text:
You are here: Home / fix / Excerpt's from Steve Smith's ECG Blog
Excerpt's from Steve Smith's ECG Blog
June 16, 2011 by CrashMaster
EMCrit.org | Emergency Department Critical Care – Dr. Smith's ECG Blog
pseudo-normalization of T waves post-mi is actually a subacute phenomena (1-2 weeks) post-MI and the t-waves will be large and hyperacute. It is an expected event for the t-waves to eventually become upright with normal sized t-waves, this is not pseudo-normalization.
Inverted T-waves in aVL is similar to Wellen's
hypokalemia-prolonged QTc, U waves,
First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved. Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia. Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs., for instance, a younger smoker). Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs. Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations). Sixth, an upright T-wave is much more likely to represent posterior MI, but probably signifies reperfusion of the artery rather than persistent occlusion. An inverted T-wave can be either subendocardial or posterior. Seventh, placement of posterior leads is very helpful. Take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in 2 consecutive leads is very accurate for posterior MI.
ECGs gathered from around the country
Circumflex Occlusion May be Subtle or Invisible on the ECG
By Steve Smith
Below are 2 cases of circumflex or obtuse marginal (branch of circumflex) occlusions showing how subtle they may be:
A 52 y.o. male presents because he "thought he might be having a heart attack." He reports intermittent CP and SOB for 2-3 days. Pain worsened and became sharper after lifting a bookcase up the stairs. He continued to have worsening pain and diaphoresis, and associated left arm pain down to the fingers. Pt. reports MI in 2001 with a stent placed in the "marginal" artery. Pain is similar, but associated with less SOB. Exam is unremarkable. Here is the EKG at 1810:
There is subtle ST elevation in II, III, and aVF. It is not 1 mm. There is no reciprocal ST depression or T-wave inversion in aVL, so the diagnosis of acute inferior MI is difficult to make by the ECG. There are, however, Q-waves in II, III, and aVF. These could be due to old or acute MI. There is no ST depression in the precordial leads, or significant ST elevation in the lateral leads, any of which would have supported the diagnosis of inferior MI. This is a non-diagnostic ECG. A repeat ECG 1 hour later is subtly changed, with some evolving T-wave inversion best seen in V5 and V6.
A stat echocardiogram would have helped to make this diagnosis and facilitate timely reperfusion. Angiography and PCI were undertake 8 hours after the initial ECG and showed a completely occluded OM-1. Echo revealed inferior-posterior wall motion abnormality and troponin peaked at 100!
It is not unusual for occlusions of the circumflex or its branches to show little on the ECG even though they represent a large amount of ischemic myocardium at risk for complete infarction. The circumflex territory is known as being "electrocardiographically silent".
How can you make the diagnosis? First, this patient had a known stent in the "marginal" artery and thought he was having a heart attack. In such a situation, when you know that the circumflex is the likely culprit artery, you may suspect that an MI will not be obvious on the ECG. In this case the ECG was very suspicious for MI, but not diagnostic. Therefore, additional diagnostic testing is warranted. Possibilities include: serial ECGs (which were done but still nondiagnostic), stat echocardiogram, or posterior ECG. Use of the PRIME ECG 80 lead body surface mapping shows great potential for improving diagnosis in such cases.
By definition, this is a non-STEMI because there is not 1 mm of ST elevation in 2 consecutive leads. However, ST elevation is only an imperfect surrogate for complete acute persistent occlusion of an epicardial coronary artery without collateral circulation. It is neither fully sensitive nor specific. Even though the patient's ECG did not meet criteria for STEMI, he had all the pathology of a STEMI.
A 38 year old male with h/o smoking only c/o a few hours of severe substernal chest pain; he thinks he is having a heart attack. The pain is very nitroglycerine responsive. The first ECG with pain (unavailable) showed T wave flattening in V2 and V3. After resolution of pain with sublingual nitroglycerine, the second ECG was changed to near normal:
There are nondiagnostic T abnormalities in I and aVL, but little to suggest ischemia except that the precordial T waves are normalized. I was suspicious of LAD disease.
73 minutes later, the patient developed pain again:
The precordial T-waves are again flattened, without any other abnormality. Nitroglycerine
again eventually resolved the pain, and the following ECG was recorded at 2234:
Now the ECG is more normal appearing than ever.
The troponin returned at 0.81 ng/ml, so the patient was started on heparin and eptifibatide, in addition to IV nitroglycerine and Metoprolol (and, of course, aspirin).
His angiogram the next day revealed a 100% mid dominant circumflex occlusion that supplied the inferior and posterior walls. There was a large LAD that collaterally supplied some of the inferior wall. Echo showed an inferior-posterior wall motion abnormality. The troponin peaked at only 13, probably because of the collateral circulation from the LAD.
How could we have gotten him to angiography and PCI faster? Patients with objective evidence of acute coronary syndrome (positive troponin or ECG) AND uncontrollable pain should get emergent PCI even if they do not have ST elevation. This patient did become pain free on maximal medical therapy, so PCI was not indicated.
Fortunately, his MI was not large by biomarkers. Although he had a wall motion abnormality, this may go away over time.
Keep New:
Posted on: Mon, Mar 2 2009 6:24 AM
Updated: Wed, Mar 4 2009 11:46 AM
Clip/Blog This
Right Bundle Branch Block with Acute ST Elevation Seen Best on Prehospital ECG
This patient is 38 years old with hyperlipidemia. He was at the gym when he had the onset of chest pain. EMS was activated and recorded the following ECG (scanned from a prehospital ECG, so the quality is not perfect):
Notice the small Q wave in V1 followed by a very large R-wave, with a prolonged QRS. There is a wide S-wave in V6. Thus, there is right bundle branch block, which should never (unlike Left BBB) have any ST elevation. But here there is a large degree of ST elevation in V2-V6, I, and aVL. RBBB in acute STEMI has a very high mortality.
The paramedics activated the cath lab from the field.
The patient had 2 ventricular fibrillation arrests during transport, but was immediately defibrillated both times, and was awake in the ED, when the following ECG was recorded:
The ST elevation has mostly resolved on this ECG, and were it not for the arrest and the prehospital ECG, this would not be a slam dunk diagnosis. There is still ST elevation in I and aVL, but it is subtle. There are abnormal T waves in V2-V4, with straightening of the ST segment which is typical of hyperacute T waves.
Angiography revealed a very tight LAD stenosis with some flow (confirming the reperfusion that we see on the ECG). A stent was placed, and the patient had an excellent outcome with no wall motion abnormality.
Learning point: the prehospital ECG is critical, as was early prehospital cath lab activation. Were it not for this prehospital ECG and the cardiac arrest, the diagnosis may have been significantly delayed. Had this happened, the artery may have re-occluded prior to angiography, with resultant recurrent cardiac arrest and/or shock and death.
Posted on: Wed, Feb 25 2009 9:57 AM
Updated: Wed, Feb 25 2009 2:19 PM
Elderly With No Symptoms, Wellens's Thus Overlooked, Then ST Elevation Doubted
Here is a case of an 89 year old woman who had syncope but no chest pain or shortness of breath. Her initial EKG (#1) shows some nondiagnostic ST depression in V4-V6, probably due to LVH. She has a troponin of 0.13 ng/ml (ref range up to 0.09).
She is admitted, her trop peaks at 0.23, her next day EKG done 8 hours later is shown below (#2) and shows some terminal T inversion in V3, consistent with the positive trop and suggesting tight LAD occlusion but open artery (T inversions are "reperfusion T waves; an inverted T wave is a sign of an open artery and an upright T wave is a sign of occlusion or re-occlusion). Echo the next day is normal. She is diagnosed with "demand ischemia" and discharged home.
The patient returned with another episode of syncope 15 days later. She had no other symptom except weakness; none whatsoever. She had the following EKG at 0700:
Here there is 4 mm of ST elevation that can only be due to myocardial ischemia. If there is any doubt, then the presence of new ST elevation and T inversion in I and aVL should erase that. If there is still any doubt, the loss of R-wave amplitude in V2 and V3 should erase that as well. The inversion of the T wave in aVL and V2 suggests an open artery. However, this is a very strange looking Wellens' T wave because of the marked ST elevation.
The treating physician contacted the cardiologist immediately, but the cardiologist was not convinced, mostly because of the minimal symptoms and partly because it is not the classic morphology of anterior STEMI due to persistently occluded LAD, which should have upright T waves.
So they recorded another EKG at 0720:
Now the ST elevation is unmistakable, even with the persistently inverted T waves. But because the patient was asymptomatic, the cath lab was not yet activated. A bedside echo suggested anterior wall motion abnormality.
Another EKG was done at 0739:
This shows even more ST elevation. The patient was still asymptomatic. An initial troponin returned at 12 ng/ml. The cath lab was activated. There was a ruptured plaque with thrombus in the LAD, with some flow still (accounting for the inverted T waves).
Fortunately, the physicians were attentive and kept ordering frequent serial EKGs.
Learning point: some EKGs represent STEMI no matter what the symptoms, until proven otherwise by angiography.
Posted on: Fri, Feb 20 2009 5:53 AM
Updated: Wed, Feb 25 2009 9:35 AM
Hyperacute T waves
Below are several examples of hyperacute T waves.
Case 1 (Hyperacute T waves with ST depression–LAD occlusion).
The following is a perfect example of Anterior MI with LAD occlusion but WITHOUT any ST elevation. This is seen commonly, but only recently reported on by de Winter, Verouden, Wilde, and Wellens' in a long letter to the New England Journal (NEJM 359(19):2071-2073; Nov. 6, 2008).
The authors reported this morphology in 2% of LAD occlusions. The morphology is as follows: 1-3 mm of upsloping ST depression in leads V1 to V6 that continues into tall, positive symmetrical T waves, with normal QRS and loss of R-wave progression and with 1-2 mm ST elevation in aVR. Interestingly, they found that this was not a transient feature that later progressed to ST elevation, but that it remained static until angiography up to 50 minutes after the initial ECG. The mean time from symptom onset was 90 minutes. K levels were normal. MI was very large as measured by high CK-MB.
Case 2 (Hyperacute T waves present AFTER ST elevation is resolving).
This is the EKG of a previously healthy 40 year old man with one hour of chest pain and profound weakness and sense of "doom". He has a history of HTN, smoking, and family history. Vital signs and exam were normal.
