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Monthly Archives: March 2017

DMD Nephrology Case 1 – Acute Renal Failure

 

You are requested to see an 80-year-old man on the surgical service because of an elevated BUN and creatinine. He had just undergone a splenectomy for thrombocytopenia secondary to splenomegaly from underlying chronic lymphocytic leukemia.  Immediately before surgery his BUN was 22 mg/dl, creatinine was 1.3 mg/dl, urinalysis was normal.  When checked two days post operatively, his BUN had increased to 40mg/dl, and creatinine was 3/0 mg/dl.  Urine output for each of the last two days was approximately 250 ml/day.

 

Discussion points:

  • Given the above information, how would you characterize this patient’s kidney problem? (Go through the differential of prerenal, renal and post renal causes of azotemia)
  • What further information do you need to get historically, through the hospital record, and on physical exam on assessing this patient’s problems?

 

The patient denies symptoms of congestive heart failure.  He has not been extremely thirsty over the last several days.  He has had difficulty urinating over the past several years with a weak urinary stream and nocturia 3-4 times per night. His doctor told him that he had BPH but no therapy was given. The patient denies leg pain or flank pain.  The hospital chart is reviewed which showed the patient had significant bleeding in the operative period with several episodes of hypotension with systolic blood pressure in the 80 range.  These episodes lasted for short periods of time less than 5 minutes and returned to normal blood pressure after that period.  His urine output was 700 ml/day immediately after surgery and dropped to 200-300 ml/day over the past two days.  For the three days after surgery his total fluid balance is positive 3 liters.  His only medication postoperatively was analgesia with Dilaudid.  He did receive one dose of Cephalothin preoperatively and none since that time.

 

Discussion point:

  • How does this historical information affect your differential? (Include possibilities of post-obstructive renal failure secondary to prostatism, and acute tubular injury secondary to hypotensive episodes.)

 

The patient’s physical exam showed his T-37 C, RR-14, BP-130/90, P-82 with no orthostatic changes.  His mucous membranes were moist.  Neck pains were 1cm above the sternal angle.  The patient’s lung exam was clear to auscultation and percussion without rales.  Cardiac exam has a normal S1, S2 without S3 or murmurs appreciated.  The patient’s abdomen was soft with slight tenderness over the surgical scar.  No ecchymosis were noted.  The patient had no CVA tenderness or ecchymosis present in the back.  A foley catheter was placed in the patient at that time which showed approximately 50 cc of urine in the patient’s bladder.

 

Discussion points:

  • How does his physical examination help you in determining the cause of this patient’s acute renal failure? (No signs or symptoms of prerenal azotemia, or post renal obstruction.  The patient could conceivably have ureteral obstructions or trauma to his ureters during surgery though both seem unlikely?
  • What laboratory tests would you order at this time?

 

A fresh specimen of the patient’s urine is examined under the microscope and showed numerous epithelial cells and brown degenerating cellular casts.  No crystals or WBC’s were noted, and only rare RBC’s were present.  The urine sodium was 40 meq/l.  Urine specific gravity was 1.01.  Repeat BUN and creatinine on the 4th day after surgery are BUN-52 mg/dl, creatinine-3.5mg/dl. Uric acid was 9.2 mg/dl.  A renal ultrasound is done, kidneys are normal in size, and no signs of obstruction are present.

 

Discussion points:

  • What is your diagnosis at this time? (ATN seems most likely secondary to the patient’s episode of  hypotension during surgery. Both physical examination and renal ultrasound confirm no signs of bladder obstruction or ureteral obstruction)
  • How would you treat the patient at this time?

 

On day 6 after surgery, the patient’s BUN is 68 mg/dl, creatinine is 4.1 mg/d.  His urinary volumes are between 300-500 ml/day.  Serum electrolytes are NA – 142 mg/dl, K-4.2 mg/dl, Cl-98 mg/dl, HCO3-23 mg/dl.  The patient is started on fluid and salt restriction but he remains oliguric. By day 8 the patient’s BUN is 85 mg/dl, creatinine is 6.3 mg/dl.

