Tuesday morning report at the VA was all about diuretics. We presented a case of a 73-year-old man with history of CHF, CKD and T2DM who presented with progressive dyspnea, bilateral lower extremity swelling, orthopnea, and abdominal distension. Physical exam showed evidence of volume overload with 3+ pitting edema, elevated JVD, and bibasilar pulmonary crackles. We considered various common triggers of heart failure exacerbation before diving into a discussion of diuretics.
Key points that we highlighted:
Decongestion with resolution of symptoms and edema is achieved through “diuresis” = loss of sodium (natriuresis) + loss of water (diuresis). That is why sodium-limited diet is crucial in treatment of fluid overload.
Loop diuretics function as “threshold” drugs that need to achieve a sufficient concentration in order to work. The natriuretic threshold is higher in patients with acute CHF than in healthy persons. That is why hospitalized patients require loop diuretic doses that are higher than stable outpatient doses.
Loop diuretics exhibit a “ceiling” effect and doses above the ceiling will not increase the amount of natriuresis. Acute CHF shifts the relation between plasma diuretic concentration and sodium excretion to the right and reduces the “ceiling.”
Patients with chronic diuretic use develop post-diuretic sodium retention and decreased efficacy with each subsequent loop diuretic dose. That is why loop diuretics are dosed multiple times daily and why patients need a net negative sodium balance each day.
Chronic loop diuretic use leads to distal tubular hypertrophy and once maximum loop diuretic effect is reached, auxiliary diuretics are sometimes used (thiazide, aldosterone antagonists, carbonic anhydrase inhibitors). We discussed specific situations you may consider using these agents.
Ethacrynic acid is the loop diuretic of choice in patients with sulfa allergy.
For further reading, check out this review from the NEJM:
Ellison DH, Felker GM. Diuretic Treatment in Heart Failure. N Engl J Med. 2017 Nov 16;377(20):1964-1975.
This morning, second year Med-Peds resident Nicky Herrick presented a great case female who presented with progressive sub acute shortness of breath. The patient’s past medical history notably included breast cancer they had been treated seven years prior with a chemotherapeutic regimen containing doxorubicin and trastuzumab. The patient was admitted to the hospital and initial work up revealed a new onset ectopic rhythm, volume overload, and pulmonary edema. Patient underwent a transthoracic echocardiogram (TTE), which demonstrated a severely depressed left ventricular ejection fraction, but no significant focal wall motion abnormalities. A CT chest with contrast was negative for pulmonary embolism. A coronary angiogram was completed showing no obstructive coronary disease. The ideology of the patient’s heart failure presentation was felt to be due to a combination of anthracycline and TKI induced cardiomyopathy.
We reviewed the broad classes of cancer therapeutics and their potential for cardiotoxicity:
While focusing on anthracycline toxicity, which is thought to be due to a the formation multimeric complex of DNA, anthracycline, and Topoisomerase causing DNA instability and subsequent cardiac myocyte apoptosis, we discussed that one of the most important determinants of whether patients would be susceptible to the short and longer term risks of cardiomyopathy are the cumulative dose of the anthracycline. It is important to know that these cumulative doses are additive across different types of anthracyclines as well. ASCO has published guidelines to help identify those patients who are at increased risk:
Finally, while anthracycline toxicity was traditionally thought to manifest in an early phase (causing dysrhythmias) and a chronic phase (causing CHF and cardiomyopathy), more recent literature suggests that LV dysfunction occurs early following exposure to such agents and adopts a indolent irreversible course. In a single prospective cohort study, ~30% of patients who received an anthracycline based chemotherapeutic regimen developed LV dysfunction as detected by surveillance TTEs done q3 months. 98% of those patients developed the dysfunction within the first year, bringing into question whether prior dogma of early and late phases of anthracycline mediated cardiomyopathy may have been a reflection of a lack of standardized monitoring, rather than a true bimodal distribution of disease.
