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| CURRICULUM IN CARDIOLOGY - CASE DISCUSSION |
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| Year : 2017 | Volume
: 3
| Issue : 1 | Page : 39-43 |
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Acute heart failure: A case discussion
Deepti Siddharthan, Sandeep Seth
Department of Cardiology, AIIMS, New Delhi, India
| Date of Web Publication | 17-Jul-2017 |
Correspondence Address:
Deepti Siddharthan
Department of Cardiology, AIIMS, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jpcs.jpcs_21_17
How to cite this article:
Siddharthan D, Seth S. Acute heart failure: A case discussion. J Pract Cardiovasc Sci 2017;3:39-43 |
| Introduction | |  |
A 45-year-old female presented with complaints of:
- Shortness of breath for 4 months
- Palpitations for 3 months.
| History of Present Illness | | |
The symptoms started with shortness of breath which was subacute in onset and progressed rapidly to New York Heart Association Class III (NYHA III) within a span of only 4 months. There was rapid worsening requiring hospitalization and subsequently mechanical circulatory support. There was a history of prolonged pharyngitis 3 weeks before the onset of the symptoms. There was also associated orthopnea. Dyspnea was not associated with cough, expectoration, or audible wheeze.
She was also having palpitations which were present for the past 3 months. These were intermittent, lasting a few minutes, not related to exertion and described as a perception of increased heart rate. These palpitations were not associated with presyncope and syncope.
There was no associated anorexia, abdomen pain, abdomen swelling, or pedal edema.
There was no history of chest pain or angina, fatigue, presyncope, or syncope. There was no history of joint pain or swelling or any abnormal movements. There was no history of receiving monthly injections in the past. There was no history of any prolonged fever requiring parenteral drugs.
There is no history of hypertension, diabetes mellitus, or smoking. There is no family history of premature coronary artery disease. She was perimenopausal. Obstetric history was unremarkable with 2 children and the last childbirth being 20 years ago. There is no history of consumption of alcohol or any other drugs.
The childhood history was unremarkable with no history of any recurrent infections.
| Discussion | | |
This is a 45-year-old female with subacute onset rapidly progressive dyspnea with orthopnea and palpitations suggestive of intermittent arrhythmias. The onset of the illness was preceded by an upper respiratory tract infection (URI). There is no history to suggest a respiratory cause for the dyspnea.
| What Would Be the Possible Causes? | | |
- Myocarditis followed by ventricular dysfunction should be kept as the first possibility in view of the short duration (2 months) and subacute onset with rapid progression with a history of preceding URI
- Coronary artery disease should always be ruled out especially above the age above 40 years in a perimenopausal woman. In the index case, the symptoms can be due to chronic ischemic heart disease or a silent myocardial infarction
- Ruptured sinus of valsalva can present with acute onset rapidly progressive heart failure even in the absence of a specific inciting event
- Rheumatic heart disease is always an important cause in India. Mitral stenosis can present with dyspnea and intermittent palpitations due to atrial fibrillation, however, the short duration of symptoms does not support this diagnosis. Regurgitant lesions like mitral and aortic regurgitation may remain asymptomatic for a long period with development of symptoms with onset of ventricular dysfunction. However, the rapid progression of symptoms is atypical for the natural course of these lesions
- Untreated and previously undiagnosed hypertension leading to heart failure may be considered. However, the progression is usually gradual
- Congenital heart diseases like atrial septal defects can also present at this age for the first time though the progression of symptoms is gradual.
| Examination | | |
On examination, the patient was in obvious respiratory distress with orthopnea. The heart rate was 110/min with frequent missed beats and the blood pressure was 86/50 mmHg. The respiratory rate was 36/min with use of accessory muscles. There was severe pallor, mild icterus, and severe pedal edema. The limbs were cold and clammy. The jugular venous pressure was elevated 6 cm above the sternal angle and both a and v waves were present. There were bilateral basal lung crepitations. The liver was enlarged 5 cm below the costal margin and was tender.
