HYPERTENSIVE CRISIS,

MALIGNANT HYPERTENSION,

HYPERTENSIVE ENCEPHALOPATHY

AND PULMONARY HYPERTENSION

SUBMITTED BY SUBMITTED TO

MISS. NICE MATHEW PROF. AGNET BEENA MANI

2ND YEAR MSc NURSING P.G COORDINATOR

BMCON BMCON

CALICUT CALICUT
INTRODUCTION

The majority of people over 65 years of age carry this diagnosis. Therefore, approximately 66.9
million people in the United States carry the diagnosis of hypertension. It is estimated that this number will
rise as the number of patients who are over the age of 65, as well as the number of patients who are obese,
continue to increase.Hypertension is the most common reason for adult office visits other than pregnancy
and has the highest use of prescription drugs. Despite the number of resources used to treat this disease, only
about 50% of hypertensives have their blood pressure under control using the definition of blood pressure
less than 140/90 (National Health and Nutritional Examination Survey[NHANES] 2005-2008).Poor
adherence to lifestyle changes and medication contribute to this poor outcome. Lifestyle changes such as a
low-sodium diet, weight loss, increased exercise and limiting alcohol abuse are difficult when there are no
symptoms of the disease until secondary problems arise. It is also difficult to continue medications when
drug-related side effects arise when the disease itself is asymptomatic. Inadequate access to medical care for
chronic disease as well as the cost of medication contribute to poor control of blood pressure.The cost of
inadequate treatment of hypertension is significant. Hypertension is a leading contributor to vascular disease
such as stroke and myocardial infarction as well as chronic kidney disease and congestive heart failure.
These diseases lead to significant medical costs as well as lost productivity in the work force.

HYPERTENSION

Hypertension or high blood pressure, is defined as a persistent SBP ≥140 mm Hg, DBP ≥90 mm Hg, or

current use of antihypertensive medication.

Systolic Pressure (mm Diastolic Pressure (mm

Terminology
Hg) Hg)

Normal < 120 < 80

Pre-hypertension 120-139 80-89

Hypertension stage 1 140-159 90-99

Hypertension stage 2 ≥ 160 ≥ 100

 Hypertensive crisis ≥ 180 ≥ 120

Hypertensive
≥ 180 ≥ 120
emergency

HYPERTENSIVE CRISIS

Definition

Hypertensive crisis is defined as an elevated blood pressure associated with evidence of acute end-organ
damage. With acute damage to vital organs, such as the kidney, heart, and brain, there is a significant risk of
morbidity in hours without therapeutic intervention.

The absolute level of blood pressure and the time course of blood pressure elevation determine the
development of hypertensive crisis. In general, with hypertensive crisis, the diastolic blood pressure is
greater than 130 mrn Hg. In children, gravid women, and previously normotensive individuals, hypertensive
crisis.

Etiology
 Noncompliance with medications
 Exacerbation of chronic HTN
 Renovascular hypertension
 Pheochromocytoma
 Drugs( cocaine, amphetamines)
 Monoamine oxidase inhibitors taken with tyramine-containing foods
 Rebound HTN (from abrupt withdrawal of some hypertensive drugs such as clonidine or beta
adrenergic blockers
 Necrotizing vasculitis
 Head injury
 Acute aortic dissection.
 Post op state
  Preeclampsia and eclampsia

Classification
Hypertensive crisis is classified by the degree of organ damage and the rapidity with which the BP must be
lowered. Hypertensive emergency, which develops over hours to days, is a situation in which a patient’s BP
is severely elevated (> 180/120mm Hg) with evidence of acute target organ damage, especially damage to
the CNS. Hypertensive urgency, which develops over days to weeks, is a situation in which a patient’s BP is
severely elevated but there is no clinical evidence of target organ damage.

Pathophysiology

The precise pathophysiology of hypertensive crisis is unknown. An abrupt increase in blood

pressure is one of the initiating events in the transition from simple hypertension or normotension to
hypertensive .crisis. The product of cardiac output and peripheral vascular resistance determines blood
pressure. The initial blood pressure increase is likely secondary to an increase in vascular resistance.
Considerable evidence suggests that mechanical stress in the arteriolar wall leads to disruption of
endothelial integrity. With disruption of vascular integrity, diffuse microvascular lesions develop.
Fibrinoid necrosis of the arterioles is seen in vulnerable organs and is considered the histologic hallmark of
hypertensive crisis. It is unclear whether hypertension alone causes the development of
hypertensive crisis or whether other factors are necessary. Increases in peripheral vascular
resistance result in part from activation of the renin-angiotensin-aldosterone system. Evidence
suggests angiotensin may injure the vascular wall directly by activation of genes for
proinflammatory cytokines (interleukin-6) and proinflammatory mediators regulated by nuclear factor-
kB. Other vascular-toxic influences may contribute to increased peripheral vascular resistance, including
hyperviscosity, immunologic factors, and other hormones (e.g., catecholamines, vasopressin, and
endothelin) .The end result of these changes is a significant increase in peripheral vascular resistance with
ischemia of heart, brain, and kidneys.
In considering hypertensive crisis and treatment, the impact of blood pressure on cerebrovascular
physiology is important. Hypertensive encephalopathy is a distinct clinical syndrome that occurs when
rapidly rising central perfusion pressure exceeds the ability of the central nervous system to autoregulate.
Autoregulation of cerebral blood flow refers to the ability of the brain to maintain a constant cerebral blood
flow as the cerebral perfusion pressure varies from 60 to 150 mm Hg. In chronic hypertension, the range of
autoregulation is increased from 60 to 150 mm Hg to 80 to 160 mm Hg. Autoregulation of cerebral blood
flow is a function of cerebral perfusion pressure (mean arterial pressurevenous pressure) and cerebral
vascular resistance:

Cerebral blood flow = cerebral perfusion pressure (mean arterial pressure - venous pressure) /
 cerebrovascular resistance
Under normal physiologic conditions the backflow in the cerebral venous system or venous pressure is near
zero, and the arterial pressure determines the cerebral perfusion pressure. With acute brain injury, as seen
with subarachnoid hemorrhage, stroke, and intracranial hemorrhage, the ability of the brain to autoregulate
and maintain cerebral blood flow is impaired. Inability to auto regulate cerebral blood flow also is seen in
hypertensive crisis when the mean arterial pressure is greater than 140 mm Hg.

