آيه طهسورة 114

آيه طهسورة 114

ByByDr. Mohamed Sayd ShorbagyDr. Mohamed Sayd Shorbagy

1. Patient planned for urgent surgery with

marked hypertension preoperatively,

blood pressure should be maintained

intraoperatively in the range of:

a) 100/60

b) 130/80

c) 150/90

1. Patient planned for urgent surgery with

marked hypertension preoperatively,

blood pressure should be maintained

intraoperatively in the range of:

a) 100/60

b) 130/80

c) 150/90

2. Most fatal hypertensive crisis

to be diagnosed

preoperatively is:

a) Acute porphyria

b) Hyperthyroidism

c) Pheochromocytoma

2. Most fatal hypertensive crisis

to be diagnosed

preoperatively is:

a) Acute porphyria

b) Hyperthyroidism

c) Pheochromocytoma

3. Most important drug to be

continued till the time of

surgery is:

a) Calcium channel blocker

b) β blocker

c) Diuretics

3. Most important drug to be

continued till the time of

surgery is:

a) Calcium channel blocker

b) β blocker

c) Diuretics

4. Patients with essential

hypertension are usually:

a) Hypovolemic

b) Normovolemic

c) Hypervolemic

4. Patients with essential

hypertension are usually:

a) Hypovolemic

b) Normovolemic

c) Hypervolemic

5. Fenoldopam is a:

a) Dopamine receptor agonist

b) Angiotensin receptor blocker

c) Brain natriuretic peptide

5. Fenoldopam is a:

a) Dopamine receptor agonist

b) Angiotensin receptor blocker

c) Brain natriuretic peptide

Classification The prevalence of hypertension (HTN) is about 20-

25% of the general population, making it the most common preoperative co-morbidity.

Isolated Systolic Hypertesion (ISD) is the most common subtype of hypertension affecting predominantly individuals older than 60 years of age with approximately half of these individuals having very wide pulse pressure (>65 mmHg) or pulse pressure hypertension (PPH).

Isolated diastolic hypertension (IDH) is most prevalent in indiviuals younger than 50 years and is an important marker of coronary heart disease.

Classification The prevalence of hypertension (HTN) is about 20-

25% of the general population, making it the most common preoperative co-morbidity.

Isolated Systolic Hypertesion (ISD) is the most common subtype of hypertension affecting predominantly individuals older than 60 years of age with approximately half of these individuals having very wide pulse pressure (>65 mmHg) or pulse pressure hypertension (PPH).

Isolated diastolic hypertension (IDH) is most prevalent in indiviuals younger than 50 years and is an important marker of coronary heart disease.

Etiology Essential hypertension. Unkown etiology.

Renal, Acute and chronic glomeruloephritis, renovascular stenosis.

Endocrine. Adrenal-Cushing’s syndrome, pheochromocytoma, hyperthyroidism.

Neruogenic. Pshychogenic, increased intracranial pressure, spinal cord section.

Miscellaneous. Coarctation of aorta, pregnancy-induced hypertension, acute porphyria, acute stress including surgery.

Etiology Essential hypertension. Unkown etiology.

Renal, Acute and chronic glomeruloephritis, renovascular stenosis.

Endocrine. Adrenal-Cushing’s syndrome, pheochromocytoma, hyperthyroidism.

Neruogenic. Pshychogenic, increased intracranial pressure, spinal cord section.

Miscellaneous. Coarctation of aorta, pregnancy-induced hypertension, acute porphyria, acute stress including surgery.

Pathophysiology The underlying mechanism of essential hypertension

is unkown may due to abnormal sympathetic nervous system activity, altered renin-angiotensin system regulation.

The characteristic hemodyanmic changes:

1. Increased systemic vascular resistance with normal COP.

2. Markedly increased sympathetic response to stress such as endotracheal intubation.

3. A greater increase in blood pressure with vasoconstriction and greater decrease in BP with vasodilation.

Pathophysiology The underlying mechanism of essential hypertension

is unkown may due to abnormal sympathetic nervous system activity, altered renin-angiotensin system regulation.

The characteristic hemodyanmic changes:

1. Increased systemic vascular resistance with normal COP.

2. Markedly increased sympathetic response to stress such as endotracheal intubation.

3. A greater increase in blood pressure with vasoconstriction and greater decrease in BP with vasodilation.

End organ damage

1. Cardiac: left ventricular hypertrophy,

infarction, arrhythmias and congestive

heart failure.

