Abstract
Heart failure (2.6% prevalent worldwide) is a complex clinical syndrome, resulting from a structural or functional cardiac disorder and impairing ventricular filling or ejection capability. The current case of a 59-year-old male patient admitted on August 18, 2016 due to worsening shortness of breath and bilateral left extremity edema (one week) involved an existing diabetes mellitus type 2 (DM2). Physical and clinical profiles indicate a comorbidity between heart failure (HF) and DM2. Laboratory and imaging findings were not indicated, while diagnosis was based on the NYHA Classification guidelines. A review of literature revealed three crucial weaknesses in the diagnosis. First, identification of precipitating causes was not performed. Second, laboratory and imaging findings (except oxygen saturation) was unreported. Third, phenotyping guidelines used were not robust to be specific and sensitive. Overall, the procedure performed in diagnosing an HF was inadequate by current best practice standards in the United States and worldwide.
1.0 Introduction
Heart failure, which has an estimated prevalence of 2.6 percent, is a complex clinical syndrome caused by a structural or functional cardiac disorder, which impairs ventricular filling or ejection capability (Kakouros & Kakouros, 2015). Acute heart failure (AHF) is largely due to deteriorating chronic heart failure (CHF) even while 40 to 50 percent of patients retained ejection fraction (EF) and the remaining cases due to de novo AHF, usually secondary to acute coronary syndromes (ACS). Close to 80 percent of AHF admissions pass the emergency department, making it necessary for emergency personnel to accurately and precisely diagnose AHF quickly.
The current case pertained to a 59-year-old male patient who was admitted on August 18, 2016 due to increased shortness of breath and bilateral left extremity edema for already a week. A case brief is provided, which consists of the chief complaint and history at admission, signs and symptoms, physical examination findings (e.g. vital signs, HEENT, abdomen, and extremities) and diagnosis. Laboratory and imaging findings had been indicated as ‘reviewed’ but not indicated in detail. To interact with the case, a review of literature explored the discussion of heart failure assessment, diagnosis, and treatment.
2.0 Case brief
[Laboratory and imaging findings: Not included but reviewed.]
Chief complaint and history: The 59 years-old male patient reported mild left knee pain (2/10) when checked at bedside. The patient had an AFIB (atrial fibrillation investigation with bidisomide); has hypertension (HPN), hyperlipidemia (HLD), type 2 diabetes mellitus (DM2), and chronic low blood pressure who was presented on August 18 for worsening shortness of breath and bilateral lower extremity edema for one week. The patient was admitted to cardiac telemetry and was then transferred to the CCU after continued hypotension even with diuresis.
Signs and symptoms: No overnight event occurred. No chest pain, shortness of breath, or palpitation was reported; neither of fever, chills, nor cough. No epigastric pain experienced after meal as well as evidence of n/y/dysuria or constipation. Net liquid input-output within the last 24 hours was -1100cc and during the length of stay was -22187 cc.
Physical examination findings: Vital Signs examination showed blood pressures ranging between 73/53(57) mmHg and 113/84(91) mmHg with a heart rate range of 64 to 87 pulses per minute. Respiratory rate ranged at 16 to 31 breathes per minute. Oxygen saturation of the arterial blood (SaO2) was 97 percent at the right atrium. HEENT examination showed normocephaly, atrauma, poor dentition, and with no jugular venous distension. His CVS showed irregular rhythm with no murmurs. Respiration is clear at lateral auscultation (CTAB) with no wheezing. Meanwhile, abdominal examination indicated abdominal softness and distension with no tenderness and rebound or guarding. Mild fluid wave was appreciated. A minor healing incision wound was found over the right lower quadrant from biopsy but non-tender. The extremities showed an anterior left knee with no tenderness, erythema, edema, or swelling. Edema on the right lower extremity was significantly improved with no calf tenderness or ulcers.
Diagnosis: The patient was diagnosed with chronic heart failure (CHF) with an ejection fraction of 10 to 15 percent (normal at left ventricle = 65%) with s/p BIV ICD and phenotype NYHA Class III [Moderate CHF: Marked limitation of physical activity with less than ordinary physical activity leading to symptoms; metabolic equivalent of 2-3 mL VO2 per min per kg BW].
Treatment plan: Dopamine gamma-glutamyltransferase was discontinued on July 27 at maps >70. D/c Metoprolol tartrate was prescribed at 25 mg q every 12 hours on August 3. Metoprolol succinate at 50 mg daily will be continued (started on August 4) with Lisinopril 5mg by mouth daily on August 16, 2016 with continued monitoring of the patient’s renal function.