Clinical features

 Head-ache, usually worse in morning. Location is occipital or anterior with a steady quality.
 Visual complaints(diplopia, hemianopsia, blindness)
 Neurological symptoms (focal deficits, stroke, TIA, confusion, somnolence)
 Ischemic chest pain
 Renal symptoms(nocturia, polyuria, hematuria)
 Back pain (aortic aneurysm)
 Gastrointestinal complaints (nausea, vomiting)
 Weight loss occurs as a result of high levels rennin and angiotensin induce a diuresis.

Diagnosis

 Hypertensive history regarding non compliance of medications, pheochromocytoma, drug

withdrawal, acute glomerulo nephritis, and preeclampsia. A medication history, including over-the-
counter medications and illegal drug use, should be obtained from every patient.
 Monitoring of BP (diastolic BP ≥120 to 130 mmHg)
 Fundoscopic examination
 Neurological examination
 Abdominal examination
 The initial laboratory evaluation should include serum sodium, chloride, potassium, bicarbonate,
creatinine, and blood urea nitrogen levels; complete blood count (with a peripheral smear to identify
schistocytes);
 electrocardiogram; and urinalysis. Evidence of intravascular hemolysis is common
 The renin-angiotensin-aldosterone axis is markedly activated, as evidenced by hypokalemia and
metabolic alkalosis.
 Blood urea nitrogen and creatinine are often elevated. Urinalysis may show small amounts of
proteinuria and hematuria with occasional erythrocyte casts.
  Marked increases in proteinuria suggest a primary glomerular process, such as glomerulonephritis,
as the cause of the elevated blood pressure.
 If hypertensive encephalopathy is suspected, magnetic resonance imaging should be performed.
With hypertensive encephalopathy, edema may occur in the posterior regions of the cerebral
hemispheres, particularly in the parieto-occipital regions, a finding called posterior
leukoencephalopathy on magnetic resonance irnaging. Brainstem involvement on magnetic resonance
imaging also has been reported.

Treatment
Goal
The primary goal of blood pressure therapy is to lower the pressure at a rate that arrests or alleviates
end-organ damage without causing ischemia of vital organs.

 Patients with hypertensive crisis are best treated parenterally with intensive care monitoring by
arterial cannulation or automated blood pressure cuff measurement. Generally the rate of blood
pressure control depends on conditions associated with the hypertensive crisis. In most settings,
blood pressure can be reduced acutely by 20% to 25% within minutes to hours. After the patient is
stabilized at this pressure, blood pressure is decreased to 160/100 to 160/110 mm Hg over the next
2 to 6 hours. If the patient is clinically stable, the blood pressure may be decreased toward a normal
blood pressure over the next 24 to 48 hours. With these decreases in blood pressure, central nervous
system blood flow autoregulation usually is maintained. In ischemic stroke, there are no large
clinical trials to support rapid reduction of blood pressure. Rapid blood pressure reduction (e.g., 15
to 30 minutes) to the normal range is indicated with acute aortic dissection or in previously
normotensive subjects with abrupt increases in blood pressure.

More rapid reduction in blood pressure also is recommended in patients with active unstable angina or
congestive heart failure with pulmonary edema. In patients with malignant hypertension or hypertensive
encephalopathy, a more controlled titration of blood pressure reduction over 1 to 3 hours is satisfactory.
Exceptions to rapid blood pressure reduction include older patients with carotid stenosis. These individuals
are particularly susceptible to central nervous system hypoperfusion. Blood pressure management in patients
with stroke or intracranial bleeding is controversial because the loss of central nervous system blood flow
autoregulation and the presence of brain edema require high systemic pressures to provide adequate cerebral
perfusion.
 Administration of antihypertensive drugs.

Drug name and mechanism of action doses

Sodium nitroprusside: Dose: Initial dose, 0.25 µg/kg/min, maximum dose 8-1
nitric oxide compound, vasodilator of µg/kg/min
arteriolar and venous smooth muscle,
increases cardiac output by decreasing
afterload

Nitroglycerin: directly interacts With Initial dose: 5µ g/min, maximum dose 200 µg/min
hit rate receptors on vascular smooth
muscle, primarily dilates venous
bed, decreases preload
Labetalol: beta-adrenergic blockade DOSe: Bolus 20 mg, then 20-80 mg every 10 min for
and alphaadrenergic blockade, maximum dose 300 mg. Infuse at 0.5-2 mg/min
alpha/beta blocking ratio 1:7

Esmolol: cardioselective beta- Dose: 200-500 µg/kg over 1-4 min, then 50 µg/kg/min for 4
adrenergic blocking agent min, and titer, then infuse 50-300 µg/kg/min.