This ECG show large symmetric T waves, best distinguished from those of early repolarization by the absence of large R-waves (in this case, the R-wave amplitude is very small). It also helps that there is inferior ST depression. There is some borderline ST elevation in leads V2 and V3. Similar to case 1, there is ST depression in leads V4-V6. This should be recognized as an EKG diagnostic for LAD occlusion.
A prehospital EKG had been done and is shown below (but has very poor quality)
This shows much ST elevation in anterior leads and illustrates an underrecognized phenomenon: hyperacute T waves are not only present early after occlusion, as the STEMI is developing, but also after the ST segment elevates AND they are present early after reperfusion as the ST segments are falling. They may be the only remaining clue to a reperfused LAD occlusion.
Case 3 (Hyperacute T waves misdiagnosed as Hyperkalemia).
49 yo man with 1 week of stuttering chest burning and tightness for 1-2 hours. Today the discomfort is associated with multiple episodes of vomiting and it is unremittant. The following EKG was obtained and hyperkalemia was diagnosed. The patient was treated with Calcium, Insulin, D50, and bicarbonate, with no change in the ECG. A bedside ultrasound revealed a possible anterior wall motion abnormality. The K returned at 2.9 mEq/L. There was an LAD occlusion that was opened and stented.
These T waves are NOT typical for hyperK. They are "fat" and wide, with a blunt peak and poor R-wave progression (especially V3). The T-waves of hyperkalemia are peaked and tented. See below:
Pure (Isolated) Posterior STEMI — not so rare, but often ignored!
Case 1.
This is a 44 yo male with h/o HTN, CABG at age 34, and 2 drug eluting stents to the first diagonal graft 3 months prior. He presented at 1810 with chest pain 5 days after stopping clopidogrel (on the instructions of another physician). The following ECG (#1) was recorded, with ECG #2 as his baseline.
#1, presenting ECG
#2, baseline from 3 months prior
#1 shows new marked ST depression in V2 and V3.
The differential diagnosis is subendocardial ischemia with probably NSTEMI vs. posterior STEMI. By ECG alone, posterior MI is more likely because of maximal ST depression in right, as opposed to left, precordial leads. However, given the history of severe 3 vessel coronary disease it is prudent to start with medical management, then observe for resolution of pain, but to also obtain an immediate echocardiogram to ascertain which wall is involved. If pain or ECG findings do not resolve, or if there is posterior wall motion abnormality, then immediate angiography with PCI is indicated.
In this case, maximal medical therapy was undertaken with Aspirin, clopidogrel, heparin, eptifibatide, metoprolol, and IV nitroglycerin and the patient was admitted to the CCU with cardiology consulted immediately. Chest pain resolved and angiogram was not done until the next day. It showed a 100% re-occluded SVG stent to D1; thrombus was suctioned out. Echo confirmed posterior wall motion abnormality. Max troponin was 47.
54 yo female with h/o smoking, DM, HTN, c/o chest pain for 3 hours, substernal radiating to both shoulders. She has an initial ECG which shows diffuse ST depression and she was treated for NSTEMI. She developed some pulmonary edema after metoprolol. ECG #2 was recorded:
ST depression is maximal from V2 to V4. This is due to posterior STEMI until proven otherwise. Unfortunately, it was treated as an NSTEMI for 2.5 hours until an echocardiogram showed a posterior wall motion abnormality. Cath revealed a 100% occluded circumflex. This was opened and stented, with the convalescent ECG below, which shows large upright posterior reperfusion T waves with a long QT.
How can such delay be avoided? By recording posterior leads V7-V9, at the level of the tip of the scapula and at the posterior axillary line (V7), a position midway between this and the spine (V8), and a paraspinal lead (V9). Also, obtaining a stat echo. Most of all, recognize this ECG pattern as being by far more likely to be posterior STEMI than due to subendocardial ischemia, which has maximum ST depression in leads V4-V6.
Here is a case of a 66 yo male with a history of CAD who presents with 1.5 hours of chest pain and is stable.
There is ST depression maximal in, again, V2-V4. The vast majority of posterior STEMI is not isolated, but rather concurrent with inferior and/or lateral involvement. In this case there is subtle ST elevtion in the inferior leads, not noticed by the treating physicians. Compare these ST segments with those of the post reperfusion ECG below:
The patient had rapid PCI of a 100% acutely thrombotically occluded mid circumflex which was opened and stented. There was 3 vessel disease.
The T-wave in posterior STEMI
Notice also that in the first (pre-reperfusion) ECG of case 3, the T wave is not upright as in previous cases. Some authors claim that the T wave must be upright for posterior STEMI. Evidence for this is lacking. In fact, an upright T wave probably indicates reperfusion of the posterior STEMI, whereas an inverted T wave is the analog of a hyperacute T wave (still occluded) but recorded from the opposite side. Either can be present in posterior STEMI, depending on the state of microvascular perfusion due to recanalization or to collateral circulation.
Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)???
This is a 46 yo male with acute onset of chest pain, in distress, who called the ambulance. He arrived and had this ECG recorded at 0118 AM:
There is 1 mm of ST elevation in V2 and V3, so this meets the criteria for reperfusion by the ACC/AHA guidelines. Unfortunately, the majority of patients who meet such "criteria" do not have MI. The most common reason for ST elevation is early repolarization.
(In this case, the limb leads are suggestive of ischemia as well, with some subtle ST depression inferiorly, suggesting pending ST elevation in aVL due to lateral MI from proximal LAD occlusion.)
I have developed a decision rule to differentiate Anterior STEMI from BER in patients who present to the ED with chest pain. These rules only apply when the DDx is Anterior MI vs. BER. A simple rule is the R-wave rule, which depends on the fact that, in BER, the R-wave is always well developed:
If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is almost certainly MI. If greater than 5 mm, it is probably BER. A cutoff of 5 mm gives a sensitivity for MI of about 70%, but a specificity of greater than 95%.
A more complex rule was derived using logistic regression, and involves 2 other variables: mean ST elevation at the J point (STEJ) from V2-V4, and computer measured QT-c (Bazett method). This relies on the findings that the mean ST elevation was higher in the MI group, and the mean QTc in BER is short (mean = 390 ms).
If the formula: (1.553 x mean STEJ) + (.0546 x QTc in ms) – (0.3813 x mean RA) is > 21, vs. less than or equal to 21, then it represents MI with high sensitivity and specificity.
In this case, the values are (1.553 x 1.0) + (.0546 x 420) – (.3813 x 1.17) = 1.553 + 22.93 – 0.3813 = 24.1
Thus, the rule predicts that this is anterior MI.
The clinicians were suspicious of MI, so they were smart to obtain serial ECGs. They obtained the second ECG at 0143:
This shows unequivocal straightening of the ST segments, compared to the first ECG. This ST straightening results in T waves which are fattened and "hyperacute". This is diagnostic of anterior STEMI.
He had a 100% proimal thrombotic LAD occlusion with TIMI-0 flow. It was opened and stented.
The followup ECG gives an idea of what this patient's T-waves looked like before his occlusion:
Posted by Steve Smith at 8:09 AM Reactions:
Tom B said…
Dr. Smith –
"If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is highly unlikely to be BER. If greater than 5 mm, it is probably MI. A cutoff of 5 mm gives a sensitivity for MI of about 70%, but a specificity of greater than 95%."
Is this a typo?
If the R-wave amplitude is greater than 5 mm, then it's probably MI? Or did you mean to say that it's probably BER?
I have two cases of anterior STEMI vs. BER, and in both cases, it turned out to be anterior STEMI.
In the first case, the mean R-wave amplitude in V2-V4 is less than 5 mm.
In the second case, the mean R-wave amplitude in V2-V4 is greater than 5 mm.
Would it be safe to say that the second case shows anterior STEMI in the presence of BER?
Thanks for another great teaching point!
Persistent ST elevation after previous MI, otherwise known as "LV aneurysm" morphology
Case 1. Classic anterior LV aneurysm morphology (Persistent ST elevation after previous MI).
This 46 yo male presented with chest pain. There is 1 mm of ST elevation in V1-V3, but there are large QS-waves preceding the STE. Such QS waves are highly suggestive of old transmural MI, with subsequent akinesis or dyskinesis of the anterior wall. Acute MI, if early in its course (first 6 hours, at least), always has tall T-waves in addition to ST elevation.
There is one retrospective study (Smith SW. American Journal of Emergency Medicine 23(3):279-287, May 2005) showing that the T/QRS ratio is significantly greater in acute anterior STEMI than in old anterior MI with persistent ST Elevation. The best criterion for differentiating was the sum of STE in V1-V4 divided by the sum of the QRS's in V1-V4 (TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4). If this value was <0.22,>0.36, then it is likely to be acute STEMI.
T-waves in aneurysm may be upright or inverted, but in neither case should they have high voltage. [Deep inversions suggest very recent NSTEMI (e.g., Wellens'). Tall T-waves suggest acute STEMI.]
The above ECG has a summed ratio of 0.05 and is clearly NOT an acute STEMI. It is important to know that only about 70%-80% of patients with the ECG morphology of "LV aneurysm" actually have an LV aneurysm, as defined by echocardiographic dyskinesis. "LV aneurysm" is far less common in this era of reperfusion, in which STEMI is not allowed to progress to full infarction (also known as "transmural" infarction, an old but useful term). The patient above had akinesis and had formerly had a mural thrombus, which is a common complication of an immobile wall which also may have post-infarction inflammation.
This patient ruled out for MI with negative troponins.
Case 2. Exaggeration of persistent STE after old MI by tachycardia
This 65 yo male presented with dyspnea but no CP. The lungs sound wet. The ECG is shown.
There is quite a bit of ST elevation in the anterior leads, but it is preceded by very deep QS waves suggestive of old MI. Previous MI can have persistent ST elevation, and just like in Left Bundle Branch block and other entities, ST elevation may be exaggerated in states of tachycardia. Therefore, the T-wave to QRS ratio may also be exaggerated. Here the formula TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4 = 0.27, substantially > 0.22, and would indicate acute STEMI. But one must be suspicous of a false positive in the presence of extreme tachycardia such as this. Also arguing against STEMI is the fact that there is no single T/QRS ratio (V1-V4) > 0.36.
The difficult decision is this: is this an old MI with exaggerated persistent STE due to tachycardia, or is it an old MI with a new STEMI superimposed? Given that the BNP was > 5000 and the patient had no chest pain, and the high likelihood that such a morphology represented the former (not the latter) diagnosis, the patient was not set up for angiogram and reperfusion.