Take Home Points:
A variety of chemotherapeutic drugs: anthracyclines, taxanes, tyrosine kinase inhibitors, checkpoint inhibitors, alkylating agents can all cause different forms of cardiotoxicity. As patients begin to live longer with more advanced chemotherapeutic options, clinicians will need to be aware of the downstream side effects that may limit patient’s survival long term.
Combinations of anthracyclines with TKIs and/or radiation to the cardiac bed may potentiate the risks of cardiotoxicity in cancer patients.
The traditional canon of different phases of anthracycline induced cardiomyopathy may occur early and more insidiously than previously thought due to closer monitoring of LV function.
Thank you Nicky for a great case, and thank you to Jason Duran for your expert input!
Today our amazing R3 Allen Jiang led us through a case of a elderly man with a history of HTN, HFpeEF, Afib and DM who came in with SOB and was found to have severe hypertension.
He had a headache and then developed respiratory failure and had a seizure and thus we were concerned for hypertensive emergency specifically for an intracranial process such as PRES.
We went over the classifications for severe hypertensive and also the mechanism of autoregulation for blood pressure for the brain to remind of how end-organ damage may manifest itself there.
Our expert discussant, Dr. Sean Evans reminded us that when BP is ultimately controlled, one might expect neurological recovery to occur within days to months, but rarely PRES is not actually reversible or there may be recurrent seizures.
Take Away Points:
PRES stands for posterior reversible encephalopathy syndrome, and is commonly associated with hypertensive emergency as well as pre-eclampsia/eclampsia as well as cytotoxic or immunosuppresive agents.
One might see white matter changes/ areas of edema on MRI specifically in the posterior or occipital regions of the brain but it is not present in all patients
Use IV labetalol or nicardipine as first line agents when treating HTN in PRES to lower the blood pressure carefully. Aim for 25% reduction in first 4 hours, as the blood pressure set point for hypotensive injury is much higher in patients with chronic hypertension!
Thanks again, Dr. Evans for your clinical pearls and to Dr. Jiang for a great case!
This morning we discussed the case of an elderly female who had a history of CAD and received a coronary artery bypass graft surgery nearly a decade ago, who presented with atypical chest pain, left arm numbness and tingling. Her admission work up revealed dynamic ECG findings indicative of ongoing ischemia and a transthoratic echocardiogram revealed new left ventricular dysfunction with a reduced ejection fraction. The patient underwent a coronary angiogram, which revealed native three-vessel disease, but patent bypass grafts. However, a 90% subclavian stenosis was visualized, as well as retrograde flow was visualized in the LIMA to LAD graft, suggestive of coronary subclavian steal syndrome.
We discussed the pathophysiology of this relatively rare complication, as well as the pertinent anatomy. Proximal left sided subclavian stenoses >75% are more likely to predispose patients to this phenomenon. However alongside left upper extremity symptoms such as claudication, paresthesias, numbness, weakness, and/or skin/temperature changes, there is an additional risk of vertebrobasilar ischemia given the location of the left vertebral artery that also sits distal to the region of stenoses. Symptoms that would be indicative of vertebrobasilar ischemia may include lightheadedness, presyncope, vertigo, ataxia, visual deficits, among other neurologic signs.
The patient underwent subclavian artery stenting, which ultimately relieved her extremity symptoms as well as her angina. Please see below.