Fenoldopam: postsynaptic dopamine- Initial dose: 0.1 /lg/kg/min with titration every 15 min, no
1 agonist, decreases peripheral bolus
vascular resistance, 10 times more
potent than dopamine as vasodilator

Hydralazine: primarily dilates Dose: 10 mg every 20-130min, maximum dose 20 mg

arteriolar vasculature
Phentolamine: alpha-adrenergic Dose- 5-15 mg
blockade

Nicardipine: dihydropyridine calcium Iniatial dose-5mg/hr to maximum of 15mg/h

channel blocker inhibits
transmembrane influx of calcium
ions into cardiac and smooth
muscle

Dose 1.25-5mg q6h

Enalaprilat:angiotensin-
converting enzyme inhibitor
 Trimethaphan: nondepolarizing
Dose-0.5-5mg/min
ganglionic blocking agent, competes
with acetylcholine for postsynaptic
receptors

 When treating hypertensive emergencies, the MAP is often used instead of systolic and diastolic
readings to guide and evaluate therapy. MAP is calculated as
(SBP+2 DBP)
MAP = 3
 Monitoring BP and pulse should be every 2-3mts during initial administration of drugs.
 Titrate the dosage of drug according to BP level
 Continual ECG monitoring for identifying dysrrhythmia
 Hourly urine output to measure renal perfusion.
 Strict bed rest to avoid cerebral ischemia and fainting.
 Frequent neurological checks, including LOC, papillary size and reaction, movement of extremities,
reaction to stimuli, help detect any changes in patient’s condition.
 Once the hypertensive crisis is resolved, it is important to determine the cause. The patient will need
appropriate management and extensive education to avoid future crisis.

MALIGNANT HYPERTENSION

Meaning
Malignant (accelerated) hypertension is a medical emergency. Presenting characteristics are as follows:

 Diastolic pressures exceeding 120 mmHg

 Retinal hemorrhage
 Rapid vascular deterioration.

Malignant hypertension is blood pressure that is so high that it is actually causing damage to organs,
particularly in the nervous system, the cardiovascular system, and/or the kidneys. 

Incidence
Malignant hypertension has a peak incidence at age 40-50 years; its occurrence in clients younger than 30
years or older than 60 years should raise the suspicion of a secondary cause of hypertension. Especially male
gender. Without treatment, malignant hypertension results in a 90 percent mortality rate within 1 year
secondary to renal or CCF, CVA, MI, or aortic dissection.

Etiology

In many people, high blood pressure is the main cause of malignant hypertension. Missing doses of blood
pressure medications can also cause it. In addition, there are certain medical conditions that can cause it.
They include:

 History of kidney disorders or failure such as pyelonephritis and glomerulonephritis.

 Taking certain drugs or medications, including cocaine, amphetamines, monoamine oxidase
inhibitors (MAOIs), and oral contraceptives
 History of collagen vascular diseases such as scleroderma
 Pregnant women with preeclampsia and eclampsia
 Pheochromocytoma
 Spinal cord disorders
 Coarctation or dissection of the aorta
 Renal artery stenosis or narrowing of the arteries to the kidneys
 Missing doses of prescribed antihypertensive medications, particularly beta-blockers or clonidine
(Catapres), which can cause a rebound effect. Medication noncompliance is the most common reason
for hypertensive emergencies.

Pathophysiology

The pathophysiology of hypertensive emergency is not well understood. Failure of normal autoregulation

and an abrupt rise in systemic vascular resistance are typical initial components of the disease process.

Hypertensive emergency pathophysiology includes:

 Abrupt increase in systemic vascular resistance, likely related to humoral vasoconstrictors

 Endothelial injury
 Fibrinoid necrosis of the arterioles
 Deposition of platelets and fibrin
 Breakdown of normal autoregulatory function

The resulting ischemia prompts further release of vasoactive substances, completing a vicious cycle. If the
process is not stopped, a vicious cycle of homeostatic failure begins, leading to loss of cerebral and local
autoregulation, organ system ischemia and dysfunction, and myocardial infarction.
It is estimated that single-organ involvement is found in approximately 83% of hypertensive emergency
patients, two-organ involvement in about 14% of patients, and multi-organ failure (failure of at least 3 organ
systems) in about 3% of patients.

The most common clinical presentations of hypertensive emergencies are cerebral

infarction (24.5%), pulmonary edema (22.5%),hypertensive encephalopathy (16.3%), and congestive heart
failure (12%). Less common presentations include intracranial hemorrhage,aortic dissection, and eclampsia.

Cerebral autoregulation is the ability of the blood vessels in the brain to maintain a constant blood flow. It
has been shown that people who suffer from chronic hypertension can tolerate higher arterial pressure before
their autoregulation system is disrupted. Hypertensives also have an increased cerebrovascular resistance
which puts them at greater risk of developing cerebral ischemia if the blood flow decreases into a
normotensive range. On the other hand, sudden or rapid rises in blood pressure may cause hyperperfusion
and increased cerebral blood flow, causing increased intracranial pressure and cerebral edema. Hypertensive
encephalopathy - characterized by hypertension, altered mentation, and papilledema- is one of the clinical
manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation.

Increased arterial stiffness, increased systolic blood pressure, and widened pulse pressures, all resulting from
chronic hypertension, can lead to heart damage. Coronary perfusion pressures are decreased by these factors,
which also increase myocardial oxygen consumption, possibly leading to left ventricular hypertrophy. As
the left ventricle becomes unable to compensate for an acute rise in systemic vascular resistance, left
ventricular failure and pulmonary edema or myocardial ischemia may occur.

