Disproportionate tachycardia and tachypnea in pulmonary tuberculosis: A marker of concurrent cardiac dysfunction :Shital Patil, Gajanan Gondhali, Manojkumar Bhadake, Journal of Association of Pulmonologist of Tamil Nadu

CASE REPORT
Year : 2022 | Volume : 5 | Issue : 3 | Page : 124--129

Disproportionate tachycardia and tachypnea in pulmonary tuberculosis: A marker of concurrent cardiac dysfunction

Shital Patil¹, Gajanan Gondhali², Manojkumar Bhadake²,
¹ Department of Pulmonary Medicine, MIMSR Medical College, Latur, Maharashtra, India
² Department of Internal Medicine, MIMSR Medical College, Latur, Maharashtra, India

Correspondence Address:
Prof. Shital Patil
Department of Pulmonary Medicine, MIMSR Medical College, Latur, Maharashtra
India

Abstract

Cardiovascular involvement in tuberculosis is not uncommon. Cardiac dysfunction is a clinical presentation due to direct or indirect affection due to tuberculosis. Cardiac dysfunction is possible without structural cardiac disease. In this case report, a 32-year-old male presented with constitutional symptoms for 6 months with acute deterioration with tachycardia and tachypnea with hypoxia 2 weeks before hospitalization. Radiological investigations documented conglomerated miliary tuberculosis and confirmed by sputum smear microscopy and Gene Xpert MTB/Rif. Cardiac investigations revealed sinus tachycardia in electrocardiogram, raised cardiac enzymes in laboratory evaluation, and “global left ventricular hypokinesia” with reduced ejection fraction in echocardiography. We have started Anti-tuberculosis treatment as per National guidelines for 6 months with steroids backup for four weeks. We have documented cardiac function improvement in one month post treatment, bacteriological cure after 2 months of ATT and near complete radiological resolution after 6 months. We recommend cardiac workup in all pulmonary tuberculosis cases with disproportionate tachycardia and tachypnea with or without hypoxia.

How to cite this article:
Patil S, Gondhali G, Bhadake M. Disproportionate tachycardia and tachypnea in pulmonary tuberculosis: A marker of concurrent cardiac dysfunction.J Assoc Pulmonologist Tamilnadu 2022;5:124-129

How to cite this URL:
Patil S, Gondhali G, Bhadake M. Disproportionate tachycardia and tachypnea in pulmonary tuberculosis: A marker of concurrent cardiac dysfunction. J Assoc Pulmonologist Tamilnadu [serial online] 2022 [cited 2023 May 29 ];5:124-129
Available from: https://www.japt.in//text.asp?2022/5/3/124/370812

Full Text

Introduction

Tuberculosis affects almost every organ in the body, but the usual site of the disease is the lungs, accounting for more than 80% of tuberculosis cases.[1] After the central nervous system, cardiovascular involvement is one of the most common extrapulmonary manifestations of tuberculosis. Cardiopulmonary tuberculosis accounts for between 1% and 2% of all tuberculosis cases in immunocompetent persons.[2] Cardiovascular involvement in tuberculosis portends an unfavorable prognosis (for example, tuberculous pericarditis is associated with a mortality rate close to 40%).[3] The “Neglected Tropical Diseases and Other Infectious Diseases Involving the Heart” (the NET-Heart Project), an initiative of the “Emerging Leaders” section of the Interamerican Society of Cardiology, aims to expand knowledge about the cardiovascular complications in these types of diseases, to help to identify barriers, and to look for possible solutions.[4],[5]

Case Report

A 32-year-old male, farmer by occupation, with no addiction history, normotensive, nondiabetic, was referred to our center by a family physician for acute febrile respiratory illness.

Further clinical details:

Fever for 6 months, intermittent, low-to-moderate grade without chills and rigors associated with minimal body ache and headache. He was treated as a case of enteric fever for 4 months by a family physician and later 2 months as jaundice without laboratory workup documentationCough for 4 months dry, intermittent, with minimal white sputum productionLoss of appetite and weight loss for 3 monthsWeakness and myalgia with fatigability for 3 monthsShortness of breath on exertion in the past 1 month.

His symptoms worsened over 6 months, and he presented with acute febrile respiratory illness with difficulty in breathing and minimal hemoptysis for 2 weeks. His shortness of breath worsened, and the family physician was referred him to our center for further workup and expert management.

Clinical examination documented as:

Restless, dry oral mucosa, cyanosis, pallor, and febrileHeart rate – 132/min, respiratory rate – 40/bpm, blood pressure – 90/70 mmHgPsO2: Eighty percent @ room air resting and 71% @ room air on exertionRespiratory system examination revealed bilateral breath sounds normal, bilateral crepitation's heard on both lung fieldsNervous system examination – higher functions normal, no neurological abnormality, cranial nerves normal, recent and past memory normal recallCardiovascular and gastrointestinal systems were normal.

