A 52-year-old man presented with worsening occipital headache, confusion over 12 hours, numbness and weakness on his right side, and blurry vision. His blood pressure was extremely high at 213/134 mm Hg. Tests found low potassium, high blood urea nitrogen and creatinine, and changes on CT scan consistent with hypertensive encephalopathy. He was admitted to the ICU and given intravenous nitroprusside, lowering his blood pressure over 3 hours and resolving his neurological symptoms within 5 hours. He was discharged on oral medications 5 days later with controlled blood pressure.
sudden spike in blood pressure to 180/120 or higher
abt how we deal with it
what we need to do immediate action
maintain ASAP blood pressure in order to save the patients
Mr. AMF 62 years presented with central chest pain on exertion for last 4 monthsHypertension(BP-220/120 mmHg) for last 4 years, taking 4 anti hypertensives.Diabetes for last 5 years (HbA1c-9.3%).Smoking for 8 years.Dyslipedemic for 3 years. H/o 5 times hospital admissions due to heart failure in last 3 years.ECG-Anterior wall ischemiaEF-58%During careful clinical exam- renal bruit on left side.Coronary angiogram done and revealed DVD. Renal angiogram showed significant left renal artery stenosis. Coronary angioplasty and left renal artery angioplasty done.
Mr AMF now have no chest pain on exertion after 3 months of coronary angioplasty.
Now BP is controlled (130/85 mm Hg), taking B blockers and ARB due to intolerance of ACE inhibitors.
No hospital admission during this period.
Diabetes and serum lipids are controlled.
sudden spike in blood pressure to 180/120 or higher
abt how we deal with it
what we need to do immediate action
maintain ASAP blood pressure in order to save the patients
Mr. AMF 62 years presented with central chest pain on exertion for last 4 monthsHypertension(BP-220/120 mmHg) for last 4 years, taking 4 anti hypertensives.Diabetes for last 5 years (HbA1c-9.3%).Smoking for 8 years.Dyslipedemic for 3 years. H/o 5 times hospital admissions due to heart failure in last 3 years.ECG-Anterior wall ischemiaEF-58%During careful clinical exam- renal bruit on left side.Coronary angiogram done and revealed DVD. Renal angiogram showed significant left renal artery stenosis. Coronary angioplasty and left renal artery angioplasty done.
Mr AMF now have no chest pain on exertion after 3 months of coronary angioplasty.
Now BP is controlled (130/85 mm Hg), taking B blockers and ARB due to intolerance of ACE inhibitors.
No hospital admission during this period.
Diabetes and serum lipids are controlled.
Wellens syndrome. Wellens syndrome (also referred to as LAD coronary T-wave syndrome) refers to an ECG pattern specific for critical stenosis of the proximal left anterior descending artery. The anomalies described occur in patients with recent anginal chest pain, and do not have chest pain when the ECG is recorded.
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...Ramachandra Barik
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Ramachandra Barik
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
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ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
2. A 52-year-old man presented to the
emergency department with
worsening occipital headache
Confusion
12 hours
numbness and weakness involving the right
side of his body
blurry vision.
Past medical history
Hypertension
hyperlipidemia..
3. On physical examination
Blood pressure was 213/134 mm Hg.
Confused.
Papilledema was seen on fundoscopic examination.
motor weakness (4/5) in the right upper extremity.
4. Laboratory studies revealed
following:
serum potassium, 3.1 mEq/L;
blood urea nitrogen, 36 mg/dL; and
serum creatinine, 2.5 mg/dL (baseline creatinine, 1.5
mg/dL).
Electrocardiogram revealed left ventricular hypertrophy by
voltage criteria and nonspecific ST-T wave abnormalities in
the lateral leads.
Computed tomography scan of the head without contrast
revealed diffuse bilateral white matter changes consistent
with hypertensive encephalopathy
5. Although not specifically addressed in the JNC 7
report, patients with a systolic BP > 179 mm Hg or a
diastolic BP > 109 mm Hg are usually considered to be
having a “hypertensive crisis”.
Crises
Emergency Urgency
6. The term malignant hypertension has been used to
describe a syndrome characterized by elevated BP
accompanied by encephalopathy or acute
nephropathy. This term, however, has been removed
from National and International Blood Pressure
Control guidelines and is best referred to as a
hypertensive emergency.
CHEST / 13 1/6/ JUNE, 2007
7. Left with 2 terms
Hypertensive Emergency
Hypertensive Urgency
8. Hypertensive emergency (crisis)
severe elevation in blood pressure (> 180/120 mm Hg)
complicated by evidence of impending or progressive target organ
dysfunction.