2. Eye : hypertensive retinopathy.

3. Renal: Nephropathy.

4. Cerebral: stroke or transient ischemic

attack.

End organ damage

1. Cardiac: left ventricular hypertrophy,

infarction, arrhythmias and congestive

heart failure.

2. Eye : hypertensive retinopathy.

3. Renal: Nephropathy.

4. Cerebral: stroke or transient ischemic

attack.

Some investigators have shown that patients with untreated, poorly controlled or labile preoperative hypertension are at increased risk for perioperative blood pressure lability, dysrhyrthmias, myocardial ischemia and transient neurologic complications.

Left ventricular hypertrophy, which signifies long-standing poorly controlled hypertension, can increase the risk of myocardial ischemia from imbalances of myocardial oxygen supply and demand regardless of the presence or absence of coronary artery disease.

Some investigators have shown that patients with untreated, poorly controlled or labile preoperative hypertension are at increased risk for perioperative blood pressure lability, dysrhyrthmias, myocardial ischemia and transient neurologic complications.

Left ventricular hypertrophy, which signifies long-standing poorly controlled hypertension, can increase the risk of myocardial ischemia from imbalances of myocardial oxygen supply and demand regardless of the presence or absence of coronary artery disease.

In hypertensive patients, autoregulation of

cerebral blood flow is reset to a higher range than

normal, and although it protects the brain against

sudden increase in pressure, it makes it more

vulneranle to hypotension. Therefore, when blood

pressure is lowered acutely, hypertensive patients

will show signs of cerebral ischemia at a higher level

of BP than normotensive patients.

So, if marked hypertension (>180/120 mmHg)

is present preoperatively, arterial blood pressure

should be maintained in the high normal range (150-

140/90-80mmHg).

In hypertensive patients, autoregulation of

cerebral blood flow is reset to a higher range than

normal, and although it protects the brain against

sudden increase in pressure, it makes it more

vulneranle to hypotension. Therefore, when blood

pressure is lowered acutely, hypertensive patients

will show signs of cerebral ischemia at a higher level

of BP than normotensive patients.

So, if marked hypertension (>180/120 mmHg)

is present preoperatively, arterial blood pressure

should be maintained in the high normal range (150-

140/90-80mmHg).

The following figure shows the renin-angiotensin systems and the mechanism

of action of antihypertensive drugs:

The following figure shows the renin-angiotensin systems and the mechanism

of action of antihypertensive drugs:

Diuretics:

They include thiazides (e.g., hydrochlorothiazide), loop diuretics (e.g., furosemide, ethacrynic acid),and potassium sparing agents (e.g., spironolactone, triametrene). All direutics initially lower the pressure (BP) by increasing urinary sodium excretion and by reducing plasma volume, extracellular fluid volume, and cardiac output. For patient with ST segment changes and evidence of pulmonary edema and hypertension or with increased intracranial cerebral pressure and hypertension, intravenous furosemide maybe appropriate.

Diuretics:

They include thiazides (e.g., hydrochlorothiazide), loop diuretics (e.g., furosemide, ethacrynic acid),and potassium sparing agents (e.g., spironolactone, triametrene). All direutics initially lower the pressure (BP) by increasing urinary sodium excretion and by reducing plasma volume, extracellular fluid volume, and cardiac output. For patient with ST segment changes and evidence of pulmonary edema and hypertension or with increased intracranial cerebral pressure and hypertension, intravenous furosemide maybe appropriate.

Antiadrenergic agents:

1. Centrally acting drugs: clonidine, dexmedetomidine and mivazerol. Stimulation of 2 receptors in the vasomotor centers of the brain reduces sympathetic outflow.

2. Peripherally acting drugs:

1 and 2 receptors phenoxybenzamine (dibenzyline), phentolamine (regitine).

1 receptor prazosin (minipress) doxazosin (cardura).

By blocking -mediated vasoconstriction, these drugs induce a fall in peripheral resistance with both arteriolar and venous dilation.

Antiadrenergic agents:

1. Centrally acting drugs: clonidine, dexmedetomidine and mivazerol. Stimulation of 2 receptors in the vasomotor centers of the brain reduces sympathetic outflow.

2. Peripherally acting drugs:

1 and 2 receptors phenoxybenzamine (dibenzyline), phentolamine (regitine).

1 receptor prazosin (minipress) doxazosin (cardura).

By blocking -mediated vasoconstriction, these drugs induce a fall in peripheral resistance with both arteriolar and venous dilation.

