevation and supplementary oxygen administration slightly improved his dyspnea, but he continued to exhibit increased work of breathing. The oral and maxillofacial surgery service was consulted to manage his head and neck injuries.
PMHX/PDHX/medications/allergies/SH/FH
The patient has a history of coronary artery disease treated with an angioplasty and a drug-eluting stent 2 years earlier for which he is on lifelong aspirin therapy. On his most recent transthoracic echocardiogram, he was found to have ejection fraction of 30% (normal, 50%–70%). He is taking lovastatin (an HMG-CoA reductase inhibitor [cholesterol-lowering medication]), furosemide (a loop diuretic), lisinopril (angiotensin-converting enzyme [ACE] inhibitor), and metoprolol (beta-blocker). He admits to poor medication compliance (risk factor for congestive heart failure [CHF] exacerbation). He also has type 2 diabetes mellitus that is managed with metformin and canagliflozin (a sodium-glucose transport protein 2 [SGLT-2] inhibitor). The patient is a current daily smoker with a 40-pack-year history (risk factor for coronary artery disease [CAD]). He has no known medication allergies. His only prior surgery was his percutaneous coronary intervention.
Coronary artery disease involves varying degrees of impaired blood supply (oxygen) to the myocardium (causing ischemic heart disease), which puts the heart at risk for ischemic events (angina, myocardial infarction), with potential functional impairment of the myocardium and subsequent systolic dysfunction. The inability to efficiently pump blood out of the heart leads to the backup of blood in the heart and lungs (congestion), which is the mechanism of CHF . Risk factors for CHF include CAD (causes 50%–75% of cases), uncontrolled systemic hypertension, valvular heart disease, cardiomyopathy (dilated or hypertrophic), stress (Takotsubo), drugs (alcohol, cocaine, chemotherapy), and infections (viral myocarditis).
There are multiple risk factors for the acute decompensation of chronic stable heart failure (HF). The most common precipitants are nonadherence to fluid restriction, sodium restriction, and medication regimens. Noncardiac causes of decompensated HF include systemic infections, which generate inflammation and an increased cardiac demand. Lower respiratory infections can further produce worsening pulmonary edema and dyspnea through capillary leakage. Cardiac arrhythmias or myocardial infarctions can rapidly impair systolic function and lead to acute decompensation. In the current case, there are multiple contributions to the patient’s acute decompensation, including noncompliance and a history of CAD.
Examination
Advanced Trauma Life Support (ATLS) primary survey. Negative except for moderate respiratory distress. The patient was immediately placed on supplemental oxygen via a face mask, however given his persistently increased work of breathing he was escalated to high-flow nasal canula (HFNC) with an improvement in oxygenation. (HFNC is less invasive than continuous positive airway pressure and bilevel positive airway pressure and can generate low levels of positive airway pressure, reduce respiratory dead space, and decrease work of breathing.)
General. The patient is awake; alert; and oriented to person, time, and place. (Confusion and altered mental status are signs of circulatory failure and cardiogenic shock.) He appears fatigued and shows increased respiratory effort.
Vital signs. Blood pressure is 90/75 mm Hg (hypotensive with a narrow pulse pressure), heart rate is 120 bpm (tachycardia), respirations are 28 breaths per minute (tachypnea), and temperature is 37.1°C.
Maxillofacial. Anterior open bite with bilateral posterior crossbite consistent with suspected Guardsman’s fracture pattern (mandibular symphysis with bilateral condylar neck fractures).
Cardiovascular. Fast but regular rhythm with normal S1 sound (closure of mitral and tricuspid valves) and S2 sound (closure of aortic and pulmonic valves). An S3 sound is auscultated at the left sternal border at the fifth intercostal space. (An S3 sound is heard in early diastole during rapid ventricular filling phase, associated with increasing filling pressures, and more common in dilated ventricles.) The point of maximum impulse (generated by the left ventricle as it touches the inner chest wall during systole) is laterally displaced with a parasternal heave (elevation of the chest wall to the left of the sternum). The jugulovenous pressure is elevated at 15 cm (normal, <9 cm) with a positive hepatojugular reflex (distension of the jugular veins on application of pressure in the right upper abdominal quadrant). Hepatojugular reflex and elevated jugulovenous pressure are signs of venous congestion observed in association with HF and volume overload.