A previous ECG was found and is shown:
It is evident that there previously was classic LV aneurysm morphology, but with much less ST elevation. The ratio here is 0.05. A previous echo had shown severe decreased LVF with an akinetic anterior wall.
Clinicians correctly interpreted the first ECG as exaggeration of ST elevation of old MI due to tachycardia, stress, and exacerbation of CHF. Treatment of CHF resulted in a slowing heart rate. Follow up confirmed all troponins negative and resolution of ST elevation when the heart rate came down.
Inferior Hyperacute T-waves
This is a 58 year old male with 40 minutes of chest pain of acute onset. He called 911 and paramedics recorded a prehospital 12 lead ECG which showed a clear inferior STEMI (not shown, tracing could not be found). He was given aspirin and sublingual nitroglycerine, which improved his pain. The cath lab was activated by the paramedics. On arrival, the following ECG was recorded.
There is 0.5 mm of ST elevation in inferior leads II, III, and aVF. In addition, the T-waves in II, III, and aVF are very large, significantly larger than normal in both height and width. To diagnose inferior MI, there must always be reciprocal ST depression or T-wave inversion or both in lead aVL. This is present here.
Hyperacute T-waves can be present early, before the ST segment elevates, but they can also be present as ST elevation is resolving from spontaneous reperfusion.
In this case the diagnosis was clear due to the prehospital ECG. But suppose there had been no prehospital ECG? Or if the first ECG had looked like this? Suppose the ST segments were on the way up rather than on the way down. Would you have diagnosed this? This identical ECG could be all the evidence you might have.
If you find yourself in this diagnostic dilemma and you are uncertain of the diagnosis, remember that you can use serial ECGs, old ECGs, and immediate echocardiography to help in the diagnosis.
Comment on Posterior STEMI
from Dr. Smith's ECG Blog by Steve Smith I had a very good question regarding the post on posterior STEMI, and I wanted to be sure that the answer gets attention:
smallville said…
While your blog does an excellent job of highlighting posterior STEMIs that were mistaken, are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI? Will posterior ST alteration always be limited to v2-v4?
This is a very good question, and not easily answered because there is very little solid research on this.
First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs., for instance, a younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).
Sixth, an upright T-wave is much more likely to represent posterior MI, but probably signifies reperfusion of the artery rather than persistent occlusion. An inverted T-wave can be either subendocardial or posterior.
Seventh, placement of posterior leads is very helpful. Take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in 2 consecutive leads is very accurate for posterior MI.
References on posterior leads:
1) Matetzky S et al. Acute myocardial infarction with isolated ST-segment elevation in posterio chest leads V7-V9: "hidden" ST -segment elevation revealing acute posterior infarction. JACC 1999;34:748-53
2) Matetzky S et al. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. JACC 1998;31 506-11.
3) Wung SF et al. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87:970-4; A4.
Pseudonormalization of T waves, Coronary occlusion without 1 mm ST elevation
This 64 year old woman presented intoxicated with nausea and vomiting and epigastric pain, with no chest pain. She has a history of a stent, but unknown in which artery. She stopped taking clopidogrel 2 weeks ago because she ran out.
Notice there is deep symmetric T inversions in inferior leads, and a large upright T wave in aVL. There is also some T inversion laterally. This is all suggestive of inferior (and lateral?) Non-STEMI, due to reperfused RCA or circ. Inverted T waves are also known as "reperfusion" T-waves. If they are in the anterior leads, they are often referred to as "Wellens' T-waves."
A troponin returned elevated, and a repeat ECG was recorded:
Now the inferior T-waves have become mostly upright, in this case biphasic. There is some ST elevation, but it is not quite 1 mm in two consecutive leads. There is new ST elevation in lead V1, which in this context is diagnostic of right ventricular STEMI.
This phenomenon is called "pseudonormalization of T-waves" because normal T-waves are upright (same axis as QRS), but become inverted in non-STEMI that is reperfused. They become deceptively upright (not normal, but "pseudo" normal) when the artery re-occludes. Thus, where reperfusion of the infarct-related artery (IRA) leads to T-wave inversion, if inverted leads become suddenly upright, this is diagnostic of re-occlusion of the IRA.
There is nothing magical about 1 mm of ST elevation. ST elevation is used as a very imperfect surrogate for coronary occlusion. Coronary occlusion that does not spontaneously reperfuse or is not compensated for by collateral circulation will quickly lead to irreversible myocardial loss. Reperfusion therapy is indicated for occlusion, even when there is not 1 mm of STE in 2 consecutive leads. However, the specificity of the ECG for occlusion becomes less as the STE is less. So expertise in interpreting the ECG is particularly important for these cases.
In this case, it was clear that there was a very unstable thrombus in the RCA or circ, and that if it was not 100% occlusive, it was very nearly so.
The cath lab was activated, a 100% proximal RCA stent thrombosis was seen and the artery was opened.
This also illustrates how chest pain or even discomfort may be completely absent in STEMI. Below is the post-cath ECG, showing T-waves are now inverted again (indicating reperfusion).
Posted by Steve Smith at 7:36 AM
Deep and widespread ST depression signifies high risk coronary lesion
This 51 yo male presented with Chest pain.
There is ST depression, greater than 3 mm in some leads, in I-III, aVF, and V3-V6. aVR also has ST elevation.
Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main origin.
This patient was treated with nitroglycerine, ASA, and heparin. His pain diminished substantially but did not go away altogether. An ED ultrasound showed an anterior, apical, and septal wall motion abnormality. Repeat ECG showed most of the ST depression resolved (but not all).
There is no ST elevation, no evidence of occlusion that will cause imminent necrosis of a myocardial wall. But there is evidence of a very unstable atherosclerotic plaque that could completely thrombose at any moment. Also, his ongoing pain signified ongoing ischemia, which is an indication for immediate angiography and PCI. Therefore he was taken emergently (in the evening) to the cath lab. There was a severe ostial LAD thrombosis that was very close to the left main.
He went for emergent bypass that evening and had a good outcome.
ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression.
Think of aVR as (-)aVR. (-)aVR is 180 degrees opposite aVR and thus is between leads I and II. Thus, if I and II have ST depression, the (-) aVR must have ST depression, and (+) aVR must have ST elevation.
Coronary occlusion need not have 1 mm ST elevation; often it does not
A 53 year old male with no previous cardiac history presented with sudden substernal chest pain with tingling of bilateral arms and dyspnea.
this is the first ECG at 1559:
There is very subtle and < 1 mm ST elevation in II, III, and aVF. The T-waves in these inferior leads are much larger than normal, with almost the same voltage as the QRS, and are "fat". These are hyperacute T waves. Just as importantly, there is minimal reciprocal ST depression in aVL, with T wave inversion. This is diagnostic for inferior STEMI, even though it doesn't meet the arbitrary criteria of 1 mm ST elevation in 2 consecutive leads.
The cath lab was activated and a distal RCA thrombus with TIMI-0 flow was seen. For technical reasons, it could not be opened. An ECG was repeated, showing the development of the inferior MI without reperfusion:
Posted by Steve S
A 32 year old male presented with a 4 day history of dyspnea, cough, palpitations, and chest pain. He had an ECG done immediately (shown above). This showed anterior T wave inversions, a QTc of 431, and also T inversion in lead III. There is sinus tachycardia and an S1Q3T3. This is all highly suspicous for pulmonary embolism. . Oxygen saturation was 95%, there were some end expiratory wheezes. D dimer was 3000. A CT pulmonary angio confirmed large central PE. . Kosuge et al. (Am J Cardiol 2007;99:817-821) compared patients with ACS and PE who had precordial T wave inversions in V1-V4. They found that in this select population, negative T waves were observed in only 15 of patient with ACS compared with 88% of patients with Acute PE. . It is tempting to diagnose Wellens' syndrome with anterior T wave inversions, but Wellens' T waves simply look different, should have a longer QTc, generally don't extend out to V6, and, most importantly, don't have T inversion in lead III. . Of course the clinical scenario is most important.
This 70 year old woman with a history of left bundle branch block presented with 10 hours of dyspnea.
Notice there is QRS widening with a wide upright R wave in lead V6. That the QRS is not similar to V6 in leads I and aVL makes this an atypical LBBB. Nevertheless,, the same rules of concordance and discordance apply: the ST-T complex should go the opposite, or discordant, direction of the majority of the QRS.
Notice there is concordant ST elevation in inferior leads.
In addition, there is less discordant ST elevation in leads V1–V3 than is normal for LBBB. A normal amount of discordant ST elevation almost always produces an ST to S ratio of less than 0.20. The mean of normal LBBB is 0.09 to 0.11, but ratios of 0.07 to 0.15 may be seen. Thus, with a 26 mm S-wave in V2, the minimum amount of normal ST elevation is 26 x 0.07 or 1.8 mm. However, there is only 1 mm of ST elevation in V1 because of relative ST depression in leads V1 to V3.
This is infero–posterior STEMI in the context of old atypical LBBB.
Inferior ST depression in ACS is reciprocal to ST elevation in aVL
from Dr. Smith's ECG Blog by Steve Smith For this topic, see also this post: http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html
This 72 yo male with h/o HTN, hyperlipidemia, and CAD, and h/o 4-vessel CABG 17 years prior presented with 8 hours of substernal chest pain radiating to upper back.
Here is his initial ECG:
Notice there is ST segment depression in II, III, and aVF. The QRS is normal, so any ST segment abnormality cannot be blamed on the QRS (i.e., ST depression is "primary", not "secondary," and the ddx of this is ischemia, hypokalemia, digoxin, and normal variant). The ST depression is somewhat "scooped" in appearance, suggesting hypoK or digoxin, but the QTc is 423 ms, so hypokalemia is unlikely (usually > 450 ms) and the patient was not taking Digoxin.
ST depression of subendocardial ischemia does not "localize". That is to say, for example, that "inferior" ST depression does not represent inferior subendocardial ischemia. When there is inferior ST depression from ischemia, it is invariably reciprocal to ST elevation in aVL (i.e., the high lateral wall). So if we look at aVL, there is indeed some ST elevation, about 0.5 mm. This is actually a significant amount of ST elevation because the R-wave is only 2 mm, and this is common in aVL.
Furthermore, there is subtle ST depression in lead V3 (0.5 mm). There should NEVER be ST depression in leads V2 and V3, there is usually some amount of ST elevation. 0.5 mm of ST depression is likely to be 1.0-1.5 mm of relative ST depression.
