Acute pressure syndromes

DR.RISHIKESAN K.V

SPECIALIST PHYSICIAN

VENNIYIL MEDICAL CENTRE SHARJAH

ACUTE PRESSURE SYNDROMES

FROM THREAT TO THERAPY

GIVING ACUTE HYPERTENSION THE HYPER ATTENTION IT DESERVES

HTN AFFECTS AT LEAST 1 BILLION INDIVIDUALS

DEFINITIONS

Hypertensive crisis, is somewhat of a generic term and

most clinicians break this into 2 categories.

The first category is referred to as hypertensive emergency. This is a severe elevation of BP, defined as >180/120 mm Hg, and it is complicated by target-organ dysfunction or damage.

Hypertensive urgency means there is a severe elevation in BP but target-organ function remains intact.

In terms of severity, pts. who have HE are in worse condition than those who have hypertensive urgency.

HYPERTENSIVE CRISES – OTHER TERMS

ACCELARATED HYPERTENSION

BP is elevated progressively, at fast pace, with retinal hemorrhage and exudates (Grade III Keith-Wagner-Barker retinopathy ).

MALIGNANT HYPERTENSION

Severe elevation BP accompanied with papilledema which may be accompanied by encephalopathy or nephropathy.

In addition to Grade IV Keith-Wagner-Barker retinopathy.

TARGET ORGAN DAMAGE / DYSFUNCTION

HE includes

Hypertensive encephalopathy,

ICH, AMI, acute LVD with pul. edema,

UA, Dissecting aortic aneurysm,

In women who are pregnant, eclampsia.

In terms of hypertensive urgency, this is stage II HTN, which may present with severe headache; shortness of breath; epitasis, or nosebleed; or severe anxiety.

HOW COMMON IT IS ? IT IS COMMON

Most of these patients :

• are generally known to have hypertension

• are oftentimes noncompliant with treatment

• or have been inadequately treated for their hypertension.

• Patients who have had hypertension for 5, 10, or 15 years and have never been well controlled are at high risk for these disorders .

EPIDEMIOLOGY

How common is this disorder?

These numbers are are somewhat suspect. It probably is underreported.

Something on the order of 3% of the patients presenting ED have hypertensive crisis ie on an annual basis, perhaps 2 to 6 out of 100,000 patients coming through EDs

Of 500,000 American patients per year who have this disorder, about 25% present to the medical section of the ED, and among these, cerebral infarction may occur in up to a quarter, along with other catastrophes like encephalopathy and ICH.

URGENCY VS. EMERGENCY

In terms of presentation, there are some differences between HU and HE, but it is not hugely different.

People who present with HE tend to be slightly older. Men slightly less commonly have HU; it is fairly equal for emergency.

If you look at the SBP, it's important to note that the BP is the same on average: 210 mm Hg.

In those in whom it is unknown whether they had hypertension in the past, urgency is a little more common than emergency.

PRESENTATION

We look at the 2 columns on the right, headache is slightly more common for pts. Who have HU compared with HE.

Epistaxis is more common. Chest pain, Dyspnoea, is more common for emergency. Psychomotor agitation is more common with urgency, and neurological deficit with emergency.

RISK FACTORS

The risk factors for developing hypertensive crises.

Having a h/o CRF, a history of heart failure, known elevations in SBP and DBP-- all of these are basically risk factors for the development of HE.

When taking a history, you probably would want to ask about these things.

PATHOGENESIS

The pathogenesis of elevations in BP is multifactorial ;

There is increases in mechanical stress and vascular wall damage which results in increase in vascular permeability,. There is cell proliferation and activation of the coagulation cascade. The endothelial cell surface lining of the vascular compartment is damaged, and when this is damaged, this leads to endothelial cell dysfunction, which further promotes vasoconstriction and platelet aggregation. There is the release of various vasoconstrictors with this situation.There is activation of the RAAS. Angiotensin II is a very potent vasoconstricting substance, but in addition, it increases the elaboration of cytokines such as IL-6 and NF-kappaB, which is a pro-inflammatory factor. There is white blood cell (WBC) adhesion, as well as proliferation of vascular smooth muscle cells. NADPH, which generates reactive oxygen species, is also increased

There is a reduction of NO, which is a protective substance, that leads to vasodilation and inhibition of platelet aggregation, and again, this leads to this inflammatory factor. So this is not a simple situation. There is not a single drug per se that attacks all of these potential targets within the cascade of hypertensive emergency.