-receptor blockers atenolol (tenormin), metoprolol (lopressor), nadol (corgard),pindolol (visken),propranolol (inderal), esmolol (breviblock). These drugs lower the BP by decreasing heart rate, contractility, cardiac output, and renin levels.

- and receptor blockers – labetalol (trandate)

Endothelin receptor antagonist: bosentan (receptor A and B antagonist) and sitaxenstan (receptor A antagonist) are examples of a few of this class of agents used in the m¬anagement of pulmonary hypertension and less so for hypertension related heart failure.

-receptor blockers atenolol (tenormin), metoprolol (lopressor), nadol (corgard),pindolol (visken),propranolol (inderal), esmolol (breviblock). These drugs lower the BP by decreasing heart rate, contractility, cardiac output, and renin levels.

- and receptor blockers – labetalol (trandate)

Endothelin receptor antagonist: bosentan (receptor A and B antagonist) and sitaxenstan (receptor A antagonist) are examples of a few of this class of agents used in the m¬anagement of pulmonary hypertension and less so for hypertension related heart failure.

Cardiovascular effects of calcium channel blockers Cardiovascular effects of calcium channel blockers

Verapamil Dilatiazem Nifedipine Nicardipine

Heart rate

Nodal conduction

or-- or-

Myocardial depression

- or -

Vasodilation

, more increase; , more decrease; increase; , decrease; -, no change.

Dopaminergic agonists:

Fenoldopam, dopamine receptor (DA1 selective) agonist, a systemic and renal vasodilator, offers significant advantages as a parenterally administered agent for the management of BP in hypertensive emergencies and in the periopertive setting.

Dopaminergic agonists:

Fenoldopam, dopamine receptor (DA1 selective) agonist, a systemic and renal vasodilator, offers significant advantages as a parenterally administered agent for the management of BP in hypertensive emergencies and in the periopertive setting.

Angiotensin converting enzyme inhibitors:

They include captopril, enalapril, lisinopril, quinapril, and ramipril. These drugs inhibit the conversion of the inactive decapeptide angiotensin I to the active octapeptide angiotensin II.

Angiotensin converting enzyme inhibitors:

They include captopril, enalapril, lisinopril, quinapril, and ramipril. These drugs inhibit the conversion of the inactive decapeptide angiotensin I to the active octapeptide angiotensin II.

Angiotensin II receptor blockers Blockade of the action of angiotensin II leads of elevation in

plasma levels of renin, angiotensin I, and angiotensin II. However, this build up of precursors does not overwhelm the receptor blockade, as evidenced by a persistent fall in both blood pressure and plasma aldosterone levels.

Angiotensin II receptor blockers Blockade of the action of angiotensin II leads of elevation in

plasma levels of renin, angiotensin I, and angiotensin II. However, this build up of precursors does not overwhelm the receptor blockade, as evidenced by a persistent fall in both blood pressure and plasma aldosterone levels.

Vasodilators Direct vasodilators: They include hydralazine, nitroprusside, nitroglycerin, and

calcium channel blockers. These drugs directly relax the smooth muscle of resistance and capacitance vessels to different degrees.

Other vasodilators: They include brain natriuretic peptides such as nestiritide that

is primarily used in acute exacerbation of heart failure to improve forward flow and reduce symptoms and signs of heart failure.

Vasodilators Direct vasodilators: They include hydralazine, nitroprusside, nitroglycerin, and

calcium channel blockers. These drugs directly relax the smooth muscle of resistance and capacitance vessels to different degrees.

Other vasodilators: They include brain natriuretic peptides such as nestiritide that

is primarily used in acute exacerbation of heart failure to improve forward flow and reduce symptoms and signs of heart failure.

Anesthetic Management Of HTN Careful control of the hemodynamic responses to

noxious stimuli such as endotracheal intubation, surgical incision and manipulation, and emergence from anesthesia is essential.

The anesthetic goal is to minimize:

1. Cerebral hypoperfusion from hypotension. Cerebral hemorrhage and hypertensive encephalopathy resulting from hypertenison.

2. Renal failure from renal hypoperfusion.

3. Myocardial ischemia from tachycardia, hypertension or hypotension.

Anesthetic Management Of HTN Careful control of the hemodynamic responses to

noxious stimuli such as endotracheal intubation, surgical incision and manipulation, and emergence from anesthesia is essential.

The anesthetic goal is to minimize:

1. Cerebral hypoperfusion from hypotension. Cerebral hemorrhage and hypertensive encephalopathy resulting from hypertenison.

