Matters of the Heart

Internal medicine meeting 8-9am

Case was an elderly patient with ischemic bowl disease. Pt had a history of CKD and Hypertensive heart disease. The systemic vascular disease led to ischemia, infarction, and ultimately necrosis. Bowl bacteria invaded in the intestinal veins and traveled into hepatic portal vein. The CT scan showed branching pattern of blackness through out the liver. I have never seen that before. It turns out to be bacterial gaseous byproduct, filling the hepatic vascular bed with gas. The attending informed the family that the mortality was 100% without operations, but mortality surgically removing the majority of small intestines will be 80%. The family opted out of the operations. One of the nephrologists led us in several interesting discussions about the intricacies of using diuretics on edematous patients. There are several pathophsyiology behind edema. For pulmonary edema, it's usually due to L heart failure. Using diuretics in CHF patients is tricky in that over-diuresis can lead to insufficient preload, decreasing Frank-Starling contractility. So for CHF, beta agonist is often used in conjunction with diuretics to ensure that contractile force and heart rate compensate for decreasing filling pressure. For LE edema and ascites, it is often due to liver cirrhosis or nephrotic syndrome. So it is likely that the effective circulating volume is higher than normal. Although often dropping oncotic pressure (due to proteinuria-induced-hypoalbuminia) can cause intravascular fluid shift into ECF, the kidney insufficiency also lead to water and sodium retention. So for chronic kidney disease, loop direuetics are the most effective, and there's less concern for hypovolumia with fluid reduction tx. For liver cirrhosis, decreased liver production of protein also reduces oncotic pressure; the other major pathophsyiology is venous flow back up. This will present with ascites and LE edema, and fluid overload as the body try to compensate for lack of arteriole blood volume. As Dr. Lopes so eloquently pointed out last semester, "fluid volume needs to be at the right location; venous blood backed up due to liver cirrhosis is not useful for perfusing the rest of the body."

A cardiologist also brought up different ways to monitor intravascular volume. Echocardiograph is non-invasive and very effective. One can check the diameter of the IVC, returning blood from the liver to the right atrium. If IVC is engorged, then there's fluid overload; if IVC collapsed, it's hypovolumia. Another more invasive constant monitoring is to measure central venous pressure.

We are curious if the massive amount of air in the hepatic vascular bed caused air emboli. Attending Dr. there were no clinical signs of emboli. The patient died, within 4 days of admission, of dropping BP and inoperable bowl infarction. We reasoned that the BP decrease due to septic shock even though the patient was too fragile to mount a typical systemic bacterial infection fever prior to shock.

Cardiology outpatient clinic with Dr. Chen (Department chief) 9-10am

We saw nearly 15 patients. Dr. Chen provides consultation on TLC, blood pressure/sugar control, and side effects management, choice and switch of medicine.

Cardiology rounds (3 cases) 10-11am
One case had aortic stenosis; I could hardly hear the systolic murmur in the room. But this made me realize that the ward is a fantastic place to practice my physical findings skills!
Another patient is 92 years old. She has complete AV block, grade III, ventricles and atria are marching to their own bands. Dr. Tu recommended PCI of setting up a pace maker for her. Sandy and I may be able to observe the procedure, yay!
The last patient was admitted due to UTI, Klebsiella pneumoniae. She was treated w/ Cefazolin; however he also suffered from HTN, CHF, and hypoglycemia. Dr. Tu stopped her glucose lowering meds. She was on both ACE-I and spironolactone. This is because long term ACE-I use will cause up-regulation of aldosterone receptor to compensate for reduced RAAS production. Spirolactone blocks aldosterone receptor and works in synergy with ACE-I. Getting to know a patient and his multiple drug list to manage intertwined co-morbidities is the best way to learn pharmacology!

Echocardiography 11-12pm, 2-5pm

We were in the ultrasound lab for several hours in the morning and in the afternoon. It was a fantastic review of some of the concepts we learned in CVRR and wonderful expansion of our currently knowledge base. Many of the patients had mitral regurgitation, but mostly mild cases. We learned to identify MR on the echocardiography. First locate the central of the valvular closure, then look at the color of the Doppler map. If there is a high frequency jet, then it is likely regurgitation. Because valvular insufficiency is similar to a slightly cracked open door, so when blood flows back through the crack, it'll be high velocity. We also learned concepts like QP/QS (pulmonary flow/systemic flow); normally, the ratio is roughly 1. However, if there is shunting, QP/QS may be greater than 1. For instance, in VSD, blood is shunted from the L side to the R due to the higher pressure in L ventricle. This will increase QP, simultaneously decreasing QS. We saw a case of mild para-menbranous VSD with incidental discovery at age 42.

Another case was really sad, a man in his 50s with H/O severe hypertension was experiencing tremendous stress at work; he was a security guard manager. One day he went to bed anxious about multiple phone calls from work reporting bad news, his middle cerebral artery ruptured. By the time his wife rushed him to the ER, 70mm of hemorrhage had been pressing on his brain. He had emergency craniotomy to remove the hemorrhage. But a couple hours later, another major artery ruptured in his brain. The trauma left him non-verbal and bed-ridden. In the matter of 7 months, he developed severe bed sore, to which repeated skin graft was rejected and detached. He now has a enormous raw spot on his buttock. He also has 3 tubes inserted, nasal-gastro-intestinal tube, fecal tube and urinary catheter. It is heart-breaking to see the condition he is in. His wife has been taking care of him since the traumatic events. I really admire her.

