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Chapter 7: Antihypertensive Drugs
|Calcium Channel Blockers
|Angiotensin Converting Enzyme (ACE) Inhibitor
Potassium Sparing
Loop Diuretics
Chlorothiazide (Diuril)
The thiazides act in the distal tubule to decrease sodium reabsorption (inhibits Na/Cl transporter).
As a result of decreased sodium and chloride reabsorption, a hyperosmolar diuresis ensues.
Delivery of more sodium to the distal tubule results in potassium loss by an exchange mechanism.
Thiazides also promote calcium reabsorption, in contrast to loop diuretics.
The initial decrease in blood volume followed by a longer-termed reduction in vascular resistance appear to account for the hypotensive effects of the thiazides.
Adverse Effects
Potassium depletion is a potentially serious side-effect that may require potassium supplementation and/or concurrent use of potassium-sparing diuretics.
Hyperuricemia may occur precipitating gout.
The increase in systemic uric acid is due to a decrease in the effectiveness of the organic acid secretory system.
Diabetic patient may have difficulty in maintaining proper blood sugar levels.
Furosemide (Lasix), Bumetanide (Bumex),Ethacrynic acid (Edecrin)
Furosemide (Lasix), bumetanide (Bumex), and ethacrynic acid (Edecrin) are "high-ceiling" loop diuretics acting primarily at the ascending limb of the loop of Henle.
The effectiveness of these agents is related to their site of action because reabsorption of about 30 - 40% of the filtered sodium and chloride load occurs at the ascending loop.
Distal sites are not able to compensate completely for this magnitude of reduction of NaCl reabsorption.
Loop diuretics increase urinary Ca2+ in contrast to the action of thiazides.
Loop diuretics also increase renal blood flow by decreasing renal vascular resistance.
These drugs are rarely used in the management of hypertension because of their short duration of action and the availability of better drugs.
Adverse Effects
Furosemide (Lasix) and ethacrynic acid (Edecrin) block renal excretion of uric acid by competition with renal secretory and biliary secretory systems.Therefore these agents can precipitate gout.
Potassium depletion.
Centrally Active
Adrenergic Neuron Blocker
Adrenoceptor Antagonists
Clonidine (Catapres) (Sympatholytic)
Clonidine (Catapres) acts in the brain, inhibiting adrenergic outflow from the brainstem. Inhibition of sympathetic outflow results in a decrease in blood pressure.
Mechanism of action: centrally acting selective a2 adrenergic agonist.
Especially effective in
management of severe hypertension or
in renin-dependent hypertension
Transdermal clonidine (Catapres) patch: useful for surgical patients unable to take oral formulation
Clonidine (Catapres) reduces cardiac output (by reducing both stroke volume and heart rate) and peripheral resistance.
Reduction in stoke volume occurs due to increased venous pooling (decreased preload).
Clonidine (Catapres) does not interfere with cardiovascular responses to exercise.
Renal blood flow and function is maintained during clonidine treatment.
Clonidine (Catapres) has minimal or no effect on plasma lipids.
Other Clinical Uses
Preservative-free clonidine administered into epidural/subarachnoid space (150-450 micrograms)-- dose-dependent analgesia
No respiratory depression, nausea, vomiting, delayed gastric emptying or pruritus -- effects associated with opioids
Probable Mechanism: activation postsynaptic a2 receptors in the spinal cord substantia gelatinosa
Clonidine (Catapres) & morphine: no cross-tolerance when used concurrently in neuraxial analgesia
Side effects of neuraxial clonidine (Catapres)
hypotension, sedation, dry mouth
Preanesthetic Medication:
Oral clonidine (Catapres) (preanesthetic medication):
Enhances intrathecal morphine + tetracaine (pontocaine) for postoperative analgesia (no increase in morphine-related side effects)
Preanesthetic clonidine (Catapres) also:
Reduces reflex tachycardia that may be caused by direct laryngoscopy for tracheal intubation
Reduces intraoperative blood-pressure heart rate lability
Reduces plasma catecholamines levels
Significantly decreases anesthetic requirements for inhaled (MAC) and injected agents.
Adverse Effects
Dry Mouth (xerostomia)
bradycardia (in patients with SA nodal abnormality)
Withdrawal syndrome upon abrupt discontinuation (increased blood pressure, headache, tachycardia, apprehension, tremors
Stoelting, R.K., "Antihypertensive Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 302-312.
Methyldopa (Aldomet) (Sympatholytic)
Methyldopa (Aldomet) is a prodrug which is metabolized to the active agent, alpha-methylnorepinephrine.
Alpha-methylnorepinephrine acts in the brain, inhibiting adrenergic outflow from the brainstem. Inhibition of sympathetic outflow results in a decrease in blood pressure.
Methyldopa (Aldomet) produces no change in cardiac output in younger patients, but in older patients a decline in cardiac output results from reduced heart rate and stroke volume.
The reduction in stroke volume occurs due to increased venous pooling (decreased preload).
Since renal blood flow and function is maintained during methyldopa treatment, methyldopa maybe valuable in managing hypertensive patients with renal insufficiency.
Adverse Effects
Dry Mouth
Parkinsonian signs
Reduced libido
Hyperprolactinemia (gynecomastia, galactorrhea)
Bradycardia (in patients with SA nodal abnormality)
Hepatoxicity (avoid in patients with hepatic disease)
Positive Coombs' test (20%)
1-5% of those with positive Coombs' develop hemolytic anemia (requiring immediate discontinuation of the drug)
Guanethidine (Ismelin)& Guanadrel (Hylorel)
Guanethidine (Ismelin) inhibits the function of postganglionic adrenergic neurons, thus inhibiting sympathetic function.
Guanethidine (Ismelin) uses the norepinephrine (N.E.) re-uptake transporter to reach its site of action, the neurosecretory vesicles.
Guanethidine (Ismelin) replaces norepinphrine in the vesicle and is released instead of the normal transmitter.
Guanethidine (Ismelin) is an inactive transmitter and the replacement of N.E. by an inactive agent is responsible for its antihypertensive effects (maintenance dosing).
Adrenergic blockade by guanethidine (Ismelin) results in post-synaptic supersensitivity.
Sympathetic blockade by guanethidine (Ismelin) produces:
reduction in cardiac output due to inhibition of cardiac sympathetic innervation
blockade of the sympathetic reflex arteriolar response to the reduction in cardiac output.
Adverse Effects
Symptomatic hypotension (due to sympathetic reflex blockade)
Sexual dysfunction (delayed ejaculation)
Guanethidine (Ismelin) effects blocked by N.E. reuptake blockers (tricyclic antidepressants, cocaine, ephedrine, amphetamine, chlorpromazine (Thorazine))
Reserpine (Adrenergic Neuron Blocker)
Labetalol (Trandate, Normodyne)
Labetalol (Trandate, Normodyne) is a competitive antagonist at both a1 and ß1-adrenergic receptors. It also has an intrinsic sympathomimetic effect at ß2 receptors
Antihypertensive effects of labetalol results from actions at both alpha1 and beta-adrenergic receptors.
alpha1 receptor blockade results in vasodilatation which is further enhanced by ß2 receptor activation.
A reduction in heart rate is mediated by beta1 receptor antagonism.
Labetalol (Trandate, Normodyne) does not alter serum lipids.
Adverse Effects
Orthostatic hypotension may occur due to alpha1 receptor blockade.
Liver injury has been reported with labetalol (Trandate, Normodyne) usage.
Labetalol (Trandate, Normodyne) metabolites: false positive for pheochromocytoma
Paresthesias (scalp tingling)
Bronchospasm -- incidence similar to that observed with metoprolol (Lopressor) or atenolol (Tenormin)
urinary retention
Stoelting, R.K., "Antihypertensive Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 302-312.
Prazosin (Minipress) (alpha1-Arenoceptor Antagonis); Terazosin (Hytrin) (alpha1-Adrenoceptor Antagonist)
Prazosin (Minipress), terazosin (Hytrin), and doxazosin (Cardura) reduce arteriolar resistance and increase venous capacitance as a consequence of alpha1 adrenergic receptor blockade.
Normal inhibition of norepinephrine-mediate inhibition through alpha2 receptors remain-- prazosin (Minipress) is a selective postsynaptic alpha1 adrenergic receptor blocker
The short-term increase in heart rate and plasma renin levels do not persist although the vasodilation continues.
Prazosin (Minipress) monotherapy --less effective than thiazide diuretics
Prazosin (Minipress) in combination with other agents: quite effective in young patients with moderately severe hypertension
Good patient compliance
Cardiovascular Effects: --
Prazosin (Minipress) reduces systemic vascular resistance without:
causing reflex-mediated tachycardia
causing increases in plasma renin {as seen with minoxidil/hydralazine}
absence of changes in plasma renin reflect continued alpha2 receptor function which normally inhibits renin release {recall that prazosin is an alpha1 selective antagonist}
Prazosin (Minipress) -- greater affinity for venular alpha receptors compared to arteriolar alpha receptors; resultant hemodynamics effect (orthostatic hypotension) --an action more similar to nitroglycerin than hydralazine (Apresoline).
Renal blood flow is maintained.
Retention of salt and water occurs.
Alpha1-adrenergic receptor blockers reduce plasma triglycerides, total and LDL-cholesterol, and increase HDL-cholesterol.
Other Therapeutic Uses:
Congestive heart failure: valuable for reducing afterload
Preoperative preparation of patients with pheochromocytoma
Treatment of benign prostatic hypertrophy in older males (drug decreases prostate size)
Adverse Effect
Inital-dose marked orthostatic hypotension is seen in about 50% of cases-- (sudden syncope; dosage dependence)
Fluid retention, vertigo
dry mouth, urinary frequency, lethargy, sexual dysfunction, nasal congestion, nightmares
Anesthetic Implications:
Prazosin (Minipress)-induced alpha1 blockade may cause exaggerated hypotension during epidural anesthesia (alpha receptor--blockade prevents compensatory vasoconstriction)
Prazosin (Minipress)-exacerbated hypotension may not be responsive to typical alpha1 adrenergic agonists (e.g. phenylephrine) dosage; epinephrine may be required to increase systemic vascular resistance & BP in this setting
The combination of prazosin (Minipress) and a beta-blocker could result in nearly refractory hypotension during regional anesthesia (diminished response to both b and alpha1 agonists)
Stoelting, R.K., "Antihypertensive Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 302-312.
|Diazoxide (Hyperstat)
|Hydralazine (Apresoline)
|Minoxidil (Loniten)
|Nitroprusside sodium (Nipride)
Diazoxide (Hyperstat), Nitroprusside sodium (Nipride)
Vasodilators used for acute management of hypertensive crisis or malignant hypertension include sodium nitroprusside and diazoxide.