 

Discussion points:

  • Is there anything else you would do to manage the patient at this point? (When do you start dialysis on a patient? What are the signs of uremia?)
  • What is the expected course of patients with acute tubular necrosis?

On day 9, postoperatively the patient’s urine output begins to rise to one liter per day, and by day 11 it is up to 3 ½ liters per day.  The patient’s BUN is up to 92 mg/dl, creatinine is 6.9 mg/dl on day 11.

 

Discussion points:

  • Given the patient is now in the polyuric phase of ATN, how would you change his fluid and electrolyte management?

On day 12 the patient’s urine output begins to decrease to 1/5 liters per day.  His BUN and creatinine begin to fall.  Fluid and salt restrictions are discontinued.  The patient is discharged from the hospital on day 14 and followed up as an outpatient. His BUN and creatinine returned to normal three weeks after surgery.

 

West Hills, Calabasas, Woodland Hils.

Assess:

  •    How do you know what your risk of having a heart attack will be? Should you be on therapy to lower your risks? What are the best ways to check your cardiovascular risks?
  •    To calculate your Heart Attack Risk, click here and have your recent Cholesterol and blood pressure numbers ready.

This calculator will give you your risk percentage of having a heart attack over the next 10 years

  •     How do you know what your cancer risk is? What are factors that increase my risk? What can I change in my life to lower that risk?

To evaluate your risk of cancer please click here.

Education

  •         Educating yourself on risk factors for having a heart attack is a crucial first step.
  •         Unsure what HDL Cholesterol or Total Cholesterol are?

o   Total Cholesterol:

  •  This is simply a total of all your cholesterol you have in your blood which includes the bad cholesterol  (VLDL and LDL) as well as the good cholesterol (HDL).
  •  What kind of numbers do you want?
  •         Anything over 240 mg/dL is considered high and puts you at twice as much of a risk of developing a heart attack
  •         At the Cardiovascular Institute we like to have our patients aim to keep their total cholesterol levels below 200 mg/dL

o   HDL Cholesterol:

  •  This is considered the good cholesterol. It is good because it carries cholesterol in your blood and brings it to the liver to remove it from your body. In doing so, HDL helps fight the “bad” cholesterol from building up in your arteries, thereby preventing strokes, heart attacks and high blood pressure.
  •  What kind of numbers do you want?
  •         Anything below 40 mg/dL puts you at risk for a heart attack
  •         At the cardiovascular Institute we like to aim to have our patient’s have levels above 60 mg/dL for optimal heart protection.

What can I do to increase my HDL cholesterol?

One of the best ways proven to increase your HDL or “good” cholesterol is exercise! Regular walking, jogging, or activity each day has been shown to increase HDL cholesterol.

  •         Unsure about blood pressure?

o   How exactly does high blood pressure affect my chances of having a heart attack?

  •  A heart attack is the result of a blocked blood supply to the heart muscle tissue. This can happen when the arteries to the heart become thicker and harder from a buildup of plaque. High blood pressure causes scarred arteries that fill up with plaque and become more prone to blood clots. Sometimes plaque or a blood clot can completely close an artery, blocking the blood flow to tissue on the other side.

High blood pressure, over time, also puts a strain on the heart and makes it work harder to pump blood out to the body. With this extra effort to pump, the heart grows in size and may compromise its ability to pump blood as well.

 

  •  What kind of numbers do you want?
  •         
Total cholesterol
Desirable Below                       Below 200
Borderline high                        200-239
High                                           240 or above
LDL (bad) cholesterol
Optimal                                 Below 70
Near/above optimal 100-129
Borderline high 130-159
High 160-189
Very High 190 or above
HDL (good) cholesterol
High 60 or above
Low Below 40
Triglycerides
Normal Below 150
Borderline high 150-199
High 200-499
Very high 500 or above

 

Up to 35% of cases of cancer have a dietary component, with some cancers being tied directly to diet. Research shows patients who follow a plant based diet that is low in fat and high in antioxidants and nutrients is associated with a lower risk of developing cancers such as colon, breast, pancreatic, and prostate cancer.

Implement:

Two of the biggest things you can do to lower your risk of both cancer and heart disease is to eat a healthy diet and exercise daily.