We also reviewed EKG. We saw a case of torsa de point. The earlier EKG strip showed warning signs of TDP, QT prolongation, which is a contra-indication for Amioderone. The cardiologist explained to us that there are 3 ways to salvage QT prolongation: Lidocaine, adminster K if hypokalemia was the cause, and beta agonist. He said that lidocain is a class Ib anti-arrthymic drug which shortens action potential by blocking Na channels. Beta agonist can also shorten action potential by increasing sinus beats. Correcting hypokalemia will also allow myocyte to depolarize more easily, increasing heart rate. We went to the ICU to check on the TDP patient; the doctor emphasized that we must switch the patient away from amioderone, as it shows both beta-blocker and K-channel blocker effects, worsening QT prolongation and TDP. Although the staff d/c Amioderone last night, they still had to defibrillate him many times due to the extremely long half life.

Other EKG features we saw were RBBB, hemiblock, L anterior fasicular block and posterior fasicular block. It's great to apply what we learned from Dr. Lope's narrated powerpoint and lab discussion real time. Dr. Tu showed us how to determine posterior from anterior fasicular block. In lead II, III, F, if the biphasic showed predominantly positive, then it is posterior fasicular block. If the biphasic ventricular QRS wave was mostly negative, then it is an anterior fasicular block. We also learned to identified and qualified locations of hyperkinesia, hypokinesia, dyskinesia, and akinesia. He said that with each contraction, the ventricular wall thickens, and then relaxes into a thinner configuration. If we see asymmetry between two ventricular adjacent to each other, the side that demonstrate lower amplitude in thickness changes is hypokinetic. This is often due to prior MI; if the MI is very severe, then the area can become akinestic (does not contract at all). Also, when one part of hear is hypokinetic or akinetic, the rest of the heart may compensate with hyperkinesia. Lastly, damaged myocyte that healed with fibrous cap becomes a ventricular or atrial aneurysm, which is dyskinetic, means that it has paroxysmal movement, bulging out when the rest of the healthy heart wall contracts. We saw a case of elderly patient, who had global hypokinesia, with severely compromised ejection fraction.

On the note of decreasing ejection fraction, I asked about what is the minimum EF that requires surgical intervention. Dr. Tu said that some virus and medications frequently cause dilated heart disease, leading to patients with 10-20% in EF. I read more about EF tonight and realized that EF can be increased with medications and mild physical therapy, life style changes, etc.

Pacemaker wound infection, case maker removal operation/wound cleaning 5-6pm

Dr. Fong, the cardiology director shared his experience of managing cardiologist patients; he also consulted us on as Dr. Tu inspect a patient’s mitral valve prolapse with U/S. They mentioned a cardiovascular surgery about to take place; Sandy and I were both excited. So I asked if it was possible for us to observe the procedure. Dr. Fong graciously made a phone call for us and took us to the operation room himself. The cardiovascular surgeon welcomed us warmly. Nicole is rotating with the CV surgeon this week, so we joined her. It was a fabulous experience. Even watching the surgeon scrubbing and dressing methodically prior to the operation was an eye-opener. He administered local Lidocaine 30-60 seconds prior to the first incision. He used an electric cauterizer, gingerly he extended the opening of the pacemaker horizontally. His goal was to remove the pacemaker and apply wet dressing to the infected, purulent wound. As soon as the patient verbalized pain, the surgeon dexterously injected additional Lidocaine, comforting the patient and then resuming excision. His plan is to apply wet dressing for a week while sterilizing the pacemaker, and then reinsert the pacemaker after infection is cleared. To insure better healing and reduce infection risk, he said that he will make a deeper pocket to house the pacemaker. Contrasted with the shallow pocket of the original pacemaker placement, this will reduce the tissue tension and promote wound healing. He emphasized that post-op healing should be one of the surgeon’s priorities, “you can be very good in surgery, but if the post-operation recovery is poor then you have mostly failed.” That ringed in my ears, resonating with “Do no harm.” At last, we asked if it is possible for us to observe the other 2-3 procedures scheduled during this week, he replied genuinely, “Any time! You can come here to learn anytime you’d like.”
After inspecting the heart in numerous ways today: from listening to heart murmurs in hospitalized patients, observing outpatient CV consultation and CV surgery, to echocardiograph, EKG, and chest radiograph, I am truly amazed at the enormity of each heart around me. Dr. Tu tirelessly answers my questions about CV epidemiology, pathophysiology, and pharmacology while performing U/S and attending to his patients; Dr. Fong support us beyond 8-5 schedule to learn; the CV surgeon welcomes us to observe the pacemaker extraction and wound cleaning. I am grateful and honored to learn from such big-hearted individuals.

“Nobody has ever measured, not even poets, how much the heart can hold.”
----Zelda Fitzgerald