Nitroprusside sodium (Nipride) is the agent of choice.
Administered by a continuously variable rate i.v. infusion pump, precise blood pressure control can be obtained.
Nitroprusside sodium (Nipride), a nitrovasodilator, is metabolized by smooth muscle cells to nitric oxide which dilates both arterioles and venules.
Side effects are mainly due to excessive vasodilation.
Much less commonly, toxicity may result from conversion of nitroprusside to cyanide and thiocyanate.
Risk of toxicity due to thiocyanate increases after 24 to 48 hours.
Nitroprusside sodium (Nipride) can worsen arterial hypoxemia in patients with obstructive pulmonary airway disease since nitroprusside will interfere with hypoxic pulmonary vasoconstriction. A result is increasing ventilation-perfusion mismatching.
Diazoxide (Hyperstat) is infrequently used unless accurate infusion pumps are unavailable.
The mechanism of action involves activation of ATP-sensitive potassium channels, hyperpolarization of arteriolar smooth muscle, relaxation and dilation.
Adverse effects include salt and water retention and hyperglycemia. Diazoxide inhibits insulin release.
Hydralazine (Apresoline) Minoxidil (Loniten)
Amlodipine (Norvasc) Felodipine (Plendil)
Highly lipid-soluble nefedipine analog
Ready access to the CNS -- reduces large cerebral arterial contraction
Clinical Use:
Cerebral Vasospasm:
Useful in preventing/reducing cerebral vasospasm associated with subarachnoid hemorrhage
Vasospasm -- mediated by calcium ion influx
Nimodipine (Nimotop) administered over a three week course (oral administration) results and decreased frequency of neurologic defects secondary to cerebral vasospasm in subarachnoid hemorrhage patients.
For comatose patients: deliver through nasogastric tube
Side effects/Concerns:
systemic hypotension (with excess nimodipine (Nimotop) effect)
possible increase in intracranial pressure -- especially in patients with decreased intracranial compliance
Stoelting, R.K., "Calcium Channel Blockers", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, p. 350.
Diltiazem (Calcium Channel Blocker)
Calcium channel blockers are effective in treating hypertension because they reduce peripheral resistance.
Arteriolar vascular tone depends on free intracellular Ca2+ concentration.
Calcium channel blockers reduce transmembrane movement of Ca2+ , reduce the amount reaching intracellular sites and therefore reduce vascular smooth muscle tone.
All calcium channel blocks appear similarly effective for management of mild to moderate hypertension
.For low-renin hypertensive patients (elderly and African-American groups), Ca2+ channel blockers appear good choices for monotherapy (single drug) control.
Diltiazem has a direct negative chronotropic effect on the heart sufficient to block reflex-mediated tachycardia secondary to the decrease in peripheral resistance.
The reflex-mediated adrenergic stimulation tends to counteract negative inotropic properties of diltiazem.
Adverse Effects
SA nodal inhibition may lead to bradycardia or SA nodal arrest.
This effect is more prominent if beta adrenergic antagonists are concurrently administered.
GI reflux.
Negative inotropic are augmented if beta-adrenergic receptor antagonists are concurrently administered.
Calcium channel blockers should not be administered if the patient has SA or AV nodal abnormalities or in patients with significant congestive heart failure.
return to Table of Contents
***angiotensin receptor blocker
Captopril and other Angiotensin Converting Enzyme Inhibitors
Pharmacological Properties
Angiotensin II, a potent vasoconstrictor, is produced by the action of angiotensin converting enzyme (ACE) on the substrate angiotensin I. Angiotensin II activity produces
a rapid pressor response
a slow pressor response and
vascular and cardiac hypertrophy and remodeling.
Antihypertensive effects of ACE inhibitors are due to the reduction in the amount of angiotensin II produced.
ACE inhibitors are efficacious in management of hypertension and have a favorable side effect profile.
ACE inhibitor are advantageous in management of diabetic patients by reducing the development of diabetic neuropathy and glomerulosclerosis.
ACE inhibitor are probably the antihypertensive drug of choice in treatment of hypertensive patient who have hypertrophic left ventricles.
Hypertensive patients who have ischemic heart disease with impaired left ventricular function also benefit from ACE inhibitor treatment.
ACE inhibitors reduce the normal aldosterone response to sodium loss (normally aldosterone opposes diuretic-induced sodium loss).
Therefore, the use of ACE inhibitors enhance the efficacy of diuretic treatment, allowing the use of lower diuretic dosages and improving control of hypertension.
If diuretics are administered at higher dosages in combination with ACE inhibitors significant and undesirable hypotensive reactions can occur with attendant excessive sodium loss.
Reduction in aldosterone production by ACE inhibitors also affects potassium levels.
The tendency is for potassium retention, which may be serious in patients with renal disease or if the patient is also taking potassium sparing diuretics, nonsteroidal anti-inflammatory agents or potassium supplements.
Captopril (Capoten): not a prodrug
Enalapril (Vasotec): prodrug
Lisinopril (Prinvivil, Zestril): not a prodrug
Ramipril (Altace): prodrug
Captopril (Capoten)
Orally effective, competitive inhibitor of angiotensin I-converting enzyme (peptidyl dipeptidase) [enzyme converts angiotensin I to angiotensin II (active)]
Decreases circulating angiotensin II & aldosterone {angiotensin II stimulates aldosterone secretion by the adrenal cortex}
Compensatory response: increase in angiotensin I & increased renin levels {loss of negative feedback control}
Decrease in aldosterone cause slight increase in serum potassium
well absorbed; 25%-30% protein bound
rapid converting enzyme inhibition (within 15 minutes following oral administration)
50% drug excreted unchanged
elimination half-life: two hours -- oxidation, real excretion
Cardiovascular Effects: captopril (Capoten)
Decrease systemic vascular resistance (secondary to a decrease in Na+ & water retention)
Prominent decrease in renal vascular resistance
Reduced systemic blood pressure: no change in heart rate & cardiac output
Absence of heart rate change despite reduced blood pressure may suggest alteration baroreceptor sensitivity
No orthostatic hypotension (captopril does not interfere with sympathetic nervous system function)
captopril may improve vasodilator drug treatment efficacy in management of CHF by blocking vasodilator-induced increases in renin secretion
Adverse Effects
Angioedema, although rare, may be potentially fatal
ACE inhibitiors should not be used during pregnancy
Dry cough
In renovascular hypertension, glomerular filtration pressures are maintained by vasoconstriction of the post-glomerular arterioles, an effect mediated by angiotensin II. Used of ACE inhibitors in patients with renovascular hypertension due to bilateral renal artery stenosis can therefore precipitate a significant reduction in GFR and acute renal failure.
Initial dose of an ACE inhibitor may precipitate an excessive hypotensive response.
Essential Hypertension (represents greater than 90% of hypertension cases)
Occurs in patients who have arterial hypertension without a clear, definable cause.
Essential hypertension is also referred to as primary or idiopathic hypertension.
Classification of Arterial Hypertension
I. Systolic hypertension (with wide pulse pressure) can be caused either by conditions of decreased aortic compliance, often due to arteriosclerosis or to increased stroke volume.
Some conditions that increase stroke volume:
Aortic regurgitation
II. Systolic and Diastolic hypertension (increased peripheral vascular resistance)
Renovascular stenosis or renal infarction
Polycystic kidney disease
Acute and chronic glomerulonephritis
Chronic pyelonephritis
Renin-producing tumors
Other severe renal diseases)
Adrenocortical hyperactivity (Cushing's disease, primary hyperaldosteronism)
Oral contraceptives
Elevated intracranial pressure
Familial dysautonomia
Increased intravascular volume
Polyarteritis nodosa
Aortic coarctation
Hypertension of Unknown Etiology
Toxemia of pregnancy
Acute intermittant porphyria
Essential Hypertension (> 90% of all cases of hypertension
Control of Blood Pressure
Arterial pressure is determined by a number of interacting factors
Physiological Factors Influencing Arterial Pressure
Preload & Contractility:
As blood volume returning to the heart increases, preload increases and there is enhanced filling with ventricular dilation.
According to Starling's Law, increased ventricular stretch usually leads to increased contractility.
Increased preload and increased contractility lead to increased stroke volume and ultimately an increase in arterial pressure, all other factors remaining equal.
Some antihypertensive drugs decrease preload.
Heart rate: Since the product of heart rate and stroke volume equals cardiac output, an increase in heart rate will increase arterial blood pressure, all other factors remaining equal.
Some antihypertensive agents decrease heart rate (ß-adrenergic receptor antagonists, e.g.).
Heart Rate X Stroke Volume = Cardiac Output
Cardiac Output X Peripheral Resistance = Arterial Pressure
Peripheral resistance: For a given cardiac output, blood pressure depends only on peripheral resistance. Some antihypertensive drugs act to reduce peripheral resistance.
Depending on mechanism of action, a given antihypertensive may:
Reduce preload
Reduce afterload
Decrease heart rate
Reduce peripheral resistance
Reduce contractility.
Many antihypertensive drugs have multiple effects.
Antihypertensive Drugs and Anesthesia
There is probably excessive concern about interaction potential between anesthetics and antihypertensive drugs.
Areas of concern for administration of anesthetic to patients treated with antihypertensive medications:
Reduced sympathetic nervous system activity--manifestations:
Orthostatic hypotension
Excessive systemic blood-pressure responses (decreases) to:
acute blood loss
body position changes
decreased venous return cause by positive-pressure ventilation
Reduced sensitivity to indirect-acting sympathomimetic agents (caused by antihypertensive drugs that deplete norepinephrine from nerve terminals
Possible enhanced response to catecholamines and direct-acting sympathomimetics following sympathetic nervous system blockade (reduced alpha-adrenergic receptor tone with loss of tonic stimulation)
Altered physiological response to sympathomimetic agents
Maintenance of antihypertensive drug treatment during perioperative time frame:
Fewer systemic blood-pressure and heart rate fluctuations during anesthesia
Decreased likelihood of cardiac dysrhythmias
Previously effective antihypertensive drug therapy should be continued during the perioperative period.