Chronic hypertension has a great impact on the renal vasculature, leading to pathologic changes in the small
arteries of the kidney. Affected arteries develop endothelial dysfunction and impairment of
normal vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted,
the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no
protection to the kidney during blood pressure fluctuations. During a hypertensive crisis, this can lead to
acute renal ischemia.

Endothelial injury can occur as a consequence of severe elevations in blood pressure, with fibrinoid
necrosis of the arterioles following. The vascular injury leads to deposition of platelets and fibrin, and a
breakdown of the normal autoregulatory function. Ischemia occurs as a result, prompting further release of
vasoactive substances. This process completes the vicious cycle.

Many factors and causes are contributory in hypertensive crises. One main cause is the discontinuation of
antihypertensive medications. Other common causes of hypertensive crises are autonomic hyperactivity,
collagen-vascular diseases, drug use (particularly stimulants,especially cocaine and amphetamines and their 
substitutedanalogues),  glomerulonephritis, head trauma,neoplasias, preeclampsia and eclampsia, and
renovascular hypertension.
During a hypertensive emergency uncontrolled blood pressure leads to progressive or impending end-organ
dysfunction. Therefore, it is important to lower the blood pressure aggressively. Acute end-organ damage
may occur, affecting the neurological, cardiovascular, renal, or other organ systems. Some examples of
neurological damage include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction,
subarachnoid hemorrhage, and intracranial hemorrhage. Cardiovascular system damage can
includemyocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and
aortic dissection. Other end-organ damage can include acute renal failure or
insufficiency, retinopathy, eclampsia, and microangiopathic hemolytic anemia. Extreme blood pressure
can lead to problems in the eye, such as retinopathy or damage to the blood vessels in the eye.

Clinical manifestations

 Diastolic pressure exceeding 120mm Hg

 Retinal hemorrhage
 Rapid vascular deterioration
 Papilledema
 Renal insufficiency or acute renal failure ( marked by proteinuria, hematuria, casts in urine)
 Encephalopathy ( marked by restlessness, decreased LOC, lethargy, dizziness, coma, seizures,
nausea, vomiting)
 LVF
 Pulmonary edema
 Hemolytic anemia
 Severe head-ache ( occipital or anterior location, steady and throbbing, worse in the morning)
 Visual blurring, reduced acuity, or blindness.

Diagnostic studies
A diagnosis of malignant hypertension is based on blood pressure readings and signs of acute organ damage.

 Recheck blood pressure and listen to heart and lungs for abnormal sounds.

 Examine eyes to check for damage to the blood vessels of the retina and swelling of the optic nerve.
 blood and urine tests that may include:
o Blood urea nitrogen (BUN) and creatinine levels, which increase if patient has kidney
damage
o Blood clotting tests
o Blood sugar (glucose) level
o Complete blood count
o Sodium and potassium levels
o Urinalysis to check for blood, protein, or abnormal hormone levels related to kidney
problems

Additional blood tests may be needed, depending on the result of the tests listed above.
The doctor will also ask for imaging tests, including:

 Echocardiogram to check heart function and blood flow through the heart
 Electrocardiogram (ECG) to check the heart’s electrical function
 Chest X-ray to look at the shape and size of the heart structures and to detect fluid in the lungs
 Other imaging tests to evaluate the kidneys and their arteries

Complications

Untreated, malignant hypertension causes death. Complications of malignant hypertension also may include:

 Aortic dissection, which is a sudden rupture of the main blood vessel leaving the heart
 Coma
 Fluid in the lungs, called pulmonary edema
 Heart attack
 Heart failure
 Stroke
 Sudden kidney failure

Treatment

Since malignant hypertension is a medical emergency, treatment needs to be received quickly. Treatment
options include the following:

 Intravenous high blood pressure medications–The specific medication will be chosen based on your
specific situation, including whether you are suffering from damage to your kidneys or other organs.
Possible medications may include:
 Sodium nitroprusside or nitroglycerin
 Beta-blockers
 Hydralazine
 Labetalol
 Vasotec (enalapril) and ACE-inhibitor
 Oral high blood pressure medicines once blood pressure has been lowered from dangerous levels
 Dialysis
 Diet and Activity

 In patients with stroke, cardiac compromise, or renal failure, appropriate consultation should be
considered. In institutions with specialists in hypertension, prompt consultation may improve the
overall control of blood pressure.
 Activity is limited to bedrest until the patient is stable. Patients should be able to resume normal
activity as outpatients once their blood pressure has been controlled.

HYPERTENSIVE ENCEPHALOPATHY
Meaning
Hypertensive encephalopathy refers to the transient migratory neurologic symptoms that are associated
with the malignant hypertensive state in a hypertensive emergency. The clinical symptoms are usually
reversible with prompt initiation of therapy.
Etiology

 Chronic renal parenchymal disease

 Acute glomerulonephritis
 Renovascular hypertension
 Withdrawal from hypertensive agents (eg, clonidine)
 Encephalitis, meningitis
 Pheochromocytoma, renin-secreting tumors
 Sympathomimetic agents (eg, cocaine, amphetamines, phencyclidine [PCP], and lysergic acid
diethylamide [LSD])
 Eclampsia and preeclampsia
 Head trauma, cerebral infarction
 Collagen vascular disease
 Autonomic hyperactivity
 Vasculitis
 Ingestion of tyramine-containing foods or tricyclic antidepressants in combination with monoamine
oxidase inhibitors (MAOIs)

Pathophysiology

Hypertensive encephalopathy is caused by an increase in blood pressure. Several conditions may evoke
blood pressure elevation: acute nephritis, eclampsia, crises in chronic essential hypertension, sudden
withdrawal of antihypertensive treatment. Additionally, hypertensive encephalopathy may occur
in pheochromocytoma, Cushing's syndrome, renal artery thrombosis.

