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Neogenesis

Neogenesis

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45 yo male in pre-op clinic for upcoming lap chole. Hx of HTN and DM. >4 METS. BP controlled 130s/70s. Normal physical exam. Approx 200lb. Pre-op EKG shows LVH. Further questioning of pt and review of old records shows worked up by cardiology approx 7 yrs ago. Echo at that time showed concentric LVH, normal EF, no LVOT obstruction or SAM. Negative stress test at that time as well. Pt was cleared by cardiology at that time for deployment (prior soldier) and note stated that he had a mild form of hypertrophic cardiomyopathy that had a very good prognosis and would not be limiting to pt in any way. EKG from 2007 apparently consistent with EKGs from 1990s per cards note, but none are available for review.

How do you proceed?

If it makes a difference, facility is a small community hospital (essentially an out patient surgery center). No ICU (step down only), cardiology, TEE, etc.
 
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Relatively gd effort tolerance. I would ask about cardiac symptoms and change in effort tolerance since the cardio work up.

What's the bmi? Assuming nothing significant from the above, i would proceed as per normal for high bmi cases.
 
Someone was worried about his heart in his late 30's to have a cardiac workup. Why?

What manifested that required an TTE, EKG and a cardiology consult to begin with. Is he out because his time was up, or was there a problem on active duty that got him out?

7 years is an awful long time for that workup, and a lot of things change. I'm embarrassed at how much weight I gained when I became more lax in the PT discipline when I got out. He also may have become lax as well, with weight gain and decreased physical activity. He may have been at a point 7 years ago where +7METS was child's play.

We all know that hemodynamics change when there is 15-18cmH2O of CO2 insufflation in the abdomen. What a cardiologist 7 years ago said about not being limiting was at that time, and not now.
 
Hawaiian Bruin said:
Proceed without further workup.
Click to expand...

Agreed, however I would like to know what prompted the initial cardiac work.

Although no SAM out lvot obstruction, what about the AOV and supravalvular aorta? He could have something more sinister (ie Williams syndrome. But, unless symptomatic currently I would not require further cardiac workup.
 
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Further info. Stress test in 2007 neg with 16.5 METS. Repeat in 2009 non-diagnostic and stopped 2/2 fatigue. Achieved 6.5 METS. Cardiac MRI was recommended but never obtained. Following repeat stress in 2009, no further cardiac testing follow up. Pt retired military in 2009.
 
Neogenesis said:
45 yo male in pre-op clinic for upcoming lap chole. Hx of HTN and DM. >4 METS. BP controlled 130s/70s. Normal physical exam. Approx 200lb. Pre-op EKG shows LVH. Further questioning of pt and review of old records shows worked up by cardiology approx 7 yrs ago. Echo at that time showed concentric LVH, normal EF, no LVOT obstruction or SAM. Negative stress test at that time as well. Pt was cleared by cardiology at that time for deployment (prior soldier) and note stated that he had a mild form of hypertrophic cardiomyopathy that had a very good prognosis and would not be limiting to pt in any way. EKG from 2007 apparently consistent with EKGs from 1990s per cards note, but none are available for review.

How do you proceed?

If it makes a difference, facility is a small community hospital (essentially an out patient surgery center). No ICU (step down only), cardiology, TEE, etc.
Click to expand...

So the echo seems normal besides LVH. But for review... these are the things you look for:

How thick was the septal hypertrophy? >15mm?
Was there a dagger shaped CWD profile? What was the peak gradient across the LVOT? What did the anterior mitral leaflet look like- was the anterior leaflet long and redundant? Was there premature closising of the aortic valve? What did M-mode through the aortic valve leaflets look like? C-sept distance? AL: PL ratio?

What drugs are you going to use and what drugs are you not going to use?

What do you do if the patient suddenly decompensates? Is epi a good idea if the BP is 50/30?
 
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lvot_cw__2_.jpg
 
You can look like a jackass and start questioning things to high heaven and possibly demand tests, or just realize that he seems to have good functional tolerance and proceed.
 
When ordering a preop test, it should be to identify a potentially dangerous modifiable condition that should be corrected before the planned procedure.