3.0 Discussion of evaluation
Initial evaluation: Initial assessment of patients with AHF involves determining the precipitating causes. Kakouros and Kakouros (2015) identified 16 precipitants of AHF, which leads to hospitalization, which includes cardiovascular (e.g. acute coronary syndrome, cardiac tamponade, uncontrolled hypertension, and tachyarrhythmia or bradyarrythmia), pulmonary (e.g. acute pulmonary embolism and exacerbated COPD), pharmacological (e.g. corticosteroids, NSAID, and negative inotropic agents), and other triggers, ranging from renal or thyroid dysfunctions to alcohol or illicit drug abuse, and dietary or medication non-compliance. These precipitants have both prognostic and therapeutic implications. Moreover, a thorough history, clinical examination, and physical examination must be complemented with chest x-ray, encephalocardiography, initial laboratory tests (e.g. blood biochemistry, cardiac and renal impairment biomarkers, and natriuretic peptides), oxygen saturation, and echocardiogram. The present case seemingly failed to establish early the precipitants, which led to the shortness of breath. Other laboratory and imaging findings cannot be reviewed here.
Meanwhile, although clinical history is the best discriminator for the acuity, etiology, and progression rate of HF, symptoms of excess fluid accumulation (i.e., dyspnea, orthopnea, edema, breathing discomfort or pain, and abdominal distension) and cardiac output reduction (i.e. fatigue) are insufficient to make an HF diagnosis (Kakouros & Kakouros, 2015). Evidence for a structural or functional cardiac dysfunction or abnormality must corroborate an HF diagnosis. Moreover, orthopnea and paroxysmal nocturnal dyspnea are more specific symptoms than many other symptoms, but they occur infrequently in HF cases, including this case; thus are not sensitive. Dyspnea on exertion and fatigue are also as highly non-specific as peripheral edema (Nohria, et al., 2003). Conversely, systolic and diastolic ventricular dysfunctions have similar symptoms. Abdominal pain in the RUQ (right upper quadrant), including nausea and abdominal discomfort, is expected in liver and gastrointestinal congestions. The absence of pulmonary rales, jugular vein distension, hepatojugular reflux, and peripheral edema also cannot rule out HF (Kakouros & Kakouros, 2015). Further, certain vital signs are inversely related with HF at presentation and mortality (in-hospital or post-discharge). Hypotension, for instance, is a deadlier sign of HF than hypertension, reflecting low cardiac output secondary to severe myocardial dysfunction, cardiac tamponade, and other HF triggers (Kakouros & Kakouros, 2015).
Diagnostic evaluation: As will be explored more in Section 4.0, a more sensitive and predictive evaluation of HF must focus on establishing the level of clinical hemodynamic and pulmonary congestion, which can be measured reliably using different methods. Currently, the gold standard in evaluating clinical congestion continued to be cardiac catheterization, which is unfortunately less popular in routine clinical practice due to its invasiveness (Kakouros & Kakouros, 2015). A more robust method, however, is pulmonary ultrasonography, using an echocardiographic probe (Ende & Fosnocht, 2002). A more recent method involved the use of thoracic lead impedance measurement using an external or implanted pacemaker (Kakouros, et al., 2014). In this approach, a reduction in the pacemaker impedance of >60 Ω from the reference value signals severe pulmonary congestion or an advance warning on a potential decompensation of HF. Meanwhile, ECG is recommended as a first line diagnostic test in most guidelines (McMurray, et al., 2012), but has a negative predictive value (98%); thus, a normal ECG makes systolic dysfunction unlikely even among acutely presenting patients.
Conversely, echocardiography is the most widely accepted (thus, commonly used) non-invasive method in detecting systolic or diastolic dysfunction, which must be performed after the initial assessment as confirmative for HF (Kakouros & Kakouros, 2015). It can effectively compensate for declining clinical examination skills of physicians and the low sensitivity and specificity of most clinical signs. Meanwhile, Kakouros and Kakouros (2015) identified highly specific clinical signs of pulmonary congestion (but low in sensitivity): S3 gallop rhythm (93%, 13%); ≥400 pg brain natriuretic peptide per mL (92%, 64% respectively); and chest radiographic findings: cephalization (96%, 41%), interstitial edema (98%, 27%), alveolar edema (99%, 6%), pleural effusion (92%, 25%), no hyperinflation (92%, 3%), and no pneumonia (92%, 4%).