Take Home Points:
Keep high index of suspicion for ischemia, particularly as females are more likely to present with atypical symptoms
Be aware of extra-coronary lesions that may result in hemodynamic changes to the coronary circulation. Coronary subclavian steal syndrome is a rare, but intervenable complication following CABG in patients with high grade subclavian stenoses
Today in Hillcrest, we discussed a patient with end-stage heart failure who was found to have RBBB+LAFB and an EF of 13%. We took this opportunity to review the conduction system, and EKG findings for bundle branch pathologies. After ruling out ischemic disease, we also explored possible etiologies for his non-ischemic cardiomyopathy with the acronym HIVEMIND (coined by CMR Gary Ma). A thorough history was key in eliminating many of the possible etiologies, and the key was his immigration from El Salvador which prompted testing for Chagas! He was ultimately diagnosed with Chagas cardiomyopathy and underwent cardiac transplantation. However, his story did not end there. After reviewing the illness script for cardiac manifestations of Chagas, which include arrhythmias, cardiomyopathy, and aneurysms, we learned that post-transplant patients still need to be regularly monitored the disease given the possibility of reactivation. This patient had not one, but two recurrences of his Chagas disease with significant conduction system disease (RBBB, 2:1 AV block) requiring multiple treatments with benznidazole and pacemaker placement!
Thank you to our discussant Dr. Anna McDivit for her insights on approaching bundle branch blocks, and for reminding us to have a lower threshold for ICD implantation in Chagas cardiomyopathy patients given their high risk for fatal arrhythmias! Thanks also to Dr. Gary Ma for his clever acronym for NICM.
Prolonged QRS intervals should prompt consideration of a bundle branch block, while axis deviations should prompt consideration of fascicular blocks.
The differential for non-ischemic cardiomyopathy is broad (think HIVEMIND!) – start with a comprehensive history to guide further testing.
Chagas disease is the most common etiology of non-ischemic cardiomyopathy in Central America. Consider Chagas disease in any patient with cardiac symptoms or EKG abnormalities from a Chagas-endemic area (particularly immigrants from El Salvador or southern Mexico).RBBB+LAFB is the most common conduction abnormality, though any can occur.
Chagas disease has an acute and chronic phase. First-line treatment for Chagas diseaseis benznidazole, although treatment is less effective for chronic infections.
Cardiac transplant is indicated in patients with Chagas cardiomyopathy and end-stage heart failure. Post-transplant patients must be monitored for disease reactivation.
Today we went through a outpatient case of a pregnant woman who comes to her primary care clinic for follow-up to acid reflux. She was thankfully doing fine but when we examined her we noticed that on her vitals she had an elevated BP, tachycardia, tachypnea, a systolic murmur and pedal edema. Should we be alarmed? Should we send her to the hospital?
We next revisited normal physiological changes to expect during pregnancy and ultimately concluded that we should be concerned about her elevated blood pressure but the rest of the physical exam findings are were normal for pregnancy. We then spend the next part of session going over the diagnostic criteria and findings for chronic hypertension, pre-eclampsia/eclampsia and gestational hypertension and the treatment option a. Our teams did a great job filling out the information and teaching each other. We were also fortunate to have our outstanding Family Medicine attending, Dr. Julie Celebi join us today to give us some expert insight regarding what she does in her practice.
Blood pressure should decrease as SVR decreases normally in pregnancy during the first trimester and then returning to prior baseline during the 2nd trimester. Elevated BP is therefore abnormal and should be concerning.
If BP is elevated prior to 20 weeks, it is likely chronic hypertension. if is elevated after 20 weeks without any lab abnormalities, it is gestational hypertension. With proteinuria, after 20 weeks, we are concerned for pre-eclampsia.
The current guidelines recommend treatment for SBPs >160, DBP >110, but for mild to moderate cases (between 140-150s/90-100s), treatment depends on patients’ co-morbidities and symptoms. First line treatment options are: PO nifedipine, IV labetalol or alpha-methyldopa. Attempt to deliver if this is a safe option for women experiencing pre-eclampsia/eclampsia.
Today, we discussed a case of a woman in her 30s who presented with chest pain. After diagnosing her with myocardial infarction, we noted she had few risk factors for obstructive CAD and broadened our differential for myocardial infarction with non-obstructive coronary arteries (MINOCA). We then reviewed her cath films, which showed a luminal narrowing in the ramus intermedius suggestive of SCAD. This prompted us to learn the illness script for SCAD, a nonatherosclerotic cause of acute coronary syndrome that primarily affects women. Expert discussant Dr. Jia Shen emphasized the risks of diagnostic and therapeutic intervention in SCAD patients, and that the main goal is conservative management unless they are at high-risk for further decompensation. Thank you, Dr. Shen, for your insights!