In this case, the condition you're concerned about is significant SAM. But this walking talking ex-soldier isn't going to have open heart surgery for a septal myectomy just so that he can then get his gallbag taken out.
 
Low suspicion for any clinically significant HOCM given his functional status but then again, the second bimodal peak for presentation is in the 30s-60s age range. Anyway, playing it safe would be pre-op 1-2L crystalloid bolus. Second pair of hands in the room. Quick asleep a-line if big old bear arms and a great pulse, awake if not. Induce with etomidate/fent/sux. Place 16-g IV. Sticks of lopressor, norepi, neo, and esmolol ready to go with ability to hang infusions quickly if needed. And a couple 5% albumins on standby for abdomen insufflation.

Still, would think twice about a plan like this at some podunk hospital in BFE given his records are 7 yrs old and the guy is possibly relatively deconditioned or has worsened hypertension now. In a situation where I couldn't just call my colleague in the other room to come drop a TEE I'd prefer an updated stress echo but probably wouldn't cancel the case.
 
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vector2 said:
Low suspicion for any clinically significant HOCM given his functional status but then again, the second bimodal peak for presentation is in the 30s-60s age range. Anyway, playing it safe would be pre-op 1-2L crystalloid bolus. Second pair of hands in the room. Quick asleep a-line if big old bear arms and a great pulse, awake if not. Induce with etomidate/fent/sux. Place 16-g IV. Sticks of lopressor, norepi, neo, and esmolol ready to go with ability to hang infusions quickly if needed. And a couple 5% albumins on standby for abdomen insufflation.

Still, would think twice about a plan like this at some podunk hospital in BFE given his records are 7 yrs old and the guy is possibly relatively deconditioned or has worsened hypertension now. In a situation where I couldn't just call my colleague in the other room to come drop a TEE I'd prefer an updated stress echo but probably wouldn't cancel the case.
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😕
How about #20 IV, GETA, go to PACU , next patient?
 
Neogenesis said:
45 yo male in pre-op clinic for upcoming lap chole. Hx of HTN and DM. >4 METS. BP controlled 130s/70s. Normal physical exam. Approx 200lb. Pre-op EKG shows LVH. Further questioning of pt and review of old records shows worked up by cardiology approx 7 yrs ago. Echo at that time showed concentric LVH, normal EF, no LVOT obstruction or SAM. Negative stress test at that time as well. Pt was cleared by cardiology at that time for deployment (prior soldier) and note stated that he had a mild form of hypertrophic cardiomyopathy that had a very good prognosis and would not be limiting to pt in any way. EKG from 2007 apparently consistent with EKGs from 1990s per cards note, but none are available for review.

How do you proceed?

If it makes a difference, facility is a small community hospital (essentially an out patient surgery center). No ICU (step down only), cardiology, TEE, etc.
Click to expand...
He needs follow up for his hypertrophied heart at some point. An echo will suffice. Might as well get it now. Otherwise what is the point of the preop clinic on a totally elective case? That's good medicine I think.
 
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Neogenesis said:
Further info. Stress test in 2007 neg with 16.5 METS. Repeat in 2009 non-diagnostic and stopped 2/2 fatigue. Achieved 6.5 METS. Cardiac MRI was recommended but never obtained. Following repeat stress in 2009, no further cardiac testing follow up. Pt retired military in 2009.
Click to expand...

The guy dropped 10 METS in 2 yrs while still in the military.
 
If this case is one that makes you afraid and forces your hand to order a million dollar work up then maybe you need to go into IM. If he is 45 yo and survived basic training and military service with HOCM then a simple lap chole isn't going to do him in. I am guessing the HOCM diagnosis is the result of an overzealous read on echo by the cardiologist. If he has no history of syncope or family history of sudden death then I wouldn't be to concerned. Basics of HOCM are keep the tank full and maximize your filling time by keeping the HR low. This is CA1 stuff.
 
PainDrain said:
If he has no history of syncope or family history of sudden death then I wouldn't be to concerned.
Click to expand...

By the time they get syncope it is too late; they can die at any moment. You want to catch them before that. This is not a clinical diagnosis.