 

Exercise

  • Daily exercise is highly encouraged. We recommend 30 minutes to 1 hour of aerobic exercise. This can include jogging, walking, swimming, or biking. The benefits of daily exercise will not only make you feel better, more confident and happier but it will ultimately prevent disease and unnecessary trips to the doctor.

Diet

  • The old saying of “we are what we eat” has truth to it. We get out of our bodies what we put into them and how we care for them. New research points to a plant based diet reducing the risk of heart disease and many cancers. We also highly encourage a diet low in salt and carbohydrates. For numerous tips on what to eat , tasty recipes, and exercise please take a look at our book online, From Our Heart To Yours,

 

Electrophysiology Study and Radiofrequency Ablation

 

What is an Electrophysiology Study with Radiofrequency Ablation?

An electrophysiology study is a procedure used to evaluate abnormal heartbeats. During the procedure Dr. Ben-Zur uses a special type of cardiac catheter to inspect the electrical activity of the heart and assess heart rhythm, rate and type of heart beat. Radiofrequency ablation is performed for many different types of heart arrhythmias such as atrioventricular reentrant tachycardia (AVRT) or AV nodal reentrant tachycardia (AVNRT), atrial flutter, atrial fibrillation, and Wolff-Parkinson-White syndrome. The radiofrequency ablation procedure blocks the electrical signals traveling through your heart to stop the abnormal rhythm and allow signals to travel over a normal pathway instead.

 

When does a patient need this procedure?

Electrophysiology study and radiofrequency ablation will be considered if you have a persistent symptomatic arrhythmia that is refractory to medications and direct current cardioversion.

Dr. Ben-Zur will determine the need for this procedure based on your symptoms, results of diagnostics and current medical condition.

 

How are electrophysiology study and radiofrequency ablation procedures done?1

Before your procedure begins a specialist will insert an intravenous line into your forearm or hand, and you will be given a sedative to help you relax. After your sedative takes effect, Dr. Ben-Zur will numb a small area near a vein on your groin. A needle will be inserted into the vein with a tube (sheath) placed through the needle. Catheters will be threaded through the sheath and to the heart. Dye may be injected through the catheter to visualize blood vessels and heart via x-ray imaging. The catheters have electrodes at the tips that will be used during the procedure. Once in place, the electrodes will send electrical impulses to your heart and record your heart’s electrical activity. This will help detect the abnormal heart tissue that is causing the arrhythmia in your heart. Once the abnormal heart tissue causing the arrhythmia is identified, heat energy is applied at the catheter tip that alters the tissue triggering your arrhythmia.

 

Cardiac ablation usually takes 2-4 hours to complete, but complicated procedures may take longer. During the procedure, it’s possible you’ll feel some minor discomfort when energy is run through the catheter tips. If you experience any type of severe pain or shortness of breath, you should alert the medical team.

 

What to expect before the procedure:

Before the procedure you will have a pre-procedure appointment. This will include obtaining labs and any necessary imaging as well as any medication adjustments that need to be made for the procedure. This is an additional opportunity to ask any questions that you may have.

 

How long will the procedures take?

An electrophysiology study and ablation usually take 2-4 hours.

 

On the day of the procedure:

  • Do not eat or drink anything after midnight the night before the exam.
  • Do not ingest any stimulants for 24 hours BEFORE the test. This includes coffee, tea, and cola drinks.
  • Wear loose fitting, comfortable clothing.
  • Do not wear necklaces or clothing with metal on it (metal buttons, sequins, brooches, etc.).
  • If you have asthma presently or previously, bring your inhaler(s) with you.
  • Bring a list of your medications with you.
  • Take your usual morning medications with sips of water on the day of your test unless directed by Dr. Ben-Zur.
  • Notify Dr. Ben-Zur if you take insulin or diabetic medication as these medications may need to be discontinued or decreased the morning of the procedure.

 

What are possible complications?