The cardiovascular examination was unremarkable. The chest was symmetrical, there was no precordial bulge. There was no evidence of cardiomegaly. There was no parasternal heave. Apex was in the 5th intercostal space in the midclavicular line and normal in character. The first sound was normal. The second sound was also normal. S3 was absent. There were no additional sounds or murmurs.
| Diagnosis | | |
Acute Decompensated Heart Failure. Cause to be ascertained with left and right heart failure, severe pulmonary artery (PA) and venous hypertension, NYHA Class IV, Anemia.
| Investigations | | |
Blood investigations
The investigations showed severe anemia with hemoglobin of 7 g/dL (microcytic and hypochromic) with evidence of iron deficiency on serum iron studies. The renal function and liver function tests were within normal limits. Cardiac enzymes were normal.
The electrocardiogram showed frequent ventricular ectopic beats. There was no evidence of any chamber enlargement. There were no ST-T changes.
The chest X-ray showed no cardiomegaly. The lung fields showed severe pulmonary venous hypertension (PVH) and pulmonary arterial hypertension (PAH).
Echocardiogram
This showed an ejection fraction of 20% with a left ventricle end-diastolic diameter of 55 mm with normal valves. The myocardium was thinned out but otherwise unremarkable. There was global hypokinesia. The right ventricular function was normal. The estimated PA pressure was 50 mmHg. The right atrium (RA) size was normal, TAPSE was 14 mm, inferior vena cava was slightly dilated but collapsing.
| Discussion | | |
At this point, the working diagnosis was:
- Acute decompensated heart failure (ADHF)
- Severe left ventricle (LV) dysfunction possibly due to acute fulminant myocarditis
- Severe PVH
- Severe PAH
- Class IV
- Normal sinus rhythm.
| Course of Disease | | |
Since a history was short and the cause was not clear, the next investigation had to be decided. A short history along with frequent ectopics favored doing a contrast magnetic resonance imaging (MRI) (recommended for investigation of recent onset heart failure).
Magnetic resonance imaging
There was evidence of myocardial edema appearing as an area of high signal intensity in T2-weighted images on MRI. Myocardial late gadolinium enhancement (LGE) reflecting irreversible myocardial injury, i.e., necrosis was also evident [Figure 1] and [Figure 2].
A coronary angiogram and endomyocardial biopsy were done. The coronary angiogram was normal, and the biopsy revealed acute fulminant myocarditis [Figure 3].
There was no improvement after 5 days of treatment (including infusions of dopamine, dobutamine, frusemide, noradrenaline along with blood transfusion and Bilevel positive airway pressure (BiPAP) ventilation) and she was assessed for end stage heart failure options including heart transplant and a left ventricular assist device (LVAD) were considered. An intra-aortic balloon pump was inserted. As the intra-aortic balloon was not enough to give support to the patient, 2 days later she was put on extracorporeal membrane oxygenation (ECMO) for better support and put on a priority heart transplant list.
As a heart transplant did not seem immediately possible, she was also evaluated for a LVAD. The right ventricular function was fairly normal, and an LVAD was implanted successfully [Figure 4]. She recovered successfully from the surgery and was discharged on the 10th day after surgery. She is currently doing well 1 year after surgery.
| Discussion | | |
This is a patient of ADHF (acute heart failure)[1] who worsened very rapidly over 4 months. The cause was fulminant myocarditis as revealed by the MRI and biopsy. It is possible that steroids might have helped her but her deterioration was too rapid to allow medical management. This case shows how rapid decision-making and quick use of mechanical assistance starting from an intra-aortic balloon pump to the implantation of a LVAD can save severe heart failure patients who otherwise cannot be managed medically.
In patients with unexplained heart failure cardiac magnetic resonance (CMR) imaging[2] is always a useful imaging investigation. Myocardial fibrosis can be picked up by LGE and T1 mapping. CMR and LGE can help distinguish ischemic and nonischemic areas and also help in the diagnosis of myocarditis, sarcoidosis, amyloidosis, hemochromatosis, and unusual diseases such as noncompaction of ventricle CMR may also help in selection of site for EM biopsy.