Rather than thinking can I get away with this case, think about what would be best for the patient.

Let's say he were your brother. Wouldn't you want to have that checked out?
 
And what are you going to do with a new echo if it says no change. Like someone above said, will he go for a septal myomecty? Probably unlikely. More likely cardiology will put him on atenolol and that's that.

What is in the two weeks this guy is getting his cards work up his gall bladder suddenly becomes emergent? What if he now has a WBC of 20 and ascending cholangitis? You will then have a patient with fluid shifts and sepsis. That makes his mild HOCM more of an issue
 
I still suspect anabolic steroids were used in the past.

Doesn't change my approach tho, proceed with case. Liberal fluids.
 
urge said:
By the time they get syncope it is too late; they can die at any moment. You want to catch them before that. This is not a clinical diagnosis.

Rather than thinking can I get away with this case, think about what would be best for the patient.

Let's say he were your brother. Wouldn't you want to have that checked out?
Click to expand...

With good exercise tolerance? No. I'd be pissed that we all took time off along with my brother so some goofball could delay the case and put more copays in the mail for the work-up while making him deal with the gallbladder discomfort longer. There is an ACC algorithm that says to proceed with surgery in this case given his good exercise tolerance. Anything less is a disservice to the patient, IMO.
 
Another one of the finer points in the case is that the stem doesn't mention whether the patient is taking a BB as part of his chronic HTN/LVH management. I'd feel a bit more uncomfortable having to give him large doses of metoprolol perioperatively to keep him slow and full if he was bb-naive on the day of surgery. ACC/AHA recommends BB be started and titrated to effect at least 1 week prior to cut.
 
vector2 said:
Another one of the finer points in the case is that the stem doesn't mention whether the patient is taking a BB as part of his chronic HTN/LVH management. I'd feel a bit more uncomfortable having to give him large doses of metoprolol perioperatively to keep him slow and full if he was bb-naive on the day of surgery. ACC/AHA recommends BB be started and titrated to effect at least 1 week prior to cut.
Click to expand...

This is the recommendation for an asymptomatic patient with (presumably) no change in condition, good exercise tolerance, and an old echo showing no LVOT?
 
Ignatius J said:
This is the recommendation for an asymptomatic patient with (presumably) no change in condition, good exercise tolerance, and an old echo showing no LVOT?
Click to expand...

The guy has HTN, diabetes, LVH, and likely some degree of diastolic heart failure. He dropped 10 METS from 2007 to 2009 and has likely deconditioned more since that time. And why did they want that cardiac MRI that was never obtained if they had no suspicion for any progressive septal hypertrophy?

I absolutely hope he would've been well beta blocked prior to surgery but it's not like any of the beta blocker guidelines are crystal clear even though there's meta analyses with 600,000 pts in them. 9999/10k times you're likely gonna get away with a lol prop sux tube plan in this patient cause he's still in relatively good shape. I just wouldn't feel great about being that cavalier in a facility with no ICU, cardiology, or TEE.

http://content.onlinejacc.org/article.aspx?articleid=1140211
Current studies suggest that beta blockers reduce perioperative ischemia and may reduce the risk of MI and cardiovascular death in high-risk patients. However, routine administration of higher-dose long-acting metoprolol in beta-blocker–naive patients on the day of surgery and in the absence of dose titration is associated with an overall increase in mortality. How should clinicians reconcile these conflicting data? Importantly, the POISE results (371) do not address continuation of beta blockers in patients undergoing surgery who are receiving beta blockers for ACCF/AHA Class I guideline indications; therefore, this continues to be a Class I recommendation for beta-blocker therapy in the present focused update. In addition, available evidence suggests but does not definitively prove that when possible and where indicated, beta blockers should be started days to weeks before elective surgery. The dose should be titrated perioperatively to achieve adequate heart rate control to increase the likelihood that the patient will receive the benefit of beta blockade, while seeking to minimize the considerable risks of hypotension and bradycardia seen in POISE (see 11.2.1.4.). Titrated rate control with beta blockers should continue during the intraoperative and postoperative period, if possible, to maintain a heart rate of 60 to 80 bpm in the absence of hypotension, because this regimen has demonstrated efficacy (59,88). However, routine administration of high-dose beta blockers in the absence of dose titration for patients undergoing noncardiac surgery is not useful, may be harmful, and cannot be advocated, which results in a new Class III recommendation for this practice. The committee continues to advocate for additional studies to address remaining issues regarding the safety and efficacy of beta-blocker therapy as outlined above.
Click to expand...
 