With any procedure there is always a risk of complications. Electrophysiology studies and radiofrequency ablations are common medical procedures. Serious complications are uncommon but may occur. If Dr. Ben-Zur determines that you are a candidate for electrophysiology study and radiofrequency ablation, he will have a long discussion with you regarding the risks, benefits, and alternatives of the procedure, including but not limited to: infection, bleeding, heart attack, stroke, death, neurologic deficit, nerve injury, lymphatic injury, venous thrombosis, pericardial effusion (blood around the heart), pleural effusion (blood around the lungs), pulmonary embolism, hematoma, pain, need for an emergent operation such as emergency coronary artery bypass grafting, possible blood transfusion and its complications, complications associated with anesthesia, drug allergies, vascular perforation, dissection, rupture, thrombosis, distal embolization, arrhythmia (irregular heartbeat) that may require a pacemaker to correct, renal insufficiency/failure, dialysis dependence, limb loss, dye allergy, discomfort and bleeding at the catheter insertion site, and radiation exposure. Your risk of having these complications may increase if you have diabetes or kidney disease.

Wound site care:

  • No stitches are needed.
  • You will have a small sterile dressing on your wound. It may be removed the next day.
  • Keep the area clean and dry.

 

Need more information?

We encourage you to ask Dr. Ben-Zur any questions and discuss concerns you have at anytime. Visit our website at www.DrBenZur.com, give us a call at (818) 986-0911, or email us at ubenzurmd@gmail.com. You may also call Dr. Ben-Zur after hours if you have any additional questions that you did not have a chance to ask during your visit.

How do I get full on vegetables? Vegetables don’t fill me up and I’m still hungry.

 

This is one of the most common things we hear when suggesting that people switch to a diet consisting of mainly or all vegetables.

 

Here are a few simple things to add to this diet to ensure you get full. These veggies are high in protein:

 

  1. Spinach. Spinach is packed with protein, especially when given the amount of protein in spinach relative to the calories of spinach.
  2. Kale. Kale has even more protein per volume than spinach!
  3. Green peas. Green peas are a great source of protein. Try to avoid canned or frozen green peas as they are high in salt and frozen vegetables lose their nutritional value over time.
  4. Broccoli. Yes, those little weird looking trees are full of delicious protein. Ever wondered what it’s like to be a giraffe eating trees? Me neither, but you can pretend you are giraffe as you fill up on this wonderful veggies.
  5. Mushrooms. Not the ones growing in your backyard or forest!
  6. Asparagus. Take out a frying pan. Fill it half to ¾ with water. Boil the water. Drop in the asparagus and let it cook for a minutes in the water. Take a fork and push on the asparagus. If your fork easily goes through the asparagus, you know it’s done cooking. Refrain from adding butter, margarine, or salt. Enjoy!

 

These simple vegetable additions to your diet can help fill you up! So sit back and treat yourself to a mouthful of yummy veggies!

 

Myocardial infarction:

Definition:

According to the third universal definition (released in 2012 by theESC/ACCF/AHA/WHF), any one of the following criteria meets the diagnosis of MI:

 

  •         Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin)

 

AND at least one of the following:

  1.   Symptoms of ischemia
  2.   Development of pathologic Q waves on EKG
  3.   New or presumed new significant ST changes or new LBBB
  4.   Identification of an intracoronary thrombus by angiography or autopsy
  5.   Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality
  6. STEMI:
  7.  Definition:  ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads is present.
  8. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia.
  9.                                    From a clinical viewpoint, the division of acute myocardial infarction into ST-segment elevation and non-ST elevation types is useful since the efficacy of acute reperfusion therapy is limited to the former group.

 

  1.  Etiology: STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis. Slowly developing, high-grade coronary artery stenoses do not typically precipitate STEMI because of the development of a rich collateral network over time. Instead, STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury. This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation. In most cases, STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted (exposing its contents to the blood) and conditions (local or systemic) favor thrombogenesis. The amount of myocardial damage caused by coronary occlusion depends on
  2.                                the territory supplied by the affected vessel
  3.                                whether or not the vessel becomes totally occluded

                         iii.      the duration of coronary occlusion

  1.                                the quantity of blood supplied by collateral vessels to the affected tissue
  2.                                the demand for oxygen of the myocardium whose blood supply has been suddenly limited

                         Vi.      endogenous factors that can produce early spontaneous lysis of the occlusive thrombus

                         vii.      the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery.

