Heart Desease Definition

The term "heart disease" is often used interchangeably with "cardiovascular disease." Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions, such as infections and conditions that affect your heart's muscle, valves or beating rhythm, also are considered forms of heart disease.

Heart disease is a broad term used to describe a range of diseases that affect your heart. The various diseases that fall under the umbrella of heart disease include diseases of your blood vessels, such as coronary artery disease; heart rhythm problems (arrhythmias); heart infections; and heart defects you're born with (congenital heart defects).

Many forms of heart disease can be prevented or treated with healthy lifestyle choices. Coronary artery disease, congestive heart failure, heart attack -- each type of heart problem requires different treatment but may share similar warning signs. It is important to see your doctor so that you can receive a correct diagnosis and prompt treatment.

Learn to recognize the symptoms that may signal heart disease. Call your doctor if you begin to have new symptoms or if they become more frequent or severe.

Symptoms and Prevention of Cardiogenic Shock

Symptoms and Prevention of Cardiogenic shock. Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most often systolic. The most common causes are serious heart complications. Many of these occur during or after a heart attack (myocardial infarction).

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction (MI). It occurs in 7% of patients with ST-segment elevation MI and 3% with non ST-segment elevation MI. It is a medical emergency requiring immediate resuscitation.

Cardiogenic shock can result from the following types of cardiac dysfunction:
Systolic dysfunctionDiastolic dysfunctionValvular dysfunctionCardiac arrhythmiasCoronary artery diseaseMechanical complications
Symptoms of Cardiogenic shock
Chest pain or pressureComaDecreased urinationFast breathingFast pulseHeavy sweating, moist skinLightheadednessLoss of alertness and ability to concentrateRestlessness, agitation, confusionShortness of breathSkin that feels cool to the touchPale skin color or blotchy skinWeak (thready) pulse
Prevention of Cardiogenic shock

Early coronary revascularisation in patients post-myocardial infarction (MI) and adequate treatment of patients with structural heart disease may help to prevent cardiogenic shock.
Better treatment of acute coronary syndrome seems to be reducing the rates of cardiogenic shock.

Breathing Problem After Cardio

Cardio is any type of exercise that elevates your heart rate and makes you breathe harder. Cardio exercise contributes to heart health and can be part of a healthy weight-loss program. Breathing issues or difficulties after a cardio workout can present a challenge. Learn how to anticipate, prevent and treat breathing issues after cardio to stay safe, healthy and comfortable.

Stress

Rapid breathing and shortness of breath can occur after cardio workouts even if you are in good physical health. Stress and anxiety contribute to a wide range of physical symptoms, including breathing issues. Exercising alone can give you time to think about events in your life, and in general physical activity is an excellent stress buster. When your life is pressure-filled, however, this alone time may not be as peaceful as you would like. If you are suffering from breathing problems after cardio due to heightened stress in your life, think about switching activities. Yoga and tai chi are quieter, more peaceful forms of exercise that can be calming to your body and brain. Engage in a team sport or another hobby with your friends to take your mind off your troubles.

Exercise-Induced Asthma

Exercise-induced asthma is one of the most common reasons that people have breathing issues after completing a cardio workout. Exercise-induced asthma is also referred to as exercise-induced bronchospasm, or EIB. During or after exercise, you may experience symptoms such as wheezing, a tightening in the chest, shortness of breath and coughing. Chest pain may accompany the other symptoms. EIB occurs when your airways become constricted, or narrowed, during exercise. Some people who have EIB also experience asthma attacks at other times, while others only experience asthma symptoms after cardio. Treatment for exercise-induced asthma includes using fast-acting inhalers prescribed by your doctor. You might also be directed to take an asthma maintenance drug to control and prevent symptoms. Exercising on warmer days or covering your nose and mouth with a scarf may control or eliminate symptoms.

Dehydration

Dehydration could cause breathing issues after cardio in children. Dehydration occurs when your body is excreting more liquid than you are taking in. Headache, dry skin and lips and decreased urine output are common signs of dehydration in adults and kids. Children may also experience a faster rate of breathing when they are dehydrated, according to BBC Health. A cardio workout makes you sweat, which means you need to replace those fluids. Drink water or a sports drink before, during and after physical activity to prevent dehydration.