Target organ dysfunction (Acute) include Emergency not defined
by a
coronary ischemia,
specific number, but
disordered cerebral function,
rather by evidence of
cerebrovascular events,
acute dysfunction in
intracerebral or subarachnoid hemorrhage or
hypertensive encephalopathy. (cerebral edema)
cardiovascular,
pulmonary edema, and
neurologic, or renal
systems
renal failure.
The rate of change in blood pressure
Dept. of Health and Human Services, National Institutes of Health,
Can Fam Physician 2011;57:1137-41 National Heart, Lung, and Blood Institute; 2004. NIH Publication No.
04–5230.
11. Hypertensive urgency,
severe elevation in blood pressure without progressive
target organ dysfunction (>160/110)
Examples
upper levels of stage II hypertension associated with
severe headache,
shortness of breath,
epistaxis, or
severe anxiety.
The Seventh Report of the Joint National Committee on
Prevention,Detection,Evaluation, and Treatment of High Blood
12. Pathophysiology
Check
Activation of Coagulation cascade and
standing
pro-inflammatory mediators BP
Underlying Precipitating
Hypertension Factor
13. Index case
The patient was admitted to the intensive care unit
and started on intravenous nitroprusside.
Blood pressure decreased to 190/100 mm Hg over the
first 3 hours and neurologic symptoms resolved within
5 hours.
He was switched to his usual oral regimen on the third
day of hospital admission and was discharged home on
the fifth day with controlled blood pressure
14. Management of Urgency
Oral antihypertensive agents in an outpatient or
observational setting
low doses
incremental doses
Avoid excessive reduction in elderly, patients with
PAD/CVD/intracranial disease
The initial goal is to reduce blood pressure to 160/110 mm Hg
over several hours to days using conventional oral therapy
(24-48 hrs)
Mean arterial pressure should be reduced by no more
than 25% within the first 24 hours using conventional oral
therapy.
15. Captopril
ACE inhibitor
onset of action 15 to 30 minutes
maximum drop in blood pressure 30 and 90 minutes
25-mg oral dose initially, followed by incremental doses of 50 to 100
mg 90 to 120 minutes later
Significant adverse effects include cough, hypotension,
hyperkalemia, angioedema, and renal failure (especially in
patients with bilateral renal artery stenosis, in whom it should be
avoided).
16.
17.
18. Nicardipine
Calcium channel blocker
oral dose is 30 mg,
Repeated every 8 hours until the target blood pressure is
achieved.
Onset of action is ½ to 2 hours.
Common adverse reactions include palpitations, flushing,
headache, and dizziness
Am Heart J 1995;129:917–23
19. Labetalol
has mixed α1- and β-adrenergic blocking
properties(1:7)
onset of action within 1 to 2 hours
Starting dose is 200 mg orally, which can be
repeated every 3 to 4 hours
Common side effects include nausea and dizziness.
20. Clonidine
central sympatholytic (α2-adrenergic receptor agonist) agent
onset of action within 15 to 30 minutes
peak effect within 2 to 4 hours
oral regimen is a 0.1 to 0.2 mg loading dose followed by 0.05 to 0.1
mg every hour until target blood pressure is achieved, up to a
maximum dose of 0.7 mg.
Common side effects include sedation, dry mouth, and orthostatic
hypotension.
Beware of “withdrawl”
21. calcium channel blocker
Peak effect within 10 to 20 minutes.
Short-acting nifedipine is not approved by the US FDA
(unpredictable drops in blood pressure and associated risk
of stroke)
In 1995, an ad hoc panel convened by the National
Heart,Lung, and Blood Institute concluded that “short-
acting nifedipine should be used with great caution (if at all),
especially at higher doses, in the treatment of hypertension.”
22. Treatment of hypertensive
emergency
Use parenteral drugs
Continuous monitoring of blood pressure.
Reduce the mean arterial pressure by 10% during the first hour and an additional 15% within the
next 2 to 3 hours
JNC VII
Reduce mean arterial BP by no more than 25 per-cent (within minutes to 1 hour),
then if stable, to 160/100–110 mmHg within the next 2–6 hours.
If tolerated further gradual reductions toward a normal BP can be implemented in the next 24–48 hours
More rapid reduction in blood pressure may result in cardiac or renal or cerebrovascular hypo-
perfusion.
altered autoregulation curve
Pressure natriuresis may cause volume depletion in patients with hypertensive emergency, and
administering vasodilator medications to these patients can lead to precipitous drops in blood
pressure. Patients with volume depletion should receive intravenous (IV) saline to restore
intravascular volume and shut off the renin-angiotensin-aldosterone system.