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vector2 said:
The guy has HTN, diabetes, LVH, and likely some degree of diastolic heart failure. He dropped 10 METS from 2007 to 2009 and has likely deconditioned more since that time. I absolutely hope he would've been well beta blocked prior to surgery but it's not like any of the beta blocker guidelines are crystal clear even though there's meta analyses with 600,000 pts in them. 9999/10k times you're likely gonna get away with a lol prop sux tube plan in this patient cause he's still in relatively good shape. I just wouldn't feel great about being that cavalier in a facility with no ICU, cardiology, or TEE.

http://content.onlinejacc.org/article.aspx?articleid=1140211
Click to expand...

I missed the follow-up to the OP. That still doesn't change in my mind. >4 mets = proceed with surgery according to simple algorithm I have burned in my brain. I am in your boat- I don't think the literature is clear on when and how much benefit INITIATING a beta-blocker is prior to surgery.

I still think having a patient reschedule, deal with ongoing discomfort, and sending some more bills his way is a disservice in this case, given the fact that the ACC/AHA guidelines says to proceed with intermediate risk surgery in a patient with >4 mets.
 
Ignatius J said:
I still think having a patient reschedule, deal with ongoing discomfort, and sending some more bills his way is a disservice in this case, given the fact that the ACC/AHA guidelines says to proceed with intermediate risk surgery in a patient with >4 mets.
Click to expand...
I think you would be right 95% of the time. I don't know the right answer in this case just as nobody does until we do the case. I hunch is, everything will be fine.
But just reading your post makes me think a bit about how we all despise protocol based medicine. It takes away our clinical judgement. It makes us lesser physicians. I didn't go into medicine to have some protocols tell me what to do.
You are correct about the ACC/AHA guidelines. But they are just guidelines and we are the physicians. And therefore, we are ultimately responsible for the outcomes. So I would lean more on experience here than guidelines.
That doesn't mean the guidelines are wrong, just that if I follow them then it is because of my experience.
 
Noyac said:
I think you would be right 95% of the time. I don't know the right answer in this case just as nobody does until we do the case. I hunch is, everything will be fine.
But just reading your post makes me think a bit about how we all despise protocol based medicine. It takes away our clinical judgement. It makes us lesser physicians. I didn't go into medicine to have some protocols tell me what to do.
You are correct about the ACC/AHA guidelines. But they are just guidelines and we are the physicians. And therefore, we are ultimately responsible for the outcomes. So I would lean more on experience here than guidelines.
That doesn't mean the guidelines are wrong, just that if I follow them then it is because of my experience.
Click to expand...

Absolutely. Don't want to portray myself as a guideline guru just taking the default route to do the case. Only using it to contribute to the argument that that is a tough case to argue cancelling. Understand that "guideline guy" is almost as bad as "what would you tell the judge" guy.

As an aside (and speaking of stupid guidelines), I was pretty perturbed that they refused to do an interscalene block on my dad's shoulder last week because (gasp) he had only been off Plavix 5 days. All he said after surgery was how he just wanted to rip his arm off. God bless those USAP Jack wagons.
 
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Ignatius J said:
As an aside (and speaking of stupid guidelines), I was pretty perturbed that they refused to do an interscalene block on my dad's shoulder last week because (gasp) he had only been off Plavix 5 days. All he said after surgery was how he just wanted to rip his arm off. God bless those USAP Jack wagons.
Click to expand...

Very weak unfortunately for your dad.
 
Arch Guillotti said:
Very weak unfortunately for your dad.
Click to expand...