We have assessed records of hospitalization as chest X-rays showing bilateral upper and middle zone inhomogeneous opacities [Figure 1] and chest X-rays done at our center during hospitalization documented new nodular opacities and increased inhomogeneous opacities as in upper, middle, and lower zones as compared to previous [Figure 2]. The duration between 2 X-rays was 2 months and the received antibiotic treatment targeting enteric fever and jaundice.{Figure 1}{Figure 2}

Laboratory examination during hospitalization documented as:

Hemoglobin – 11.1 gm%, total white blood cells – 10,000/mm3, polymorphs – 70%, platelet count – 90,000/uLC-reactive protein (CRP) – 212 mg/L (0–6 mg/L), random blood sugar level –134 mg% HbA1C-5.60%Lactate dehydrogenase – 1680 IU/L (70–470 IU/L), uric acid – 3.4 mg (3.5–7.5 mg/dL)Serum electrolytes: Sodium – 134 meq/L (135–145 meq/L), potassium – 3.7 meq/L (3.5–5.5 meq/L,) ionic calcium –1.39 meq/L (1.09–1.36 meq/L)D-dimer – 810 ng/ml (<500 ng/ml)Interleukin – 6–4.75 pg/ml (0.00 – 7.00 pg/ml)Serum creatinine – 1.3 mg/dL (0.7–1.4 mg/dL)Liver function tests – NormalThyroid functions – NormalSputum examination documented acid-fast bacilli and tuberculosis (TB). Gene Xpert Mycobacterium TB (MTB)/rifampicin were documented MTB genome and rpo-b mutation negativeElectrocardiogram (ECG) showed sinus tachycardia [Figure 3].Pro- B-type natriuretic peptide – 66 pg/ml (<125 pg/ml)CPK-MB test (creatine phosphokinase-MB) – 76.22 IU/L (0–25 IU/L)Trop-I- (cardiac troponin) – 359.6 ng/L (0–19 ng/L)COVID-19 Reverse transcription polymerase chain reaction test and results documented negative for SARS-CoV-2.{Figure 3}

Echocardiography was done to rule out myocarditis and structural heart disease in the presence of sinus tachycardia and raised cardiac enzymes. Echocardiography examination showed dilated left ventricle, global left ventricular dysfunction with reduced ejection fraction and without structural pericardial or myocardial abnormality.

High-resolution computed tomography thorax suggest bilateral, peripheral multifocal nodular opacities in the upper middle and lower lobes [Figure 4]. Nodular opacities were isolated, randomly placed at some point, and in groups forming conglomerated appearance to consolidations involving upper and middle lobes predominantly with decreasing frequency to lower lobes [Figure 5] and [Figure 6].{Figure 4}{Figure 5}{Figure 6}

During hospitalization, emergency care management was done with oxygen supplementation with nasal cannula to achieve target oxygen saturation of 91%. We have started injection methylprednisolone 40 mg three times, and antibiotics as meropenem 1 gram intravenously 8 hourly and linezolid 600 mg intravenously 12 hourly. We have stopped antibiotics after sputum examination documented as tuberculosis and started Anti-tuberculosis treatment (ATT) as per weight band with isoniazid, rifampicin, pyrazinamide, ethambutol. Cardiac enzymes were raised, and ECG showed sinus tachycardia; the cardiologist consultation suggested adding metoprolol 25 mg OD (Once in a day) to control the heart rate. He was tolerating ATT without any liver or renal dysfunctions; the dose of methylprednisolone decreased from 40 mg three times to time daily after 1 week after stabilization of heart rate and decrease in oxygen requirement. His improvement in oxygen saturation, no oxygen requirement, and normal heart rate (60–90 beats/minute) took 10 days in the intensive care unit. He was discharged to home after 2 weeks of treatment, with four drugs ATT and oral methylprednisolone 40 mg tapered over to 8 weeks to 4 mg daily. After 2 months of treatment, the radiological response was documented with clearance of radiological abnormalities. Radiological response documented as a significant decrease in nodular opacities in bilateral lung fields [Figure 7].{Figure 7}

After completion of the intensive phase, she was shifted to the continuation phase with isoniazid, rifampicin, and ethambutol without steroids. We have done a radiological response assessment by performing follow-up chest X-ray at 4 months. Chest radiological evaluation shown near complete resolution of opacities in upper, middle, and lower lung fields [Figure 8]. He had abnormal renal functions initially during hospitalization; we recommended monthly follow-up in the outdoor unit with kidney function and liver function tests monitoring. He tolerated the complete course of ATT for 6 months as per National guidelines and documented “cure” of tuberculosis. Microbiological response to ATT was documented by analysing sputum examination at 2 and six months. We have documented microbiological 'cure' with the absence of acid fast bacilli in sputum examination and Gene Xpert MTB/Rif negative for MTB (mycobacterium tuberculosis) genome. Clinical and radiological response documented after completion of ATT with complete resolution of radiological abnormalities in chest X-ray [Figure 9]. Echocardiography done after completion of ATT documented normal cardiac chambers, normal systolic and diastolic left ventricular function with normal ejection fraction and without structural pericardial or myocardial abnormality.{Figure 8}{Figure 9}