Aging

Breathing issues after cardio could simply be a sign of aging. As you age, your lung function could decrease, according to the National Institutes of Health. This is especially true of older adults who also have heart disease. Lower levels of oxygen in the body can make you less tolerant to exercise, creating breathing difficulties during and after a workout. Keep your lungs healthy by not smoking. Participate in low-impact aerobic exercise as much as you can to stay healthy. Walking and swimming are examples of cardio that may not contribute to breathing issues. In the case of asthma, swimming can strengthen your upper body without triggering breathing symptoms.

Myocardial Infarction In Nursing Plan

Myocardial Infarction In Nursing Plan. Nursing care plan to the patients with Myocardial Infarction. Patients who suffer Myocardial Infarction they have many symptom include chest pain, shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom. In physical examination to the patient with Myocardial Infarction cases appear some of general symptom like comfortable, or restless and in severe distress with an increased respiratory rate.

The Nurse in medical care to take an action as nursing intervention they will collecting data and priority nursing care plane according to the patients condition. This is some nursing care plan (NCP) for patients with Myocardial Infarction related to patient condition :

1. Nursing care plan for chest discomfort (pain) due to an inbalance Oxygen (O2) demand supply.
- Asses the severity, location & duration of pain (report)
- Administer O2 with semi-fowler's position
- Obtain a 12 lead ECG during pain
- Monitor vital signs
- Administer Nitroglycerine & Narcotic analgesics as ordered
- Administer & Monitor Thrombolytic therapy
- Ensure rest & sleep, provide a comfortable environment
- Monitor patient's response to drug therapy

2. Nursing care plan for potential Arrhythmias related to decrease cardiac output.
- Monitor cardiac rate, rythm & conduction (report any change)
- Observe vital signs, ECG, urine output, skin temp & colour
- Administer prophylactic anti-arrhythmic & other drugs as ordered
- Administer IV fluids
- Promote physical & mental rest & comfort
- Monitor laboratorium result
- Keep anti-dysrhythmic drugs & defibrillator ready

3. Nursing care plan for respiratory difficulties (dyspnoea) due to decrease CO
- Asses for any dyspnoea, abnormal breath sound (report)
- Ensure propped up position, rest & comfort
- Administer O2 & drugs as ordered
- Psycological support, give liquid diet

4. Nursing care plan for anxiety & fear of death
- Encourage patient & family to express fear or anxiety by interest, listening, caring
- Explain the procedures being done on him
- Psycological & spiritual support
- Administer morphine or other anti-anxiety drug

5. Nursing care plan for activity intolerance related to limitations imposed by Myocardial Infarction
- Explain to the patient if he need Bed rest to decrease O2 consumption
- give liquid diet & stool softners to avoid constipation
- help for personal hygienic activity
- Watch for dyspnoea, chest pain during activity
- Administer O2 as needed

6. Nursing care plan for potential for complications of thrombolytic therapy
- Watch for sign & symptom of bleeding, arrhythmias ect
- Fix cannula for IV medication & blood collection
- Protect patient from any injury
- Monitor bleeding time & coagulation profile
- Keep anti-coagulant antidote ready (protamine sulphate ect)
- Monitor vital signs

7. Nursing care plan for discharge medications, follow up & Health teachings
- Explain the name, purpose & side effect of each medicine
- Ask for regular follow up & continuing medications at home
- Teach about management of chest pain at home
- Teach how to take Nitroglycerine
- Explain diet to avoid large meals, rest after meals
- Ask to seak immediate medical aid if chest pain not relieved after taking GTN and rest.