Yeah. He wasn't too happy. Neither was I. An interscalene with u/s is basically a SQ injection. Nothing against USAP (they are the staff at this hospital and it is just an opportunistic jab), but being on the other side you can really see how what we do makes a difference. My dad was miserable.
 
Ignatius J said:
As an aside (and speaking of stupid guidelines), I was pretty perturbed that they refused to do an interscalene block on my dad's shoulder last week because (gasp) he had only been off Plavix 5 days. All he said after surgery was how he just wanted to rip his arm off. God bless those USAP Jack wagons.
Click to expand...

So they were OK proceeding with the case but not doing a ISB?? :bang::boom:
 
SaltyDog said:
So they were OK proceeding with the case but not doing a ISB?? :bang::boom:
Click to expand...

Yep, very annoying.

As an aside, this all started out when he had a syncopal episode out trimming hedges complete with my mom doing chest compressioins until paramedics arrived. Negative MI/CVA but subsequently got cathed and received a BMS for a 99% blockage in the LCx. His cardiologist was on top of it as his orthopedist told him permanent functioning would deteriorate the longer and longer they waited. So he did BMS > waited one month > Plavix/AsA 325mg. Off Plavix for surgery and then resumed thereafter. My dad said he was in for an appointment and heard the cardiologist yelling at the orthopod about why he refused to stop aspirin. Ended up doing an open procedure. Going to be a long recovery but thankful to still have him. Tough being in the medical field and not dictating your family's care.
 
pgg said:
Sucks. Thank ASRA and their dumb guideline revision a couple years ago.
Click to expand...

I would really like the ASRA to change that. Lots of people may not be getting optimal post-op pain control because of it. We put CVCs in vasculopaths on all sorts of crazy blood thinners all the time, but we have to follow neuraxial guidelines with a 21G needle which is essentially tissue infiltration? Makes no sense.
 
Well you don't HAVE to follow ASRA guidelines. That's why the are called guidelines. That's why they are called guidelines and not standard of care rules. I have no problem doing a superficial block on someone on anticoagulation as long as 1) I think benefit outweighs risk, and 2) I give the patient a choice and discuss the risks/benefits with them. If they wish to proceed I think its reasonable, and i'm sure some day i'll end up holding pressure for 30 minutes after I end up hitting a vessel... but that's why I use ultrasound.
 
Ignatius J said:
Absolutely. Don't want to portray myself as a guideline guru just taking the default route to do the case. Only using it to contribute to the argument that that is a tough case to argue cancelling. Understand that "guideline guy" is almost as bad as "what would you tell the judge" guy.

As an aside (and speaking of stupid guidelines), I was pretty perturbed that they refused to do an interscalene block on my dad's shoulder last week because (gasp) he had only been off Plavix 5 days. All he said after surgery was how he just wanted to rip his arm off. God bless those USAP Jack wagons.
Click to expand...

5 days without any plavix is more than enough to do an ISB under U/S. I'd even do it after being off Plavix for 3 days with a normal verify now test or you just catch me in a good mood.
 
To the OP, if I saw this patient preop or in holding I'd want an Echo of his heart (within the past 12 months). I'd like to know his current EF, any valvular dysfunction or IHSS. He most likely has some degree of diastolic dysfunction. At my hospital I can get a TTE in about 30-45 minutes after calling the Echo tech. I have the option of being at the bedside/stretcher to see the Echo and get the results immediately.
 
A total of 127 subjects (case) with type 2 diabetes of more than five years duration were studied. Total 100 healthy subjects were included as the control group. Echocardiography was performed to assess left ventricular diastolic function.

Results:
Out of the total 127 subjects, 69 (54.33%) from the case group had diastolic dysfunction, and 11% amongst 100 in the control group population showed the diastolic dysfunction (P < 0.001). Patients with a longer duration of DM (of 11 to 15 years) had a higher prevalence of diastolic dysfunction (P < 0.02). Subjects with high waist circumference and high waist to hip ratio had statistically significant diastolic dysfunction with ‘P’ =0.001 and ‘P’ = < 0.02 respectively. Subjects with HbA1c > 7.5% had a higher prevalence of diastolic dysfunction than subjects with HbA1c < 7.5% (P < 0.02). Diastolic dysfunction was present in majority of the subjects with autonomic neuropathy and retinopathy.