The pharmacology of the particular antihypertensive drug should be considered in the development of the anesthesia plan.
Stoelting, R.K., "Antihypertensive Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 302-312.
Considerations: Anesthetic Management in Hypertensive Patients
Hypertension: Organ Systems Effects
Normal control of BP: sympathoadrenal axis-- response to a decrease in BP
Sensed by Central baroreceptors {heart & great arteries}
Stimulation of ß-adrenergic systems
increased heart rate (positive chronotropic response)
increased force of contraction (contractility, positive inotropic response)
increased renin secretion {juxtaglomerular renal cells}
Stimulation of alpha-adrenoceptor systems: causes vasoconstriction
With essential hypertension, above mechanisms function inappropriately
Excessive sympathetic activation
Elevated norepinephrine may promote through vascular endothelium injury:
vascular hypertrophy
ß-adrenergic receptor down-regulation
Reduced endothelium-mediated vascular relaxation
Consequence: increased vasoconstrictive tone (chronic vasoconstriction)
Excessive sympathetic activation promotes enhanced peripheral vascular resistance in hypertensive patients
Hypertension and the kidney:
ß-adrenergic receptor stimulation leads to increased renin secretion which in turn leads to increased angiotensin II levels
Increased angiotensin II levels promotes an increase in BP by means of:
direct vasoconstriction
increasing renal cortical {zona glomerulosa}aldosterone production which causes intravascular volume expansion
Hypertension associated with elevated renin levels may predispose patients to myocardial infarction {compared to those patients with normal/decreased renin levels}
Hypertension associated with elevated renin levels is amenable to treatment with ACE inhibitors {e.g., captopril (Capoten)}
"Pressure-naturesis"-dysfunctional in hypertensive kidneys {Definition of pressure-naturesis: increasing Na+ & H2O excretion by the kidney with increased blood-pressure}
Frequency: 4%-5% of hypertensive patients
Principal causes:
Endocrine causes of secondary hypertension
Cushing's Syndrome--Cortisol overproduction
Adrenal hyperplasia:
Secondary to excessive pituitary ACTH production
Pituitary-hypothalamic dysfunction
Pituitary ACTH-producing micro-or macroadenomas
Secondary to ACTH or CRH producing nonendocrine tumors
Bronchogenic carcinoma
Thymic carcinoma
Pancreatic carcinoma
Bronchial adenoma
Adrenal nodular hyperplasia
Adrenal neoplasia
Exogenous, iatrogenic causes (most common cause)
Long-term glucocorticoid use
Long-term ACTH use
bilateral adrenal hyperplasia due to pituitary adenoma (basophilic tumor)
about 20 to 25 percent of Cushing's syndrome patients have adrenal neoplasm
"Adenoma composed of basophilic cells (blue with H&E stain) in Cushing disease."
(c) 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.
Cushing's disease-Presenting Symptoms:Hypertension, Truncal obesity, Glucose intolerance, Muscle weakness, Striae*
*"Stretch marks on the skin with a silvery-white hue. Often the result of stretching the skin in pregnancy. Heavy or long-term
corticosteroid use (cream or oral forms) can cause striae formation.-on-line medical dictionary" (http://www.graylab.ac.uk/omd/)
Twice as common in women as in man
Most often presents between 30 in 50 years of age
Adrenal adenoma -- excessive aldosterone production
unilateral adenoma (usually small; either side)
Conn's syndrome (primary hyperaldosteronism;Two types of abnormalities are noted: (1) benign tumor of one adrenal (adenoma) or (2) hyperplasia., a general enlargement of both adrenals.
hyperplastic adrenal glands -- abnormal secretion
malignant tumor
adrenal carcinoma (rare)
Physiological Effects of aldosterone hypersecretion:
increased renal distal tubular exchange of sodium for secreted potassium and hydrogen ions -- body potassium depletion/hypokalemia
diastolic hypertension (no edema)
renin hyposecretion (low plasma renin activity)
renin secretion does not increase with volume depletion
aldosterone hypersecretion that is not suppressed with volume expansion
Diastolic hypertension (not very severe)
secondary to increased sodium reabsorption/volume expansion
Polyuria, polydipsia
impairment of urinary concentrating ability
due to effects of potassium depletion
Electrocardiographic changes -- consistent with potassium depletion (hypokalemia-- which increases ectopy)
prominent U waves
cardiac arrhythmias
premature contractions
Many effects secondary to potassium loss associated with:
may be severe (< 3 mmol/L)
hypernatremia-- due to:
sodium retention
water loss from polyuria
metabolic alkalosis-- due to
urinary hydrogen ion loss
movement of hydrogen ion into potassium-depleted cells
alkalosis enhanced by potassium deficiency which increases proximal convoluted tubule capacity to reabsorb filtered bicarbonate.
Occurs as:
a singular tumor or as
an element of multiple endocrine neoplasia {including thyroidal medullary carcinoma and hyperparathyroidism}
Associated with elevated catecholamine levels
Surgical manipulation {during tumor removal} is likely to cause a rapid increase in blood-pressure due to releases of catecholamines.
Patients with pheochromocytoma may have reduced blood volume-a factor to consider in perioperative management
Undiagnosed pheochromocytoma in patients presenting intraoperatively with hypertension is associated with high mortality {50%}
Pharmacological management prior to tumor removal
alpha & ß-adrenoceptor blockers (a blockers to reduce vasoconstriction; ß-blockers decrease heart and contractility, also reducing blood pressure) -- both groups of adrenergic blocking agents protect against the effects of elevated circulating catecholamines due to tumor.
alpha-adrenergic blockade should precede beta-receptor blockade in order to prevent severe hypertension due to unopposed (ß-receptor-mediated) a receptor mediated vasoconstriction.
alpha-adrenergic blockers--Phenoxybenzamine (Dibenzyline) or phentolamine (Regitine): used to control blood pressure prior to definitive surgical treatment
"Catecholamine-secreting pheochromocytoma of adrenal medulla gross. Note spherical enlargement of the adrenal medulla in this cross section of adrenal."
(c) 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.
- Hulyalkar, A. R., and Miller, E.D., Evaluation of the Hypertensive Patient in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 157-165, 1998.
- Goldfien, A.,Adrenocorticosteroids and Adrenocortical Antagonists, in Basic and Clinical Pharmacology, (Katzung, B. G., ed) Appleton-Lange, 1998, pp 635-650.
- Williams, G. H and Dluhy, R. G. , Diseases of the Adrenal Cortex, In Harrison's Principles of Internal Medicine 14th edition, (Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L., eds) McGraw-Hill, Inc (Health Professions Division), 1998, pp 2035-2056.
Chronic Hypertension: Effects on Cardiac function
Early Cardiac problems associated with chronic hypertension
Diastolic relaxation abnormalities (may be subclinical)
Such diastolic dysfunction may manifest during surgical stress
Identification of diastolic dysfunction: echocardiography (Pulsed-wave Doppler)
Abnormal filling characteristic secondary to diminish left ventricular compliance (increasing ventricular wall stiffness)
May occur in the absence of coronary vascular disease-- secondary to reduced coronary flow reserve
Transient myocardial ischemia may occur in the absence of coronary vascular disease in these patients {frequency = 50%}
Probable mechanism: abnormal coronary flow reserve {ischemia unrelated to left ventricular hypertrophy}
Left ventricular hypertrophy:
Reversibility: dependent on antihypertensive protocol
ACE inhibitors (e.g. captopril (Capoten)) or the calcium channel blocker verapamil (Isoptin, Calan): effective in reducing left ventricular hypertrophy
Other agents useful in left ventricular hypertrophy management:
Methyldopa (Aldomet)
Calcium channel blockers
Methyldopa (Aldomet)
Methyldopa (Aldomet) is a prodrug which is metabolized to the active agent, alpha-methylnorepinephrine.
Alpha-methylnorepinephrine acts in the brain, inhibiting adrenergic outflow from the brainstem. Inhibition of sympathetic outflow results in a decrease in blood pressure.
Methyldopa (Aldomet) produces no change in cardiac output in younger patients, but in older patients a decline in cardiac output results from reduced heart rate and stroke volume.
The reduction in stroke volume occurs due to increased venous pooling (decreased preload).
Since renal blood flow and function is maintained during methyldopa (Aldomet) treatment, methyldopa maybe valuable in managing hypertensive patients with renal insufficiency.
Calcium channel blockers
Calcium channel blockers are effective in treating hypertension because they reduce peripheral resistance.
Arteriolar vascular tone depends on free intracellular Ca2+ concentration.
Calcium channel blockers reduce transmembrane movement of Ca2+ , reduce the amount reaching intracellular sites and therefore reduce vascular smooth muscle tone.
All calcium channel blocks appear similarly effective for management of mild to moderate hypertension.
For low-renin hypertensive patients (elderly and African-American groups), Ca2+ channel blockers appear good choices for monotherapy (single drug) control.
Interactions with Anesthetics:
In anesthetized patients with preexisting left ventricular dysfunction--
verapamil (Isoptin, Calan) administration results in:
myocardial depression
reduced cardiac output
In patients with depressed left ventricular function, anesthetized with a volatile anesthetic,and undergoing open-chest surgery:
IV verapamil (Isoptin, Calan) or diltiazem (Cardiazem) further decreases ventricular function
In patients with preoperative cardiac conduction anomalies, treated with combined calcium channel blockers and beta-adrenergic receptor blockers: condition not associated with perioperative cardiac conduction abnormalities.
Interactions with neuromuscular-blocking drugs:
Calcium channel blockers potentiate depolarizing and nondepolarizing neuromuscular-blocking drug effects.
Similar to effects produced by "mycin" antibiotics in the presence of neuromuscular-blocking drugs (mycins:decrease acetylcholine release, e.g. gentamycin; tetracyclines - chelate calcium and decrease acetylcholine release)
Note that verapamil (Isoptin, Calan) possesses local anesthetic properties -- due to sodium channel blockade -- in effect which contributes to neuromuscular-blocking drug effect potentiation
Neuromuscular effects of verapamil (Isoptin, Calan): more likely to be evidenced in patients with reduced neuromuscular transmission margin of safety.