2. Renal failure from renal hypoperfusion.

3. Myocardial ischemia from tachycardia, hypertension or hypotension.

Preoperative evaluation and preparation

In addition to the routine systemic preoperative physical examination and history, special attention should be paid to the following: etiology and severity of hypertension, the subtype of hypertension, current therapy (hypokalemia and hypomagnesemia with diuretics) and the end-organ damage by chronic hypertension (for cardiac evaluation: ECG and Echo, for renal evaluation: serum creatinine and blood urea nitrogen).

Failure to diagnose a pheochromocytoma preoperatively, may prove fatal crisis.

Preoperative evaluation and preparation

In addition to the routine systemic preoperative physical examination and history, special attention should be paid to the following: etiology and severity of hypertension, the subtype of hypertension, current therapy (hypokalemia and hypomagnesemia with diuretics) and the end-organ damage by chronic hypertension (for cardiac evaluation: ECG and Echo, for renal evaluation: serum creatinine and blood urea nitrogen).

Failure to diagnose a pheochromocytoma preoperatively, may prove fatal crisis.

Elective surgery should be delayed for patients with severe hypertension (diastolic BP> 115 mmHg) or with severe isolated systolic hypertension (ISH) (systolic BP> 200 mmHg) until the BP is below 180/110 mmHg. If time permits, The blood pressure should be lowered over 6 to 8 weeks to less than 140/90 mmHg. Acute control within several hours is inadvisable before elective surgery, because this practice may put the cerebral circulation at risk for ischemia.

Elective surgery should be delayed for patients with severe hypertension (diastolic BP> 115 mmHg) or with severe isolated systolic hypertension (ISH) (systolic BP> 200 mmHg) until the BP is below 180/110 mmHg. If time permits, The blood pressure should be lowered over 6 to 8 weeks to less than 140/90 mmHg. Acute control within several hours is inadvisable before elective surgery, because this practice may put the cerebral circulation at risk for ischemia.

Current opinion generally favors continuation of

antihypertensive medication, especially β-blockers,

up to the time of surgery. The withdrawal

syndrome of beta blocker is characterized by an

enhanced sensitivity to sympathetic stimulation due

to increased β-receptor density.

Preoperative control of

hypertension:

1. A single dose of clonidine, 5μg per kg orally, 2

hours before surgery significantly decreases

anesthetic requirements and hemodynamic lability

in patients with mild-to-moderate hypertension.

Current opinion generally favors continuation of

antihypertensive medication, especially β-blockers,

up to the time of surgery. The withdrawal

syndrome of beta blocker is characterized by an

enhanced sensitivity to sympathetic stimulation due

to increased β-receptor density.

Preoperative control of

hypertension:

1. A single dose of clonidine, 5μg per kg orally, 2

hours before surgery significantly decreases

anesthetic requirements and hemodynamic lability

in patients with mild-to-moderate hypertension.

2. A single small oral dose of a β-adrenergic blocking

agent such as labetalol. Atenolol, or oxpernolol

given preoperatively to untreated, asymptomatic

mildly hypertensive patients.

3. The premedication with diazepam, lorazepam, or

midazolam can be regulated to have the patient

arrive in the operating room sedated.

Controlled hypotensive technique for hypertensive patients:

Uncontrolled or untreated severe hypertension is a

contraindication to controlled hypotension.

2. A single small oral dose of a β-adrenergic blocking

agent such as labetalol. Atenolol, or oxpernolol

given preoperatively to untreated, asymptomatic

mildly hypertensive patients.

3. The premedication with diazepam, lorazepam, or

midazolam can be regulated to have the patient

arrive in the operating room sedated.

Controlled hypotensive technique for hypertensive patients:

Uncontrolled or untreated severe hypertension is a

contraindication to controlled hypotension.

Intraoperative management

Regional anesthesia: These patients should have intravascular fluids given

prior to the regional anesthetic, regional blocks should be administered to an adequately medicated and sedated patient to prevent stress-related release of catecholamines.

Monitoring:

1. Electrocardiogram (ECG). Simultaneous leads V5 and II, multiple leads ST analysis

2. Blood pressure (BP).

3. Pulse oximeter.

4. End-tidal CO2 analyzer.

Intraoperative management

Regional anesthesia: These patients should have intravascular fluids given

prior to the regional anesthetic, regional blocks should be administered to an adequately medicated and sedated patient to prevent stress-related release of catecholamines.