 

  1.        Signs and sxs:
  2.                           Pain is the most common presenting complaint in patients with STEMI. The pain is deep and visceral; adjectives commonly used to describe it are heavy, squeezing, and crushing. Typically, the pain involves the central portion of the chest and/or the epigastrium, and, on occasion, it radiates to the arms. Less common sites of radiation include the abdomen, back, lower jaw, and neck. It is often accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom. The pain may commence when the patient is at rest, but when it begins during a period of exertion, it does not usually subside with cessation of activity, in contrast to angina pectoris.

 

  1.       Diagnostics:
  2.                              EKG:   Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential. Such changes cause a voltage gradient between normal and ischemic zones. As a consequence, current flows between those regions. These currents of injury are represented on the surface ECG by deviation of the ST segment. When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone.
  3.                                    Serum Biomarkers:  Certain proteins, called serum cardiac biomarkers, are released from necrotic heart muscle after STEMI. The rate of liberation of specific proteins differs depending on their intracellular location, their molecular weight, and the local blood and lymphatic flow. Cardiac biomarkers become detectable in the peripheral blood once the capacity of the cardiac lymphatics to clear the interstitium of the infarct zone is exceeded and spillover into the venous circulation occurs. The temporal pattern of protein release is of diagnostic importance. The criteria for AMI require a rise and/or fall in cardiac biomarker values with at least one value above the 99th percentile of the upper reference limit for normal individuals.

 

  1.   Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino-acid sequences different from those of the skeletal muscle forms of these proteins.  These differences permitted the development of quantitative assays for cTnT and cTnI with highly specific monoclonal antibodies. Since cTnT and cTnI are not normally detectable in the blood of healthy individuals but may increase after STEMI to levels many times higher than the upper reference limit  the measurement of cTnT or cTnI is of considerable diagnostic usefulness, and they are now the preferred biochemical markers for MI.

 

  1.  CK rises within 4–8 h and generally returns to normal by 48–72 h. An important drawback of total CK measurement is its lack of specificity for STEMI, as CK may be elevated with skeletal muscle disease or trauma, including intramuscular injection. The MB isoenzyme of CK has the advantage over total CK that it is not present in significant concentrations in extracardiac tissue and, therefore, is considerably more specific. However, cardiac surgery, myocarditis, and electrical cardioversion often result in elevated serum levels of the MB isoenzyme.

                                              

iii.    Imaging:  Abnormalities of wall motion on two-dimensional echocardiography are almost universally present. Although acute STEMI cannot be distinguished from an old myocardial scar or from acute severe ischemia by echocardiography, the ease and safety of the procedure make its use appealing as a screening tool in the Emergency Department setting. When the ECG is not diagnostic of STEMI, early detection of the presence or absence of wall motion abnormalities by echocardiography can aid in management decisions, such as whether the patient should receive reperfusion therapy

 

  1.  Treatment:  

INITIAL THERAPY — The patient with acute ST elevation myocardial infarction (STEMI) should have continuous cardiac monitoring, oxygen, and intravenous access. Therapy should be started to relieve ischemic pain, stabilize hemodynamic status, and reduce ischemia while the patient is being assessed as a candidate for fibrinolysis or primary percutaneous coronary intervention (PCI), with a goal of initiating PCI within 120 min of first medical contact.. Other routine hospital measures include anxiolytics, serial electrocardiograms, and blood pressure monitoring.

 

MONA:

  1.   M:  Morphine may be given for the relief of chest pain in the setting of acute myocardial infarction. We generally reserve its use for patients with an unacceptable level of pain, due to evidence of worse outcomes in patients receiving the drug. We give intravenous morphine sulfate at an initial dose of 2 to 4 mg, with increments of 2 to 8 mg repeated at 5- to 15-minute intervals.
  2.   O:   Oxygen, when hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction.
  3.   N:  Nitrates, intravenous nitroglycerin is useful in patients with persistent chest pain after three sublingual nitroglycerin tablets, as well as in patients with hypertension or heart failure. Nitrates must be used with caution or avoided in settings in which hypotension is likely or could result in serious hemodynamic decompensation, such as right ventricular infarction or severe aortic stenosis. In addition, nitrates are contraindicated in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction (or pulmonary hypertension) within the previous 24 hours.
  4.   A:  Aspirin, There is strong evidence to support the early initiation of dual antiplatelet therapy with aspirin and a platelet P2Y12 receptor blocker, irrespective of treatment strategy (fibrinolysis, PCI, or medical therapy), in patients with acute-STEMI.