A colleague showed me this and I said that, because there is ST elevation in aVL and ST depression in V3, it is probably an obtuse marginal (OM) branch (of the circumflex) or near-occlusion.
Appropriate management is to treat maximally for ischemia with ASA, heparin or enoxaparin (depending on institutional preference), clopidogrel if institutionally acceptable and epitifibatide if not. If the pain does not resolve, go urgently to the cath lab. If the pain and ECG findings resolve, then next day cath is acceptable.
The patient had initial symptom control and was put in the ICU, but symptoms recurred and were refractory, so he was taken urgently to cath and was found to have ACS of the saphenous vein graft to the obtuse marginal. This was stented, and flow was TIMI-III after the procedure. Pre-procedure flow was not documented, but pain was resolved afterwards. Troponin I peaked at 8.5 ng/ml. Post-procedure ECG showed prominent T-wave inversion in aVL (analogous to Wellens' T-waves in the anterior leads). Notice the ST depression in V3 is gone, but the ST elevation in aVL is more pronounced, as is the reciprocal ST depression.
A 56 yo f with h/o HTN and hypercholesterolemia called EMS from home after onset of L chest pain radiating to the left arm. Before EMS arrived, she had "seizure activity" and became unresponsive. She was defibrillated successfully from ventricular fibrillation and developed a perfusing rhythm. She was intubated. She arrived comatose and in cardiogenic shock and the following ECG was recorded.
There is a bradycardic rhythm of uncertain etiology, possibly a sinus pause with escape, and occasional PVCs.
There is ST elevation in II, III, and aVF, but also ST elevation in V1, but also in V2 and V3. This is diagnostic of Right ventricular MI. RVMI that has ST elevation in V1 all the way to V3 is referred to as "pseudoanteroseptal MI," and is distinguished from LAD anterior MI by the inferior ST elevation (although a "wraparound" LAD can do this) and by the fact that there is more ST elevation in V1 than in V4. That this is an RVMI is confirmed with the following right sided ECG:
Now it can be seen that most of the precordial ST elevation is in V4R, much more than is present on the left side of the heart (V1R, which is equivalent to V2 on the left sided ECG.
She was bradycardic and hypotensive. Normal saline bolus was given, with improvement in BP. .
Pressors were required, and the patient was transported to the cath lab with a door to balloon time of 60 minutes, where a proximal dominant RCA occlusion was opened and stented.
She underwent therapeutic hypothermia, and emerged from coma.
She awoke and was discharged to home with no disability
Steve Smith said…
There was a comment with a couple inaccurate statements:
1) "In RVMI, you normally see STE in lead III higher than II, and normally you'd see ST depression in V1-V3…"
RVMI is always a result of RCA occlusion, and it is true that STE in lead III is usually higher than in lead II in RCA (as opposed to circumflex) occlusion, as seen here.
ST depression in V1-V3 is only present if the RCA has branches to the posterior wall, which happens < 50% of the time.
When there is concomitant RVMI and posterior MI, ST segment in V1 may be either elevated or depressed, depending on which dominates.
Cardiac Arrest suddenly after blood loss, is it due to MI? Also, when the rhythm looks like torsade, it is usually not.
from Dr. Smith's ECG Blog by Steve Smith A 74 yo f with ESRD on dialysis and h/o CAD bumped her access fistula and began to bleed profusely. She had a prehospital BP of 60, pulse 70, and this remained the same in the ED. The bleeding was controlled. She was asymptomatic. Hgb was 10 and fluids were given, and the BP rose to 80 systolic. An ECG was recorded (below, 1st ECG):
This shows sinus rhythm with LVH and typical LVH repolarization abnormalities, with no evidence of acute ischemia. QTc = 440 ms.
Suddenly she became bradycardic and lost pulses. CPR was begun. She was given atropine 1 mg, Epi 1 mg, and Calcium chloride 1 "amp". Moments later, this rhythm was recorded:
This shows polymorphic ventricular tachycardia or ventricular fibrillation. There appear to be "turning of the points," but torsade de pointes can only be diagnosed in the presence of a long QT on the preceding ECG. Polymorphic v tach may be torsade, but we know this case is not because the previous QTc was 440 ms. Torsade would be due to one set of circumstances (electrolytes, congenital, drugs). More commonly, however this polymorphic v tach is NOT torsade; in fact, ventricular fibrillation looks like this as well. In the case of v fib or non-torsade polymorphic v tach, the most likely etiology is ischemia. . So this 12-lead was recorded:
This shows Left Bundle Branch Block (new), with concordant ST elevation in II, III, aVF, V5 and V6, and also concordant ST depression in V2. This is diagnostic for transmural ischemia of the infero-postero-lateral wall. This explains the cardiac arrest. . Notice also the PVC (1st complex in V1, V2 and V3). It shows discordant ST depression that is EXCESSIVELY discordant. Thus, it is a PVC complex that reveals posterior STEMI. . Is this transmural ischemia due to hypotension from fluid loss? Unlikely, because the previous ECG, taken after quite a period of hypotension, showed no ischemia. . Is this due to ACS (plaque rupture with MI)? It seems unlikely only because it would be a coincidence. . The bleeding from the fistula has stopped. It is controlled. There is no risk now that it will bleed if anticoagulants and antiplatelet agents are given. . The patient should go immediately to the cath lab. . It seemed incredible to the physicians caring for the patient that she could be having an acute MI, and the LBBB confused them as well, so that there was some delay in cath lab activation, during which time a much more obvious ECG was recorded and an echocardiogram confirmed what an astute electrocardiographer would already know: there were new wall motion abnormalities. . At cath, an occluded circumflex was found and stented.
Dr. Smith's Rule to differentiate BER from LAD occlusion
There is 2-3 mm of ST elevation in leads V2-V4, and also ST elevation in V5, V6, I, II, and aVL. However, the ST elevation in anterior leads looks very much like early repolarization. I have derived and validated a 3 part rule to differentiate early repol from acute LAD occlusion (paper submitted). If 2 of the following 3 questions are answered "yes", then it is MI with an accuracy of about 85%: 1) is the QTc > 392 ms? (here, yes) 2) Is the ST elevation at 60 ms after the J-point in lead V4 > 2mm (here, yes) 3) Is the R-wave in V4 < 13 mm (here, no). So by this rule, the ECG leans toward acute LAD occlusion.
LAD occlusion in the setting of paced rhythm
An 80 yo male presented with chest pain.
There is clearly a ventricular paced rhythm. Normally in a paced rhythm, the QRS is usually all negative from V1-V6 because the pacing wire is in the apex of the RV and thus all depolarization goes away from the apex.
In the above ECG, the QRS in V2 is positive and all others are negative, as in the patient's previous ECG below. This implies some problem with lead placement. Nevertheless, leads V1, V3, and V4 have excessively discordant ST segments.
Though there is not a lot of data to support it, the ratio used for left bundle branch block seem to be applicable to paced rhythm. An ST/S ratio in V1-V4 > 0.20 I believe to be quite specific for LAD occlusion. V2, though suspect because of the positive QRS, has a concordant ST segment, which is diagnostic of STEMI.
The emergency physician needed to do some persuasion with the interventionalist, but succeeded and the patient was taken for angiography and PCI of a 100% LAD occlusion.
This is the ECG 2 days later:
This is a much more difficult ECG because only complexes 4 and 5 are paced now. The precordial leads have an RBBB morpholoyg, with some minimal persistent ST elevation in v2 and V3 with T-wave inversion, suggestive of reperfusion.
Ischemic symptoms and a paced ECG with excessive discordance in V1-V4, with ST/S ratio > 0.20, is anterior STEMI until proven otherwise.
Filed Under: fix


text:
Home/News & Analysis/WWE 2K game coming to Android soon
WWE 2K game coming to Android soon
Shubham Mishra Follow on Twitter April 1, 2015 5:38 pmLast Updated: April 1, 2015 5:38 pm
This is only the second ever WWE 2K game to be launched for mobile users. The game will feature aspects from the console versions
Mobile gamers and WWE lovers have something to look forward to. 2K Sports has announced that a WWE mobile game is coming soon. According to the company, this is the "first simulation-based WWE video game," and it is due to launch soon on Android and iOS devices for $8 (Rs. 500 approx.).
The official title of the game will be WWE 2K and it will have features similar to the console versions (read: WWE 2K15 review) that we've seen till now. This includes unlockables, create-a-character mode, live multiplayer and some other features. The player roster will include pro-wrestling mainstays like Daniel Bryan, John Cena, Triple H, Sting, Hulk Hogan, Undertaker, Roman Reigns, Seth Rollins, Bray Wyatt and Dean Ambrose.
In addition, 2K Sports has also announced that the game will have three match types, full ring entrances for superstars and their particular move sets. There will also be a career mode in the game.
This will be the third WWE game that has hit the mobile space, after WWE 2K Supercard game, which was launched in August last year, and WWE Immortals.
Honor 20i With Triple Camera Setup, Kirin 710 SoC Launched in India
Oppo F19 Pro And Oppo F19 Pro+ Launched In India: Price, Specifications & Features
Asus ZenFone Max Pro M1 Gets Price Cut in India, Available at Rs. 7,999
Moto G5 Plus With Metal Body Launched in India

redpajama_set_name: RedPajamaCommonCrawl


Medical Science Monitor, 2009, v. 15 n. 8, p. MT105-MT112 How to Cite?
Background: Gait analysis techniques guide the use and design of functional electrical stimulation (FES) systems for paraplegic walking. However, published studies on dynamic gait stability for the effective use of FES are limited. This paper introduces a new risk-tendency graph (RTG) technique to analyze and process gait stability in FES-assisted paraplegic walking. Material/Methods: The main instrument was a specialized walker dynamometer system based on a multi-channel strain-gauge bridge network affixed to the frame of the walker. This system collects force information for the handle reaction vector (HRV) between the patient's upper extremities and the walker during walking. The information is then converted into a walker tipping index (WTI), which is an indicator of the patient's walking stability. Dynamic gait stability is then combined with spatio-temporal locating methods for WTI and visually described as morphological curves in the temporal and spatial domains, namely RTGs. Results: To demonstrate the potential usefulness of RTG in gait analysis, a preliminary clinical trial was conducted with one male paraplegic patient who was undergoing FES walking training. The gait stability levels for the patient under different stimulation patterns were quantified using the results of temporal and 3-D spatial RTG. Relevant instable phases in the gait cycle and dangerous inclinations of the patient's body while walking were also clearly identified. Conclusions: The new RTG technique is a practical method for distinguishing useful gait information from the viewpoint of stability and may be further applied in FES-assisted paraplegic walking rehabilitation. © Med Sci Monit, 2009.


