Pressure difference between Supine and Sitting

elderly lady,chulha worker,presented with chronic cough and dyspnea,which is increased since a month.non dm,no major illness in the past.sr creat 1.2,sputum AFB negative.RV neg. o/e bil wheezing with reduced breath sounds. HR 110/min,spo2 44%,no cyanosis clubbing. BP 110/60 mmHg.with 1/2 lit oxygen,spo2 remains 96%. plz suggest further management.

37 year old male came with the c/o burning sensation in the epigastric region and history of regurgitation of food. No h/o palpitations, exertional chest discomfort, sweating. Not a K/c/o T2DM,HTN,IHD. No significant family history. Smoker and alcoholic. HR-92 BPM Bp-200/110 mmhg Spo2-98% at RA RS,CVS,P/A,CNS are NAD

A 48yrs old male presented to ED having H/o sudden onset LOC and seizure with multiple episode of vomitting.K/c/o HTN not on regular treatment as advice by his family doctor.O/e CNS - conscious,alert,oriented,Right UMN facial palsy,Both pupils are normal in size.GCS-E3V4M4,Bp-170/90mmhg.Diagnosis?

Management of Acute pulmonary edema Treatment of pulmonary edema should be focused on ‘fluid redistribution’ and not ‘fluid removal’. First line: Nitroglycerin and NIV (start ASAP) Second line: ACE-I (in addition or instead of NTG) Third line: Diuretic like furosemide Morphine has NO ROLE in modern management of cardiogenic pulmonary edema NIV decreases work of breathing, improves O2/ CO2 exchange, reduces length of stay, reduces hospital costs, reduces need for intubation, and may decrease mortality. Early NIV usage is a must! . Nitroglycerin should be the FIRST line drug for treatment of moderate CHF and pulmonary edema. Being Aggressive! Starting at 50-60 microgram/min (NOT at 2.5-5mcg/min) and escalating 10-20mcg/min (upto 400mcg/min). Another way of optimising hemodynamics is thru a NTG bolus of 0.5 - 2mg. Multiple studies like Cotter et al 1998, Beltrame et al 1998, Kruas et al 1990, Hoffman et al 1987, Nelson et al 1983 have proved the importance of high dose nitroglycerin over smaller dosages. The oral dose of NTG is 0.4mg or 400mcg is approximately equal to 80mcg/min infusion. Therefore, starting an infusion at 5mcg/min after administering 0.4mg sublingual dose leads to a dramatic dose reduction. Take caution if the patient is hypotensive, acute mitral regurgitation, aortic stenosis, pulmonary hypertension and patients on sildenafil Diuretic effect is delayed if administered alone and can be detrimental in first 30-60 minutes. Furosemide activates the renin angiotensin aldosterone system and increases the afterload, causing more harm than good in pulmonary edema patients. So, when the patients undergo preload and afterload reduction, furosemide works immediately as the kidneys are perfused. If pre-medicated with nitrates and captopril, furosemide had an immediate and sustained effect on pulmonary capillary wedge pressure. More than 50% of patients in cardiogenic pulmonary edema are euvolemic. Fluid is excess in the wrong bucket.( I. e lungs) . Hence treatment should be focussed towards ‘fluid redistribution’ and not ‘fluid removal’.

40 yrs old female pt.came to opd with c/o giddiness nausea and high grade fever(102 F),her BP 190/110 mmHg(1st time detected),her CBC,s. create,rbs,lipid profile,s. tsh,s.electrolyes are in normal limit,urine routine&micro shows plenty of pus cells,her ecg shows T inversion in inferior wall. iv Anti biotics and supportive Rx given,for htn oral Anti htn not work so I started inj.lobet via infusion for 24 hours.her bp was 160/100 while infusion was running.but when it stoped than after 1 hr it increase to 190/110 mmhg.I started tab lobet(100) tds.but not work.than next day I started inj.nitroglycerin via infusion initially 5 mcg/min than increase to 10 mcg/ min,than pt bp was 150/90mmhg.after 24 hrs pt.get severe headache so I slowly tapered and stop infusion than after 2 hours bp increase to 190/110 mmHg. plz give ur opinion for further Ix and Rx