 

STEMI EKG Changes:  

The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process (reversible [i.e., ischemia] versus irreversible [i.e., infarction]), the duration (acute versus chronic), the extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).           

 

Acute ischemia causes a current of injury. With predominant subendocardial ischemia (A), the resultant ST vector will be directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. With ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.

ST-elevation MI evolution — The classic (but not invariable) sequence of ECG changes in patients with STEMI is as follows:

 

  1.  The first change may be a hyperacute T wave. It is tall, peaked, and symmetric (the normal T wave is asymmetric with an upstroke that is slower than the downstroke) in at least two contiguous leads.

 

  1.  Initially, there is elevation of the J point and the ST segment retains its concave configuration but may become convex or rounded upward.

 

  1.   Over time, the ST-segment elevation becomes more pronounced and the ST segment changes its morphology, becoming more convex or rounded upward.

 

  1.   The ST segment eventually merges with the T wave and the ST-segment and T wave become indistinguishable. The QRS-T complex can actually resemble a monophasic action potential. This is a “current of injury” or so-called “tombstone” pattern. Reciprocal ST-segment depressions are usually observed in other leads.

 

  1.   The ST-segment returns to baseline, an initial Q wave develops, and there is a loss of R wave amplitude. When the ST segment elevation persists for greater than three weeks after the event, a ventricular aneurysm in the area may be suspected.

 

  1.   The T wave becomes inverted and it may remain inverted or return to upright

 

  1.   Over time, there is continued evolution of ECG changes. The R wave amplitude becomes markedly reduced, the Q wave deepens, and the T wave remains inverted or becomes positive. These changes generally occur within the first two weeks after the event; however, in some patients, they occur within a few hours of presentation.
  2.   LOCATION OF ST CHANGES IN RELATION TO LOCATION OF INFARCT:

ST-segment elevation, associated with epicardial coronary vasospasm or actual occlusion, is a relatively specific sign of acute transmural ischemia. ST-T wave abnormalities that are suggestive of acute myocardial ischemia in the earliest phase of ST elevation MI are usually localized to those leads that reflect the involved regions of the myocardium:

  1.        V1-V2 – Anteroseptal
  2.       V3-V4 – Anteroapical
  3.        V5-V6 – Anterolateral
  4.       I, aVL – Lateral
  5.       II, III, aVF – Inferior

 

  1.       Acute Anterior Wall MI:  An acute anterior wall MI presents with the changes in some or all of the precordial chest leads V1 to V6. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting most often as depressions of the ST segments in the inferior leads (II, III, and aVF). Reciprocal changes are actually the same ST segment shifts as seen from a different angle or direction.

 

  1.   Anteroseptal MI:  An acute anteroseptal MI presents with the changes in leads V1 to V2. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segments in the inferior (II, II, aVF) or lateral leads (I, aVL, V5, and V6).
  2.   Anterioapical wall MI:  An acute anteroapical MI presents with the changes in leads V3 and V4. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF).

 

  1.  Anterolateral wall MI :   An acute anterolateral MI presents with the changes in leads V5 and V6, often in association with changes in leads I and aVL (waveform 6). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF), and in some cases in leads V1 and V2.

 

  1.  Lateral wall MI:   An acute lateral MI presents with the changes confined to leads I and aVL (waveform 7). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as ST segment depressions in the inferior leads (II, III, and aVF) or leads V1 and V2.