An endomyocardial biopsy should be done in all new-onset dilated cardiomyopathy of less than 6 months' duration, which is associated with either a failure to respond to usual care, sustained or symptomatic ventricular tachycardia, or high-degree heart block. This is a Class I indication[3] because it may indicate giant-cell myocarditis. Giant cell myocarditis is usually fulminant and should be considered for a transplant or LVAD but may respond to immune suppression like cyclosporine.
The second indication is fulminant heart failure[4] (<2 weeks duration) associated with hemodynamic collapse requiring inotropes or balloon pump support in the setting of a nonischemic cardiomyopathy. This is suggestive of fulminant myocarditis. Fulminant myocarditis has a good chance for recovery so every effort should be given to provide temporary mechanical support if needed.
Sometimes, sarcoidosis may be diagnosed on EM biopsy where treatment with steroids and immunosuppressive agents may alleviate the symptoms. Eosinophilic myocarditis also responds to steroids.
Management of the patient
ADHF can be categorized into hemodynamic stages[5] depending on cardiac index (CI) and pulmonary capillary wedge pressure. The stages are classified as the Forrester Hemodynamic subsets. CI indicates the degree of perfusion; patients are characterized as either “warm” or “cold” depending on the presence of hypoperfusion. A CI of <2.2 L/min/m2 warrants a classification of “cold,” indicating hypoperfusion. Signs and symptoms consistent with hypoperfusion include fatigue, hypotension, cool extremities, decreased renal function, and altered mental status. Patients are classified as either “dry” or “wet” depending on the presence of edema. Signs and symptoms of volume overload include cough, dyspnea, paroxysmal nocturnal dyspnea, elevated jugular venous pressure, peripheral edema, ascites, hepatomegaly, and splenomegaly. The most common presentation, constituting two-thirds of ADHF admissions, is warm and wet. In comparison to warm and dry, the subset which is cold and wet increases the rate of death by two and one-half times.
This patient was wet (pedal edema) and cold (low perfusion). Such patients are treated with diuretics and vasodilators and inotropics agents.
Intravenous loop diuretics are the mainstay of treatment for patients presenting with fluid overload. Bolus doses of loop diuretics are preferred. Furosemide is most commonly used; however, bumetanide and torsemide are equally efficacious. If patients have inadequate response to the maximum recommended bolus dose of a loop diuretic, continuous infusion of furosemide may be started at 5 mg/h and titrated to 20 mg/h as needed. The Diuretic Optimization Strategies Evaluation trial did not show a significant difference between safety and efficacy endpoints, but smaller studies have indicated a small increase in urinary output with continuous infusion.
If the blood pressure is less than 90 mm systolic then vasodilators cannot be given, and a vasopressor is added and diuretic added when the pressure is corrected. Dobutamine and milrinone are the inotropes of choice. Milrinone should be chosen to treat patients receiving concomitant beta-blockers since it exerts an effect on cardiac output and systemic vascular resistance via phosphodiesterase inhibition. Dobutamine, however, is the best choice for hypotensive patients, combined with dopamine, as milrinone can cause significant drops in blood pressure.
Patients who do not stabilize on drugs should be considered for mechanical circulatory support
These devices primarily provide circulatory support, unload the ventricles, and drive coronary perfusion and myocardial perfusion by increasing coronary blood flow.
Devices are broadly categorized into pulsatile and nonpulsatile.
The pulsatile device is the intra-aortic balloon pump.[6] The primary function of the intra-aortic balloon pump is to augment diastolic pressure and, as a result, drive coronary perfusion. The augmented mean arterial pressure is driven primarily by augmented diastolic pressure.
The continuous-flow devices can be further categorized into “axial-flow devices” or “centrifugal-flow pumps.” An example of axial flow pumps is the Impella axial flow catheter. This works by taking blood from the LV and directly ejecting that blood into the aorta. That's done through what's called a rotodynamic pump, so it's continuous flow.