text:
Marine Le Pen tacks further towards far-Right in final rally before French presidential election
Marine Le Pen after addressing supporters at a campaign rally in Marseille Credit: Paul Durand/EPA
Oscar Lopez, Marseille
Rory Mulholland, Paris
20 April 2017 • 9:18am
Oscar Lopez
French presidential election
Marine Le Pen focused on Islamist terrorism and the threat to France from immigrants on Wednesday night in her final rally before this weekend's fiercely contested french presidential election first round.
The Front National leader targeted security concerns as she addressed supporters in Marseille, the multi-ethnic southern city where two men were arrested on Tuesday on suspicion of planning to attack a presidential candidate.
Her rival candidates were happy to let "immigrants turn France into a gigantic squat," she argued.
"Are we going to be able to live as French for much longer when entire neighbourhoods are taken over by foreigners?" she said, adding to wild applause and cheering. "A multicultural society is a multi-conflict society."
Supporters cheer and wave as they listen to Le Pen Credit: Paul Durand/EPA
Ms Le Pen has spent years trying to broaden support for the party founded by her father, Jean-Marie Le Pen, but she appears to have suspended much of that approach in the final days of rallying before Sunday's first round of voting.
The new hardline tack has met with approval from her fans, with many at the Marseille rally chanting "la France aux français" (France for the French) , an old slogan associated with the xenophobia and anti-Semitism that infected the Front National when it was led by Mr Le Pen.
For André Boyer, 75, it was immigration above all else that secured his vote for Ms Le Pen. "We're not even in our own country anymore," he said as he waited for the Front National leader to take the stage.
"We're being invaded by migrants. Meanwhile we have seven million people without work," he said.
Ms Le Pen's anti-elite and anti-globalisation rhetoric also plays well with her supporters and she spent much of her Marseille rally denouncing the unbridled free market and calling for "economic patriotism" and "intelligent protectionism".
Marion Marechal Le Pen also appeared on stage at the rally Credit: Jeff J Mitchell/Getty Images
Globalisation "wants to make of the world a giant supermarket where everything is for sale, where everything is bought, including people, including workers. Well France is not for sale, the French people are not for sale," she said.
Ms Le Pen's promises to pull France out of the euro, slash immigration, make it harder to get French nationality and to get tough on suspected Islamists, have kept her in joint top place in the presidential race in most of the latest polls.
But the polls show a four-way race has developed between her, Mr Macron, the scandal-scarred conservative candidate François Fillon, and far-Left firebrand Jean-Luc Mélenchon.
French election grid
Just two will go through to the second and final round of voting on May 7 after what has been the most unpredictable French presidential election in decades that came in the wake of the UK's decision to leave the European Union and Donald Trump's presidential triumph in the US.
Security has been stepped up at all election events after police arrested the two terror suspects in Marseille on Tuesday and found an arsenal of weapons and bomb-making equipment in their flat along with an Islamic State (Isil) flag.
Masked youths walk behind a banner as they campaign against Marine Le Pen Credit: Philippe Laurenson/Reuters
It quickly emerged that police had been watching the pair for several weeks before they finally detained them on suspicion of plotting "an imminent and violent attack" in the run-up to Sunday's first-round vote.
It was not clear who or what the target was but sources said Mr Fillon was a possibility, according to media reports.
French election postcards
Profile | Marine Le Pen
Tory leadership latest: Boris Johnson refuses to commit to reducing net migration levels in final head-to-head debate
Jeremy Corbyn calls special frontbench meeting on anti-Semitism as MPs warn 'racists are not being dealt with'
Jeffrey Epstein had fake passport with Saudi Arabian address, prosecutors claim
Comment: Brexit isn't some imperial fantasy – it just means we want to be ourselves
Tim Stanley
Profile: Assistant Commissioner Neil Basu, the man who quietly rose to become Britain's anti-terror chief


What do You Want to see on The Quiet Branches 2017?
I have questions for you, the readers (& anyone interested in plant science) as I consider my 2017 schedule for the blog and start to plan content for the year. So everyone knows (& can possibly help me), I will be moving onto a new job I still need to find within the first 3 … More What do You Want to see on The Quiet Branches 2017?
Leave a comment What do You Want to see on The Quiet Branches 2017?


text:
Sunshade geoengineering people apparently have been in the midday sun too long
Anthony Watts / October 21, 2012
From the Carnegie Institution , not just aerosol injections, but effective aersol injections. Law of unintended consequences be damned.
Improving effectiveness of solar geoengineering
Washington, D.C.— Solar radiation management is a type of geoengineering that would manipulate the climate in order to reduce the impact of global warming caused by greenhouse gasses. Ideas include increasing the amount of aerosols in the stratosphere, which could scatter incoming solar light away from Earth's surface, or creating low-altitude marine clouds to reflect these same rays.
Research models have indicated that the climatic effect of this type of geoengineering will vary by region, because the climate systems respond differently to the reflecting substances than they do to the atmospheric carbon dioxide that traps warmth in Earth's atmosphere. New work from a team including Carnegie's Ken Caldeira uses a climate model to look at maximizing the effectiveness of solar radiation management techniques. Their work is published October 21st by Nature Climate Change.
Attempting to counteract the warming effect of greenhouse gases with a uniform layer of aerosols in the stratosphere, would cool the tropics much more than it affects polar areas. Greenhouse gases tend to suppress precipitation and an offsetting reduction in amount of sunlight absorbed by Earth would not restore this precipitation. Both greenhouse gases and aerosols affect the distribution of heat and rain on this planet, but they change temperature and precipitation in different ways in different places. Varying the amount of sunlight deflected away from the Earth both regionally and seasonally could combat some of this problem.
By tailoring geoengineering efforts by region and by need, the team—led by California Institute of Technology's Douglas MacMartin—was able to explore ways to maximize effectiveness while minimizing the side effects and risks of this type of planetary intervention.
"These results indicate that varying geoengineering efforts by region and over different periods of time could potentially improve the effectiveness of solar geoengineering and reduce climate impacts in at-risk areas," Caldeira said. "For example, these approaches may be able to reverse long-term changes in the Arctic sea ice."
The study used a sophisticated climate model, but the team's model is still much simpler than the real world. Interference in Earth's climate system, whether intentional or unintentional, is likely to produce unanticipated outcomes.
"We have to expect the unexpected," Caldeira added. "The safest way to reduce climate risk is to reduce greenhouse gas emissions."
David Keith of Harvard and Ben Kravitz, formerly of Carnegie but now at DOE's Pacific Northwest National Lab, are co-authors on the study.
The Carnegie Institution for Science is a private, nonprofit organization headquartered in Washington, D.C., with six research departments throughout the U.S. Since its founding in 1902, the Carnegie Institution has been a pioneering force in basic scientific research. Carnegie scientists are leaders in plant biology, developmental biology, astronomy, materials science, global ecology, and Earth and planetary science.
Here's another similar press release on the same topic, sort of a "climate justice" spin:
Targeting solar geoengineering to minimize risk and inequality
New study suggests that solar geoengineering can be tailored to reduce inequality or to manage specific risks like the loss of Arctic sea ice
Cambridge, Mass., and Washington, D.C. – October 21, 2012 – By tailoring geoengineering efforts by region and by need, a new model promises to maximize the effectiveness of solar radiation management while mitigating its potential side effects and risks. Developed by a team of leading researchers, the study was published in the November issue of Nature Climate Change.
Solar geoengineering, the goal of which is to offset the global warming caused by greenhouse gases, involves reflecting sunlight back into space. By increasing the concentrations of aerosols in the stratosphere or by creating low-altitude marine clouds, the as-yet hypothetical solar geoengineering projects would scatter incoming solar heat away from the Earth's surface.
Critics of geoengineering have long warned that such a global intervention would have unequal effects around the world and could result in unforeseen consequences. They argue that the potential gains may not be worth the risk.
"Our research goes a step beyond the one-size-fits-all approach to explore how careful tailoring of solar geoengineering can reduce possible inequalities and risks," says co-author David Keith (pictured at right), Gordon McKay Professor of Applied Physics at the Harvard School of Engineering and Applied Sciences (SEAS) and Professor of Public Policy at Harvard Kennedy School. "Instead, we can be thoughtful about various tradeoffs to achieve more selective results, such as the trade-off between minimizing global climate changes and minimizing residual changes at the worst-off location."
The study—developed in collaboration with Douglas G. MacMartin of the California Institute of Technology, Ken Caldeira of the Carnegie Institution for Science, and Ben Kravitz, formerly of Carnegie and now at the Department of Energy—explores the feasibility of using solar geoengineering to counter the loss of Arctic sea ice.
"There has been a lot of loose talk about region-specific climate modification. By contrast, our research uses a more systematic approach to understand how geoengineering might be used to limit a specific impact. We found that tailored solar geoengineering might limit Arctic sea ice loss with several times less total solar shading than would be needed in a uniform case."
Generally speaking, greenhouse gases tend to suppress precipitation, and an offsetting reduction in the amount of sunlight absorbed by Earth would not restore this precipitation. Both greenhouse gases and aerosols affect the distribution of heat and rain on this planet, but they change the temperature and precipitation in different ways in different places. The researchers suggest that varying the amount of sunlight deflected away from the Earth both regionally and seasonally could combat some of this problem.
"These results indicate that varying geoengineering efforts by region and over different periods of time could potentially improve the effectiveness of solar geoengineering and reduce climate impacts in at-risk areas," says co-author Ken Caldeira, Senior Scientist in the Department of Global Ecology at the Carnegie Institution for Science.
The researchers note that while their study used a state-of-the-art model, any real-world estimates of the possible impact of solar radiation management would need to take into account various uncertainties. Further, any interference in Earth's climate system, whether intentional or unintentional, is likely to produce unanticipated outcomes.
"While more work needs to be done, we have a strong model that indicates that solar geoengineering might be used in a far more nuanced manner than the uniform one-size-fits-all implementation that is often assumed. One might say that one need not think of it as a single global thermostat. This gives us hope that if we ever do need to implement engineered solutions to combat global warming, that we would do so with a bit more confidence and a great ability to test it and control it."