For ACS patients without significant risk factors for obstructive CAD, broaden your differential to consider “MINOCA” etiologies by coronary (vasopasm, dissection, microvascular dysfunction) and non-coronary causes (eg myocarditis, Takutsubo cardiomyopathy, etc)
Remember the 3 F’s of SCAD risk factors: Female, Fertility (ie pregnancy), and Fibromuscular dysplasia
DAPT and beta-blockers are the mainstay of medication management for SCAD – consider ACEI or statin if other indications. Reserve PCI or CABG for high-risk, hemodynamically unstable patients.
Today, PGY-2 Jenny Zhou presented an intriguing case of a woman in her early 20s who had been sent to the ED for a new murmur. She had a couple months of subjective fevers, fatigue, night sweats, weight loss dyspnea on exertion. Physical exam revealed a 4/6 holosystolic murmur heard best at the apex. Blood cultures grew 1/4 strep sanguinis. Surface echocardiogram showed a large vegetation on her mitral valve with severe mitral regurgitation. We took this opportunity to review Duke’s criteria, as well as some key differences between subacute and acute bacterial endocarditis. The echo also left clues suggesting some chronicity, prompting us to learn more about MR classification and severity. The 3-D echo revealed aneurysmal destruction of the leaflet, which led us to reflect on indications for surgery in endocarditis patients. This patient ultimately underwent valve replacement with tissue cultures confirming strep sanguinis as the culprit. The patient Spontaneous guest discussant and esteemed chief resident/HC attending Sean Kenmore added some great clinical pearls regarding about the patient’s blood cultures and EKG findings to look out for. Thanks, Dr. Zhou and Dr. Kenmore!
Subacute bacterial endocarditis presents with indolent, non-specific symptoms (subjective fevers, night sweats, weight loss) over weeks/months which may often lead to a delayed diagnosis and subsequently very large vegetations. It is often caused by different organisms than acute bacterial endocarditis, so ask the micro lab to run blood cultures for a longer time period!
Mitral regurgitation is classified by primary (valvular abnormality) or secondary (maladaptive changes) which helps guide the approach to management.
Look at ejection fraction with a different lens for patients with severe MR because of the volume lost to regurgitant flow back into the left atrium. For asymptomatic patients with severe MR, an EF of <60% is a class I indication for surgical intervention.
Our awesome PGY-2 and RACE tracker Averie Tigges presented a great case on a patient in their 50s who presented with shock of unclear etiology. We reviewed the different etiologies of shock, and a CT A/P incidentally found a large pericardial effusion. However, we recalled that tamponade cannot be diagnosed from a CT! In order to evaluate whether the patient’s pericardial effusion may be causing the hemodynamic instability, we reviewed various diagnostic tools to aid in what is ultimately a clinical diagnosis. In particular, we reviewed how to do a pulsus paradoxus, and our expert discussant Dr. Kahn discussed key echocardiographic findings such as RV diastolic buckling, IVC dilation, and mitral inflow variation.
The patient was found to have equivocal findings on bedside echo. However, in light of his Beck’s triad on physical exam, relatively low voltage on EKG, and subsequent cardiac arrest without other likely etiology, his shock was attributed to cardiac tamponade and an emergent pericardiocentesis was performed with 1L drained. The patient achieved ROSC and was ultimately discharged from the hospital.
Keep a broad differential for shock, as it may not always be so straightforward.
A large pericardial effusiondoes NOT equaltamponade. Utilize physical exam findings, EKG findings, pulsus paradoxus, echocardiographic findings to evaluate for tamponade.
Cardiac tamponade is a clinical diagnosis. No single diagnostic tool can confirm or rule out tamponade.