Conclusions:
; subjects and, this finding was correlated with the duration of diabetes, HbA1c levels, obesity indices and diabetic microangiopathies. We conclude that early diagnosis and instPresent study reveals high incidence of diastolic dysfunction in asymptomatic diabeticitution of treatment will reduce morbidity and improve the outcomes, and prevent future heart failure.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224441/
 
We conclude that early diagnosis and institution of treatment for diastolic dysfunction in the form of ACE inhibitors, angiotensin II receptor blockers, aldosterone antagonists, diuretics etc. depending on clinical scenario, will reduce the morbidity and improve the outcome of diastolic HF. In order to improve the current poor prognosis in subjects with DM, the treatment of diastolic HF must be optimised. Subjects with DM type 2 should be screened for sub clinical diastolic dysfunction by echocardiography.
 
Editor's key points


  • Management of antiplatelet therapy in patients undergoing neuraxial injections is controversial.

  • The time course for recovery of platelet function was monitored in 13 patients undergoing epidural steroid injection.

  • All subjects had <30% platelet inhibition after discontinuation of clopidogrel for 5 days.

  • This small preliminary study suggests that 5 days might be sufficient for platelet recovery after clopidogrel before a neuraxial injection.

http://bja.oxfordjournals.org/content/107/6/966.full
 
Abstract Title: Spinal Anesthesia Five Days After Discontinuation of Clopidogrel: The Role of PFA II and P2Y12 Assays
Authors: Honorio T Benzon, MD, Chicago, IL
Robert Fragen, MD, Chicago, IL; Hubert A Benzon, MD, Chicago, IL; Jennifer Robinson, CRNA, Chicago, IL
Poster Type: Either


ABSTRACT BODY
Introduction: We report an uneventful spinal anesthesia 5 days after clopidogrel was stopped and after the PFA II and P2Y12 assays showed minimal or no residual antiplatelet activity.

Case Report: A 68–year old man sustained a fracture of his left femoral neck and was scheduled for a hip hemiarthroplasty. He has ankylosing spondylitis and coronary artery disease. In June 2007, his CABG surgery was cancelled because of the inability of the anesthesiologist or surgeon to intubate him. Instead of the planned surgery, three bare metal coronary artery stents were placed and he has been on clopidogrel 75 mg and ASA 81 mg daily since. He had normal neuro examinations with severely limited ROM of his neck. His surgery was 5 days after discontinuation of his clopidogrel and aspirin, he took his aspirin the day of surgery. The PFA II was 87 sec (range: 41-134 sec) and the P2Y12 assay results were 8% platelet inhibition and a platelet reaction unit (PRU) of 250 (range: 194-418). A spinal anesthesia was performed with a 25 G 3 ½ inch needle, 12 mg hyperbaric bupivacaine was injected and a sensory level of T4 was noted. Intraoperatively, he had propofol infusion, fentanyl, and midazolam. His BP was maintained at or above 100/50 mm Hg with intermittent IV ephedrine. He was brought to the PACU with a sensory level of T5, this regressed to T10 after 1 h, to L2 after 2 h and there was complete sensory and motor recovery at 5 ½ h after the spinal was started. He was started on enoxaparin 40 mg on POD1, the plan was to continue the drug daily until his INR is 2.0; warfarin 5 mg was given the night of POD1 with planned daily doses of 4 mg. His sensory and motor examinations were normal and he was able to walk with a cane on POD1. There was no bruising at the site of the spinal anesthesia. The rest of his postoperative recovery was uneventful.