The authors declare no competing financial interests.
October 21, 2012 in Aerosols, Geoengineering. Tags: Carnegie Institution for Science, climate change, greenhouse gas, Ken Caldeira, Solar radiation management
Jet contrails will likely affect climate by 2050
Cooling effect of preindustrial fires on climate underestimated
Study: dust guided by meandering jet stream has big impact on Arctic melt
← Weekly Climate and Energy News Roundup
Tornado Report – September 2012 →
41 thoughts on "Sunshade geoengineering people apparently have been in the midday sun too long"
higley7 says:
Alas, another means of wasting money. Not by geo-engineering, but by studying geo-engineering, wasting time, energy, and money—other people's money no less!
How will they explain to their grandchildren around the old glacier face in the back yard that they spent their careers studying how to cool the planet, based on pseudoscience and government/political funding? "Grandpa! How could you be THAT stupid! You want this glaciation!"
Richdo says:
"Further, any interference in Earth's climate system, whether intentional or unintentional, is likely to produce unanticipated outcomes."
Except for increasing CO2 of course, we know every outcome there Bubba!
"greenhouse gases tend to suppress precipitation"
There's a good one. Water vapor (a greenhouse gas AFAIK) thends to suppress precipitation. Who'd a thunk it?
After they solve the problem of incoming sunlight, they should tackle shutting down a major volcano!
The anthropocentric hubris of the Gore crowd knows no limits!
R Taylor says:
No government will let these naifs have anything sharp to play with. The only "solution" government wants is another stream of tax revenue.
davidmhoffer says:
They used a model.
A SINGLE model.
Given that the various models use a wide range of forcing for aerosols, it is safe to bet that had they used two or more models, the results would have been all over the map and they would have looked utterly ridiculous.
Not to mention that the IPCC rates the Level of Scientific Understanding of direct aerosols (per AR4 Ch 2) as "medium to low", of cloud albedo (all aerosols combined) as "low", black carbon aerosols on snow as "low", and volcanic aerosols as "low".
No wonder they caution about actually doing anything of the sort! They know very well that they're bee essing. They'd pee their pants if they thought anyone was actually going to do it on any scale large enough to matter.
Rhoda Ramirez says:
Anyone proposing geoengineering solutions should be placed against a wall and shot. To preserve the gene pool, if nothing else.
Dennis Nikols says:
Totally unreliable and foolish. The models are useless and the variables are as unknown and misunderstood as most of them being used in climatology. This stuff is nice science fiction at best and pure hubris at worst. Many unkind terms come to mind about this stuff and people that foster it. I suspect charlatan is as good as any.
ntesdorf says:
These are some of the most foolish of the CAGW Insane Clown Posse. They are tinkering round with computer models that fail every test and these same models are useless at predicting anything as they are mainly based on a false premise. All their variables are unknown and totally misunderstood. This sort of science fiction dream is one of the most dangerous spin-offs of the CAGW fiasco. Their funding should be terminated immediately.
Sparks says:
Let's intentionally do something to the climate and spend hundreds of years predicting what we've done to it.
Geo-engineering is not possible.
We have been geo-engineering for 70 years by the various cloud seeding operations. Not to mention the cirrus cloud (contrail) formation by thousands of planes and the millions of tons of aerosols they dump into the atmosphere every year.
The 'it all could go horribly wrong' angst is overdone IMO. And these kinds of experiments would lead to more precise quatification of aerosol and cloud effects, which would lead to a more accurate (lower) GHG forcing, and could well be the final nail in the coffin of the model-driven CAGW cult.
So, I say, go for it.
GeoLurking says:
Risk? Like the risk of screwing with biosphere and potentially making it totally uninhabitable because the model didn't include some obscure relationship that they overlooked?
"Inequality" Un-equal how? Where in the genome of any organism or individual is the sequence that codes for "equalness?" Hint… the world is not equal, period. All critters are by design, whether intelligent or evolved, to exploit any nuanced benefit from their environment that they can gain. "Equal" has Jack[censored] to do with it.
Who decides what is equitable? What gives them that right? (ans: No one and nothing.)
Mark.R says:
If this dose work then they will be cutting the UV we need to make vitamin D thus we shall die younger.
dp says:
These people need to be jailed before they do something irreversibly dangerous. We've already had the iron sulphate dumper off the coast of Canada. They can share a cell – that would be very green.
mjk says:
For once I agree with the sceptics. Geo-engineering solutions are absolute madness. They should not even be studied.
MJK
I've been trying to find references in scientific papers to airplanes dumping aerosols in the upper atmosphere that people don't know is happening, what are those aerosol chemicals and why are they doing that? Are they Metallic chemicals?
Possible influence of anthropogenic aerosols on cirrus clouds and anthropogenic forcing
"and from aircraft that deposit their aerosols directly in the upper troposphere"
http://www.atmos-chem-phys.net/9/879/2009/acp-9-879-2009.html
I found in the studies, "We use sulfate aerosols as a proxy for pollution aerosols". Why not metallic types of aerosols?
Anthropogenic aerosols may have increased upper tropospheric
humidity in the 20th century
http://www.atmos-chem-phys.net/11/4577/2011/acp-11-4577-2011.pdf
This is interesting;
"Present US aerosol concentrations are sufficiently low that future air quality improvements are projected to cause little further warming in the US (0.1 °C over 2010–2050). We find that most of the warming from aerosol source controls in the US has already been realized over the 1980–2010 period."
Climatic effects of 1950–2050 changes in US anthropogenic aerosols – Part 2: Climate response
http://www.atmos-chem-phys.net/12/3349/2012/acp-12-3349-2012.html
So much goo reading on anthropogenic aerosols at ACP site.
An Interactive Open Access Journal of the European Geosciences Union
http://www.atmos-chem-phys.net/full_text_search.html?q=anthropogenic+aerosols&x=3&y=6
I think this is the smoking gun though;
Dr. Jasper Kirkby Explains Prior and Ongoing Atmospheric Geo Engineering by Jet Airplanes
In the beginning of this video to 21 seconds in, you can see him pointing with his laser pointer to an image example of what cloud patterns look like, that are formed in the sky as a result of, "jets dumping aerosols into the upper atmosphere." Quote is Dr Jaspery Kirkby from CERN, the European Organization for Nuclear Research, Geneva, Switzerland.
"There's plenty of evidence that large regions of the climate are lacking sufficient aerosol to form clouds. Contrails are a well known example of that. These are not smoke trails, these are clouds which are seeded by jets dumping aerosols into the upper atmosphere."
Full lecture here;
Cosmic rays and climate
http://cdsweb.cern.ch/record/1181073
Here's another smoking gun;
Atmospheric Geoengineering with Aluminum Aerosols.mov
J Martin says:
Given the current woeful lack of understanding of the climate as witnessed by the poor accuracy / skill of climate models, added to the fact that we know the sun is entering a quiet phase of unknown depth and extent, then any attempt to geo-engineer the environment can only be described as
suicidally stupid.
michael hart says:
What happens in the models, stays in the models.
Why not just turn down the water vapor feedback-amplification in the models? Problem fixed. No need to write all those extra lines of code.
Mike McMillan says:
davidmhoffer says:	October 21, 2012 at 8:28 pm
Yes, but it's a "state of the art" model.
Let's save the geo-engineering for the next ice age.
The difference between genius and stupidity is that genius has its limits." – Copy to Clipboard — Albert Einstein
Disputin says:
A Swedish chemists shop:
"I'd like to buy a deodorant"
"Yes Sir, ball or aerosol?"
"Neither. I want it for my armpits."
What they are proposing is balls.
John Marshall says:
Atmospheric engineering is a stupid, stupid idea from people who know very little about the atmosphere.
Rowland (UK) says:
Aren't they doing something already? Expanding and long lasting vapour trails from aircraft occur over Colchester, Essex, UK very reguarly. While these are normally produced by high flying aircraft, I witnessed one being caused by a turbo-prop aircraft at much lower altitude below the cloud base just the other day. In fact, I believe that this followed at least two previous passes judging by remnants of trails in the same direction. Meanwhile, the sky is presently 100% cloudy and therefore is obscuring any spraying that might be occurring while the number of aircraft flying over seems to have increased inordinately in the last few days.
This is yet another reason to believe that climate change is truly the greatest danger confronting mankind.
But it's not the climate itself that is the danger, provided we do not enter an era of global cooling. The danger is that governments will do mad things that will make us – and our children – far poorer and may even cause the very climate instability that they thought they were trying to stop.
Complete and utter madness….
dave38 says:
This sort of science fiction dream is one of the most dangerous spin-offs of the CAGW fiasco. Their funding should be terminated immediately.
No! Not just the funding: [snip . . yes it is inline with the 10/10 nonsense but we didn't approve of that either . . mod]
Pour encourager les autres
Primarily black carbon, which in climate science terminology is an aerosol, but plenty of sulphates and nitric/nitrous oxides.
Just google, airplane black carbon climate.
And black carbon eventually gets back to the surface decreasing snow and ice albedo – warming the surface.
Tom in Florida says:
"The safest way to reduce climate risk is to reduce greenhouse gas emissions."
So now it is "climate risk".
richardscourtney says:
michael hart:
At October 22, 2012 at 12:14 am you say
Oh, it can be done more simply than that.
Each model 'runs hot': i.e. it provides more warming over the twentieth century than was observed. This is compensated by inputting an amount of assumed aerosol cooling.
But each model 'runs hot' by a different amount and, therefore, the amount of assumed aerosol cooling used in any one model is different from the amount used in every other model. See
http://img36.imageshack.us/img36/8167/kiehl2007figure2.png
(ref. Kiehl JT,Twentieth century climate model response and climate sensitivity. GRL vol.. 34, L22710, doi:10.1029/2007GL031383, 2007).
Adjust the assumed aerosol cooling and you get whatever rate of warming you want in any model. And the assumed 'aerosol cooling' is input as a 'fudge factor' which can be varied to provide any warming you want.
So, the solution to the problem is already 'built in' to each model as a single datum which is an adjustable input parameter of assumed magnitude that has known effect on warming.
Incidentally, the fact that each model 'runs hot' by a different amount can only mean that all except at most one – and probably all – of the models emulates a different climate system than exists on the real world.
Gary Pearse says:
Hmm…they're not suggesting that the sun, of all things, is a significant contributor to GW?