The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial.
Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilate arterioles in
response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This
autoregulation falters when hypertension becomes excessive. According to the over-regulation conception,
brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic
edema. According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate,
leading to vasogenic edema. Cerebral edema can be generalized or focal. Brain ventricles are compressed,
cortical gyri flattened.

Clinical features

 occur 12–48 hours after a sudden and sustained increase in blood pressure.
 The first manifestation of these symptoms is a severe headache. 

 restless.
 Alterations in consciousness may follow several hours later, which include impaired judgement and
memory,confusion, somnolence and stupor.
 the condition is not treated, these neurological symptoms may worsen and ultimately turn into a
coma.
 increased irritability, vomiting, seizures, twitching and myoclonus of the limbs.
 Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness)
are common.

Diagnostic studies

o History

o physical examination,

o blood pressure measurement,

o blood sampling

o ECG

o  EEG,

o chest X-ray

o urinalysis

o arterial blood gas analysis

o cranial CAT scans

o  MRI. ---Brain MRI scans have shown a pattern of typically posterior (occipital greater than
frontal) brain edema that is reversible. This usually is termed reversible posterior
leukoencephalopathy or posterior reversible encephalopathy syndrome (PRES).

Treatment

 Acute cases of hypertensive encephalopathy require urgent treatment, preferably in intensive care
units where vital signs and electroencephalographic characteristics can be monitored.
  The first measure is to lower blood pressure with drugs.

  Blood pressure reduction is monitored to avoid damage from excessive reduction. Excessively
reduced blood pressure may result in cerebral infarction, blindness and cardiac ischemia.

 Intravenously injected diazoxide is effective in 80% of the patients with hypertensive

encephalopathy. It normalizes blood pressure within 3-5 min, and the effect lasts 6–18 hours. One
benefit of diazoxide is that it does not cause drowsiness and thus does not affect the patient’s state
of consciousness. Reflex tachycardia caused by this drug is the major disadvantage which limits its
use in patients with ischemic heart disease. 

 Furosemide injected simultaneously with diazoxide enhances both the antihypertensive effect and
its duration.

 Hydralazine is also administered intravenously or intramuscularly to reduce the blood pressure. Its
action is similar to that of diazoxide, but less consistent.

 Another drug which is used to reduce blood pressure is sodium nitroprusside which is delivered
continuously through intravenous infusion.

 Nitroglycerine is also used to decrease blood pressure in patients with hypertensive encephalopathy

 Another class of drugs that are used to reduce blood pressure in hypertensive encephalopathy are
ganglionic blocking agents:pentolinium and trimethaphan. These agents have rapid effect, and they
do not cause drowsiness. However, they may have side effects, such as bowel and bladder atony.
These drugs, with the exception of labetalol, are not used if hypertensive encephalopathy is
associated with prepartal eclampsia because they may harm the fetus.

 Reserpine, methyldopa and clonidine are less applicable to hypertensive emergency because their

effect starts slowly (in 2–3 hours after administration) and they affect the patient's consciousness.

 Oral antihypertensive drugs are administered after the patient recovers from the most severe
symptoms, and intravenous injections are no longer necessary.

 In addition to antihypertensive drugs, anticonvulsant drugs, such as phenytoin, may be given to the

patient with seizures. However, typically anti-hypertensive medication is sufficient for treatment of
neurological symptoms.

PULMONARY HYPERTENSION
Meaning
Pulmonary hypertension (PH) is an increase of blood pressure in the pulmonary artery, pulmonary vein, or
pulmonary capillaries, together known as the lung vasculature, leading to shortness of
breath, dizziness, fainting, leg swelling and other symptoms. Pulmonary hypertension can be a severe
disease with a markedly decreased exercise tolerance and heart failure. 
Pulmonary hypertension is defined as a pulmonary artery mean pressure (PAPm) of 25 mm Hg or greater
and may be precapillary or postcapillary in etiology.

Etiology

Postcapillary causes include processes affecting the left side of the heart (e.g., left ventricular svstolic or
diastolic dysfunction, mitral stenosis or regurgitation, aortic valvular disease) or, more rarely, the pulmonary
veins (pulmonary veno-occlusive disease).

Precapillary causes pulmonary hypertension, or pulmonary arterial hypertension (PAH), can be idiopathic
(IPAH-previously known as primary pulmonary hypertension [PPH]) or may occur in association with a
variety of underlying disease processes such as collagen vascular disease, portal hypertension, congenital
systemic to pulmonary shunts, drug or toxin exposure, or HIV infection. PAH/PPH is principally a disease
of young women, but it can affect all age groups and both sexes.

Pathophysiology

Whatever the initial cause, pulmonary arterial hypertension involves the vasoconstriction or

tightening of blood vessels connected to and within the lungs. This makes it harder for the heart to pump
blood through the lungs, much as it is harder to make water flow through a narrow pipe as opposed to a wide
one. Over time, the affected blood vessels become both stiffer and thicker, in a process known as fibrosis.
This further increases the blood pressure within the lungs and impairs their blood flow. In addition, the
increased workload of the heart causes hypertrophy of the right ventricle, making the heart less able to pump
blood through the lungs, ultimately causing right heart failure (a condition known as cor pulmonale). As the
blood flowing through the lungs decreases, the left side of the heart receives less blood. This blood may also
carry less oxygen than normal. Therefore it becomes harder and harder for the left side of the heart to pump
to supply sufficient oxygen to the rest of the body, especially during physical activity.

