From our anonymous insider…
Heart failure week begins Sunday evening. Jane and I watch (at 1.75x speed) three hour-long lectures on hypertension and ischemic heart disease (due to obstructed arteries the heart is starved for oxygen causing chest pain d). The lecturer is a 35-year-old cardiologist who comes in Monday morning for a two-hour case workshop. “I get excited when I see 30-year-olds with hypertension. I can change their lives. When I see a 70-year-old patient with three decades of uncontrolled hypertension, the damage is already done.”
Hypertension is categorized by disease acuity. Malignant hypertension is a severe acute elevation of blood pressure that causes end organ damage, particularly in organs with dense capillaries, e.g., the kidneys and retina. Benign hypertension, over 95 percent of cases, is a progressive mild elevation of blood pressure. Our lecturer explained that Amazonian tribes with no exposure to Western diet typically show blood pressures of 80/50. Normal blood pressure for an occasional McDonald’s customer is 120/80. Greater than 140/90 mmHg constitutes benign hypertension. Over 200/120 mmHg is malignant.
“The vast majority of benign hypertension is simply caused by chronic excess of salt intake,” said the cardiologist. “Our bodies have evolved complex mechanisms to retain fluid by holding onto salt. Recommended salt intake is about 4 grams; most Americans consume about 10 grams per day.” About 30 percent of the US adult population has hypertension compared to 45 percent of the Japanese adult population with their salt-heavy fish diet.
He explained that, although salt intake is a serious driver, “there are many risk factors that interplay with this volume overload state. It is well-established that African Americans have an increased risk of hypertension. The current theory is that there was an evolutionary adaptation to holding onto salt in Sub-Saharan Africa. These adaptations helped individuals survive as young children in a dry environment with little access to salt.” He continued, “The unintended consequences of chronic hypertension that develop when you are 50 do not really matter from an evolutionary standpoint. Our genetics are most adapted to getting to reproductive age.” There is nothing that humans can do after age 50 to increase their genetic success? “I would like to think there is some selection that occurs during your 50s as you take care of your child, perhaps even into grandchildren-rearing age.”
Why is hypertension bad? “A misconception about hypertension is that the heart is at fault. Hypertension is not a disease of the heart, but a disease of the vasculature and kidneys. Cardiologists get stuck dealing with many of the serious complications.” The endothelial cells and smooth muscle cells of vessels do not respond well to chronically elevated hypertension. Over time, the increased pressure within the vessels hardens and narrows both large and small arteries (atherosclerosis and arteriosclerosis, respectively). The increased resistance decreases perfusion to tissues and increases the risk for thrombus (clot) formation leading to embolic events such as heart attack and stroke. Further, the left ventricle undergoes hypertrophy (thickening) as it struggles to pump against an increased total peripheral resistance.
“For most of my patients, losing weight is the most effective method,” said the cardiologist. “Unfortunately, only six percent of patients told to lose weight actually keep weight off at one year. I give HTN medications first and tell them that they can get off them once they lose the weight.” What about reducing salt? “Americans are so far to the extreme that taking away the salt shaker will do nothing. Shake away. Chronic benign hypertension needs antihypertensive medications.”
Where is HTN treatment going? “We are in the dark ages of hypertensive treatment and pharmacology in general. Most of us hope that in twenty years we will have a renaissance in pharmacogenetics to personalize treatment. Right now it is just black or white.” (White patients may respond to single drugs, but certain monotherapies are contraindicated in African Americans due to poor response rates. Black patients will be started on lisinopril in combination with a diuretic.)
The cardiologist concluded: “On a brighter note, we are at a unique point in human history that we are no longer dying from microbes and predators. Instead, we are eating, drinking and smoking our way to death. Not bad.”
The rest of the week was dedicated to the diagnosis and management of heart failure. First we learned multiple classifications:
- Diastolic v. systolic (relaxation versus contraction)
- Ischemic versus non-ischemic (oxygen supply to the heart muscle)
- Preserved versus decreased ejection fraction (percentage of blood pumped out of heart)
- Hypertrophic cardiomyopathy versus dilated cardiomyopathy
Retired Navy Physician: “Cardiology is not rocket science. It is just common sense.”
We were prepared for our patient case with a lecture on dilated cardiomyopathy, a systolic non-ischemic problem. The heart is enlarged due to growth of muscle cells, but the resulting thin-walled muscle is unable to pump enough blood. This can be caused by genetic defects, viruses (Coxsackie B), parasites (Trypanosoma cruzi causing Chagas disease), alcohol abuse, cocaine, and poorly understood autoimmune mechanisms.
For the most part, we’re not working with cadavers this year, However, this week we go into the anatomy lab to dissect the preserved hearts that we removed from our cadavers last year. Several students expressed frustration that they had to resurrect their anatomy outfits. Pinterest Penelope: “I thought we were done with anatomy lab. Another pair of scrubs will be tossed.” Our favorite trauma surgeon and an M4 helped with the dissection. We first weighed each heart and found that two-thirds weighed more than the normal 500 grams. The trauma surgeon attributed this to “pervasive hypertension”.