Neuromuscular-blockade antagonism: possibly impaired by reduced acetylcholine presynaptic release in the presence of a calcium channel blocker (presynaptic calcium influx is typically required for neurotransmitter release)
Risks associated with hypertensive cardiomyopathy and caused by myocardial ischemia {secondary to increased myocardial oxygen demand & reduced coronary flow reserve
Sudden Death
Ventricular Tachyarrhythmias
Abnormal ventricular compliance: major characteristic of hypertensive cardiomyopathy
Systolic function significantly limited in end-stage disease
Sequence in chronic hypertension:
Slow increase in left ventricular diastolic pressure (preload) leads to reactive fibrosis + hypertrophy [Increased hypertrophy reduces wall tension] which causes monocyte necrosis & reparative fibrosis {ACE inhibitors, e.g. lisinopril (Prinvivil, Zestril) may prevent reactive fibrosis but reparative fibrosis may be irreversible}
Ventricular hypertrophy -- significant wall thickening -- predisposes to ventricular arrhythmias
Hypertrophic & fibrotic myocardium associated with patients who have both diabetes & hypertension
ACE inhibitors
Angiotensin II, a potent vasoconstrictor, is produced by the action of angiotensin converting enzyme (ACE) on the substrate angiotensin I. Angiotensin II activity produces
a rapid pressor response
a slow pressor response and
vascular and cardiac hypertrophy and remodeling.
Antihypertensive effects of ACE inhibitors are due to the reduction in the amount of angiotensin II produced.
ACE inhibitors are efficacious in management of hypertension and have a favorable side effect profile.
ACE inhibitor are advantageous in management of diabetic patients by reducing the development of diabetic neuropathy and glomerulosclerosis.
ACE inhibitor are probably the antihypertensive drug of choice in treatment of hypertensive patient who have hypertrophic left ventricles.
Hypertensive patients who have ischemic heart disease with impaired left ventricular function also benefit from ACE inhibitor treatment.
ACE inhibitors reduce the normal aldosterone response to sodium loss (normally aldosterone opposes diuretic-induced sodium loss).
Therefore, the use of ACE inhibitors enhance the efficacy of diuretic treatment, allowing the use of lower diuretic dosages and improving control of hypertension.
If diuretics are administered at higher dosages in combination with ACE inhibitors significant and undesirable hypotensive reactions can occur with attendant excessive sodium loss.
Reduction in aldosterone production by ACE inhibitors also affects potassium levels.
The tendency is for potassium retention, which may be serious in patients with renal disease or if the patient is also taking potassium sparing diuretics, nonsteroidal anti-inflammatory agents or potassium supplements.
Hulyalkar, A. R., and Miller, E.D., Evaluation of the Hypertensive Patient in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 157-165, 1998. Stoelting, R.K., "Calcium Channel Blockers", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, p. 352-353.
Chronic Hypertension: CNS Effects
Hypertension & Stroke
Reduction in BP reduces stroke incidence
Hypertension predisposes to both ischemic & hemorrhagic stroke
Hypertension damages vascular endothelium and in turn damaged endothelial cells promote:
(1) localized platelets aggregation
(2) thrombus formation and
(3) atheromatous plaque formation
Plaque formation reduces distal flow
Reduced vessel lumen dimension promotes turbulent blood flow which causes further injury
Smooth muscle media hypertrophy may weaken vascular integrity, increasing the likelihood of hemorrhagic stroke
Thrombotic Stroke
Acute thrombus at site of vessel narrowing
If a portion of the thrombus breaks off, distal vessel plugging results in embolic stroke
Predisposing factors for embolic stroke:
Cardiac arrhythmias
Atrial fibrillation (myocardial thrombus formation leading to cerebral emboli)
Hypertension predisposes the myocardium to arrhythmias
Infarcts secondary to hypotension, when BP falls below range of cerebral autoregulation
{Watershed infarcts = insufficient systemic blood-pressure for arterial blood to reach the end of vascular branches-- in particular poor cerebral cortical perfusion of a susceptible "watershed zone" between anterior & middle cerebral artery or middle & posterior cerebral artery may result in linear infarcts}
In the chronically hypertensive patient, a greater blood-pressure is required to maintain adequate cerebral perfusion compared to normal patients
Watershed Infarct image courtesy of the Digital Slice of Life Cooperative Project (http://medstat.med.utah.edu/kw/sol/sss/index.html)
Chronic Hypertension: Renal Effects
Chronic renal injury
Intimal hyperplasia
Afferent arteriolar sclerosis
Parenchymal fibrosis
secondary to reduced blood flow
Reduced renal function as a result of hypertension is characterized by a gradual degradation in renal function {benign nephrosclerosis}, leading to ultimately a rapid and irreversible renal failure {malignant nephrosclerosis}
Characteristics of benign nephrosclerosis
Renal dysfunction probably due to compensatory hyperfiltration by normal glomeruli
Increase glomerular pressure is associated with proteinuria
Hyperfiltration of certain glomeruli tends to induce sclerosis of otherwise normal glomeruli
Malignant Nephrosclerosis
Renal manifestation of malignant hypertension
If untreated (initially with IV vasodilators), malignant hypertension will precipitate renal failure within days-weeks
Treatment: typically IV vasodilators initially {e.g., nitroprusside sodium (Nipride), nitroglycerin}
Three renal histological changes associated with malignant hypertension
Arteriolar fibrinoid necrosis
Hyperplastic arteriosclerosis {arteriolar "onion-skinning"-note the vessel in the center of the image below}
Glomerulitis in the hypercellular glomerulus {screen position: 7 o'clock position below}
Description and image: courtesy of The Urbana Atlas of Pathology, use with permission
Malignant Nephrosclerosis Images
Image contribution by Saint Francis Hospital
Hulyalkar, A. R., and Miller, E.D., Evaluation of the Hypertensive Patient in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 157-165, 1998.
Chronic Hypertension: Perioperative Issues
Increased intraoperative blood-pressure lability in patients not receiving their antihypertensive medication: Recommendation -- administer medications on the day of surgery
-- Exception: possibly diuretics
Concerning elective surgery in patients with uncontrolled hypertension:
Surgery not associated with elevated incidence of perioperative cardiac morbidity if preoperative diastolic pressures were less than 110 mm Hg with careful perioperative blood-pressure monitoring
Preoperative approaches to the hypertensive patients:
Factors that increase risk of myocardial ischemia intraoperatively
uncontrolled hypertension or hypertension control solely with diuretics {compared to patients treated with atenolol (Tenormin)}
myocardial ischemia --most likely occurs during:
emergence from anesthesia
Intraoperative ischemia: primary association = tachycardia
Special considerations:
Diabetic patients with hypertension (noncardiac surgical procedures)
Predictors of postoperative ischemia/infarction
Preoperative cardiomegaly (demonstrate radiographically)
Previous myocardial infarction
Intraoperatively events predictive of postoperative for cardiovascular complications {renal/cardiac morbidity}
intraoperative hypotension (> 20 mm Hg decrease in mean arterial pressure (duration > 1 hour))
intraoperative hypertension (> 20 mm Hg increased in mean arterial pressure (duration > 15 minutes )) alternating with hypotension
Hypertension & organ transplantation
Occurs only in some patients
Hypertension increases the likelihood of renal failure in the transplanted kidney
Antihypertensive drug treatment: no improvement in graft survival
Post-organ transplantation hypertension probably due to immunosuppressive drugs:
Glucocorticoids -- Na+/H2O retention
Cyclosporine (Sandimmune, Neoral): increased sympathetic nervous system activity (suggested factor)
Perioperative issues in managing patients with cerebrovascular disease/hypertension:
Aneurysmal subarachnoid hemorrhage patients
Hypertension management may reduce re-bleeding
Hypertension management, however may increase cerebral infarction risk
Surgical intervention for aneurysmal subarachnoid hemorrhage in patients who have had hypertension: associated with increased seizure risk.
Diastolic pressures: best maintained in a range of 95-105 mm Hg
Post-operative control of BP & vasospasm-- nimodipine (Nimotop)
Nimodipine (Nimotop)
Hypertension & Anesthetic management
Elective surgery issues:
Cancel elective surgery if diastolic pressure > 115 mm Hg {until evaluation & treatment result in controlled pressure}
Emergency surgery issues:
Intraoperative management of BP with--
Short-acting parenteral drugs, e.g. nitroprusside sodium (Nipride), nitroglycerin, esmolol (Brevibloc)
Nitroprusside (Nipride)
Overview:nitroprusside (Nipride)
Direct-acting, nonselective peripheral vasodilator--NO mediated
Relaxation of arterial and venous vascular smooth muscle
ferrous iron center complex with five cyanide moieties and a nitrosyl group (44% cyanide by weight)
Immediate onset of action
Short duration (requires continuous IV administration to maintain effect)
requires careful dosage titration
frequent systemic blood pressure monitoring -- often by intra-arterial catheter
Mechanism of Action: nitroprusside
nitroprusside interacts with oxyhemoglobin, forming methemoglobin with cyanide ion and nitric oxide (NO) release
NO activates guanylyl cyclase (in vascular smooth muscle);resulting in increased intracellular cGMP
cGMP inhibits calcium entry into vascular smooth muscle (may also increase calcium uptake by smooth endoplasmic reticulum): producing vasodilation
Mechanisms by which cGMP relaxes vascular smooth muscle remain to be elucidated. cGMP does, however, activate K+ channels (hyperpolarizing effect), activate a cGMP-dependent protein kinase, , decrease IP3, and inhibit calcium entry into the smooth muscle cells.
NO: active mediator responsible for direct nitroprusside vasodilating effect.