Pathogenesis in pulmonary venous hypertension is completely different. There is no obstruction to blood

flow in the lungs. Instead, the left heart fails to pump blood efficiently, leading to pooling of blood in the
lungs. This causes pulmonary edema and pleural effusions.

In hypoxic pulmonary hypertension, the low levels of oxygen are thought to cause vasoconstriction or
tightening of pulmonary arteries. This leads to a similar pathophysiology as pulmonary arterial hypertension.

In chronic thromboembolic pulmonary hypertension, the blood vessels are blocked or narrowed with blood
clots. Again, this leads to a similar pathophysiology as pulmonary arterial hypertension.

Diagnosis

Symptoms , signs and clinical history

Because of the insidious onset of symptoms, PAH is often advanced at the time of diagnosis.
Dyspnea on exertion is a common presenting symptom, but it is sometimes attributed to deconditioning or
other cardiorespiratory ailment. Chest pain, mimicking angina pectoris, may occur. Patients with advanced
disease may present with syncope or signs and symptoms of right-sided heart failure, including lower
extremity edema, jugular venous distention, and ascites.

The clinical historv should focus initiallv on the exclusion of underlying causes of pulmonary hypertension.
Important clues to an underlying condition might include a previous history of a heart murmur, deep venous
thrombosis or pulmonary embolism, Raynaud's phenomenon, arthritis, arthralgias, rash, heavy alcohol
consumption, hepatitis, heavy snoring, daytime hypersomnolence, morning headache, and morbid obesitv, A
careful family history should be taken. Medication exposures, particularly to appetite suppressants and
amphetamines, should be noted. Cocaine is a powerful vasoconstrictor and may contribute to the
development of pulmonary hypertension. Intravenous drug abuse has been associated with the development
of PAH.

Physical examination

Signs of PAH may not become apparent until late 'in the disease. Findings such as an accentuated second
heart sound, a systolic murmur over the left sternal border, jugular venous distention, peripheral edema,
and/or ascites might suggest the presence of pulmonary hypertension and right ventricular dysfunction.
Associated systemic diseases, such as collagen vascular disease or liver disease, may also become apparent
during routine examination.

Laboratory evaluation

Laboratory evaluation can provide important information in detecting associated disorders and contributing
factors. A collagen vascular screen, including antinuclear antibodies, rheumatoid factor, and erythrocyte
sedimentation rate, is often helpful in detecting autoimmune disease, although some patients with
IPAH/PPH will have a low titer positive antinuclear antibody test. The scleroderma spectrum of disease,
particularly limited scleroderma or the CREST syndrome, has been associated with an increased risk for the
development of PAH. Liver function tests (aspartate aminotransferase, alanine aminotransferase, alkaline
phosphatase) may be elevated in patients with right ventricular failure and passive hepatic congestion but
may also be associated with underlying liver disease. Liver disease with portal hypertension has been
associated with the development of pulmonary hypertension. Thyroid disease may occur with increased
frequency in patients with IPAH/PPH and should be excluded with thyroid function testing. HIV testing and
hepatitis serologic studies should be considered in patients at risk. Routine laboratory studies such as the
complete blood cell count, complete metabolic panel, prothrombin time, and partial thromboplastin time are
recommended during the initial evaluation and as indicated to monitor the patient's long term clinical status.
Echocardiography

Doppler echocardiography is useful in estimating the severity of pulmonary hypertension and detecting left-
sided heart disease. Findings may include enlargement of the right ventricle, flattening of the
interventricular septum, and compression of the left ventricle. Bubble contrast echocardiography may detect
a right-to-left shunt, but exclusion of a left-to right intracardiac shunt may require cardiac catheterization
with an oximetry series.

Radiographic evaluation and exclusiojn of thromboembolic disease

Chest radiography may reveal enlargement of the central pulmonary vessels and evidence of right
ventricular enlargement. Evidence of parenchymal lung disease may be apparent. When parenchymal lung
disease is suspected, pulmonary. function testing and high-resolution computed tomography (CT) of the
chest may be indicated. Ventilation-perfusion lung-scanning should be performed in an attempt to exclude
chronic-recurrent pulmonary thromboembolic disease, which is among the most preventable and treatable
causes of pulmonary hypertension. Diffuse mottled perfusion can be seen in IPAH/PPH, whereas larger
segmental and subsegmental mismatched defects are suggestive of chronic recurrent pulmonary
thromboembolic disease. Intermediate results on ventilation-perfusion lung scanning may require
pulmonary arteriography to obtain a definitive diagnosis. Although contrast medium-enhanced CT has been
popularized recently for the diagnosis of acute pulmonary thromboembolic disease

Pulmonary function testing

Pulmonary function testing is indicated to detect underlving parenchymal lung disease. The diffusing
capacity is often reduced in pulmonary vascular disease, consistent with impaired gas exchange. Oximetry
testing of patients at rest with exertion, and nocturnally, is useful in detecting hypoxemia and the need for
supplemental oxygen.

Right sided heart catheterization and vasoreactivity testing

Right-sided heart catheterization remains an important method of the evaluation. Left-sided heart
dysfunction and intra cardiac shunts can be excluded, the degree of pulmonary hypertension can be
accurately quantified, and the cardiac output can be measured. Pulmonary vascular resistance can then be
calculated. Acute pulmonary vasoreactivity can be assessed using a short-acting agent such as prostacyclin
(epoprostenol inhaled nitric oxide, or intravenous adenosine.