We used a scalpel to open the right atrium. We used angled probes to identify the veins draining the body: inferior vena cava, superior vena cava, and the barely visible coronary sinus. We then opened the left atrium with its four pulmonary veins draining oxygenated blood from the lungs. One student found a patent foramen ovale (PFO) type of atrial septal defect (ASD). You could see a hole connecting the left atrium to the right atrium. (The trauma surgeon expected more: “I would expect to have several PFOs. It is expected to be present in 25 percent of the population. Look closer!” We then opened the left and right ventricles to observe the heart strings connecting to the valves. Afterwards we went over to the “Tray of Horrors,” collected over multiple years. We looked at the severely dilated thin walls of dilated cardiomyopathy, a bicuspid aortic valve, and a heart with several stents in the left anterior descending coronary artery. “Good haul!, I am very impressed,” said our trauma surgeon. She suggested that our class contribute to the school’s archive: “Put the mechanical aortic valve and aortic dissection on the tray.”
Our patient case: Jonathan, 53-year-old construction manager and father of two, presents to the ED for progressive shortness of breath and swelling in his legs associated with a 15-pound weight gain over two weeks. Lung auscultation (listening with a stethoscope) reveals bibasilar (base of both lungs) crackles. Heart auscultation reveals a S3 gallop, an extra heart sound that sounds like a horse’s gallop, suggestive of rapid ventricular filling.
Feeling for the location of the heart under Jonathan’s left nipple revealed a laterally displacement. Chest xrays showed an enlarged cardiac silhouette and bilateral infiltrates (pathy whiteness at the base of the lungs) with accentuated vasculature at the hilum (connective tissue where the pulmonary artery, pulmonary vein and bronchi pierce through the pleura). EKG shows sinus rhythm with a left bundle branch block, left ventricular hypertrophy, and biatrial enlargement. An echocardiogram (ultrasound of the heart) shows dilation with a 30 percent ejection fraction (normal > 55 percent). Jonathan is diagnosed with dilated cardiomyopathy secondary to viral myocarditis (infection of heart). (“Viral myocarditis and dilated cardiomyopathy,” Kearney, et al. Post-Graduate Medical Journal, 2001 ).
Jonathan, his wife, and their 25-year-old son were joined by his cardiologist. Jonathan and the son rarely spoke; the wife, a middle school teacher, led the conversation. “We did not know what hit us. It came out of nowhere,” explained the wife. “I did not know what to say to my children or husband for weeks.” The son was clearly uncomfortable. When asked about his perspective on two separate occasions, he repeated: “I try to stay optimistic, and hope for the best. I just have to believe my father will pull through this.”
Jonathan’s symptoms rapidly deteriorated at the hospital to a point he underwent a LVAD (left ventricular assist device) implantation to improve his cardiac output while he waits for a heart transplant. “We would have liked to do the surgery at a larger hospital that does maybe 100 per year. There was just no time, he was on his deathbed,” explained the wife. “The surgeon had done maybe two in his life. We put our faith in him, and it fortunately went great.”
Jonathan has been on the heart transplant list for five years. He appears tired, worn out, although he still looks imposing in his burly 6’5″ frame. “It is hard to find a heart that fits his size,” added the cardiologist. His wife is convinced he will get one soon. She recounted the scariest day in her life: “I got a phone call from my husband telling me he got in a car accident. A truck veered into his lane, striking the car in front of him. He swerved off the road hitting a tree. “I believe God has a plan for him. He wouldn’t have come out of that car accident without any scars.” Jonathan: “I am realistic. I have lowered my expectations.” There is clearly a disconnect.
Jonathan’s symptoms have improved remarkably from his deathbed with the LVAD. His progress has pushed him down in the transplant list for more urgent cases. He is maintained on diuretics and antihypertensive medications. He quickly gets out of breath from walking. He has had to retire on disability, while his wife has picked up hours working at Starbucks after her job.
A student directly asked Jonathan, “Are you depressed?” “I feel like a failure. My whole life I provided for my family. Now I just sit and wait.” Several students went up afterwards to thank the family and look at the numerous batteries and charging devices for the LVAD. Mary asked to listen to his LVAD. “It sounded like a fish-tank pump.”
Our ethics lecturer and facilitator returned this week to introduce the topics of beneficence and nonmaleficence (do no harm). Lecture opened with the classic ethics train dilemma. “There are five people on the track who will die unless you pull the lever to divert it to the side track where one person will die. Would you pull the lever?” Most students responded via the iClickers, “Yes”. “Now you have five patients that need a transplant and a healthy tourist comes to town? Should you harvest the tourist’s organs to save your five patients?” The class responded “No”. Asked to justify the different answers, one student responded “The guy on the track got into his unfortunate situation, the tourist did not.” Lanky Luke: “Is that victim blaming?”
In our small groups, we went over the Jesica Santillan case. Jesica Santillan was treated for anemia in her hometown of Guadalajara, Mexico with iron supplements, but over the years her conditioned worsened and a heart murmur was found. She was diagnosed with restrictive cardiomyopathy, a genetic disorder requiring heart transplant. She crossed the border illegally to stay with a family member living in North Carolina and sought treatment at Duke. After she was denied Medicaid coverage, a local business owner and the community donated $500,000 to pay for a transplant. A heart and lung transplant was performed at Duke in February 2003. Unfortunately, she probably would have been better off getting the transplant in her native Mexico. The American transplant surgeon, James Jaggers, assumed that the organ program would not have contacted him unless the donor and Jesica were a match. Her body rejected the new
Full post, including comments