Note that organic nitrates (e.g. nitroglycerin) require thio-containing agents to generate NO
The reaction: nitroprusside interacts with oxyhemoglobin, leading to methemoglobin formation with cyanide ion and nitric oxide (NO) release produces an unstable nitroprusside radical
nitroprusside radicals decomposes releasing five cyanide ions (one cyanide reacts with methemoglobin to form cyanomethemoglobin)
remaining free cyanide ions (following reaction with hepatic & renal rhodanase) are converted to thiocyanate {thiosulfate donor: body sulfur stores are sufficient detoxifying about 50 milligrams nitroprusside})
Organ System Effects: Nitroprusside
Overview: Principal effects referable to:
Cardiovascular system
Cerebral blood flow
Hypoxic pulmonary vasoconstriction
Platelet aggregation
Cardiovascular Effects: Nitroprusside
Direct venous/arterial vasodilation; rapid decrease in systemic blood-pressure
Reduced systemic vascular resistance (arterial vasodilation; venous capacitance vessel vasodilation)
Positive inotropic & chronotropic responses: reflex-mediated secondary to hypotensive response
Net increase in cardiac output due to:
increase contractility
decreased left ventricular ejection impedance
Hypotensive response: associated with reduced renal function; renin release occurs (explains over shoot upon nitroprusside discontinuation {ACE inhibitor-sensitive, i.e. an ACE inhibitor will prevent this overshoot effect})
Nitroprusside: may worsen myocardial infarction damage due to "coronary steal", blood flow directed away from ischemic areas by arteriolar vasodilation
Cerebrovascular Effects:
Increased cerebral blood flow, volume.
with decreased intracranial compliance, increased intracranial pressure results
Generally, increases in intracranial pressure are most apparent when systemic mean arterial pressure decreases by less than 30%
if systemic mean arterial pressure decreases by > 30%, intracranial pressure decreases below the awake level.
Nitroprusside contraindicated in patients with known inadequate cerebral blood flow (e.g. high intracranial pressure; carotid artery stenosis)
Hypoxic Pulmonary Vasoconstriction
Nitroprusside infusion (and other vasodilators) causes decrease in PaO2
Mechanism: vasodilator-mediated reduction in hypoxic pulmonary vasoconstriction
Clinical Uses: -- nitroprusside (Nipride)
Control hypotension during anesthesia and surgery
Rapid, predictable vasodilation & decrease in BP allows a nearly bloodless surgical field, required in some operations: spine surgery, neurosurgery (also reduces transfusions)
Other drugs that might be chosen to produce controlled hypotension, nitroprusside is most likely to ensure adequate cerebral perfusion (mean arterial pressure's of 50-60 mm Hg can be maintained without apparent complications {in healthy patients})
The potential for cyanide toxicity can be diminished by:
Use of other cardiovascular depressant drugs which reduce nitroprusside requirements
These drugs include: volatile anesthetics, beta-adrenergic antagonists, calcium channel blockers; note that beta adrenergic antagonists may cause a decreased cardiac output-- a potential problem in patients with diminished the ventricular reserve.
Treatment of hypertensive emergencies
Acute & chronic heart failure
Reduction of afterload may be important for patients with CHF, mitral or aortic regurgitation, acute myocardial infarction with left ventricular failure
Role of nitroprusside in chronic, congestive heart failure -- advantageous because:
reduced ventricular ejection impedance (injection at lower end-diastolic volumes
preload reduction (secondary to blood pooling in venous capacitance vessels -- reflected in decreased ventricular and-diastolic volume)
Surgical indications:
Aortic surgery
reduction of proximal hypertension associated with aortic cross-clamping (thoracic aortic aneurysm, dissections, coarctations)
distal hypotension may occur (relative to clamp location)
Cardiac surgery necessitating cardiopulmonary bypass
Activation of renin-angiotensin system may cause systemic hypertension during cardiac surgery
Nitroprusside is effective in reducing such increases in BP
Following cardiopulmonary bypass {re-warming phase}, nitroprusside-mediated vasodilation facilitates heat delivery to tissues {reduces nasopharyngeal temperature decline after bypass}
Nitroprusside is effective in managing pulmonary hypertension after valve replacement
Pheochromocytoma resection
Vasodilators used for acute management of hypertensive crisis or malignant hypertension include sodium nitroprusside and diazoxide.
Nitroprusside sodium (Nipride) is the agent of choice-- advantages
Rapid onset
Effect diminishes rapidly upon drug discontinuation
May also be used (rapid injection) to reduce systemic blood-pressure associated with direct laryngoscopic tracheal intubation
Administered by a continuously variable rate i.v. infusion pump, precise blood pressure control can be obtained.
Nitroprusside sodium (Nipride), a nitrovasodilator, is metabolized by smooth muscle cells to nitric oxide which dilates both arterioles and venules.
If patients have controlled hypertension, anxiolytics may be appropriate {preoperative medication}
diazepam (Valium); oral
midazolam (Versed); intramuscular
Patients managed with diuretic drugs for hypertension:
Diuretics not given on same day of surgery
Patients may be volume depleted
Patients whose hypertension is managed with diuretics may have to be dehydrated prior to the surgical procedure {remaining antihypertensive medications, i.e. non-diuretics should be administered on the surgical day.}
Management of hemodynamic variability during anesthetic induction/emergence:
Reduction of variability
Esmolol (Brevibloc) {short-acting ß-receptor blockers}
Effective in management of sinus tachyarrhythmias & hypertension in cardiac & noncardiac surgical patients
Lidocaine (Xylocaine)
Nicardipine (Cardene)-management of perioperative hypertension
Choice of anesthetic for maintenance:
Any agent reasonable except for ketamine (Ketalar)
Ketamine (Ketalar) associated with hypertension, increased intracranial pressure & tachycardia
Intraoperative management of acute blood pressure increases:
Prior to antihypertensive drug administration, rule out:
inadequate anesthetic depth
Hulyalkar, A. R., and Miller, E.D., Evaluation of the Hypertensive Patient in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 157-165, 1998. Stoelting, R.K., "Calcium Channel Blockers", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, p. 350; Stoelting, R.K., "Antihypertensive Drugs", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 302-312;and "Peripheral Vasodilators", in Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, 315-322.
Pharmacological Management of Hypertension
Non-pharmacological interventions: Diet, Stress reduction, regular aerobic exercise, weight reduction as needed, control of other risk factors (blood lipids, smoking)
Diet involves several aspects that may include:
reduction of sodium intake
caloric restriction for obese patients
restriction of cholesterol and saturated fat intake.
Pharmacological Management
Pharmacological interventions in essential hypertension management is based on selecting often a single initial agent and evaluation of patient response. Unless clinical conditions require immediate reduction in blood pressure as in hypertensive crisis, the first step may involve the use of :
a calcium channel blocker or beta-blocker, or angiotensin converting enzyme inhibitor (ACE inhibitor). The specific clinical presentation may favor one choice over another.
For example, in patients with asthma or chronic obstructive pulmonary disease (COPD) the use of a beta-adrenoceptor antagonist may be contraindicated since agents belonging to this drug class may cause bronchoconstriction.
Alternatively, a patient with marginal left ventricular function, predisposed to congestive heart failure, may not tolerate beta-blockers or calcium channel blockers because both mediate a negative inotropic effect (reduced myocardial contractility). At this step, beginning with a low dosage first is usually appropriate.
Thiazide diuretics has been often used in the past as the first drug given.
Thiazides may be added if adequate blood pressure control by a calcium-channel blocker, a beta-blocker, or an ACE inhibitor has not been achieved.
Thiazides promote potassium loss and increases in serum lipids.
If control has not been achieve with the above drugs at optimal dosages, a antiadrenergic drug may be added (such as a central or peripheral-acting sympatholyic). Peripheral vasodilators may also be used at this stage.
The general idea is to use a single agent before progressing to multiple agents and then stronger multiple drugs. Often the side-effect profile becomes less favorable as more and stronger drugs are added.
Note the progression of antihypertensive medication
At each step dosages are reviewed and if the patient's hypertension is controlled then therapy may be continued with review for possible removal of medication.
Figure adapted from Harrison's "Principles of Internal Medicine, Thirteenth Edition, p. 1128
For hypertensive emergencies/crises sodium nitroprusside is the agent of first choice.
Hypertensive Crisis
Definition: diastolic pressure > 130 mm Hg
Malignant hypertension (evidence of end-organ damage): Medical emergency-requires immediate treatment
Malignant hypertension requires the use of parenteral agents with intra-arterial BP monitoring
Without end-organ damage present, oral or sublingual antihypertensive drugs might be used
Factors causing a rapid increase in BP:
Elevation of intracranial pressure (increased blood pressure allows maintenance of cerebral perfusion)
Neurological causes of hypertensive crisis:
intracranial hemorrhage
head trauma
CNS tumor
thromboembolic stroke
subarachnoid hemorrhage
Cautious management for patients with hypertensive crisis --hypertensive drugs given in severe hypertension (> 200/130 mm Hg)
Nitroprusside sodium (Nipride) -- careful administration {may increase intracranial pressure and patients with reduced intracranial compliance)
Beta adrenergic receptor blocking drugs: Not recommended; may cause cerebral vasospasm
Centrally acting drugs {e.g., clonidine (Catapres); methyldopa (Aldomet)}: not recommended for hypertensive crisis as a result of neurological cause
Hemorrhage, Subarachnoid, Hypertensive Vessels (left); Hemorrhage, Intraventricular Medulla, Extension into Lateral Recess and Subarachnoid Space (right): Courtesy of Digital Slice of Life (http://medstat.med.utah.edu/kw/sol/sss/index.html)
Cardiovascular causes of hypertensive crisis:
Myocardial infarction
Dissecting aortic aneurysm
Therapeutic Objectives:
20%-25% reduction in diastolic or pressure (100 mm Hg)
For dissecting aortic aneurysm cases, reducing the arterial pressure rate of rise may prevent aneurysmal rupture-{nitroprusside sodium (Nipride) + ß-adrenoceptor blocker is a useful combination}
In myocardial infarction, maintenance of coronary perfusion is critical as systemic pressure is reduced-Useful drugs include:
calcium channel blockers
ß adrenoceptor blockers
Renal causes of hypertensive crisis:
Renal artery stenosis
Parenchymal renal disease
Therapeutic objectives:
maintain renal perfusion while decreasing BP to prevent fibrinoid necrosis
Useful drugs:
Nitroprusside sodium (Nipride)
Calcium channel blockers
Other interventions:
the combination of renal failure & malignant hypertension may require dialysis
Special cautions:
Thiocyanate levels must be monitored when nitroprusside sodium (Nipride) is used at high doses for extended periods of time
ACE inhibitors should not be used if bilateral renal artery stenosis suspected/confirmed:
Mechanism -- glomerular filtration is dependent on post-glomerular arteriolar constriction, which is maintained by angiotensin II. Renal failure can be induced if post-glomerular arterial constriction is lost.