Elliot WJ. Clinical features and management of selected hypertensive
emergencies. J Clin Hypertens (Greenwich)
2004;6:587–92
23. Exceptions to treatment of
Emergency
Aortic dissection
Pulmonary edema
Stroke
Patient requiring thrombolysis
24. Hypertension in the setting of an intracerebral bleed
Treat only when blood pressure is more than 180/ 105
mm Hg.(or 200/110)
MBP should be maintained <130 mm Hg
Ischemic stroke,
Observe first 1 to 2 hours to determine if it spontaneously
decrease s
Only a persistently MAP>130 mm Hg or a SBP> 220 mm Hg
or DBP >120, should be carefully treated.
Mean arterial pressure should be lowered by 15% to 20% (10-
15% JNC VII) over 24 hrs
Bring BP <185/110 for thrombolysis. Maintain at <180/105
Labetelol,Sodium Nitroprusside , nicardipine, enalipritat
used
American Heart association recommendation
Adams HP Jr, Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic stroke: a scien-tific
statement from the Stroke Council of the American Stroke Association. Stroke 2003; 34:1056 –1083
The European Stroke Initiative Executive Committee andthe EUSI Writing Committee. European Stroke
Initiativerecommendations for stroke management: update 2003.Cerebrovasc Dis 2003; 16:311–337
25. Acute aortic dissection,
IV β-blocker (eg, labetalol or esmolol) followed by a
vasodilating agent, classically IV nitroprusside.
lower the SBP to a goal of < 120 mm Hg within 20
minutes (MAP <80).
26. Acute stroke with accelerated htn well within accepted
range but with concomitant noncerebral acute
organ damage .
What next?
Blood pressure should be reduced carefully
beyound the accepted values using emergency
guidelines, with careful monitoring of
neurological status
27. Acute Postoperative Hypertension
early onset, (within 2 h after surgery)
Typically of short duration, (treatment for ≤ 6 hrs)
Complications of APH may include hemorrhagic stroke, cerebral
ischemia,encephalopathy, myocardial ischemia, myocardial
infarction, cardiac arrhythmia, CCF with pulmonary edema,
failure of vascular anastomoses, and bleeding at the surgical site
Most commonly associated with cardiothoracic, vascular, head
and neck, and neurosurgical procedures.
Activation of the sympathetic nervous system, increase in
afterload, increase in SBP and DBP with or without tachycardia
28. Post cardiac surgery, treatment is recommended for a
BP > 140/90 or a MAP of > 105 mm Hg. Other
conditions the goal may vary
Rule out Pain,anxiety, hypothermia with shivering,
hypoxemia, hypercarbia, and bladder distension
Labetalol, esmolol, nicardipine, and clevidipine have
proven effective
30. The Seventh Report of the Joint National Committee
on Prevention,Detection,Evaluation, and Treatment
of High Blood Pressure
31. The current AHA
guidelines recommend the
use of Labetalol or
nicardipine if the SBP is
>220 mm Hg or the DBP is
from 121 to 140
mm Hg, and nitroprusside
for a DBP > 140 mm Hg
The diagnosis and management of hypertensive crises.
Chest 2000
33. 5 patients arrive with identical vital signs: heart rate of 100 beats/min, blood pressure
(BP) of 209/105 mm Hg, respiration rate of 20 breaths/min, and temperature of 36.9oC
Patient A is a 65-year-old man with nausea, Intravenous labetalol, bolus or infusion.Target:
vomiting, and confusion and papilledema Reduce MAP by 20% to 25% over 2 to 8 hours
Nitroglycerin infusion; intravenous
Patient B is a 73-year-old woman with sudden enalaprilat or sublingual captopril.
shortness of breath, pink sputum, and heavy Furosemide will work only after adequate
chest pain and LVH decrease in preload and afterload
Urgent imaging with simultaneous decrease in
Patient C is a 56-year-old man with sharp, BP. Nitroprusside and esmolol infusion;
tearing chest and back pain and diastolic labetalol boluses or infusion.Target: Rapidly
murmer reduce systolic BP to 110 mm Hg if there is
no evidence of hypoperfusion
No treatment.Reduce BP only if it is greater
Patient D is a 64-year-old woman with a 6- than 220/120 mm Hg (embolic) or greater
hour history of right-sided weakness. NCCT than 180/105 mm Hg (hemorrhagic)
no hemorrage. Thrombolysis not
contemplated
Restart the medications she was on (Diuretic
Patient E is a 51-year-old woman with a mild
headache, concerned about her history of and ARB). Ask her to follow up in OPD
hypertension.Poorly compliant. LVH +
Headache and altered level of con-sciousness are the usual manifestations of hyperten-sive encephalopathy.25,26 Focal neurologic findings,especially lateralizing signs, are uncommon in hyper-tensive encephalopathy, being more suggestive of acerebrovascular accident. Subarachnoid hemorrhageshould be considered in patients with a sudden onsetof a severe headache.