Pulmonary. Use of the accessory muscles of respiration (sternocleidomastoid, scalenes, pectoralis major and minor, and serratus anterior muscles). Dyspnea is exacerbated when the patient assumes the supine position (orthopnea). Bilateral basilar rales (fluid in the alveolar spaces) with dullness to percussion (caused by pleural effusions) in the lung bases. (Fluid accumulation in the lungs is secondary to left-sided HF.)
Abdominal. Nontender and nondistended with hepatomegaly. The liver was percussed at 10 cm below the costal margin (hepatic congestion caused by right-sided HF).
Extremity. The extremities are cool to the touch (suggesting diminished perfusion). The lower extremities show 3+ pitting edema at the ankles up to the midshin (significant fluid in the extravascular compartments caused by venous congestion, causing capillary leakage; this is usually first noted in the lower extremities because of the added effect of gravity; Fig. 97.1 ).
Imaging
A chest radiograph is the minimum imaging modality for the evaluation of CHF exacerbation. This is valuable for the evaluation of pulmonary edema and infiltration and for the approximation of the heart size. Echocardiography (transthoracic or transesophageal) is also useful for the evaluation of ventricular and valvular function and determination of the ejection fraction. The earliest finding of left-sided HF on the chest radiography is cephalization of the pulmonary vessels. Normally, the vessels in the lung bases are larger and more numerous than those in the lung apices. This is secondary to the effects of gravity and the anatomically larger volume of the lungs at the base. With the progression of HF, the increased pressure is transmitted “backward” to the pulmonary veins and capillaries (hence the term “backward failure”). The lung bases are affected first; therefore, blood is preferentially “shunted” to the upper, or more cephalad, lobes, giving the radiographic appearance of cephalization. If the pressure in the vessels continues to rise, the fluid in the interstitium becomes radiographically evident as interstitial edema, bronchial wall thickening, and interlobular septa. The most noticeable are the Kerley B lines. These are short, thin, perpendicular lines extending to the pleura at the lung bases on a chest radiograph. The following imaging findings were noted for the current patient.
Chest radiograph. Bilateral blunting of the costophrenic angles with pronounced infiltrates in the lower lobes (consistent with bilateral pleural effusions and pulmonary edema).
Cephalization of the pulmonary vessels bilaterally. Increased cardiac silhouette. (An increased cardiac silhouette, spanning more than one-third of the thoracic cavity on an anteroposterior film, is indicative of an enlarged heart or dilated cardiomyopathy.)
Transthoracic echocardiography. Dilated left ventricle consistent with dilated cardiomyopathy with decreased wall motion (systolic dysfunction) and mild mitral regurgitation. The pulmonic, aortic, and tricuspid valves were without stenosis or regurgitation. The ejection fraction was estimated at 25% (compromised ventricular function). No pericardial fluid and normal wall thickness were seen in all four chambers. Moderate elevation of the pulmonary artery pressure was noted.
Computed tomography (CT) (maxillofacial and neck). Bilateral medially displaced condylar neck fractures with a mildly displaced and widened symphysis fracture. Cervical spine without any abnormalities. (A CT scan of the chest can also be used to further evaluate the pulmonary parenchyma and cardiac structures.)
Labs
Brain natriuretic peptide (BNP) level was 2000 pg/mL (normal, <100 pg/mL).
With CHF, increased pressure and workload on the heart trigger the myocardial cells to secrete natriuretic peptides. Atrial myocytes secrete increased amounts of atrial natriuretic peptide, and the ventricular myocytes secrete both atrial and BNPs in response to the high atrial and ventricular filling pressures. Both of these peptides work as natriuretic, diuretic, and vasodilator agents and help reduce both preload and afterload. The plasma concentrations of both hormones are increased in patients with asymptomatic and symptomatic CHF. Of note, natriuretic peptide levels can be normal in HF with preserved ejection fracture (HFpEF) because there is less myocardial stretch.
Electrocardiogram findings
The electrocardiographic findings for the current patient were as follows:
-
Rate. Tachycardic at 120 bpm.
-
Rhythm. Regular; each P wave followed by a QRS complex; each QRS complex preceded by a P wave; QRS complexes occurring at regular intervals.