Other causes of hypertensive crisis:
Ingestion of tyramine-rich foods in patients taking MAO inhibitors
Recreational drug use
Hyperautonomic syndromes {chronic smoke or dysfunction}
Pheochromocytoma-massive release of endogenous catecholamines by tumor.
Hulyalkar, A. R., and Miller, E.D., Evaluation of the Hypertensive Patient in Principles and Practice of Anesthesiology (Longnecker, D.E., Tinker, J.H. Morgan, Jr., G. E., eds) Mosby, St. Louis, Mo., pp. 157-165, 1998.


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Medea filmmaker is a role model for independent artists struggling to raise funds
I consider Tyler Perry an inspiration and a role model. And I say that without ever having seen any of his films. As entertainment goes, they're not to my taste. I'm sure that's fine with Mr. Perry, because he didn't make them to please snobs like me. He made them to please his audience. Tyler Perry knows, likes and respects his audience of church-going, (mostly) African-Americans from working poor to emerging middle class, and he gives them what they want without pretense or condescension. As a result, he is a critic-proof, hit-generating machine. He is one of the few figures in the movie industry who can green-light himself. So, if he's not my inspiration as an auteur, he certainly is as an entrepreneur. He has been a model for Christian filmmakers, who have gotten support from local congregations to fund their projects. But everyone in Hollywood, from the sniveling film-school graduate, laboring to give birth to a delicate art house examination of the ethereal blending on adolescent angst and Marxist dialectic, to the cynical exec chasing the next of iteration of Michael Bay meets Mattel, should take note: Know your audience. Like your audience. Respect your audience. Deliver what the audience wants.
It wouldn't hurt also, if you happened to like your fellow man, which is another quality Mr. Perry seems to possess in abundance. Hence the marketing campaign for his new film, Good Deeds. The press release for the film reads:
Tyler Perry's GOOD DEEDS is very happy to announce Good Deeds: Great Needs, an initiative to support Covenant House, a non-profit organization that provides for homeless youth. Through GiftCardGiver.com, Good Deeds: Great Needs will be collecting unused gift cards and donating all collected to Covenant House.
In addition, Lionsgate will be making a financial donation to Covenant House for every share of the GOOD DEEDS trailer! So make sure to watch and share the video!
To learn more and share Good Deeds: Great Needs, visit www.gooddeedsgreatneeds.com
GOOD DEEDS also presents fans the opportunity to win a Valentine's Date Night! Just head over to the GOOD DEEDS Facebook page and submit your "love story" for the chance to win a $500 Visa Gift Card!
Contest can be found here.
I'm not presenting this information to plug a film I probably won't see. What interests me is the skill with which the film is being marketed. By associating it with a worthy cause, Covenant House, Perry may boost his social networking chances substantially and garner good will from prospective viewers. This may translate into better box office. I can't help but wonder if this can be applied to artists struggling to fund their independent projects.
I get a lot of kickstarter.com requests to support my friends' artistic projects. For those of you who haven't heard, kickstarter is a website which features video pitches for artistic projects and processes donations. If an artist hits his goal, he gets the funds, minus the kickstarter cut. If he falls short of his goal, the credit cards are not processed, and he gets nothing. Most people I know who have tried kickstarter.com have not made their goals. That may be due to the size of their social network or the attractiveness of their project or the goodies they offer as rewards. But I think associating themselves with a larger purpose than the project itself might give the extra nudge they need.
That's exactly what Tyler Perry is doing with this campaign. Whether it succeeds and whether it could be adapted to work by lesser known artists who don't have Lionsgate behind them is something to be seen. But I think all artists have a connection to some charity or network thereof, which might just help an artist break through and get the financing he needs to launch a project and a career.

subset: commoncrawl


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I've been using Snapseed as the primary photo editing app on my phone for some time. It's powerful and easy to use, more so than the default photo editing app that comes with my Samsung phone. Amateur Photographer just published a detailed review. If you have an Android or Apple phone, I'd definitely recommend it.
Nik Software has been developing a range of excellent plug-ins and standalone software for photographers since the 1990s. Most famous for its image-editing program Snapseed, the company was acquired by Google in 2012 and its focus was steered towards mobile image editing. The desktop version of Snapseed was dropped in 2013 and the mobile app began having bigger and better updates.
Skip forward to April 2015 and Snapseed 2.0 was released in the Google Play and Apple App Store. This new update was a complete overhaul. The user interface changed and the toolset became more comprehensive than ever, making it one of the most sophisticated editing apps available – all for free!
It's available on iOS and Android, and both versions work similarly across both platforms, with the same feature set. The interface is also consistent between tablets and phones. Once the app is open, users can edit images from albums on their smart device. When an image is open, there are a few options. By double-tapping the screen, users can zoom into the image and move around using the navigator in the bottom left of the screen. When zoomed out, users can toggle a histogram on or off in the bottom-left corner. In the top right is a menu that allows users to undo, redo, revert a recent adjustment, share the image, or look at the details of the file including camera, shutter speed, aperture and more. The most important element, though, is the Pencil icon in the bottom right, which marks all the editing functions available. These are in two sections: Tools and Filters.
Read more at http://www.amateurphotographer.co.uk/accessory_reviews/snapseed-2-0-review-69151#r81duH73xamXMCok.99


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Despite Collision, Jackson Bend Feisty and Fit for Forego
In the aftermath of a violent collision on Saratoga's Oklahoma training track, some wondered whether or not Nick Zito's five year old Jackson Bend would survive, let alone race again. But remarkably, when the gates swing open for Saturday's Grade One Forego, just two weeks after that training accident, the five year old fighter will be in the mix.
On August 18th, the normal hustle and bustle of Saratoga Race Course's Oklahoma training track gave way to paralyzing fear, as a forceful collision between two horses left one of them laying on the track, unable to get up for more than five minutes. It was Nick Zito's multiple Grade One winning Jackson Bend down prone, having been clobbered head-on by the Anthony Quartarolo trained Little Nick, who stepped onto the track, spooked, and bolted under his jockey.
The collision was enough throw Jackson Bend's exercise rider, Carlos Correa, over the top and onto the dirt. It was there that horse and rider lay for a number of minutes, both trying to catch their breath. "I was disgusted for him," said Correa, who, when asked, said he thought the horse wouldn't survive the ordeal. "It was a hard impact, you know? I thought he might have broken his shoulder."
Trainer Nick Zito echoed the grim thoughts. "I was horrified. I said 'Oh please, no. It can't be him.'" But while those on the scene simultaneously hoped for the best and prepared themselves for the worst – and while Zito attempted to contact the horse's owners, Robert LaPenta and Fred Brei – the horse simply stood up; and after being vanned back to Zito's barn and examined by doctors, seemed, astoundingly, fine.
"It's an amazing story," said Zito, who spoke at length defending his decision to run Jackson Bend on Saturday. "All I can do is take all the tests, and I did. And they all came back good," he said. Unfolding a printed sheet of paper and turning it for us to see. He continued, "See [the blood work results]?" indicating the paper, "This is Jackson Bend. Know when this was taken? Yesterday. You know what it is? Perfect." "I ask [exercise rider Carlos Correa] every day, if he said no, it'd be no," he finished.
For his part, Correa agrees, saying that the horse is "over it," and specifically mentioning how well he's trained of late, "It's scary the way he's been going, like his old self."
Attempting to explain away the horse's impressive resiliency, both trainer and rider noted his toughness, calling him feisty and fearless. But perhaps it was Zito who put it best when he said simply, "He's a tough little bastard."
And so against all odds, Jackson Bend will race on Saturday. He's been installed a 7/2 second choice in Saturday's Grade One Forego, and will likely have to rely on that grittiness to score a win. With plenty of front-running speed joining him in the starting gate, he'll likely sit near the back and rely on a ferocious closing run – and if the fight he's displayed battling through an ordeal that would have doomed lesser horses is any indication, I wouldn't ignore him when stepping up to the betting window. Why would you want to anyway? A horse like this? He's one to root for. Go get 'em Jackson Bend.


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So journals it is. If argument journals aren't your cup of tea, or you'd like more options employ a close reading journal. One of my favorite resources for this type of journaling is found in Nancy Dean's Voice Lessons. Her lessons are invaluable. She has already selected non-fiction and prose "snippets" and created questions. As a teacher, all you have to do is choose. Dean's questions often ask about the impact of specific syntax and diction. Each quote is usually followed by two questions. Choose the ones you like, copy and have students answer the questions as one journal reflection. Even students who struggle can understand the power of word choice and the way that Nancy Dean constructs her questions reaches a range of students. A teacher, especially in light of common core expectations couldn't ask for a better resource.
Since Voice Lessons is such a fabulous resource, I could end the post right there. However, if you'd like to kick the exercises up a bit examine Maria Popova, of Brain Pickings fame, and her Literary Jukebox. Each day a quote from a book is posted along with a thematically chosen song. Some of my favorites include:
- Cat's Cradle, Kurt Vonnegut
- Adam Bede, George Eliot
- Sense and Sensibility, Jane Austen
- The Glass Menagerie, Tennessee Williams
Use Popova's quotes in the same way you would with Voice Lessons except ask your students to identify the words upon which the sentences turn. Then have them discuss the meaning, power and effect of those words in their journals. Feel like they need more? Have them listen to the song Popova has partnered with the quote and ask them to write about why the partnership works for the second part of their response.
Need a quick journal rubric? Here is a Close Reading Rubric that can be adapted for any type of classroom journals.


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May 1, 2005
AMHERST, MA - The Amherst College softball team was eliminated from playoff contention with a pair of losses to visiting Williams College on Sunday afternoon in a matchup that was originally scheduled for Williamstown but moved to Amherst at the last minute due favorable field conditions. Williams (20-12/7-1 NESCAC West) took the opener 5-4, clinching a berth in the NESCAC Postseason Championship Tournament, and then won the second game, 9-6.