Discussion: Clopidogrel is prescribed after coronary stent placements(1). Clopidogrel inhibits platelet aggregation by inhibiting the effects of ADP. There has been a case report of an epidural hematoma in a patient who was on clopidogrel and underwent a cervical ESI (2). ASRA recommends the discontinuation of clopidogrel for 7 days before a neuraxial injection (3). There is a case report of a safe removal of an epidural catheter in a patient 24 hours after discontinuation of the clopidogrel (4) and a case report of a caudal ESI 5 days after discontinuation of the clopidogrel, no test of platelet function was performed (5). The cut-off values for residual platelet reactivity are > 68 seconds for the PFA II and a PRU > 264 for the P2Y12 assay (6). Our patient’s PFA and P2Y12 PRU signified minimal or no residual antiplatelet activity of the clopidogrel. We recommend the PFAII and P2Y12 assays if a neuraxial injection is performed between 5 and 7 days after the clopidogrel is discontinued.

References:
1. Grines CL et al. Circulation 2007;115:813-8
2. Benzon HT et al. Anesthesiology 1999;91:1558-9
3. Horlocker TT et al. Reg Anesth Pain Med 2003;28:172-97
4. Bergman L et al. Reg Anesth Pain Med 2007;32:354-7
5. Broad L et al. Br J Anaesth 2007;98:19-22
6. Panicia R, et al. Thromb Haemost 2007;5:1839-47
 
It was also noted that there was a better correlation of the P2Y12 assay with light transmission aggregation than the PFA test.2 The PFA test cost $154.00, whereas the P2Y12 assay costs $459.00. Another test, the platelet mapping portion in the thrombelastography, has been used, but limitations in its clinical usefulness have been noted.3 Our 1 case of an uneventful spinal anesthesia does not guarantee the safety of neuraxial injections 5 days after clopidogrel is stopped. If a neuraxial injection has to be performed before 7 days after clopidogrel is stopped, then either the PFA II or the P2Y12 assay, preferably the P2Y12 assay if available, should be considered to determine the residual antiplatelet activity of clopidogrel. Further studies are required to determine the clinical appropriateness of these tests
 

Fig. 5
Transmitral diastolic Doppler in flow patterns are obtained across the open mitral valve leaflets. Here, we see a normal E:A ratio (A) associated with pseudonormalization and the subsequent demonstration of moderate DD using a Valsalva manoeuvre in the same patient (B). The third trace shows how the E and A waves change with advancing disease (C).
 
There are four basic Echocardiographic patterns of diastolic heart failure, which are graded I to IV:

  • The mildest form is called an "abnormal relaxation pattern", or grade I diastolic dysfunction. On the mitral inflow Doppler echocardiogram, there is reversal of the normal E/A ratio. This pattern may develop normally with age in some patients, and many grade I patients will not have any clinical signs or symptoms of heart failure.
  • Grade II diastolic dysfunction is called "pseudonormal filling dynamics". This is considered moderate diastolic dysfunction and is associated with elevated left atrial filling pressures. These patients more commonly have symptoms of heart failure, and many have left atrial enlargement due to the elevated pressures in the left heart.
Grade III and IV diastolic dysfunction are called "restrictive filling dynamics". These are both severe forms of diastolic dysfunction, and patients tend to have advanced heart failure symptoms:

  • Class III diastolic dysfunction patients will demonstrate reversal of their diastolic abnormalities on echocardiogram when they perform the Valsalva maneuver. This is referred to as "reversible restrictive diastolic dysfunction".
  • Class IV diastolic dysfunction patients will not demonstrate reversibility of their echocardiogram abnormalities, and are therefore said to suffer from "fixed restrictive diastolic dysfunction".
The presence of either class III and IV diastolic dysfunction is associated with a significantly worse prognosis. These patients will have left atrial enlargement, and many will have a reduced left ventricular ejection fraction that indicates a combination of systolic and diastolic dysfunction.

Imaged volumetric definition of systolic heart performance is commonly accepted as ejection fraction. Volumetric definition of the heart in systole was first described by Adolph Fick ascardiac output. Fick may be readily and inexpensively inverted to cardiac input and injection fraction to mathematically describe diastole. Decline of injection fraction paired with decline of E/A ratio seems a stronger argument in support of a mathematical definition of diastolic heart failure.

Another parameter to assess diastolic function is the E/E' ratio, which is the ratio of mitral peak velocity of early filling (E) to early diastolic mitral annular velocity (E'). Diastolic dysfunction is assumed when the E/E' ratio exceed 15.[5]
 
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