Why Man in His 60's with Very Subtle ECG and Pain not Controlled with Medical Therapy

Why Man in His 60's with Very Subtle ECG and Pain not Controlled with Medical Therapy. A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain.  Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG.  The patient had never had pain like this before.  The pain improved from 9/10 to 3/10 after NTG.  Here is the initial ED ECG:

QRS axis = 11, T-wave axis = 13.  There are very subtle signs of ischemia here: minimal ST elevation in I and aVL with minimal reciprocal ST depression in lead III.  Most specific is the abnormal ST segment and T-wave in aVF: it is downsloping with a subtly biphasic (down-up) T-wave.   There is also poor R-wave progression in anterior leads, but no ST elevation to suggest acute anterior MI.  This could be, however, evidence of old anterior MI.  Also, the T-waves in V4-V6 are taller than they should be relative to the R-wave amplitude.

This ECG, especially along with the very typical history, was very worrisome, but not absolutely diagnostic of, ischemia.  Several serial ECGs showed no change, even after the pain finally resolved to 0/10 after NTG.

He was given aspirin, clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was called and notified that this patient was very high risk and needed close attention.  He readily agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063 ng/ml (upper limit of normal = 0.025 ng/ml).  Repeat ECG remained unchanged.

He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on medical therapy with plan for angiogram in the morning.

Just before admission to the hospital, the patient admitted to recurrent pain and appeared uncomfortable.  Therefore, the cath lab was activated urgently.

The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or subtotal occlusion.

At cath, there was a 95% proximal LAD stenosis, proximal to a large diagonal.  A stent was placed and the patient became pain free.

The ECG the next AM is here:

QRS axis = 50, T-wave axis = 42.  The T-wave inversion in III is resolved, but this may be only due to a change in QRS axis.  In any case, there is minimal T-wave inversion in aVL and the ST elevation is resolved.  The ST depression in III is resolved.  The abnormal ST-T complex in aVF is resolved.

The troponon I peaked at only 1.117 ng/ml.  Echo the next AM showed a new Regional Wall Motion Abnormality of the distal septum, apex, and anterolateral wall with an estimated EF of 55%.  This anterior WMA is probably stunned myocardium that will recover (although the poor R-wave progression is consistent with previous completed infarction of the anterior wall).  This patient was at risk of a very large anterolateral STEMI and loss of large amount of myocardium.

Learning Points

1. Subtle ECG findings led to very rapid evaluation and treatment of this high risk ACS
2. The ECG alone is not an indication for urgent cath.
3. The entire clinical picture was then made more clear by an elevated troponin
4. The indication for urgent cath was uncontrolled ischemia in spite of maximal medical therapy in a patient with objective evidence of ACS as the etiology of the symptoms.

When there is not a STEMI, what are the indications for emergent cath?

The indications are uncontrolled ischemia, with objective evidence of ongoing ischemia.


I.   Objective evidence of ischemia
     1. Ischemic ST elevation; ST elevation known to be due to ischemia though not diagnostic of STEMI.
            a. Not ST elevation due to a normal variant or to LVH or LBBB etc. OR
            b. Dynamic ST elevation
     2. Ischemic ST depression (see the 5 primary patterns of ischemic ST depression)
            a. Not ST depression due to hypokalemia or LVH or LBBB
            b. Dynamic ST depression
     3. Positive troponin (this is a late finding!)
     4. New wall motion abnormality on ultrasound

Ischemic T-wave inversion is not necessarily evidence of ongoing ischemia!  Rather it is often a sign of reperfusion, even if evolving on serial ECGs!

II. Inability to control the ischemia with medical therapy alone (Ongoing ischemia)
     1.  Continued, refractory ischemia on the ECG or
     2.  Continued, refractory symptoms of ischemia (espeically chest pain) or
     3.  Shock, venticular dysrhythmias, pulmonary edema


In cases in which the ECG shows active ischemia, resolution of pain may be very deceptive.  Ischemia can be symptom free.  Studies of patients with known ischemia proven by dynamic ST segments on 12-lead ST segment monitoring show frequent periods of ischemia, including ST elevation and depression, not associated with symptoms.  Thus, if there is known ischemia manifesting on the ECG, these ECG findings of ischemia must resolve along with the symptoms.

Inferior lead & early repol & Diagnosed. Is it?

A 20-something male presented from an outside facility with Chest pain.  Vital signs were normal.

History: Onset of CP 2.5 hours prior to ED arrival.  "Tight and pressure, radiates to right arm, + nausea, + SOB.  No thromboembolism risks, not pleuritic, no radiation to the back.  No cardiac risk factors, no cocaine use.