Amherst (14-12-1/4-4 NESCAC West) trailed 4-2 in Game 1, but knotted the score with a pair of runs in the top of the seventh as junior Laura Trigeiro led off with a single and scored on a fielder's choice, and sophomore Annalise Rodli plated another run with an RBI single. Williams then won the game with a two-out rally in the bottom half of the inning when Laura Noel reached on an error, and pinch runner Melissa Vandermyn trotted home on a pinch-hit single by Taryn Goodman.
Amherst junior hurler Miya Warner struck out four and surrendered four hits and four earned runs before moving to second base in the seventh. Rookie Samantha Miller pitched the final frame and took the loss to fall to 0-4. Trigeiro and first-year Ralina Shaw each singled twice for the Jeffs, while Kelly King singled and drove in a pair of runs.
Alana Frost, Katie Powers and Noel each homered for Williams. Starting pitcher Clara Hard went the distance and improved to 7-3 with the win.
Frost and Beth Lorge each homered for Williams in the nightcap, while Liz Gluck tossed a complete game, upping her pitching record to 3-5.
Trigeiro paced Amherst in defeat with a trio of singles. Shaw added a pair of doubles and two RBIs. Hilary Little drew the start and took the loss to drop to 3-4.


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Good platform for rolling out mobile data units.
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Avg. Customer Rating: (45 customer reviews)
The most favorable review
Good platform for rolling out mobile data units.
The most critical review
Dented back panel
Our company has purchased quite a few of these cabinets, however, the most recent one received had a dented back panel.
Mobile Computer Cabinet
Your review: We currently have close to 15 of these cabinets that we have purchased over the years. They are used in diesel truck shops for diagnostic PC's. They have performed well and we are still using the initial ones we bought. Assembly is easy and the cabinet provides a safer/cleaner environment for our shop computers.
Pros: Good quality, solid protection for PC's and monitors and easy to move within our shops.
Cons: Would prefer that one key opened all locks instead of needing to keep up with three.
Not bad, does as intended
Your review: This cabinet is a bit on the cheesy side, definitely seen worse though. It will do the job, seems slightly expensive for what it is. Also waiting for a replacement caster, 1 original was built wrong and didn't spin.
Pros: the drawer and shelf slides are good quality. Works nice with no slop.
Cons: I think the gauge of steel should be thicker. Don't let it fall over.
Good Product
Your review: This is the second mobile security cabinet we have purchased. Assembly went smoothly and it has a decent amount of space for the computer and additional devices. I don't like the plastic screen for the lcd compartment. I have since replaced them both with glass to avoid scratches which limits the viewability.
Mobile Security Cabinet
Your review: Bought this cabinet to house an end of line test system for our factory floor. Fairly solid, lots of assembly, but places everything in easy to use position for the operator. I would give it five stars but out of all of the key locks, all of the keys matched except the bottom cabinet which is a different key.
Mobile Security LCD Computer Cabinet and Sidecar
Your review: We were happy, as always, with the prompt delivery and the quality of the cabinet. We were, however, disappointed that there were several dents in the cabinet; not quite enough damage for us to send the item(s) back but still disappointing.
Mobile Work Station
Your review: Over all a very good product that I would recommend.
Pros: Easy to assemble and comes with the ability to store multiple peripherals and secure them. Access to both sides makes wiring/installations easy and painless.
Cons: Easy to stand and work next to yet slightly more difficult to sit next to it and work comfortably due to configuration. Screen to protect LCD monitor is made from a plastic material that scratches easily and glares heavily under direct lighting.
Nice Cabinet
Your review: This cabinet works great in our shop environment. I was very impressed with the quality and durability of this product as well. We needed a well constructed work station for a shop that is typically very dusty and dirty and this has provided a great solution.
Great Cabinet for the price
Your review: We bought 3 cabinets for our cadillac dealership. The price was awesome. The cabinets are a nice quality. The only thing I would change is the wire grommet placement for the monitor. They have it centered in the rear of the monitor area and all the monitor bases cover the grommet and there is no space to feed the wires. but...that is the only thing I can pick apart, I would buy this product again
There are 45 questions and 3 answers for this product.
Is the metal window panel holding the glass removable?
Question Asked By: Bill , Tucson, AZ , May 22, 2017
What is the country of origin?
Question Asked By: Anonymous , April 12, 2016
what is the joules protection?
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Exco plea to power firms to cut rises
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Top government officials have made an unprecedented appeal to the city's two power firms to cut price increases next year.
They say the planned rises are 'excessive' and fear they could accelerate inflation.
Hongkong Electric said it had responded to the government's appeal by announcing a 6.3 per cent increase. It would not say by how much it had cut the planned rise.
But CLP Power says capital expenditure and a three-fold increase in its fuel costs means it will charge customers an average 9.2 per cent more. This will push up the monthly bill for most households by about HK$25. CLP said it had little room to manoeuvre. Managing director Richard Lancaster said: 'A 9.2 per cent increase is the best we can do, and we have tried our best to minimise the impact.'
The increases will enable the two firms to earn the maximum allowable return of 9.99 per cent on their net fixed asset values - specified in their scheme of control agreed with the government - which could be the highest in a decade.
Secretary for the Environment Edward Yau Tang-wah reported the issue to the Executive Council yesterday morning. 'The council has expressed reservations about the excessive tariff hikes,' he said, adding that it had asked both firms to reconsider their positions.
Speaking at a meeting of the Legislative Council's economic development panel yesterday, Yau said the increases did not take into account the public's ability to pay or the impact on society.
He said CLP could consider following Hongkong Electric's example of delaying the recovery of its fuel costs from consumers. But CLP said its costs, which will rise from HK$4 billion to HK$12 billion next year, were too big for it to shoulder alone.
Lancaster said CLP would introduce a two cents per kilowatt hour basic tariff reduction, excluding fuel costs, for low-consumption residential households for the first 400 units used. Those using more than 2,600 kilowatt hours would pay more.
At the same time, the company will abolish discounts for non-residential users who reach a certain level of consumption and introduce a flat rate to promote energy conservation. CLP said most small businesses would pay less than HK$131 more on their monthly bill.
CLP's increase will add HK$50 to the two-monthly bill of households using 500 units of electricity a month, which accounts for about 70 per cent of its domestic customers.
Yau questioned whether CLP had done enough to control its rising operating costs and wondered why the firm had taken into account some unnecessary or untimely capital spending.
Billy Mak Shui-choi, from the Department of Finance at Baptist University, said the direct impact on inflation would be minimal because power costs were a small part of household expenditure.
'There might be a knock-on effect on heavy power users like the trams, the MTR or restaurants which will pass on the extra costs to consumers. But it is difficult to quantify the impact now,' he said.
Political parties slammed the increases. 'These firms are wolves which completely ignore if the people can bear the increase and how the tariff hike will trigger inflation,' said unionist legislator Lee Cheuk-yan.
CLP Power's rise will add HK$50 to the two-monthly bill of those using 500 units of electricity a month - this percentage of domestic customers
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Don't dump it, donate it!Monday, August 20th, 2007
UNE has signed up to a mobile phone recycling program. This means reducing waste, pollution and raising money for a good cause.
In 2002 75% of Australian households had at least one mobile phone. Like other new technologies there's pressure on mobile phone users to constantly upgrade their phone. That means that there's millions of old mobiles heading into landfill.
Throwing a mobile into the bin is particularly worrying given the toxic chemicals that are common mobile phone components. Arsenic, Beryllium, Cadmium, Copper, Lead, Lithium, Mercury and Zinc are all commonly found in mobile phones.
Clean up Australia in association with Aussie Recycling has set up a mobile phone recycling program that ensures that no mobile phone waste will make it into landfill. This means no toxins in the environment – but wait there's more. The recycling program will help to raise funds for The Spastic Centre – helping to provide services for children and adults with cerebral palsy. The program also helps to provide affordable communication to developing countries.
To donate your old mobile just pop in to the service desk and pick up a yellow phone recycling satchel. This provides free postage for your old mobile.


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Magic Snitch Pocket Watch
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The Magic Snitch Pocket Watch has a perfectly designed Full Hunter cover which mimics the prestige and character of the magic snitch as inspired by the Harry Potter series, making it the perfect gift for any occasion. The polished face and back cover give it a refreshing feel that any pocket watch lover would enjoy.
A Full Hunter Pocket Watch is a classic style that includes a pocket watch cover that entirely hides the face of the watch. The Magic Snitch Full Hunter Pocket Watch also includes a chain and Bold Numeral Dial for an elegant finish that would add class to any man's wardrobe.


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The national survival rate for breast cancer patients is 91 percent. Kaiser Permanente's patients' survival rate is 93 percent, noted Dr. Hong Yoon Plurad.
Plurad, a surgeon and director of the Breast Center at Kaiser Permanente Baldwin Park (KPBP) Medical Center, said that small increase in the survival rate is the result of several efforts by Kaiser Permanente.
One of those is by getting each eligible patient screened early. KPBP's Breast Center leads the nation with 90 percent screening of eligible patients.
The medical center offers walk-in mammograms without an appointment and KP's advanced electronic health information system, Kaiser Permanente HealthConnect, allows receptionists to check a patient's full medical record including any exams that may be due or upcoming, including a mammogram, when they check in for any other appointment.
"I've gotten (a mammogram) - it ruins your day, I know," said Plurad. "But it's always better to know and to get it found early. The survival rate increases, the sooner it's found and treated."
Another important tool for KP breast cancer patients is a multidisciplinary conference. Every patient's care is designed to incorporate multiple disciplines - surgery, oncology, radiology and pathology. Each patient's case is discussed by all practitioners that would be involved in their care, before surgery is done, if needed.
"In some cases, a patient has surgery and then meets with their oncologist or other doctor and finds out they may have had other options for treatment," said Plurad.
As a surgeon, Plurad said it is disheartening to learn that surgery may not have been necessary and sees how patients' care is better because of the conference.
"It's all standardized," she said. "All of this is so we don't miss anything, nothing slips through the cracks."
For Covina resident Mary Gonzales, all these efforts were worth it for her when she realized she had breast cancer in 2007.
"I went to see my allergist and (Susan Salas) was the receptionist," said Gonzales, 72.
Gonzales admits she had been putting off getting a mammogram for a while because she said she just got busy.
After much insistence from Salas, Gonzales agreed to schedule an appointment and within weeks had her mammogram done.