 

  1.  Inferior wall MI – An acute inferior wall MI presents with the changes in leads II, III, and aVF. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting with ST segment depressions in leads I and aVL. The ST segment depression in the precordial leads V1 to V2 may be reciprocal, but more likely represents true posterior wall involvement (which may be diagnosed by ST elevation in leads V7 to V9) [4]. In addition, there may be the presence of ST elevation in the precordial chest leads V1 to V2. Involvement of the right ventricle may occur with an inferior wall MI and is confirmed by the presence of ST segment elevation in V3R and V4R. The duration of ST elevation in the right precordial leads may be shorter compared to the inferior leads, and, therefore, a right-sided ECG should be obtained as soon as possible after inferior wall ST elevation is noted.
  2.  Posterior wall MIAn acute posterior wall transmural MI reflecting left circumflex coronary artery involvement may be missed on a typical ECG. Posterior lead ECG (leads V7 to V9) should be completed if there is a high degree of suspicion or if ST depression is present in V1 to V3. The criteria for ST elevation in leads V7 to V9 are ≥0.05 mV in men over 40 years and women and ST elevation of ≥0.1 mV for men <40 years.

CONGENITAL HEART DISEASE

  1. Pulmonic Stenosis-
    1. Essentials of Dx
      1. Asymptomatic unless lesion is at least moderately severe.
      2. Severe cases may present with right-sided heart failure.
      3. High-pitched systolic ejection murmur maximal in the second left interspace with radiation to the left shoulder.
      4. P2 delayed and soft or absent.
      5. Ejection click often present and decreases with inspiration—the only right heart sound that decreases with inspiration; all others increase.
      6. Echocardiography/Doppler is diagnostic.
      7. Patients with peak pulmonic valve gradients greater than 60 mm Hg or a mean of 40 mm Hg by echocardiography/Doppler should undergo intervention regardless of symptoms. Otherwise, operate for symptoms.
      8. A dysplastic pulmonary valve usually requires surgical treatment, while a domed pulmonary valve stenosis usually can be treated with balloon valvuloplasty.
      9. RV outflow tract obstruction due to conduit stenosis, homograft stenosis and some prior bioprosthetic valve dysfunction may be treated with a percutaneous pulmonary valve replacement.
    2. Fun pictures for our edification

 

    1. Signs/Symptoms-
      1. Mild cases = asymptomatic; Moderate to Severe = symptoms of dyspnea on exertion, syncope, chest pain, and eventually RV failure.
      2. Palpable parasternal lift due to right ventricular hypertrophy (RVH)
      3. Loud, harsh systolic murmur and occasionally a prominent thrill are present in the left second and third interspaces parasternally.
      4. Murmur radiates toward the left shoulder (d/t the flow pattern) and increases with inspiration
      5. Loud ejection click CAN precede the murmur
      6. Right S4 gallop may be heard in the right subclavicular area
    2. Diagnostics Tests
      1. EKG–right axis deviation or peaked P waves give evidence of right atrial overload
      2. CXR–may show prominent RV or RA
      3. Echo–Test of choice
    3. Treatment
      1. mild pulmonic stenosis may be asymptomatic early in life and progressively get worse with age–important to monitor.  It can cause right sided heart failure in ages 20-30s.  
      2. percutaneous balloon valvuloplasty–treatment of choice
        1. indications–peak pulmonary valve gradient is greater than 60mmHg or mean gradient greater than 40 mmHg
  1. Coarctation of the Aorta
    1. Essentials of Dx
      1. usual presentation is systemic hypertension
      2. echocardiography/doppler is diagnostic: gradient over 20 mmHg may be significant due to collaterals around the coarctation
      3. associated bicuspid aortic valve (in 50-80% of patients)
      4. systolic pressure is higher in upper extremities than lower extremities; diastolic is similar
      5. pulse in femoral artery delayed compared to brachial artery
    2. symptoms and signs
      1. if cardiac failure does not occur in infancy, there are no symptoms until the hypertension produces LV failure or cerebral hemorrhage occurs
      2. strong arterial pulsations seen in the neck and suprasternal notch
      3. hypertension is present in the arms, but the pressure is normal in the legs and difference exaggerated by exercise
      4. femoral pulsations are weak and delayed compared to brachial or radial pulse.
      5. in severe cases–a continuous murmur heard superiorly and midline in the back or over the left anterior chest
    3. Diagnostic Studies
      1. ECG–shows LV hypertrophy
      2. CXR–”scalloping” of the ribs due to enlarged collateral intercostal arteries
      3. Echo–is diagnostic
      4. MRI and CT
    4. Treatment
      1. endovascular stenting is treatment of choice
      2. self expanding and balloon expandable covered stent
      3. surgical resection (end to end anastomosis)
        1. if untreated patients die of hypertension, rupture of aorta, infective endarteritis, cerebral hemorrhage before the age of 50
  2. Atrial Septal Defect and Patent Foramen Ovale
    1. Essentials of Dx
      1. often asymptomatic and discovered on routine physical examination
      2. RV lift; S2 widely split and fixed
      3. echocardiography/doppler is diagnostic
      4. All atrial septal defects should be closed by a percutaneous device or by surgery if there is any evidence of an RV volume overload regardless of symptoms
      5. A patent foramen ovale, present in 25% of the population, rarely can lead to paradoxic emboli.  Suspicion should be highest in patients who have cryptogenic stroke before age 55 years.
    2. symptoms and signs

