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Archive for the ‘critical care ccu’ Category

An elderly man  with past H/o CAD  was admitted with ischemic LVF and hypotension .Blood pressure was  90/60 mmhg  and pulse rate was 140 . Urine urine output  in the immediate past hour was 50 ml . Saturation was 95 % .He had fairly extensive  crackles in both lung fields.

A bed side echo showed  moderate LV dysfunction , with wall motion defect in LCX territory and  mild  MR .A dignosis of post  MI -ischemic LVF was made .

He  was  put on intensive anti failure protocol. I asked my  fellow to administer IV NTG  and left the ward .

On my next visit after few hours  . . . the patient was in much bad shape  , and when I enquired , I learnt  NTG was never administered . I was curious to know why the fellow  dis- obeyed my instruction .

He felt sorry  .  .  . But he earnestly told me  , he  could not comprehend the principle of administering NTG in a  patient  with shock ! . I was happy  to  note his  genuine concern  for   the patient  !  But  . . . I had to take a brief  lecture to convince the importance of NTG in some forms of shock !

What is the cause for hypotension in ischemic LVF ?

Lungs are flooded due to  very high LVEDP . Blood  not only struggles to  enter the LV  but also finds difficult to   leave the LV ,  former due to defective relaxation later due to poor pumping.

The extremely high pre-load actually stuns the left ventricle in diastole . (Primarily diastolic stunning  )  . Here is a hemodynamic paradox . Excess pre-load  occurs in  terms of pressure , but  in terms of volume there is miniscule amount  blood  that  traverses LV  .

This is pre-load mismatch  at play .Empty ventricles with high wall stress  and that is reflected in aortic afterword as well .

We have to some how reduce the  very high levels of LVEDP . IV NTG can  dramatically  reduce the pre load  ( and reduce the LVEDP .) The other major  benefit is ,  NTG   can reduce the MVO2 by improving sub endocardium coronary perfusion and de-stress the heart.

Once  LVEDP  is  lowered  , the ventricle will tend to recover and gain at least some  original elasticity ( Frank starling forces) . Of course it will be defective due to ongoing ischemia . Even slight fall of LVEDP (say from 25 to 18 mmhg  can have  significant benefits as the LV function curve labors on the steep shoulder region !) .

This is one situation where NTG can increase the blood pressure once the hemodynamics is favorably altered.

*Yes  . . . heavy doses  of  Frusemide injection can do the same job but it largely depends the kindey’s cooperation to flush out fluids  .In a shock like situation one can trust the kidney perfusion  !

Additional benefits of NTG

Mitral  regurgitation  is a serious destabilizer of LV function .NTG can reduce the regurgitant fraction in acute MR effectively .

Caution

NTG may worsen the hypotension of RV infarction . Make it very sure , you are not dealing with this unique  pre-load dependent circulation.

What happened to this patient ?

He  did show  improvement with IV NTG . Of course it was not dramatic as I have projected in this article .Still it was really helped him .He required simultaneous dobutamine infusion as well .The BP did not fall  further and lung congestion was relieved  .He went on to recover fully by 48 hours and was posted for elective cath study .

Final message

                                             We tend to  worry  more about falling blood pressure  when administering  NTG. . .It is a wonderfully effective drug especially in the setting of ischemia and cardiac failure  even if  the blood pressure is low !

Acute cardiac hemodynamics  is  complex phenomenon .No one has mastered it .Paradoxes are common . Hypotension in the back ground of  acute pulmonary edema  especially due to ischemic LVF  can be corrected by NTG . Of course physicians  need  some  courage to administer NTG in patients  with a systolic pressure of  80-90mmhg.

This should ideally be done with intra arterial line in place and a simultaneous inotropic line (Doubtamine /Nor-epinephrine ) back up in case of worsening perfusion pressure .

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A 60 year old man with chest discomfort and severe breathlessness  and  blood pressure of 160/110 was  wheeled into CCU. A diagnosis of  acute anterior  STEMI was made and he  was about to be  thrombolysed . Since  his blood pressure was high they were waiting for it to come down with IV  Nitrglycerin

I was called to see this  patient  .Here is his ECG .