Discussion

Tuberculosis is a communicable disease caused by the bacillus MTB. It is the leading cause of mortality from an infectious disease and is among the top 10 leading causes of death worldwide, particularly in low- and middle-income countries, where it generates a significant burden of disease.[6] Although tuberculosis has been considered a global public health emergency for the past 25 years, it remains poorly controlled. India, China, Indonesia, South Africa, and Nigeria rank first to fifth, respectively, in terms of incident TB cases.[7] According to an estimate by the WHO, between 1999 and the year 2020, nearly 1 billion more people will be newly infected, 200 million will get sick and 70 million will die from TB, if the control measures are not strengthened.[8]

Disproportionate tachycardia may be defined as pulmonary tuberculosis cases with resting heart rate above 100/min or a heart rate above 130/min with minimal exertion without causing hypoxia or oxygen saturation <90% or more than 5% fall from resting saturation. Tachypnea is defined as pulmonary tuberculosis cases with resting respiratory rate above 20 breaths per minute or a respiratory rate above 40/min with minimal exertion without causing hypoxia or oxygen saturation <90% or more than 5% fall from resting saturation. Hypoxia is defined as pulmonary tuberculosis cases with resting oxygen saturation <90% at room air and falls to more than 5% with minimal exertion and will take more than 5 min to return to normal or more than 90%.

Tuberculous myocarditis is a very rare disease, with only a few reported cases in the literature. Tuberculous myocarditis usually results from the spread of mycobacterium tuberculosis bacilli to the myocardium either through hematogenous route or direct extension from pericardium or retrograde lymphatic spread from bronchial and mediastinal lymph nodes due to pulmonary tuberculosis.[9],[10] Myocarditis is assumed to involve both ventricles diffusely or, less commonly, the right ventricle alone. In one of the studies with endomyocardial biopsy, biventricular involvement was noted in approximately 70% of patients and alone right ventricular myocarditis in 8%.[11]

Myocardial involvement may be identified by aberrant ECG changes, transient localized and global wall motion abnormalities, and increased cardiac enzyme levels, as we have documented in the present study. Myocarditis is a challenging diagnosis to establish, and there is no clear in vivo gold standard since a negative endomyocardial biopsy result does not exclude the diagnosis. In recent years, abnormal myocardial mechanics, mainly left ventricular global longitudinal strain, have been extensively studied to diagnose cardiac dysfunction in various cardiovascular diseases.[12] Although echocardiography is the preferred imaging modality for the heart, computed tomography and Magnetic resonance (MR) imaging are likely underutilized due to their capacity to increase lesion visibility and characterization. In the present study, cardiac MR (CMR) is not performed due to cost constraints. CMR outperforms echocardiography in detecting tuberculous myocardial involvement, analogous to what has been reported in the Western European series on myopericarditis.[13],[14] Based on the 2013 European Society of Cardiology Working Group on Myocardial and Pericardial Diseases guidelines, patients with inflammatory myocarditis may benefit from immunosuppressive or immunomodulatory therapies, and those with an ejection fraction <40% should be treated with guideline-based heart failure therapy.[15]

Issues need further global research

Is cardiac dysfunction possible without the direct involvement of heart or structural heart disease in pulmonary tuberculosis?Whether systemic inflammatory surge is leading cause of cardiac dysfunction as measured by CRP titer in pulmonary tuberculosis?Whether direct and or indirect myocardial involvement due to tuberculosis pathology leading to cardiac dysfunction?Direct involvement due to TB is underestimated due to less expertise in invasive diagnostic modalities as myocardial samplings and reliability of these modalities is a real concernIndirect myocardial involvement occurs due to inflammatory surge and adrenal suppression. Adrenal suppression is common with or without adrenal involvement, resulted into cardiac dysfunctionWhether steroids should be added with ATT in these cases? As steroids will help in two ways, first cutdown inflammatory surge and second adrenal supportGlobal hypokinesia is the hallmark of cardiac dysfunction, especially in these cases with myocardial suppression and cardiac pump failure resulting into tachycardia and shock.