He came with this ECG from the outside facility, recorded 1 hour after pain onset:

There is at least 2 mm of inferior ST elevation, with reciprocal ST depression in aVL, ST flattening in V4-V6, and T-wave inversion in V2.

Is this inferior ST elevation due to "early repolarization"?

No.  Why not? We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics.

1. There is reciprocal ST depression in aVL.  This occurred in 0 of 66 cases of early repolarization, and 99% of patients with inferior STEMI.
2. There is too much ST elevation.  In only 1 of 66 cases of early repol was there one lead with at least 2 mm STE.
3. Absence of ST elevation in V5 and V6.  In our group with inferior early repolarization, 53 of 66 had at least 1 mm of STE in V5, and 61 of 66 had at least 0.5 mm in V5.  64 of 66 had at least 1 mm of STE in V6 and 58 of 66 had at least 0.5 mm in V6.  In other words, when there is normal variant ST elevation in inferior leads, there is usually also normal variant ST elevation in V5 and V6.
4. T-waves are too tall.  T-waves in inferior leads are hyperacute, out of proportion to those in early repol
5. T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia.

95 minutes later, the patient arrived in the ED and here is the triage ECG:

There is 2-2.5 mm of ST elevation in inferior leads.  There is reciprocal ST depression in I and aVL, with T-wave inversion in aVL.  There is relative ST depression in V2 (isoelectric: in a young man it there should be at least 1 mm of ST elevation), thre is also flattening of the ST segment in V2.  There is ST depression from V3-V6.  There is a negative T-wave in V3, and biphasic T-waves in V4-V6.

There should be no doubt that this is STEMI.  All of the above 5 points apply, but now all the features have evolved and are more apparent. In addition, there is ST depression, diagnostic of ischemia, in V3-V6.

Nevertheless, the cardiologist consulted diagnosed early repolarization.  The patient did not undergo immediate cath.

22 minutes later, another ECG was recorded:

It is slightly changed.  See next image for side by side comparison

Side by side comparison of leads II and III on the first two ECGs:

ST elevation is higher on the repeat ECG than on the first, especially in proportion the the R-wave.  There appears to be a diminution of the T-wave amplitude; however, not when the R-wave amplitude is taken into account.

First troponin I returns + at 0.252 ng/ml.

191 minutes after first ECG:

There is resolution of ischemic findings, spontaneously.  There are no Q-waves.  There appears to have been spontaneous reperfusion.  The minimal remaining inferior ST elevation is now consistent with early repolarization

Heparin drip started.  CCU consulted.  Admitted to CCU.  Integrilin given.  Not take directly to cath lab.

A second troponin returned at 1.71 ng/ml 3 hours later.

The patient was not taken to cath for another 6 hours after this last ECG.  It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch.  A coronary aneurysm was found.  TIMI flow not reported.

Troponin I peaked at 75 ng/ml.



Next ECG available - 2 week followup:

There are inferior Q-waves of infarction, with T-wave inversions typical of completed inferior transmural MI.

This ECG, and the very elevated troponin, strongly suggest that the artery re-occluded during the extra 6 hour delay. 



Lessons:
1. Young people do have MI
          a. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated  with coronary aneurysms (left out to maintain anonymity) in this case.  Young women, when they have STEMI, often have coronary dissection.
          b. Nevertheless, even young people have atherosclerosis and plaque rupture.  We have seen many, such as this young woman.    And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"

2. When the ECG is unequivocally diagnostic, don't let young age or other atypical features deter you.

3. Know the features of STEMI look-alikes.  In this case, early repolarization was diagnosed by the cardiologist, who clearly was unaware of important differentiating features of inferior early repol from inferior STEMI (see above)

4. Once STEMI is diagnosed, the patient should go immediately to the cath lab even if the ST elevation resolves, because the risk is so high.  In this case, however, the diagnosis was also simply missed.
See this case to demonstrate the danger of reperfused STEMI!