Diuretics are indicated in patients with evidence of right ventricular failure and volume overload (i.e.,
peripheral edema and or ascites). Careful dietary restriction of sodium and fluid ir cake is important in the
 management of patients with PAH with right-sided heart failure. Rapid and excessive diuresis mar
produce systemic hypotension, renal insufficiency, and syncope. Serum electrolytes and measures of renal
function should be followed closely in patients receiving diuretic therapy.
Although not extensively studied in PAH, digitalis is sometimes utilized in refractory right ventricular
failure or atrial dysrhythmias. Drug levels should be followed closely, particularly in patients with
impaired renal function.
Because of the potentially devastating effects of respiratory infections in PAH, immunization against
influenza and pneumococcal pneumonia is recommended.
Treatment

General care

Warfarin, oxygen, diuretics, digoxin and vaccination

Improved survival has been reported with oral anticoagulation in IPAH/PPH. The target International
Normalized Ratio in these patients is 1.5 to 2.5. Anticoagulation of patients with PAH occurring in
association with other underlying processes, such as scleroderma or congenital heart disease, is
controversial. Generally, patients with PAH treated with chronic intravenous epoprostenol are
anticoagulated in the absence of contraindications, owing in part to the additional risk of catheter-associated
thrombosis.

Hypoxemia is a pulmonary vasoconstrictor and can contribute to the development or progression of

PAH. It is generally considered important to maintain oxygen saturations at greater than 90% at all times.
Supplemental oxygen use is more controversial in patients with Eisenmenger physiology but may decrease
the need for phlebotomy and potentially reduce the occurrence of neurologic dysfunction and complications.

Diuretics are indicated in patients with evidence of right ventricular failure and volume overload
(i.e., peripheral edema and or ascites). Careful dietary restriction of sodium and fluid ir cake is important
in the management of patients with PAH with right-sided heart failure. Rapid and excessive diuresis mar
produce systemic hypotension, renal insufficiency, and syncope. Serum electrolytes and measures of renal
function should be followed closely in patients receiving diuretic therapy.
Although not extensively studied in PAH, digitalis is sometimes utilized in refractory right
ventricular failure or atrial dysrhythmias. Drug levels should be followed closely, particularly in patients
with impaired renal function.

Because of the potentially devastating effects of respiratory infections in PAH, immunization against
influenza and pneumococcal pneumonia is recommended.

Calcium channel blockers

Patients with IPAH/PPH who respond to vasodilators and calcium channel blockers-v generally have
improved survival.
Prostanoids
Prostacyclin, a metabolite of arachidonic acid produced primarilv in vascular endothelium, is a potent
systemic and pulmonary vasodilator that also has antiplatelet aggregatory effects. A relative deficiency of
prostacyclin may contribute to the pathogenesis of PAH.

Eg:-Epoprostenol, Treprostinil, Inhaled lloprost, Beraprost

Endothelin receptor antagonists

Endothelin-1 is a vasoconstrictor and a smooth muscle mitogen that may contribute to the pathogenesis of
PAH.40 Endothelin-1 expression, production, and concentration in plasma, and lung tissue are elevated in
patients with PAH, and these levels are correlated with disease severity.

Eg: Bosentan- Bosentan is a dual endothelin receptor blocker that has been shown to improve pulmonary
hemodynamics and exercise tolerance and delay the time to clinical worsening.

Phosphodiesterase inhibitors

Phosphodiesterases (PDEs) are enzymes that hydrolyze the cyclic nucleotides, cyclic adenosine
monophosphate (cAMP) and cvclic guanosine monophosphate (cGMP), and limit their intracellular
signaling. Drugs that selectively inhibit cG~!P-specific PDEs (or type 5, PDE5 inhibitors) augment the
pulmonary vascular response to endogenous or inhaled nitric oxide in models of pulmonary hypertension.

Eg:- Dipyridamole, Sildenafil

Nitric oxide

Nitric oxide contributes to maintenance of normal vascular function and structure. It is particularly
important in mal adaptation of the lung circulation at birth, and impaired nitric oxide production may
contribute to the developrnent of neonatal pulmonary hypertension. L-Arginine is the sole substrate for nitric
oxide synthase and thus is essential for nitric oxide production.

Lung transplantation

Special situations in the ICU

DVT
patients with PAH are likely at increased risk for the occurrence of deep venous thrombosis (DVT) and are
certainly at increased risk for poor outcomes as a consequence of the development of DVT. Patients with
PAH are prone to a more sedentary lifestyle and to chronic venous congestion of the lower extremities
owing to increased right-sided cardiac filling pressures. Hospitalization in the ICU, often with discontin-
uation of anticoagulation in anticipation of invasive procedures, likely places these patients at even higher
risk for DVT. For these reasons, meticulous attention must be paid DVT prophylaxis.
Procedures and surgery