In the present case report, we have documented cardiac dysfunction in radiologically advanced lung disease with disproportionate tachycardia and tachypnea with hypoxia. Abnormal cardiac enzymes, sinus tachycardia in ECG and abnormal echocardiography confirmed myocarditis as the cause for cardiac dysfunction. We have successfully treated with steroids and ATT with the radiological resolution, bacteriological cure in pulmonary tuberculosis and normal cardiac function after 6 months.

Key learning points from this case report are:

More awareness regarding constitutional symptoms of pulmonary tuberculosis as majority of these cases were treated as enteric fever or jaundice and is the main reason for the delay in diagnosisCardiac dysfunction in active pulmonary tuberculosis is underestimated and less evaluated routinelyDisproportionate tachycardia and tachypnea with or without shock are clinical indicators to suspect early, especially in cases with risk factors like advanced pulmonary TB on chest radiographs with abnormal cardiac enzymesEchocardiography examination showed normal cardiac chambers, global left ventricular dysfunction with reduced ejection fraction and without structural pericardial or myocardial abnormalityTreatment with a short course of steroids with ATT backup is showing significant improvement in clinical status and have a significant impact on the final cardiac outcomeWe recommend always looking for cardiac dysfunction in pulmonary TB cases in cases with unstable cardiorespiratory parameters. Echocardiography is basic bedside noninvasive, reliable tool to diagnose cardiac dysfunction in expert handsThe learning point from this case report is never hesitated to give steroids even in advanced cases with ATT backup, which will significantly impact the final outcome in both TB and cardiac dysfunctionCardiac dysfunction is not rare; actually, it is double trouble in sick and critical cases with pulmonary tuberculosis cases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1	Adewole OO, Erhabor GE, Ogunrombi AB, Awopeju FA. Prevalence and patient characteristics associated with pleural tuberculosis in Nigeria. J Infect Dev Ctries 2010;4:213-7.
2	Anders JM. Tuberculosis of the myocardium. J Am Med Assoc 1902;39:1081-6.
3	Mayosi BM. Contemporary trends in the epidemiology and management of cardiomyopathy and pericarditis in sub-Saharan Africa. Heart 2007;93:1176-83.
4	Burgos LM, Farina J, Liendro MC, Saldarriaga C, Liprandi AS, Wyss F, et al. Neglected tropical diseases and other infectious diseases affecting the heart. The NET-Heart Project: Rationale and design. Glob Heart 2020;15:60.
5	Ortiz HI, Farina JM, Saldarriaga C, Mendoza I, Sosa Liprandi A, Wyss F, et al. Human African trypanosomiasis & heart. Expert Rev Cardiovasc Ther 2020;18:859-65.
6	World Health Organization. Global Tuberculosis Report; 2019. Available from: https://www.who.int/tb/publications/global_report/tb19_Exec_Sum_12Nov2019.pdf?ua=1. [Last accessed on 2020 Mar 10].
7	World Health Organization. Global Tuberculosis Control: Surveillance, planning, Financing: WHO Report 2008. Geneva: World Health Organization; 2008.
8	Bawri S, Ali S, Phukan C, Tayal B, Baruwa P. A study of sputum conversion in new smear positive pulmonary tuberculosis cases at the monthly intervals of 1, 2 & 3 month under directly observed treatment, short course (dots) regimen. Lung India 2008;25:118-23.
9	Rose AG. Cardiac tuberculosis. A study of 19 patients. Arch Pathol Lab Med 1987;111:422-6.
10	Liu A, Hu Y, Coates A. Sudden cardiac death and tuberculosis – How much do we know? Tuberculosis (Edinb) 2012;92:307-13.
11	Yilmaz A, Kindermann I, Kindermann M, Mahfoud F, Ukena C, Athanasiadis A, et al. Comparative evaluation of left and right ventricular endomyocardial biopsy: Differences in complication rate and diagnostic performance. Circulation 2010;122:900-9.
12	Kalam K, Otahal P, Marwick TH. Prognostic implications of global LV dysfunction: A systematic review and meta-analysis of global longitudinal strain and ejection fraction. Heart 2014;100:1673-80.
13	Imazio M, Brucato A, Barbieri A, Ferroni F, Maestroni S, Ligabue G, et al. Good prognosis for pericarditis with and without myocardial involvement: Results from a multicenter, prospective cohort study. Circulation 2013;128:42-9.
14	Syed FF, Aje A, Ntsekhe M, Mayosi BM, Moosa S, Tshifularo M, et al. Resolution of nodular myocardial tuberculosis demonstrated by contrast-enhanced magnetic resonance imaging. Cardiovasc J Afr 2008;19:198-9.
15	Caforio AL, Pankuweit S, Arbustini E, Basso C, Gimeno-Blanes J, Felix SB, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: A position statement of the European society of cardiology working group on myocardial and pericardial diseases. Eur Heart J 2013;34:2636-48, 2648a-2648d.