Pamela Gray says:
Tell it to the winegrowers and then wait and see if the government that thought this one up gets re-elected. If you like your wine, you don't want to be shading the sun. And you think they won't try it? Base your answer on windmills and solar panels rotting in the ground.
David L says:
Key word here: "Models". Translation: "junk science"
gator69 says:
When you consider how poorly they understand climate, this really scares the Hell out of me.
Pooh, Dixie says:
Does this come with an "UnDo" button?
Goode 'nuff says:
The Geminids meteor shower is said to be growing in both size of the meteors and numbers. Some other meteor showers are said to be doing the same. Problem solved.
http://adsabs.harvard.edu/full/1969SSRv….9…58R
I haven't reached for sunglasses in four years. That corresponds with solar and volcanic cycles.
Don't know much about wine,
Do millions of miles traveling under the sun's vine,
at times it's a blinding light,
a sheer tornado of pain,
like a whiskey fury,
pounding like the devil's rain…
Well, I don't know how to fix that link. It's all about stratospheric dust.
Billy Liar says:
They're out to get you. Make sure you look behind the shrub in the garden before you go to work.
PS You may notice the same vapor trails coming from vehicle exhausts on cool damp mornings. All part of the same plot.
I honestly think Geo-engineering is not possible when I think of it in terms of energy displacement, it is like straping on a set of massive rocket boosters to the planet and moving it into an orbit further from the sun, that's if the planet gets warm and then doing the same again to move the planet into an orbit closer to the sun if it gets too cold.
Clive Williams says:
Does CAGW stand for Computer Assited Global Warming?
Does CAGW stand for Computer Assisted Global Warming?
Sorry for my typo. I spell quite well when I write by hand.


We had the most amazing lunch on the beach, seriously, I might have found my new favourite Thai dish.
I climbed to the top of this gorgeous mountain/cliff to see a lovely little temple with a stunning view and hung out with some cheeky monkeys.
Teacher Ann took me to her favourite beach, which was in this beautiful sound; we also say this weird zoo/farm thing (for lack of a better word), that had an ostrich, turkey, and deer hanging out, which is not something you see everyday.
She took me to her favourite cake shop which she said was famous in Prachuap and with good reason; holy moly was it yummy.
Last, but not least I got my work permit and got to have a nap on the ride home!
Sometimes it's the days and things that you least expect that end up meaning the most to you. Life really does surprise you in the best ways when you least expect it.


text:
Pentagon Recognizes "Officially" that Israel is a Nuclear Power. Declassified Document
Region: Middle East & North Africa
Theme: Militarization and WMD
In-depth Report: Nuclear War
The Institute for Defense Analyses (IDA), an entity on contract to the US Department of Defense has released a previously classified military document which confirms Israel's nuclear weapons program.
This is considered to be a landmark decision, widely interpreted as constituting a semi-official recognition by the US Department of Defense that Israel is a bona fide nuclear power. While the document confirms what is already known regarding Israel's nuclear arsenal, the political implications are potentially far-reaching, particularly in relation to the ongoing negotiations pertaining to Iran's alleged nuclear program."
Who Threatens Whom in the Middle East:
A de facto acknowledgement by the US that Israel is a nuclear power threatening the Middle East in contrast to Iran's non-existant nuclear weapons program
Moreover, as detailed below, the IDA report tacitly portrays Israel's nuclear weapons program as an extension of that of the United States.
This 386-page 1987 report entitled "Critical Technological Assessment in Israel and NATO Nations" provides details regarding Israel's weapons systems including the development of the hydrogen bomb.
Click image to access the complete 387 page 1987 report
While the report was written 28 years ago, it confirms Israel's capabilities to develop nuclear weapons, with an explosive capacity equivalent to 1000 times a (Hiroshima) atomic bomb:
that in the 1980s Israelis were reaching the ability to create bombs considered a thousand times more powerful than atom bombs.
The report also states that:
"[Israel is] developing the kind of codes which will enable them to make hydrogen bombs. [1980s] That is, codes which detail fission and fusion processes on a microscopic and macroscopic level,".
The report also notes that research laboratories in Israel "are equivalent to our Los Alamos, Lawrence Livermore and Oak Ridge National Laboratories," the key labs in developing America's nuclear arsenal. (quoted in Israel National News, March 25, 2015)
Israel's nuclear infrastructure is "an almost exact parallel of the capability currently existing at our National Laboratories,"
The report intimates that Israel's weapons industry including its nuclear program is essentially an extension of that of the US, developed with the active support and collaboration of US military research labs and US "defense contractors".
In this regard it also dispels the notion that the US was not made privy to Israeli classified information concerning its nuclear program, which in the earlier period was developed with the support of France.
The report also reveals that the Pentagon was fully informed regarding the intimate details of the Israeli program, which also suggests that it was developed in active collaboration with the US
The complete report can be consulted at http://cryptome.org/2015/03/ida-ctaiiann.pdf
The original source of this article is Global Research
Copyright © Prof Michel Chossudovsky, Global Research, 2015
Articles by: Prof Michel Chossudovsky
Michel Chossudovsky is an award-winning author, Professor of Economics (emeritus) at the University of Ottawa, Founder and Director of the Centre for Research on Globalization (CRG), Montreal, Editor of Global Research. He has taught as visiting professor in Western Europe, Southeast Asia, the Pacific and Latin America. He has served as economic adviser to governments of developing countries and has acted as a consultant for several international organizations. He is the author of eleven books including The Globalization of Poverty and The New World Order (2003), America's "War on Terrorism" (2005), The Global Economic Crisis, The Great Depression of the Twenty-first Century (2009) (Editor), Towards a World War III Scenario: The Dangers of Nuclear War (2011), The Globalization of War, America's Long War against Humanity (2015). He is a contributor to the Encyclopaedia Britannica. His writings have been published in more than twenty languages. In 2014, he was awarded the Gold Medal for Merit of the Republic of Serbia for his writings on NATO's war of aggression against Yugoslavia. He can be reached at [email protected]


text:
Trump Leaves Israel in the Lurch
The president's precipitous decision to withdraw U.S. troops from Syria provided many Israelis with a rude awakening.
By Daniel Shapiro
A Trump supporter during a convention organized by the Israeli branch of the U.S. Republican Party in Jerusalem on October 26, 2016 (Ammar Awad / Reuters)
Ask Israelis what they appreciate about President Donald Trump, and they can tick off a substantial list: the long-sought move of the U.S. embassy to Jerusalem; the abandonment of the much-maligned Iran nuclear deal; the lack of pressure (so far) on Israel to curtail settlement expansion or make concessions to the Palestinians; and the absence of tensions with Israel's leaders, which plagued the relationship between former President Barack Obama and Prime Minister Benjamin Netanyahu.
But dig a bit deeper, and you hear something else, best captured in a phrase used frequently by young Israelis I meet who consider themselves Trump fans: gever-gever, a real man. Something about the Trump style appeals to an Israeli sense of machismo, an appreciation for direct, gut-level expressions of toughness, such a contrast from the more analytical Obama.
Trump's sudden decision this month to reverse course and announce the withdrawal of the 2,000 U.S. troops in Syria, though, forced Israelis to recognize, in many cases for the first time, both their policy differences with Trump and the downsides of his stylistic idiosyncrasies. The implications, for Israel's strategic interests in the region and for its management of its relationship with the United States, are broad.
Start with the way the decision was made. Trump had signaled months ago his preference for a prompt declaration of victory over ISIS and the return of U.S. troops from Syria. But persuaded by his national-security team, including Secretary of Defense James Mattis, Secretary of State Mike Pompeo, and the special representative for Syria engagement, James Jeffrey, he reversed course. Netanyahu also called for maintaining the U.S. deployment. The presence of U.S. forces meant that Israel did not feel left to manage the threat entirely on its own, or appear to others to be doing so, even as it conducts its ongoing campaign of air strikes in Syria against Iranian military entrenchment.
Reuel Marc Gerecht and Mark Dubowitz: Trump delivers a victory to Iran
Trump's sudden about-face, announced by tweet on December 19, so shocked and upset his own national-security team that Mattis and the special envoy for the counter-ISIS campaign, Brett McGurk, resigned. Netanyahu reportedly received a heads-up in a phone call with Trump two days before the announcement, but failed to dissuade Trump; he was not, in any meaningful sense, consulted. Israel's tight-lipped statements calling it a "U.S. decision" that would in no way constrain Israel's own actions betrayed Netanyahu's unhappiness.
Surprises are bad enough. I know it firsthand, having informed the Israeli government in August 2013 of Obama's decision to strike Syrian targets in response to Syrian President Bashar al-Assad's use of chemical weapons, only to have Obama pull back to seek congressional approval. In that case, the surprise stung and left lingering region-wide doubts about the willingness of the United States to use military force. But at least then, a plausible policy alternative emerged: an agreement with Russia that led to the removal and destruction of 1,300 tons of Syrian chemical-weapons stocks. Israel endorsed the new approach.
The problem for Israel today, though, goes beyond the surprise. If Obama was too cautious for many Israelis, Trump has now shown them how his approach to foreign policy—impulsive, isolationist, transactional, turning on a dime with no alternative in place—can work against their interests. And Netanyahu—who praised Trump in almost messianic terms and who knows how poorly he responds to criticism—now has few tools at his disposal to object to this policy. Israelis can only shake their heads at the absence of any strategy as they survey the regional fallout.
Take ISIS. By every account, the battle to destroy ISIS is not finished. The removal of U.S. forces will put at risk the gains of the campaign's first three years, and could facilitate the group's regeneration. Israel is not threatened by ISIS in an existential sense, but preventing Sunni jihadist terrorists from harassing Israel's borders and undermining its neighbors is undoubtedly an Israeli interest.
Kori Schake: Trump just messed up the one thing he did better than Obama
And who persuaded Trump to make the ill-advised move? None other than Netanyahu's regional nemesis, the Israel-bashing Turkish strongman Recep Tayyip Erdogan. Netanyahu has seemed unconcerned as Trump cozied up to the international club of autocrats—Putin, Orbán, Duterte, Bolsonaro, Mohammed bin Salman—and has even taken a swim in the same pool. Now he sees what happens when Trump strikes a deal with the local Islamist member of this club, who harbors ambitions for regional leadership. Obama may have hung in too long with Erdogan as he dismantled Turkish democracy. But Trump, knowing who Erdogan really is from the start, sees it as no impediment to doing deals. A Trump-Erdogan bromance is the stuff of Netanyahu's nightmares.