5.  Finally, YOU have to be the expert and YOU have to advocate for the patient.  Cardiologists don't know everything, and in particular they don't know YOUR job, which is to differentiate the patients with benign symptoms (the vast majority) from those with Serious pathology.  If the cardiologist disagrees and is incorrect, the only way the patient will get good care is if YOU are the expert, YOU know what findings are true positives and true negatives, and YOU can explain why you are right and Advocate.

Cardiologists need to know a whole lot, but they don't do our everyday job of screening hundreds of symptomatic patients to find the one with the real thing.  They cannot be experts at that; you must be the expert.  They are much more likely to demand proof of disease than emergency physicians.  We demand proof of absence of disease.  And the cardiologists' opinions are of course often, or even usually, correct, but insist on a respectful conversation in which reasoning and evidence, rather than authority, direct the outcome.  That can only happen if YOU are well informed.


Here are two examples of early repolarization in the inferior leads:

First:

1. There is inferior ST elevation without reciprocal  ST depression in aVL.  This is because the ST axis is leftward, not down or to the right.  And thus the ST elevation in lead III is always less than or equal to that in lead II.  2. There is anterior and lateral ST elevation also; isolated ST elevation in inferior leads is relatively rare in limb lead early repol.        3. There are, in this ECG, well formed J-waves in leads V4-V6.  4. The QTc is less than 390, though we did not find this to be an accurate distinguishing feature of inferior ST elevation.  5. The ST elevation is at most 1 mm in inferior leads.

Second:

Slightly different, but the generalizations above apply here, too.

Found a great site for beginners in ECG, also good for experienced readers!

It's an Irish site.  It has excellent video demonstrations of the underlying pathophysiology of ECG findings correlated with simultaneous video of ECG evolution.

http://www.ecgteacher.com/

Increasing ST Elevation. STEMI vs Dynamic Early Repolarization vs Pericarditis.

Increasing ST Elevation.  STEMI vs Dynamic Early Repolarization vs Pericarditis.. Here is a series of ECGs with increasing ST elevation (STE).  They are of a young male with pleuritic, but not positional, chest pain.

Time zero:

NSR.  No remarkable findings.  Minimal STE in V2, V3, and I.  QTc 383.  LAD occlusion, early repol formula = 18.1


Time = 4.5 hours:

New, diffuse ST elevation. QTc 384, formula 19.1.  The ST axis is about 30 degrees (towards leads I and  II, such that there is STE in aVL, I, II, and aVF, but not III) and there is no reciprocal ST depression except in lead aVR).  This is very typical for pericarditis or diffuse early repolarization.  Pericarditis does not usually have T-wave voltage this high; a high T/ST ratio is more likely to be early repolarization.  Additionally, there are very well formed J-waves, typical of early repolarization.  It is highly unlikely to be acute STEMI.


There was no pericardial friction rub and echo revealed no pericardial fluid and no wall motion abnormality, and normal EF.

Time = 5.2 hours:

More ST elevation, especially in lead V2.  QTc 389, formula 20.56


Time = 7.2 hours:

No change.  QTc 389, formula 19.96



He ruled out for MI.

Diagnosis: probable dynamic early repolarization.  Could it be pericarditis?  Yes, but if there is no pericardial effusion and there is good cardiac function with negative troponins (not myocarditis with myocardial dysfunction), then pericarditis would be treated with Nonsteroidal antiinflammatory medications only.

In other words, the really important differential is this: is this STEMI, or is it a more benign etiology?  And to make this determination, it is important to know that early repolarization may be dynamic (1, 2).  And it may even change from hour to hour, or with heart rate or exercise.   We have seen this many times, though it is not common.

The use of the LAD-BER formula may be of great help and lead one to obtain an echocardiogram rather than activating the cath lab.

1. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61. 

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.


2. Mehta MC. Jain AC.  Early Repolarization on the Scalar Electrocardiogram.  The American Journal of the Medical Sciences 309(6):305-11; June 1995. 

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

What You Need to Know About Angina Pectoris

What You Need to Know About Angina Pectoris. Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand.