-
Axis. Positive deflection in lead I; negative deflection in lead aVF (indicative of left-axis deviation secondary to left ventricular hypertrophy).
-
Intervals. PR interval less than 0.20 second, or 5 small boxes on electrocardiograph paper (>5 small boxes is consistent with first-degree atrioventricular node block); QRS complex less than 0.12 second, or 3 small boxes (>3 small boxes indicates widened QRS complex); QT interval less than half the distance from QRS complex to QRS complex (normal).
-
Infarctions. Q waves in leads V 1 through V 5 (hallmark of old anteroseptal myocardial infarction); no flipped T waves, and no ST-segment elevation or depression (signs of acute ischemic events).
-
Other. Loss of precordial R wave progression in leads V 1 through V 6 (suggestive of old anteroseptal MI and loss of anterior electrical forces).
Assessment
A 65-year-old male status after a mechanical fall with a history of heart disease now presenting with acute CHF exacerbation and a complex mandible fracture.
Treatment
The cardiology service was consulted for management and preoperative optimization, and the patient was treated with aggressive fluid and salt restriction and intravenous Lasix (furosemide, a loop diuretic). His home metoprolol was temporarily held because of its negative inotropic effects; likewise, the home lisinopril was held because of the hypotension and concern for renal injury. Inotropic support was considered because of the relative hypotension and cool extremities on examination; however, it was not required because of the good urine output and mental status which argued against the presence of cardiogenic shock. The patient’s cardiovascular symptoms and findings gradually improved within 36 hours (decreased shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea; resolution of peripheral edema and pleural effusions; decrease in cardiac biomarker BNP level). He remained chest pain free and hemodynamically and electrically stable (no arrhythmias). After his volume status normalized, he was restarted on his home regimen of lisinopril and metoprolol. After a careful perioperative cardiac risk assessment, the patient was taken to the operating room for open reduction and internal fixation of the mandibular fractures under general anesthesia.
Discussion
Heart failure can result from any structural or functional cardiac disorder that impairs the ability of the heart to pump blood ( Fig. 97.1 ). It is characterized by several symptoms, such as dyspnea, fatigue, edema, and weight gain. There are several causes of HF, including myocarditis or endocarditis (viral or bacterial infections), ischemic heart disease, infiltrative disease (amyloidosis, sarcoidosis), peripartum cardiomyopathy, hypertension, human immunodeficiency virus infection, connective tissue disorders, substance abuse, certain chemotherapy drugs, and idiopathic origin.
Fluid retention in HF is initiated by the fall in cardiac output, leading to edema and decreased effective arterial volume. The reduction of cardiac output sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of the renin–angiotensin–aldosterone and sympathetic nervous systems. Although initially beneficial in the early stages of HF, these compensatory mechanisms eventually lead to a vicious cycle of worsening HF, fluid retention, and volume overload.
The classification systems used for the management of CHF are based on the severity of the condition, systolic versus diastolic dysfunction, and left-sided versus right-sided failure. The two main classifications of HF are the New York Heart Association (NYHA) classification (most commonly used) and the American College of Cardiology/American Heart Association (ACC/AHA) classification.
The NYHA classifies patients into one of four functional categories based on the amount of effort needed to elicit HF symptoms. The NYHA also includes an objective assessment to stratify the clinical extent of heart disease regardless of symptomatology. This objective assessment of cardiovascular disease is determined using data from electrocardiograms, stress tests, echocardiograms, and radiologic imaging. Therefore, the comprehensive classification includes a description of both the functional capacity and the objective assessment (e.g., Functional Capacity IV, Objective Assessment A).
Functional classification
- •
Class I: symptoms of HF only at levels that would limit normal individuals
- •
Class II: symptoms of HF with ordinary exertion
- •
Class III: symptoms of HF on less than ordinary exertion
- •
Class IV: symptoms of HF at rest
Objective assessment
- •
Class A: no objective evidence of cardiovascular disease
- •
Class B: objective evidence of minimal cardiovascular disease
- •
Class C: objective evidence of moderately severe cardiovascular disease
- •
Class D: objective evidence of severe cardiovascular disease
The ACC/AHA classification is based on the chronology of disease progression and provides accompanying treatment guidelines for each stage. The most recent 2022 ACC/AHA classification and treatment guidelines can be found in Table 97.1 .