The centrifugal-flow pumps are different. They include the (CardiacAssist) TandemHeart device, which, for left ventricular support, is a left-atrial-to-femoral-artery bypass device and also venoarterial (VA) ECMO.[7] Those two devices are different from the other devices because the pump sits outside the body, so it's extracorporeal. Essentially, there are two cannulas in those configurations. In the tandem configuration, blood is taken from the left atrium and circulated into the systemic circulation. In the ECMO configuration, blood is taken from the RA, oxygenated, and put into the systemic circulation. VA-ECMO is indicated in patients with refractory cardiogenic shock who have an underlying potentially reversible heart condition, although it can also be used as a bridge to a ventricular assist device or cardiac transplantation. Patients with irreversible organ damage, multiorgan failure, or those who are not candidates for transplantation will usually not benefit from ECMO support. ECMO is not generally recommended in patients who cannot be anticoagulated and severe aortic regurgitation or aortic dissections are contraindications for VA-ECMO.
In patients with cardiogenic shock or postcardiotomy syndrome, many short-term mechanical devices provide biventricular support. For chronic patients with Stage D HFrEF who are not transplant candidates, the only mechanical device option is LVAD support.[8],[9]
Indications for left ventricular assist device are
Patients with NYHA functional Class IV symptoms who have failed to respond to optimal medical management, including angiotensin-converting enzyme inhibitors or beta-blockers, for at least 45 of the past 60 days, or have been intra-aortic balloon pump-dependent for 7 days or IV inotrope-dependent for 14 days;
Left ventricular ejection fraction <25%; and functional limitation with a peak oxygen consumption <x;14 ml/kg/min, unless on an intra-aortic balloon pump, IV inotropes, or physically unable to perform the exercise test.
The protocol for selecting patients for an [Figure 5] is shown below:
The indications for destination therapy for LVAD include:
- Elderly
- Diabetes with multiple complications
- Pulmonary hypertension
- Renal dysfunction
- Recent malignancy.
Contraindication to LVAD is listed below:
Extreme body mass indices—that is, being extremely underweight or extremely overweight—are considered contraindications to LVAD implantation. The most important contraindication for LVAD therapy is a right ventricle (RV) that is unable to support LVAD flows. If one has a high suspicion of RV failure (based, e.g., on severe dysfunction with a low right ventricular stroke work index and high right atrial pressures), the best options are biventricular assist devices, total artificial heart replacement, and transplant. Furthermore, contraindication to anticoagulation is also a contraindication to LVAD implantation.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Gheorghiade M, Zannad F, Sopko G, Klein L, Piña IL, Konstam MA, et al. Acute heart failure syndromes. Circulation 2005;112:3958-68.  |
| 2. | Laissy JP, Messin B, Varenne O, Iung B, Karila-Cohen D, Schouman-Claeys E, et al. MRI of acute myocarditis: A comprehensive approach based on various imaging sequences. Chest 2002;122:1638-48. [ PUBMED] |
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| 4. | McCarthy RE rd, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Hare JM, et al. Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis. N Engl J Med 2000;342:690-5. |
| 5. | Nieminen MS, Böhm M, Cowie MR, Drexler H, Filippatos GS, Jondeau G, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: The Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J 2005;26:384-416. |
| 6. | Oshima K, Morishita Y, Hinohara H, Kadoi Y, Hayashi Y, Tajima Y, et al. Prolonged use for at least 10 days of intraaortic balloon pumping (IABP) for heart failure. Int Heart J 2005;46:1041-7. [ PUBMED] |
| 7. | Marasco SF, Lukas G, McDonald M, McMillan J, Ihle B. Review of ECMO (extra corporeal membrane oxygenation) support in critically ill adult patients. Heart Lung Circ 2008;17 Suppl 4:S41-7. [ PUBMED] |
| 8. | Oz MC, Rose EA, Levin HR. Selection criteria for placement of left ventricular assist devices. Am Heart J 1995;129:173-7. [ PUBMED] |
| 9. | Ammirati E, Oliva F, Cannata A, Contri R, Colombo T, Martinelli L, et al. Current indications for heart transplantation and left ventricular assist device: A practical point of view. Eur J Intern Med 2014;25:422-9. [ PUBMED] |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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