PATHOGENESIS

Vasoactive substances Vasoa

ctive substances

Sheer stress of high pressure

UNCONTROLLED HYPERTENSION

• Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled BPs lead to progressive or impending EOD. In these conditions, the BP should be lowered aggressively over minutes to hours. With the advent of anti hypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1% of patients with hypertension .

• In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriate medical treatment.

ADAPTIVE VASCULAR CHANGES

• A PATIENT WITH CHRONIC HTN IS LIKELY TO HAVE ADAPTIVE VASCULAR CHANGES WHICH PROTECT END ORGANS.

• CONVERSELY PTS. WITH NO H/o HTN LACK THESE PROTECTIONS AND MAY DEVELOP A HE AT A SURPRISINGLY LOW BP (FOR EG. ACUTE GLOMERULONEPHRITIS, ECLAMPSIA IN PREGNANACY

TREAT THE PATIENT AND NOT THE NUMBER

• The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of end-organ dysfunction. Many patients present to the ED with elevated BPs; however, only a small proportion of patients will require emergency treatment.

• An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

IF YOU DETERMINE A HU ( NO EVIDENCE OF END ORGAN DAMAGE )

• Rapid reduction can induce cerebral or myocardial ischemia

• Goal BP, safe level in 6 hrs, 160/110 over 12-24 hrs with conventional oral therapy

• Identify the cause and give appropriate TTT.

• can give extra or double dose of what the patient is already on.

• Patients can be sent home.

• Oral agents may be used in hypertensive urgency, but they are discouraged in hypertensive emergency.

HYPERTENSIVE EMERGENCIES

• Admission to a CCU

• Hemodynamic monitoring (ECG, CVP and arterial line).

• Ensuring proper ventilation, free air way, control of seizures and adequate urinary output are important

• The initial goal is to lower the arterial BP by no more than 25% within an hour after the patient is seen and then, if the patient is stable, to titrate the BP to the range of 160/100-110 mm Hg diastolic within the next 2 to 6 hours.

• We do not want to lower the BP in the first 5 minutes.

• Avoid excessive reduction, because this can precipitate changes in blood flow to vital organs, such as the kidney, brain, or coronary arteries

WHY NOT ENTERAL OR INTRAMUSCULAR

Oral absorption or absorption through other routes, is not dependable in this situation.

Someone having HE probably does not have normal blood flow to the gut nor the skin; the same would be true for the muscles.

Pts. with HE are volume depleted. They are pumping blood at the kidney at an accelerated rate, meaning high RBF, and essentially pts. are salt and water depleted secondary to having very high renal blood flow.

NEUROLOGIC EMERGENCIES

Rapid BP reduction is indicated in HTNVE encephalopathy, acute ischemic stroke, acute ICH,SAH.

In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours.

Labetalol, Nicardipine , Esmolol are the preferred medications;

However, Nitroprusside and Hydralazine should be avoided

• What you see here is a so-called U- or J-shaped curve: for DBPs >105 and <70 mm Hg, the 90-day death rate is higher, whereas if the diastolic is in the range of 70 to 105 mm Hg, you have the lowest death rate. For SBP there is a very similar relationship: having a systolic >220 mm Hg is bad, but having a systolic in the range of 155 to 220 mm Hg gives you the best outcome.

HTN IS NOT BAD IN AIS

ACUTE ISCHAEMIC STROKE

ICH AND SAH

• PREFERRED MEDICATIONS ARE

• LABETALOL,NICARDIPINE AND ESMOLOL

• IN CASE OF INCREASED ICP

• MAINTAIN MAP < 130 mmHg or SBP < 180mmHg FOR THE FIRST 24 HOURS

• IF NORMAL ICP MAP <130mmHg OR SBP<160mmHg

SAH

PREFERRED AGENTS ARE AGAIN

LABETALOL, NICARDIPNE AND ESMOLOL.