An episode of angina is not a heart attack. Having angina means you have an increased risk of having a heart attack.
A heart attack is when the blood supply to part of the heart is cut off and that part of the muscle dies (infarction).Angina can be a helpful warning sign if it makes the patient seek timely medical help and avoid a heart attack.Prolonged or unchecked angina can lead to a heart attack or increase the risk of having a heart rhythm abnormality. Either of those could lead to sudden death.

People who are at risk of angina are:
Men above 55 years old,Women above 65 years old,Obese or overweight,Cigarette smokers,Having high blood pressure,Having high cholesterol levels,Physically inactive,Having kidney disease,Having diabetes mellitus, andHaving family history of premature cardiovascular disease (men who suffer from heart disease below the age of 55 or women who suffer from the same disease below 65 year old).

Generally, angina pectoris is recognized in two types:
Stable angina is found more often in people. The symptoms of this type occur regularly and are predictable. Usually, people with this type suffer from the chest discomfort during exercise and stress, or after consuming heavy meals. Generally, the symptoms last not more than five minutes and improve when the patient rests or takes medications such as nitroglycerin, amlodipine besylate, or ranolazine.Unstable angina is found less often but more serious than the first type. Unlike the stable one, the occurrence of unstable angina cannot be predicted. The symptoms of this type also tend to be more severe. Unstable angina usually creates more pain and occurs longer and more frequent. Usual medication or resting cannot improve the symptoms. While unstable angina differs from heart attack, it is often noted as the precursor to heart attack.

Your doctor or nurse will examine you and measure your blood pressure. Tests that may be done include:
Coronary angiographyCoronary risk profile (special blood tests)ECGExercise tolerance test (stress test or treadmill test)Nuclear medicine (thallium) stress testStress echocardiogram
Your doctor may give you one or more medicines to help prevent you from having angina.
ACE inhibitors to lower blood pressure and protect your heartBeta-blockers to lower heart rate, blood pressure, and oxygen use by the heartCalcium channel blockers to relax arteries, lower blood pressure, and reduce strain on the heartNitrates to help prevent anginaRanolazine (Ranexa) to treat chronic angina

A Tough ECG, But Learn From It!

A Tough ECG, But Learn From It!. I have to tell this story from my point of view because I don't want anyone to think that the recognition of LAD occlusion was made in retrospect.  I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG.

The Case:

I was reading dozens of leftover ECGs from over a weekend and saw this one:

There are symmetric T-waves and poor R-wave progression.  There is 1 mm of ST elevation at the J-point in leads V2 and V3.  This formerly met "criteria" for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific.  It is nonspecific because normal variant ST elevation can be even much greater.  However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke.  See image below:

Slow upstroke, fast downstroke.  Asymmetric.

This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion.  So I went to look at the chart and here is the history:

This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.

This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:  

His pain continued and his ECG was read as normal.  His first troponin was normal.  He was admitted to the hospital for a "rule out."  His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml.  His ECG was repeated at this point:

This shows a well developed anterior STEMI.

The cath lab was activated and an LAD occlusion was opened.  The peak troponin I was over 100.  On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.

I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4).  The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.

To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.  

It is not a missed STEMI, but it is a missed coronary occlusion.  As you can see, the subtle findings are apparent and, with a prepared mind, can be detected.  Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation.  This is because of subtle ECG findings.  These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.


This patient had continued and ongoing pain.  If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.  

Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB.  In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve. 

Hyperkalemia and ST Segment Elevation

Hyperkalemia and ST Segment Elevation.A male in his 60's presented with weakness.  Here is his initial ECG.  He had no chest pain:

Probable junctional rhythm, with wide QRS (162 ms) and peaked T-waves.  Obvious hyperkalemia.  But there is also ST elevation in III and aVF, with reciprocal ST depression in I and aVL, and ST depression in V2 and V3.  Is there also an infero-posterior STEMI?

The K returned at 9.4 mEq/L.  He was treated with 5 g of calcium gluconate, 20 units of insulin and 100 ml of 50% dextrose and 100 mL of 8.4% bicarbonate.  Here is the second ECG 60 minutes later, with a concurrent K of 7.4 mEq/L:

Sinus rhythm with a normal QRS at 94 ms, with hardly any change in the serum potassium.  All the difference is in calcium administration.  The ST elevation is gone.