procedures and surgery in patients with PAH can be associated with substantially increased operative and
perioperative risks, and appropriate precautions should be undertaken to optimize outcomes. As always,
careful consideration should given to whether an invasive procedure is absolutely necessary.
Vasovagal events
Patients with severe PAH are particularly prone to vasovagal events, which can lead to severe
consequences, including syncope, cardiopulmonary arrest, and death. Pain, nausea, .vomiting, or even a
bowel movement can lead to a vasovagal event in patients with severe PAH. Cardiac output may be
particularly dependent on heart rate in this situation, and bradycardia and systemic vasodilatation that
accompany vasovagal event can therefore result in an abrupt decrease in systemic arterial pressure. Patients
should therefore have close monitoring of their heart rate during invasive procedures, with ready availability
of atropine or a similar agent.
Avoidance of hypoxemia and hypercarbia
hypoxernia and hypercarbia are both pulmonary vasoconrictors and can contribute to the worsening
of pulmonary hypertension. Oversedation can lead to ventilatory insuffiencv and precipitate clinical
deterioration. Caution should be utilized in laparoscopic procedures in which carbondioxide is used for
abdominal insufflation, because absorption can lead to hypercarbia. The induction of anesthesia and intuba-
on for surgical procedures can be a particularly high-risk for patients with PAH, because they are at risk for
vagal vents, hypoxemia, hypercarbia, and shifts in intrathoracic pressure with associated changes in cardiac
filling pressures.
Pregnancy
The hemodynamic changes in pregnancy are substantial, and volume shifts occur immediately post
partum, with cardiac filling pressures increasing as a result of decompression if the vena cava and the return
of uterine blood into the systernic circulation. The changes induced by pregnancy impose a significant
hemodynamic stress in women with PAH/PPH, leading to an estimated 30% to 50% mortality rate. Because
of high maternal and fetal morbidity and mortality rates, most experts recommend effective contraception
and early fetal termination in the event of pregnancy. There have been case reports of successful treatment
of pregnant IPAH/PPH patients with chronic intravenous epoprostenol , inhaled nitric oxide,86-88 and oral
calcium channel blockers. In general, management includes early hospitalization for monitoring, supportive
therapy with cautious fluid management, supplemental oxygen, diuretics, and dobutamine, as needed. The
use of a pulmonary artery catheter for close hemodynamic monitoring and for titration of vasodilator and
cardiotonic therapy has been recommended.

Portopulmonary hypertension
 Patients with chronic liver disease have an increased prevalence of pulmonary vascular disease. Two
forms of pulmonary vascular disease can complicate chronic liver disease: the hepatopulmonary syndrome
and portopulmonary hypertension. Both tend to occur in patients with chronic, late-stage liver disease, and
each may increase the risk associated with liver transplantation.
Hypoxemia and intrapulmonary shunting characterize the hepatopulmonary syndrome. Shunting may be
manifest echocardiographically by the late appearance (after three to five cardiac cycles) of bubble contrast
in the left side of the heart. Treatment is generally supportive, with supplemental oxygen. The syndrome
may improve in some patients after liver transplantation. Severe hepatopulmonary syndrome may increase
the risk associated with undergoing liver transplantation.

Portopulmonary hypertension occurs in patients with chronic, late-stage liver disease and/or portal
hypertension. Portopulmonary hypertension often differs hemodynamically from IPAH/PPH, and these
differences may affect the approach to therapy. Patients with portopulmonary hypertension have lower
pulmonary arterial diastolic and mean pressures, higher cardiac outputs, and lower pulmonary and systemic
resistances.. Later-stage patients may develop hemodynamic findings more similar to those of patients with
IPAH/PPH, and this group may have a poorer prognosis and be at higher risk with attempted liver
transplantation. It is occasionally possible to make a borderline candidate for liver transplantation an
acceptable one through aggressive treatment of the PAH. Supplemental oxygen should be used as needed to
maintain saturations greater than or equal to 91 % at times. Diuretic therapy should be utilized to control
volume overload, edema, and ascites. Anticoagulant therapy has not been carefully studied in this
population and should probably be avoided in patients with significant coagulopathy due to impaired
hepatic synthetic capability and in patients at increased risk of bleeding due to gastroesophageal varices.
There have been a number of case reports and small case series describing the use of intravenous
epoprostenol for treatment of porto pulmonary hypertension. Interestingly, some patients may demonstrate
improvement in their pulmonary hypertension after liver transplantation. Other patients may develop
worsening of their pulrnonarv hvper tension well after transplantation. It may be possible to wear; an
occasional patient off epoprostenol after liver transplantation. This should probably be done very graduallv.

Intravenous antihypertensive therapy

Affected organ Complications Therapeutic Contraindicated
considerations
Aorta Dissection Labetalol/Esmolol +
Fenoldopam/Nitroprusside
Brain Ischemic stroke Labetalol/Fenoldopam Nitroprusside
Brain Intraparenchymal Labetalol/Fenoldopam Nitroprusside
hemorrhage
Brain Hypertensive ACEI and/or labetalo Nitroprusside
 encephalopathy
Heart ACS Nitroglycerin + Nitroprusside
labetalol/esmolol/ACEI
Heart HF/ pulmonary edema Nitroglycerin/nitroprusside labetelol
+ loop diuretic
Placenta Eclampsia, Magnesium sulfate + ACEI/Nitroprusside
preeclampsia Labetalol/Nicardipine
kidney ARF, hematuria, ACEI/Boluses ACEI/Nitroprusside
proteinuria Labetalol/fenoldopam
perfusion

CONCLUSION
Once blood pressure is at goal and stable, the patient should be seen at a minimum once a year by the
clinician to assess patient adherence, patient satisfaction and any changes in target organ status. Patients'
comorbidities such as heart failure, associated diseases such as diabetes, and need for laboratory tests
influence the frequency of visits (Chobanian, 2003 [Guideline]). Lifestyle modifications should be
reviewed, reemphasized and documented annually. Patients should monitor blood pressure more frequently
by home monitoring or by other allied health professionals.
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 en.wikipedia.org/wiki/Hypertensive_emergency
 www.mayoclinic.com › ... ›
 www.webmd.com/hypertension-high-blood.../guide/hypertensive-crisis
 www.mayoclinic.com/health/pulmonary-hypertension/DS00430
 www.phassociation.org/