MAINTAIN SYS.BP <160 mmHg UNTIL THE ANEURYSM IS TREATED OR

CEREBRAL VASOSPASM OCCURS

ACUTE CARDIOPULMONARY COMPROMISE

NICARDIPINE

• Nicardipine is good because

• It doesn't depend on renal function or in terms of liver function for its excretion . It can be given as an IV bolus or constant infusion, and so it is very useful

• Dose: 5–15 mg/ hr IV .Onset 5–10 min Duration13–30 min, may exceed 4 hr

• AE :Tachycardia, headache, flushing, local phlebitis

• Indication : Most HE except acute heart failure;

• Caution: coronary ischemia

FENOLDOPAM

• Fenoldopam mesylate

• Dose 0.1–0.3 µg/kg/min as IV infusion. onset of action <5 min . Duration 30 min .

• AE: Tachycardia, headache, nausea, flushing

• Indication Most HEs; Caution with glaucoma

• Fenoldopam, I think, is a very expensive alternative drug for the treatment of hypertensive urgency; again, it must be given by constant infusion.

• There were reportedly advantages in terms of preserving renal function

SNP

Sodium nitroprusside is a very quick-acting , quick both in terms of onset and offset.

It is good for many situations, but it requires very careful monitoring, usually within arterial lines, to make sure that you are measuring the true BP.

The drug should not be used in pts. who have renal insufficiency because the metabolic pathway for SNP leads to -CN, and -CN, of course, is very toxic.

So in pts. with renal insufficiency, avoid this drug

• NOTE THAT DIURETICS ARE GENERALLY AVOIDED IN HTNVE EMERGENCIES AS MANY PTS.ARE HYPOVOLEMIC DUE TO PRESSURE INDUCED NATRIURESIS.

• EXCEPTIONS ARE PATIENTS WITH HEART FAILURE AND OR PULMONARY EDEMA

DIURETICS

BETABLOCKERS , ALPHA BLOCKERS

• The adrenergic inhibitors include the beta-blockers labetalol and esmolol and the alpha-blocker phentolamine

• Labetalol is useful in terms of being both an IV bolus with a constant infusion and then potentially a follow-up oral therapy

• Esmolol, of course, is ultra-short-acting. It is very useful in critical care situations in surgery, but certainly not a very useful long-term drug. Adverse effects apply for all beta-blockers in patients who have bronchospastic disease, and please note, this means asthma patients, not chronic obstructive pulmonary disease (COPD) patients.

• And lastly, phentolamine is a very special-use drug. It specifically blocks the alpha receptor and is particularly useful in situations such as pheochromocytoma, in which the secretion of catecholamines such as epinephrine and norepinephrine are responsible for severe swings in hypertension. This drug is only given IV and is actually somewhat difficult to find.

IV labetalol and hydralazine are considered first-line Rx for the management of acute-onset, severe hypertension in pregnant and postpartum women. Second line alternatives to consider include labetalol or nicardipine by infusion pump .SNP should be reserved for extreme emergencies and used for the shortest amount of time possible because of concerns about cyanide and thiocyanate toxicity and increased ICP with potential worsening of cerebral edema in the mother

THAT IS NOT A GOOD IDEA ……….

S/L NIFEDIPINE

There are studies for captopril, nifedipine, and prazosin given orally.

These drugs should be avoided. Even though the stuff is out there, it is not really a good idea, especially for nifedipine We had several disasters with sublingual administration of nifedipine.

You poke a hole in the capsule for the immediate-release nifedipine and you squirt it under the tongue.

We had several patients who developed severe hypotension and had to be given IV fluids and pressors to get their BP back.

CLEVIDIPINE

Clevidipine, an intravenous CCB, was approved by the FDA in August 2008 for the management of acute, severe hypertension .

A 3rd generation DHP CCB that inhibits L-type calcium channels . A short half life of 1 to 2 minutes, a quick onset of action of 2 to 4 min. and a short duration of action of 5 to 15 min.

Clevidipine lowers SVR , it has greater effects on arterial vasodilatation

CLEVIPREX

The antihypertensive efficacy of intravenous clevidipine was compared with a placebo in cardiac surgery patients in 2 randomized, double-blind multicenter studies.

• These studies showed that clevidipine was effective in the treatment of both acute preoperative and postoperative hypertension.

• The antihypertensive efficacy of clevidipine was also compared with the efficacies of nitroprusside, nitroglycerin, and nicardipine.

• Overall the blood pressure control was similar among the 4 treatments.

CLEVIDIPINE