The first victims of Erdogan's empowerment, of course, will not be Israelis. They will be Kurds. Kurdish fighters—who make up the Syrian Democratic Forces (including, it must be acknowledged, some affiliated with the anti-Turkish terrorist group the PKK)—have led the battle on the ground against ISIS, liberating city after city in northeastern Syria. With no U.S. troops to coordinate with and protect them, they will be left to Erdogan's tender mercies.
Israelis see the Kurds—a moderate, pro-Western, Muslim community that eschews anti-Israel sentiment, and with whom Israel has worked quietly—as exactly the kind of element that the Middle East needs more of. They constantly press for more American support for the Kurds. Israel, against American wishes, encouraged the Kurds of northern Iraq in their ill-advised independence referendum of 2017. For Israel, the U.S. abandonment of the Kurds represents both a strategic and an emotional blow.
The blow is that much more painful for what it says about U.S. staying power in the Middle East. This concern did not originate with Trump, of course. Obama, too, was criticized by Israelis for withdrawing troops from Iraq, for failing to strike Syria in response to chemical-weapons use, and for his perceived reluctance to use force against Iran's nuclear program. But Trump, the gever-gever, Israelis hoped, would reverse the trend. Instead, Trump is doubling down on reducing U.S. involvement in the Middle East in an even more brutal fashion: bashing regional allies as freeloaders, demanding payment for U.S. protection, and loudly declaiming against any plausible logic for a U.S. military presence in the region. America's friends, including Israel, feel a chill wind at such talk.
Conor Friedersdorf: What the Syria hawks refuse to acknowledge
Meanwhile, its adversaries take heart. The main source of Israel's concern in Syria is the continuous effort by Iran to transfer ever more sophisticated weapons to Hezbollah in Lebanon, and to deploy its own forces and weapons against Israel from Syria. U.S. troops in eastern Syria have not been directly involved in Israel's campaign against such threats, but their presence denies Iran access to certain locations in Syria, including the key border-crossing between Syria and Iraq at al-Tanf.
More broadly, they signify a U.S. interest in what happens in Syria and provide a measure of leverage in the diplomacy that will help shape postwar arrangements. Once they are gone, the U.S. voice demanding Iran not be permitted to use Syria as a venue to threaten Israel will weaken. The rest of Trump's vaunted "maximum pressure" strategy against Iran will weaken along with it. U.S. sanctions remain, but U.S. seriousness is in question. Netanyahu claimed that Obama's nuclear deal empowered Iranian aggression across the region. Any serious analyst would make the same assertion about Trump's latest move.
The other major beneficiary of the U.S. withdrawal is Russia, now the unchallenged power in Syria, with influence that radiates out throughout the region. Declining U.S. involvement and increasing Russian dominance empower Russian President Vladimir Putin. When it suits Russia's interests, he may attempt to constrict Israeli freedom of action against targets in Syria. On cue, Moscow blasted this week's Israeli strike on Iranian-Hezbollah weapons facilities and the Syrian air-defense units that protect them with the dubious claim that Israeli pilots endangered civilian airliners.
Israel has maintained effective communication and deconfliction with Russia in Syria for three years, but it can expect more such Russian bullying tactics with the United States out of the picture. Israelis who complained that Obama "allowed" Russia to deploy heavily to Syria in 2015 can hardly feel better about Trump's decision.
A more dominant Russia in Syria means a reinforced Assad regime. That process was happening anyway, much to the chagrin of Israeli strategists and anyone with a moral conscience. But the folding of the U.S. tent cements the outcome. Where Turkey does not wipe out the Kurds, Russian-backed Syrian forces will mop them up. The Tehran-Damascus-Hezbollah weapons highway will be disrupted only by Israeli action. Other Arab states, long funders of anti-Assad opposition groups, have given up and are welcoming Syria back to the fold. Syria's prospective invitation to the Arab League summit, the visit of Assad's security chief to Cairo, and the reopening of the UAE embassy in Damascus mark Syria's best week diplomatically since the war began in 2011.
Following Trump's tweet announcing the U.S. withdrawal, Netanyahu told the Israeli people there was no cause for alarm. In the big picture, he's right. Israel can and will defend itself against the array of threats it faces. U.S. military assistance to Israel and diplomatic support at the United Nations are not in jeopardy.
But management of the conversation about the region between these two allies is now hobbled. A planned coordination visit to Israel by Mattis was scotched. Multiple conversations with a range of American envoys, premised on the continuation of the U.S. presence in Syria, have proved worthless. Israelis now know the dread of Trump's Twitter feed that has tormented many other U.S. allies.
And most of all, Israel's confidence in the robust, muscular backing of the gever-gever in the White House must now be tempered by a new understanding. Trump's disdain for any American military role in the Middle East, his eagerness to cut deals with his autocratic friends, and his lack of any sense of obligation toward U.S. allies should prepare Israelis for the bitter truth that the second half of Trump's term could look quite different from the first.


Mayor Bill de Blasio said Friday the city won't be going after vehicles clogging bike lanes because it doesn't have adequate "resources" for such a crackdown.
"We don't have the resources to do that right now in the way I think … the bicycle community would like to see, but we do believe that anybody who is parked in the bike lane, of course, is going to be summonsed and there will be consequences," de Blasio said during his weekly appearance on WNYC radio.
De Blasio responded that bus lanes are a higher priority because "of the sheer number" who use them, meaning the 2.5 million daily passengers.
His comments came a day after de Blasio announced that seven NYPD tow teams would be dedicated exclusively to clearing bus thoroughfares.
Of course this would not be complete without another incriminating display of his brazen sense of entitlement and defiant hypocrisy, for he's also a recidivist scofflaw concerning this pervasive issue.
How about a towing crackdown on all the cars with no plates and expired out of state plates all over the place?
Fair. Equal. Just. Accountable. Transparent.
Sure, but after a cyclist was killed by a hit and run driver in the bike lane on 8th Ave in Hells Kitchen, they found the resources to crack down on cyclists for such non existent infractions such as riding without a helmet.
Thank G-d this turd can't run for another term, But watch out that doesn't mean his wife can't. Look at what the Barrons, Charles anbd Inez have done. He's term limited, so he runs for office in Albany and pretty much turns his council seat over to his wife Inez. Nothing illegal there. Could BDB do it with his wife? Is the electorate dumb enough to allow it to happen? Stay tuned. BDB is weighing a run for president.
Perhaps the assets could be paid for by registering bicycles as moving vehicles and taxing the rider in much the same way they do for automobiles?
Anonymous!!! That would be racist & biased to POC & illegal aliens- how could you- person of privilege dare suggest that the law be applied equally? Don't you know that there was slavery in this country? Let's forget about all those white would be indentured servants who were sold into slavery! They couldn't read or write & couldn't sign their names to the identures- when they got off the ships they were sold to pay for their ship tickets & accomodations.
Crack down on double parking!
"Perhaps the assets could be paid for by registering bicycles as moving vehicles and taxing the rider in much the same way they do for automobiles?"
Why not tax my feet? Taxing something will not fix things !
This is surprising. I fully expected the mayor to pull cops off of patrols and responding to crimes in order to give out more bus lane tickets.


text:
LAURA VALLADAO
Laura Valladao is a Cinematographer based in Brooklyn, New York. Her passionate interest in light and deep connection to community inspires storytelling rich with honest and stunning visuals. She shot the feature film, "Premature", Directed by Rashaad Ernesto Green, which premiered in the NEXT program at Sundance 2019 as well as the short film "My Nephew Emmett", directed by Kevin Wilson Jr., which won the Student Academy Award in 2017 and went on to be nominated for an Oscar. Laura's documentary credits include "Outlaws: The Saga of Tupac and Afeni Shakur" directed by Allen Hughes and her commercial work has received awards from the AICP. Her work on Danish TV series "Limboland" directed by Rikke Schdt, helped season one to win TV Prisen for Best Television Series, Short Form.
Laura holds an MFA in Cinematography from New York University and loves to work in new places whenever the opportunity presents itself.
@lvalladao
Allison Irvin
airvin@zerogravitymanagement.com
Ajay Ghosh
aghosh@zerogravitymanagement.com


Successful operators know, that they are only as good as their weakest employee.
In this competitive industry, mediocracy just doesn't cut it. Let us work with your team to properly train and educate your staff on everything car wash. When you succeed, we succeed!
We are your training partner every step of the way. No matter your experience level, Mike's is here to assist you with putting together a comprehensive training program that fits your specific needs. Learn how to manage systems, procedures, equipment and chemicals, all while balancing costs and customer expectations.
Investing in your staff is investing in the future of your business. Here at Mike's Car Wash Solutions we have access to the best trainers in the biz. We can provide training for management, service advisors and detail staff. Mike's does free on-site demonstrations, provides sales guidance and techniques, product knowledge, equipment troubleshooting and maintenance, detailing and much more!


It all started with a trip to Charleston in East Sussex. "I took my parents there last year, and it was a dream—couldn't have been more up my street," says Alexa Chung from her design studio in North London. It's the evening after the 2018 Brit Awards, and, after a "very late night," the style polymath is nursing a tiny cup of espresso in a very large leopard-print coat. "I mean, the details of that place are just so beautiful: the painted cabinets, the ceramic light fixtures—I even bought a lamp," she adds, her voice slightly hoarse.
The much-admired museum, which preserves the home of British artists Vanessa Bell and Duncan Grant—pioneers of the Bloomsbury group—prompted Chung to immerse herself in the history of the Bloomsbury movement. "I found it so interesting because here were these incredible writers, artists, and philosophers all holed up in a house, refusing to go to war and having to farm in these romantic clothes," she explains.
Her Spring 2018 see-now-buy-now collection (the fourth outing from her eponymous label) is a clever distillation of that free-spirited Bloomsbury sensibility and her own much-imitated aesthetic. There are silky pajama-style trousers with matching tops, high-neck dresses in duck egg–blue lace, and a milky-colored linen suit, which Chung remarks is "totally Duncan lounging in the sitting room." She singles out a long white cotton smock dress with rickrack trims. "Everything is dreamy, comforting, and also weirdly reminds me of Florence Welch," she laughs. "That whole poetic Pre-Raphaelite vibe." Welch would undoubtedly look a picture in that piece or any number of the line's standout looks: the belted paisley gown, the Prince of Wales check blazer with ditsy floral embroidery, or those kick-flare dungarees that sit snuggly on the waist.