4.0 Discussion of diagnosis
It is crucial that an AHF diagnosis is established early as any delays in diagnosis will also delay therapy, which can result to worse treatment outcomes (Kakouros & Kakouros, 2015). Establishing HF diagnosis had followed different guidelines in determining the HF severity level. The case followed the New York Heart Association (NYHA) Classification (CHFGEWP, 2011), which is graded based on the patients’ capability to perform physical activity. This guidelines consists of four severity classes, which are quantitated using the metabolic equivalent (MET) of a 40-year-old male with 70-kg weight. It includes an asymptomatic pre-CHF category: Class I (Asymptomatic left ventricle dysfunction, MET= >7; No limitations).
Kakouros and Kakouros (2015) mentioned two other guidelines: the European Society of Cardiology (ESC) guidelines, which relies on the effusion fraction (EF); and the Killip classification, which provided prime importance on cardiac decompensation. The ESC Guidelines (McMurray, et al., 2012) categorize HF into two groups based on specific signs and symptoms: (A) HF with reduced EF (e.g. typical HF signs and symptoms) and (B) HF with preserved EF (e.g. typical HF signs and symptoms; normal to mildly reduced left ventricle EF; non-dilated left ventricle; and at least a relevant structural heart disease, such as left ventricle hypertrophy, left atrium enlargement, and/or diastolic dysfunction).
Meanwhile, the Killip Classification includes a No Heart Failure classification (Stage I: No clinical signs of cardiac decompensation). The rest follows: Stage II (HF: Diagnostic criteria, e.g. rales, S3 gallop, pulmonary venous hypertension); Stage III (Severe HF: Marked pulmonary edema in all lung fields); and Stage III (Cardiogenic Shock: Signs of hypotension [systolic blood pressure of ≤90 mmHg] and vasoconstriction [e.g. oliguria, cyanosis, and diaphoresis]) (Kakouros & Kakouros, 2015; cf. Schmitt, Kushner, & Wiener, 1986).
Evidently, the NYHA Classification helped in the case gross screen for HF, but could not specifically diagnose HF due to its reliance on symptoms (e.g. dyspnea, fatigue, and even pulmonary edema), which have no prognostic value without left ventricular systolic (LSV) function data. Leier and Chatterje (2007) noted that patients with pulmonary edema, secondary to severe hypertension but with normal LSV function, had far excellent prognosis compared to those with moderate dyspnea but with severe LSV dysfunction. Thus, the Killip Classification is relatively more robust due to its pulmonary congestion determination emphasis, which determines high left ventricular diastolic pressure (LVDP). Moreover, the NYHA Classification apparently has no global or even national acceptance as a standard in clinical practice. A global survey (Ponikowski, et al., 2014) noted that only two guidelines are widely recognized in the United States in 2015 (the American College of Cardiology Foundation [ACCF]/ the American Heart Association [AHA] and the Heart Failure Society of America [HFSA]).
Overall though even the most sophisticated diagnostic laboratory tests (e.g. blood tests) contribute to HF diagnosis, but cannot positively identify patients who have; thus, leaving the burden of diagnosis to the clinical judgment of an experienced physician (Ponikowski, et al., 2014). The statistical methods known as risk stratification methods, however, hold a promise in identifying potentially specific and sensitive HF risk determinants in the future. However
5.0 Discussion of Treatment
In managing an HF case, the initial therapy must address the removal of a precipitant or trigger (Kakouros & Kakouros, 2015). Current medications, however, had been found unable to address the underlying causes of heart failure (Ponikowski, et al., 2014). The World Heart Failure Alliance (WHFA) believed that the best approach to ‘treating’ HF is through preventive medication, which should be the focus of research and development efforts in the future. Meanwhile, the WHFA observed no ground breaking development in the new treatment modalities for HF to date, which contrasted with strong developments in the long-term care (e.g. remote monitoring, telephone support, and specialized community-based care) or self-care of patients who survived HF incidents (Ponikowski, et al., 2014).
Conclusion
The present case, as reviewed, presented at least three crucial shortcomings in assessing, diagnosing, and treating an accurately appreciated HF case. First, the attending physician failed to identify at least one precipitating cause for the development of the patient’s symptom (i.e. worsening shortness of breath). Comorbidity can be observed in the case, such as diabetes mellitus, type 2m which can explain certain signs and symptoms (e.g. hypertension, bilateral lower extremity edema for one week). Second, the laboratory and imaging findings (except for the oxygen saturation) should be recorded in the case summary to assist potential reevaluation of the case when potential misdiagnosis occurs. Third, the phenotyping guidelines used in diagnosing HF, which was the NYHA Classification, was evidently not a robust set of guidelines for a specific and sensitive diagnosis of HF. The Killip Classification should have worked better but would have required more robust laboratory and imaging diagnostic tests to be carried out, which cannot be established here. Overall, the diagnostic handling of the patient was inadequate.
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