Q-LVH INCOMPLET LBBB STEMI DIFFERENTIAL DIAGNOSIS 2

Though   ECG  suggested anterior  STEMI  , I  was  fairly  convinced  it  was  in fact  LVH and  incomplete  LBBB.

I confirmed with the  patient  about the onset of symptoms . It was primarily  breathlessness and only a  vague discomfort .Meanwhile , the troponin came as positive and CPK MB    was  normal. The combined troponin  positivity  and ST elevation  almost confirmed the STEMI ,  and  the  urgency for  thrombolysis was  intensified . One resident suggested  an  emergency PCI.

My self ,  in spite of  being a cardiologist was isolated among the physician team .  I  had to  urgently  prove to them it is indeed  not STEMI !  I did a bed side echo and showed  the  physician colleagues   a vigorously contracting  hypertrophied  left ventricle  with a EF of 68 % . There  was  negligible wall motion defect  . . .  if at all any !

They were still far from convinced ?  They  were  sort of  amused .There is   ST elevation ,  there is  troponin  positivity. . . what else you want  . . . they seemed to ask  ?

I asked them  . . . How can an  acute  extensive anterior   MI contract so well ,  without a trace of   wall motion defect ?

It took me considerable time and effort  to  convince them  that the whole thing was not a STEMI.  Finally they agreed .It was  a simple LVH with secondary ST elevation  due to incomplete  LBBB .  Troponin elevation  simply  represent minor myocardial  injury associated  with hypertensive  LVF . This  patient was discharged within 24 hours  in perfectly stable  condition . Since he had mild elevation of creatinine and was  sent for  nephrology  work up.

Final message

LVH with secondary  ST elevation in V1-V4 is a common situation that mimics  acute STEMI . Cardiac failure can result in non ischemic troponin  release .  Acute medicine is  an unique art . Some times it demands all your senses to be on alert mode . Realise ,  in the above case ,   in spite of the   the classical   triad of  chest pain ,    ST elevation , troponin positivity  it  almost led to a wrong diagnosis of  acute myocardial Infarction .

After thought : What  if they had thrombolysed this patient or taken for a PCI ?

When  the clinical suspicion is high and  circumstantial evidence  point to an ACS   ,   this error can be  justified . After all ,  5 % of   famous ISIS  study population were not suffering from STEMI  but got thrombolysis !

* One real possibility in this ECG is  old AWMI with re-infarction  or a dyskinetic septum lifting the ST segment .But both were excluded by the rapid bed side echo.

 

 

 

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Acute stroke /ICH/SAH/ Blood pressure is 210 /120 !

You are called in to control the BP  . . . What will you do ?

Basics

Neurogenic HT is adrenergic dependent /stress related .It is  often volume independent .Nitroglycerin worsens adrenergic  hypertension by reflex tachycardia even though it may drop the initial BP .Sustained reduction won’t happen with NTG .Further , nitroglycerine is known to elevate the intra cranial pressure and worsen  the stroke laden  cortical / brain-stem  ischemia

Best drugs

  1. Alpha methyl dopa
  2. Metoprolol
  3. Labetalol

Not best ( Worst ? )

  1. Nitroglycerine ( I guess  most  would disagree with this !  how dare you call NTG useless for   controlling HT )*
  2. Calcium blocker (It is still useful for spasm prevention in SAH)
  3. Diuretics

* IV NTG is useful in some of these patients for a instant effect. However , It has a huge risk of raising intra- cranial pressure .

Final message

Control of neurgenic HT requires correction of the primary trigger namely  the neural insult .The second best option is to stop the effects  neural signal outflow  .Adrenergic  blockers are the best way to do it . All other drugs like calcium/Nitric oxide /diuretics  are non specific  and only  provide a transient relief  and may in fact aggravate sympathetic mediated hypertension.There is no harm in giving  calcium blockers but it should always be accompanied by beta blockers to bring aggressive control .

Finally , controlling hypertension in stroke is to be done  with frequent confabulations !  with neurologists ,  as blood pressure  lowering modalities  has a competing interest with brain perfusion !