Dietary sodium should be reduced tono more than 100 mmol per day (2.4 g of sodi-um).94–
Emergencycharacterized bysevere elevations in BP (>180/120 mmHg) compli-cated by evidence of impending or progressive tar-get organ dysfunction (jnc 7)Examplesinclude hypertensive encephalopathy, intracerebralhemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable anginapectoris, dissecting aortic aneurysm, or eclampsiaChronic Target Organ Damage (JNC VII)HeartLVHAngina/prior MIPrior coronary revascularizationHeart failureBrainStroke or transient ischemic attackDementiaCKDPeripheral arterial diseaseRetinopathydecompensation of vital organ functionwhereas in children and pregnantwomen, encephalopathy may develop with a DBP ofonly 100 mm Hg.
Htnenchephalopathy is vasodilation, edema, and increased intracranial pres-sure. Clinically, patients present with headache, visual changes, nausea, and vomiting. They might complain of transient and migrating nonfocal neurologic deficits, and might progress to seizures and coma.
Some patients with hypertensive urgencies maybenefit from treatment with an oral, short-actingagent such as captopril, labetalol, or clonidine followed by several hours of observation.The reason for a stepwise reduction in blood pressure is the fact that patients with chronic hypertension have an altered autoregulation curve. Acute normotension would lead to hypoperfusion in these patients. Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Patients with hypertensive urgency should have theirBP reduced within 24 to 48 h, whereas patients with
require immediateBP reduction (not necessarily to normal) to pre-vent or limit target organ damage (jnc 7)The initialgoal of therapy in hypertensive emergencies is toreduce mean arterial BP by no more than 25 percent (within minutes to 1 hour), then if stable, to160/100–110 mmHg within the next 2–6 hours.. There are exceptions to the above recommendation—patients with anischemic stroke in which there is no clear evidencefrom clinical trials to support the use of immediate antihypertensive treatment, patients withaortic dissection who should have their SBP lowered to <100 mmHg if tolerated, and patients inwhom BP is lowered to enable the use of thrombolytic agents (see Stroke).return the BP to a level where autoregulation restores normal perfusion pressure to vital organs, not to “nor-mal” BP levels.
Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Aortic dissection SBP < 100Pulmonary edema rapid decrease required
SBP ≥180mmHg or DBP ≥105 mmHg usually necessitatestherapy with intravenous agents to prevent intracerebral bleeding (jnc 7)Aortic dissection 75% die in 2 wks without treatment or 75% survive over 5 yrs with treatment. Left ventricular Force of ejection has to be decreased. Only vasodilator will cause tachycardia and propogation of dissectionThe elevated BP is not a manifes-tation of a hypertensive emergency but rather aprotective physiologic response to maintain cerebralperfusion pressure to the vascular territory affectedby ischemia.
Considering the potential for severe toxicity withnitroprusside, this drug should only be used whenother IV antihypertensive agents are not availableand then only in specific clinical circumstances andin patients with normal renal and hepatic function.68The duration of treatment should be as short aspossible, and the infusion rate should not be 2 g/kg/min. An infusion of thiosulfate should be usedin patients receiving higher dosages (4 to 10 g/kg/min) of nitroprusside.7Nitroglycerin reduces BP by reducingpreload and cardiac output; undesirable effects inpatients with compromised cerebral and renal per-fusion Diuretics should beavoided unless specifically indicated for volumeoverload, as occurs in renal parenchymal disease orcoexisting pulmonary edema.
Pulmonary edema also start positive pressure ventilation before furosemide. More rapid decrease is permitted but not very severe decrese. More often decrease should be titrated as per symptomsNitroprusside has a rapid onsetof action, and provides both arterial and venous dilation. Heart rate control with β-blockers must be initiated first to avoid reflex tachycardia that will propagate the dis-section. Alternatively, labetalol, with its a -blocking andβ-blocking properties, is a relatively user-friendly option for controlling heart rate and BP simultaneously.); if a thrombolytic is given, reduce BP to 180/105 mm Hg before treatment and 180/100 mm Hg after treatmen