The troponin was normal.  All ST elevation was due to hyperkalemia.




A woman in her 40's was found down:

Sinus rhythm with wide QRS at 133 ms and obvious Peaked T-waves with obvious hyperkalemia.  But there is also significant ST elevation in V1-V3.  Is there anterior STEMI?

The K = 8.1.

After treatment with 3 g of calcium gluconate, 10 units of insulin, and 50mL of 8.4% bicarbonate (at 100 minutes), the K was measured again and was 6.5 mEq/L and this ECG was recorded:

QRS = 88 ms and ST elevation is now normal, not excessive.   


 The troponin was normal.

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hosting companies and a part of hosting services's analytics. The information inside the log files includes internet protocol (IP) addresses, browser type, Internet

Service Provider (ISP), date/time stamp, referring/exit pages, and possibly the number of clicks. This information is used to analyze trends, administer the site,

track user's movement around the site, and gather demographic information. IP addresses, and other such information are not linked to any information that is

personally identifiable.
Cookies and Web Beacons
http://cardio-help.blogspot.com uses cookies to store information about visitors' preferences, to record user-specific information on which pages the site visitor

accesses or visits, and to personalize or customize our web page content based upon visitors' browser type or other information that the visitor sends via their

browser.

DoubleClick DART Cookie


→ Google, as a third party vendor, uses cookies to serve ads on http://cardio-help.blogspot.com.

→ Google's use of the DART cookie enables it to serve ads to our site's visitors based upon their visit to http://cardio-help.blogspot.com and other sites on the

Internet.

→ Users may opt out of the use of the DART cookie by visiting the Google ad and content network privacy policy at the following URL -

http://www.google.com/privacy_ads.html
Our Advertising Partners

Some of our advertising partners may use cookies and web beacons on our site. Our advertising partners include .......


GoogleWhile each of these advertising partners has their own Privacy Policy for their site, an updated and hyperlinked resource is maintained here: Privacy Policies.

You may consult this listing to find the privacy policy for each of the advertising partners of http://cardio-help.blogspot.com.
These third-party ad servers or ad networks use technology in their respective advertisements and links that appear on http://cardio-help.blogspot.com and which are

sent directly to your browser. They automatically receive your IP address when this occurs. Other technologies (such as cookies, JavaScript, or Web Beacons) may also

be used by our site's third-party ad networks to measure the effectiveness of their advertising campaigns and/or to personalize the advertising content that you see on

the site.
http://cardio-help.blogspot.com has no access to or control over these cookies that are used by third-party advertisers.

Third Party Privacy Policies

You should consult the respective privacy policies of these third-party ad servers for more detailed information on their practices as well as for instructions about

how to opt-out of certain practices. http://cardio-help.blogspot.com's privacy policy does not apply to, and we cannot control the activities of, such other

advertisers or web sites. You may find a comprehensive listing of these privacy policies and their links here: Privacy Policy Links.
If you wish to disable cookies, you may do so through your individual browser options. More detailed information about cookie management with specific web browsers can

be found at the browsers' respective websites. What Are Cookies?

Children's Information
We believe it is important to provide added protection for children online. We encourage parents and guardians to spend time online with their children to observe,

participate in and/or monitor and guide their online activity.
http://cardio-help.blogspot.com does not knowingly collect any personally identifiable information from children under the age of 13.  If a parent or guardian believes

that http://cardio-help.blogspot.com has in its database the personally-identifiable information of a child under the age of 13, please contact us immediately (using

the contact in the first paragraph) and we will use our best efforts to promptly remove such information from our records.


Online Privacy Policy Only

This privacy policy applies only to our online activities and is valid for visitors to our website and regarding information shared and/or collected there.
This policy does not apply to any information collected offline or via channels other than this website.
Consent

By using our website, you hereby consent to our privacy policy and agree to its terms.



Update
This Privacy Policy was last updated on: Wed, Aug 7th, 2013.
Privacy Policy Online Approved Site
Should we update, amend or make any changes to our privacy policy, those changes will be posted here.