Hold on to your Heart: A cautionary tale

 

As an advocate for lifestyle optimization, I have seen that for many patients, changes are often not made until the heart disease has progressed to a life-threatening level. My hope is that through sharing my these patients’ stories, that others may learn and avoid the need to put their own lives on the line to take the message to heart. It is my great privilege and joy in life to be practice medicine and bring health to my patients. Yet through my years of training and experience, I have come to realize the limitations of our medical tool box. I have come to see time and time again, that the lasting life changing improvements I’ve helped to bring to patients lives’ were achieved through diet and exercise.  

 

Case#1 -Hold onto your heart

 

I was a person who considered french fries my daily vegetable intake. I figured if it can’t run or fly and be doused with BBQ sauce, it wasn’t worth eating. My exercise consisted of picking up the remote control from the counter and sitting back down on the couch to watch TV. I was used to my high intake, low output lifestyle, but he was ignoring the signs of my heart. After years of doctors visits and medications, my His heart had given up trying to tell Bob that it wanted to be fed with fresh nutrients, free of fats, that it wanted to pump to make Billy move and enjoy life. Through this neglect, the processes of hypertension and atherosclerosis quickly took hold and soon, Billy’s heart was nothing more than a lump in his chest taking up space.

 

By the the time Bob finally started listening to the pain his dying heart was sending him, and came to see me, there was little we could do. Bob came to me morbidly obese, his heart was so diseased that the only possible solution would be to take out his heart and replace it with a new one. A dangerous procedure with long-term complications. However, it was the only way to save Bob’s life. Yet there was one problem. Bob had become so obese, that the surgeons could not operate on him unless he could lose some weight.

 

This is the point my counseling with Bob began to transform his life. He realized he had passed a point of no return and he could choose to allow life to keep happening to him as he always had, or he could take a stand to make some positive changes in his lifestyle. With my guidance, Bob took responsibility for himself and started to cultivate a new outlook and self discipline. By adopting a vegan diet and starting to get real forms of exercise, Bob was able to lose the 40lbs he needed to undergo his surgery.

 

Bob waited until the last possible moment after years of ignoring the information and warning signs around him, such as his shortness of breath with activity and lying down at night, the occasional chest pains, and the increased swelling in his legs.  He was able to prolong his life from the age of 50, but not without first losing his own heart. The effect of diet and exercise is never too late to change a life, but had it been incorporated by Bob just a few years earlier, he may have avoided the risky and complicated procedure all together.
I share this information not to blame Bob for what he went through, but to applaud him for having the courage to make lifestyle changes before it was too late; and with the hope that others may listen to their hearts and give their bodies the nutrition and activity it needs long before their body’s most important muscle dies of neglect. Celebrate your body by choosing to eat an informed  balanced diet high in vegetables, fruits and plant-based protein. Express your bodies innate abilities to move through exercise that makes you feel good. You will find that you will be more in tune with your heart and that your life will be infused with new vitality and passion. You will find that by nurturing a rejuvenated body, you will be able to avoid putting in someone else’s old heart.


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