Monitoring:

1. Electrocardiogram (ECG). Simultaneous leads V5 and II, multiple leads ST analysis

2. Blood pressure (BP).

3. Pulse oximeter.

4. End-tidal CO2 analyzer.

Induction:Deeper anesthesia with potent inhalation agents to

attenuate tachycardia and hypertension should be done with caution because of higher incidence of hypotension arising from both vasodilatation and cardiac depression.

Intubation:

Laryngoscopy time should be 15 seconds or less to minimize BP elevation. Other measures are described as follows:

1. lidocaine, 1.5 mg per kg is given 2 minutes before intubation and using it in topical airway anesthesia.

Induction:Deeper anesthesia with potent inhalation agents to

attenuate tachycardia and hypertension should be done with caution because of higher incidence of hypotension arising from both vasodilatation and cardiac depression.

Intubation:

Laryngoscopy time should be 15 seconds or less to minimize BP elevation. Other measures are described as follows:

1. lidocaine, 1.5 mg per kg is given 2 minutes before intubation and using it in topical airway anesthesia.

2. Esmolol, 2 mg per kg.

3. Labetalol, 0.15 to 0.45 mg per kg.

4. Nicardipine, 1 mg intravenously 2 minutes before tracheal intuabtion.

Hypotension after induction of anesthesia usually can be easily corrected by volume replacement and simultaneous titration of vasopressors such as ephedrine 5 to 10 mg or phenylephrine in 0.1 mg inrements.

Maintenance of anesthesia:Potent inhalation anesthetices or narcotics should

be titrated to the desired level of central nervous system depression while the blood pressure (BP) is monitored continuously.

2. Esmolol, 2 mg per kg.

3. Labetalol, 0.15 to 0.45 mg per kg.

4. Nicardipine, 1 mg intravenously 2 minutes before tracheal intuabtion.

Hypotension after induction of anesthesia usually can be easily corrected by volume replacement and simultaneous titration of vasopressors such as ephedrine 5 to 10 mg or phenylephrine in 0.1 mg inrements.

Maintenance of anesthesia:Potent inhalation anesthetices or narcotics should

be titrated to the desired level of central nervous system depression while the blood pressure (BP) is monitored continuously.

The combination of nitrous oxide and low to moderate doses of narcotics and potent inhalation agents may provide the most stable intraoperative couuse.

Fluid therapy:Patients with essential hypertension are usually

hypovolemic because of vasoconstriction and diuretic therapy.

Overhydration should be avoided because it may contribute to postoperative hypertension when the vasodilating effects of anesthetics are gone. Careful estimation of fluid intake and output is essential.

The combination of nitrous oxide and low to moderate doses of narcotics and potent inhalation agents may provide the most stable intraoperative couuse.

Fluid therapy:Patients with essential hypertension are usually

hypovolemic because of vasoconstriction and diuretic therapy.

Overhydration should be avoided because it may contribute to postoperative hypertension when the vasodilating effects of anesthetics are gone. Careful estimation of fluid intake and output is essential.

Intraoperative hypertension (causes and management):

Differential diagnosis of intraoperative hypertension:

Intraoperative hypertension (causes and management):

Differential diagnosis of intraoperative hypertension: Related to preexisting disease

Chronic hypertension, increased intracranial pressure, aortic dissection, early acute myocardial infarction.

Related to surgery

Prolonged tourniquet time, post-cardiopulmonary bypass, aortic cross-clamping, postacarotid endarerectomy.

Related to anesthetic

Pain, inadequate depth of anesthesia, catecholamine release, malignant hyperthermia, shivering, hypoxia hypercarbia, hypothermia, hypervolemia, improperly sized (too small) blood pressure cuff, intra-arterial transducer positioned too low.

Related to medication

Rebound hypertension (from discontinuation of clonidine, btea blockers, or methyldopa), systemic absorption of vasoconstrictors intravenous dye (e.g, indigo carmine)

OthersBladder distention, hypoglycemia.

Postoperative management:

The causes of postoperative hypertension include pain, emergence excitement, hypoxemia, hypercarbia, reaction to endotracheal tube, full bladder, hypothermia, relative hypervolemia from intraoperative administration of excess fluids. The most common cause of postoperative hypertension is incisional pain.

Postoperative management:

The causes of postoperative hypertension include pain, emergence excitement, hypoxemia, hypercarbia, reaction to endotracheal tube, full bladder, hypothermia, relative hypervolemia from intraoperative administration of excess fluids. The most common cause of postoperative hypertension is incisional pain.