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Conventionally  pulmonary embolism is classified as massive, sub massive  based on

  1. Severity of obstruction
  2. Level of  obstruction in pulmonary anatomy (MPA,Branch PA, Segmental etc )
  3. Thrombus burden
  4. Quantum  of pulmonary vascular bed  compromised

But it is always intriguing ,    the clinical outcome was not linearly  correlating with the above parameters.

Instead the outcome seemed more dependent on the following .

  1. Degree of RV dilatation
  2. Systemic hypo-tension
  3. RV shock

Image courtesy .www.smartdraw.com

So ,  whatever be the quantum of pulmonary embolism , it is the behavior of RV that is going to determine the outcome.  The current  wisdom   demands , all hemo-dyanmically unstable pulmonary embolsim may be considered as massive or high risk pulmonary embolism and  aggressive treatment  is  to be undertaken.

Counter point

There is  one major diagnostic issue  if we depend more on hemo-dynamic instability . What is that ?

There is no valid method to identify Acuteness / chronicity of   RA, RV dilatation . Consider this  example , a patient with chronic thrombo -embolic PAH presents with  acute deterioration  due to a transient arrhythmia  or  non cardiac  cause of hypotension . He is at  risk of being labeled as  acute pulmonary embolism  since he may  show   some thrombus  in his pulmonary circulation in  CT scan .  However ,  no great harm is done as long as he receives only heparin.

Reference

http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-APE-FT.pdf

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Up to 24 hours

  • Failed thrombolysis and persistent infarct related chest pain
  • Prolonged  Infarct pain  in spite of successful thrombolysis (Rare)
  • Dual STEMI and Dual ACS ( Combination of STEMI/NSTEMI)  *

* Generally  until   after  24 hours one should not make a second coronary syndrome  though  logically  it is possible ( Dual acute coronary syndrome)

After 24 hours -up to 2 weeks

  • Post MI angina  – IRA related (Re-occlusion, Threatened reocclusion)
  • Post MI angina -Non IRA related ( Critical  non -IRA lesion)
  • Thrombus migration /Side branch occlusion
  • Re infarction -Same territory
  • Re-infarction-Remote territory
  • Infarct extension, Infarct expansion , Dyskinetic segments  ( Acute ventricular  remodeling  has a potential to generate pain )
  • Combinations of the above

Caution

24 hour is  arbitrary cut off .There can be spill overs and over laps

*Refractory non ischemic  chest pain often atypical not relieved by anti anginal  medication   – Pericardits, Coronary dissections , myocardial /Pap muscle  tears .

After thought

Do we need to break our brain  to  find  the source of angina  following STEMI ?

Principles of scientific medicine  would demand it  . However   in this era of  hyper active interventional  cardiologists  there is little purpose  as they  tend to  open up all occluded arteries   guided by the  their  ignorance about the source of chest pain.

Reference

Video on Dual  coronary syndrome

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This  is the ECG  of  a  45 year old man with  H/O hypertension  and  chest pain .The general practitioner who first saw him alerted this  patient about a possible  heart  attack  asked to meet a cardiologist immediately. The cardiologist who  saw  this ECG   tended to confirm  the diagnosis  and advised admission in  a coronary  care unit .

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

  • Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
  • Bi-phasic  T wave in v1 to v3
  • ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

  • LV strain  pattern normalises ?
  • Further ST depression  occurs ?
  • No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

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Most important MCQ in clinical cardiology

Many cardiologists  would love to do away with detailed  clinical examination because  . . .

  1. They think it is an inferior job to do  . By skipping  it , they get a false sense of superiority.
  2. It is a time killer  and eat into precious cath-lab  time
  3. They no longer believe in  these “perceived – primitive” medical methods.
  4. Fear of colleagues making  fun of hem if they  indulge  in detailed clinical examination.( At-least in India ! )
  5. To give more job opportunities  to para medics.
  6. They are no longer confident about making a good clinical examination as they  are neither  trained  adequately nor interested in it !

Answer :  All of the above can be true .  The 6th response is  likely to be  more  correct !

While cath labs can prevent few deaths occasionally . . . it is the general wards and OPDs that add life every day

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