Gonzales was called in for another exam and then an ultrasound in October before she began to wonder what was going on.
"They had me go talk to a doctor and they told me they found a spot (in my breast). They wanted to do a biopsy, did it the next day, and within a couple days they made an appointment for surgery," said Gonzales.
In November 2007, Gonzales had a mastectomy.
"I had two kinds of cancer," she said. "One of the cancers was a deadly one that can get into the bloodstream - once it gets into the bloodstream, it's deadly."
Gonzales said she thanks Salas for insisting on getting a mammogram.
"Thanks to her, I had more time to spend with my family," said Gonzales.
To show her thanks, Gonzales sent Salas a gift with a thank you note to her office. The note eventually made it up the ranks of supervisors and soon Gonzales was asked to help promote screenings by taking part in informational and educational videos.
On Oct. 1, Gonzales's story debuted in a national television commercial as part of KP's Thrive campaign.
"When I was asked to do a TV commercial, I told Susan, `We made it to Hollywood!'," said Gonzales.
For Susan Cohen-Rooks, a KP member since she was 16, mammograms were routine since she was 28 years old. The San Gabriel resident had a spot in her breast and her doctor had it checked every 6 months, luckily with no change for years.
Then in 2009, her general practitioner called to remind her she hadn't had her scheduled mammogram.
"(In the mammogram,) they saw something that wasn't there before, not what I had there before," said the 59-year-old.
After a simple biopsy results were inconclusive, Cohen-
Rooks had a more advanced biopsy that confirmed she had cancer.
"I was shocked, scared, really scared," she said. "It was small, I never would have found it by doing a self exam."
Cohen-Rooks had early stage 1 breast cancer and had surgery with Plurad in March 2010 to remove a tumor and a lymph node. She required radiation for about six weeks.
"I felt I got off easy compared to others in (my) support group meetings," she said. "If my general practitioner wasn't on top of things, we wouldn't have caught it early. Thank you Dr. Pham."
Cohen-Rooks is now a big advocate with coworkers, friends and family about getting their mammograms done on time.
Plurad said word of mouth is great but having general practitioners who are well informed is also key.
"General practitioners know about the breast center and I think they feel better knowing we're there so they can get information and ask questions for their patients," she said.
Through the breast center, each patient has a specialized nurse in breast cancer guiding them through their individual breast cancer journey. Patients have access to social workers specializing in breast cancer care and a monthly support group for breast cancer patients is offered on site.
KPBP Medical Center held its fifth annual "Celebrate Life" Breast Cancer Survivor's Luncheon featuring Jovana Lara, ABC7 Eyewitness News co-anchor, as emcee, and several cancer survivors.
KPBP also held a special tree planting ceremony at the medical center campus on Oct. 2 to commemorate breast cancer survivors. Participants at the Breast Cancer Survivor's luncheon placed their names on a ribbon to be hung on the tree.
"I'm always impressed with (survivor groups), they continue to exercise and be physical," said Plurad. "You see people persevering."
For more information on KPBP's Breast Center, visit www.kp.org.
626-962-8811, ext. 2110


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If you're anything like me (which chances are you're not because I'm one in a million) you hate when people ask you, "What was the last book you read?" If I were honest, I would answer, "To Kill a Mockingbird in the seventh grade." But as that's a little too accurate to be funny, I usually just come up with one of the many titles that have made their way under my bed. I have every intention of finishing a book but I just don't think it's for me. I read the first few chapters then get bored. Maybe if we have a hurricane (here's hoping!) this year I will finally finish one.
Don't be too quick to judge my intelligence though, you bookworms. I do my fair share of reading, but in a way that's appropriate for me. Short, sweet and fabulous.
My abbreviated collection of Domino and House Beautiful
I seriously need a new camera. This is foul.
I like magazines. There's nothing better than picking up your mail and seeing a perfect bound glossy magazine just waiting to be discovered. I usually fumble all my other mail around and struggle to hold Watson's leash as I tear through the first few pages. Ah, now that's the kind of "reading" I can get on board with.
Here Lies Domino
The most fabulous publication to ever bless my life
Unfortunately the publishing world lost one of it's gems, Domino, last year due to the heartless recession. I remember where I was when I got the news. The editor sent out a painful message to their avid subscribers with the sad news that Domino would be no more. I was at work, let out one of my classic overdramatic puffs for air and had to hold back tears. Really. I wanted to cry. As I was still the "new girl" I refrained until I got home.
The more I revisit my issues of Domino the more upset I get that it's not around anymore. It really challenged me to think out of the box and design a space that reflects "me". As that never happened, you can imagine how sad I am that it's not around to give me the encouragement I so desperately seek in terms of my interior decisions.
I also discovered that it was said that Domino is for the woman who "wants to have fun on the never-ending search for items for her home." Well now I might just cry again. That's what Semi-Designed Life is all about!! I am not and will never be satisfied with the space I'm living in. I believe your space should evolve and grow as you do. You should be surrounded by things that make you happy every day. Your space should reflect you at every stage of your life. Right now, my space is screaming, "Broke 20-Something" and I love it. Well, until I get the hankering to recover a chair in a Schumacher fabric. Then I get depressed and consider mowing lawns for some extra spending money.
But anywhoozies, Domino was an amazing magazine and if you never got the pleasure of reading it, try to snag some issues off Ebay. I know I'm going to try and expand my collection that way. Let the bidding wars begin...
House Beautiful
That magazine euphoria I previously mentioned has been restored with House Beautiful. If I weren't so freakishly obsessed with Domino the past few years, House Beautiful would have made a special place in my heart a lot sooner. Offering the same kind of funky offerings Domino provided me, HB gives me that fix I so desperately crave.
They do a great job of incorporating affordable finds with the ridiculous so I don't feel so bad about myself by the time I get to the back cover. But really, HB is an incredible resource and provides amazing inspiration whether it's for arranging your artwork or bookcases or for tantalizing you with pretty dishes or linens. It's consumer friendly and is laid out in a way that allows you to "shop" through the entire magazine.
House Beautiful, please make it through the recession. I can't lose another friend.
Hello Lonny my new friend
Enter Lonny. Lonny has been up and running since October 2009. Former Domino employees and activists started this genius new platform that allows junkies (like moi) to get their fix via the web! It's a smart new solution that allows you to hover over and click on anything that catches your fancy and it takes you immediately to a link where you can purchase that sparkly something. Now THAT is consumer friendly! Or consumer dangerous. Pick your poison.
And finally, that familiar Domino je ne sais quoi is back. The quirky is here to stay and nothing tickles me more. I finally have something that makes me question the "me-ness" of my living space! So glad something has me doubting myself again.
I urge all of you to go out and pick up one of my favorite "books" and try to discover what your space says about you. And next time someone asks me, "What was the last book you read?" I will proudly answer, "DOMINO AND HOUSE BEAUTIFUL AND LONNY. WHAT OF IT?!?"


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Guys. I'm gonna be straight with you. Invincible is, hands down, the best superhero comic book I have ever read. Ever. Now that I have that out of the way....I have never really been able to read many comics. I don't have a comics shop anywhere around me, and no bookstore near me even sold the things. So as much as I love comic books, me buying one was few and far between. Then I got an iPad. And then, I learned of these little things called apps. And then I learned of these apps that allowed you to read comics. So obviously I get the Marvel and DC apps so I can read my Batman and Deadpool which I have actually been keeping up with (Sidenote: The runs of those comics that are going on now are probably the best iterations of the heroes I have personally ever read. Snyder does Batman like no one else and Gerry Dugan and Brian Posehn treat Deadpool like their horiffically deformed and twisted baby and holy crap it's so good.....okay moving on). So I've been able to get a good bit of comic reading done on the ole iPad and it's been amazing. Then, I found more comic apps. The first was IDW, not much interested me there, except for a little comic called Locke and Key by Joe Hill, Stephen Kings son. As an avid reader of Mr. King I obviously had to pick it up. I read the entire series in two weeks. Thank goodness the volumes were relatively cheap. It was only about thirty-six issues though so no big deal. Anyway, I finally found the Image comics app. And as I scrolled through the app looking at prospective comics I come across a comic called Invincible, and didn't even take a second to look at it, I scrolled right passed it! Oh how dumb I was, didn't even give it a second though for MONTHS. Then one day at work I was listening to the GameOverGreggy show, and Nick and Greg I believe start talking about Invincible and how Nick just picked it up and couldn't stop reading it. Now I'm not saying that I do everything the GameOverGreggy guys tell me to do, but Nick and Greg both said how anyone listening needed to pick up Invincible as soon as they could, so I obviously bought it on my lunch break. I read volume one right then and there, all of it. Then I bought volume two. I read that in one sitting when I got home. Eight comics down, hundred something to go. My new obsession was found.
Invincible is a comic written by Robert Kirkman, best known for his Walking Dead series. Kirkman along with his friend and artist Cory Walker decided way back when to create their own version of a superhero tale. And this being Kirkman, it was obviously an incredibly twisted and emotion one. Invincible is a story about Mark Grayson, a normal teenager who has no idea what incredible gift and/or curse he is about to recieve....PSYCHE! Mark totally knows that he would soon be getting super powers! Why? Because his dad, Nolan Grayson, is the most powerful superhero on earth Omni-Man. And Mark has known that he has the possibility to gain powers since he was seven. Nolan is actually an alien from a planet called Viltrum, and is actually sent to Earth to be it's protector by his planet's government....sort of. I'm not going to ruin anything here but you really need to pick up the first few volumes to get the whole story. Anyway, Mark is working one day when his powers finally kick in. And after weeks of trying to control his powers, Invincible is born. As I read the first volume of Invincible which I believe had comics 1-6 in it, I couldn't help but feel disappointed. It seemed like a generic superhero story. Kid gets superpowers in a world where superpowers are a common thing. He joins a small team of teen heroes and fights a bunch of bad guys with nothing but his fists and cheesy banter. However then I start reading volume 2 and eventually I get to Issue 7. This is where things start to get a little twisted. You see we finally meet the big bad superhero team the Guardians of the Globe. And not to ruin anything but something really out of the ordinary happens. And then we forget about this for the next 5 issues. Volume 3 is where everything changes. And I do mean everything. Marks life starts to spiral out of control. And it's really hard for me not to spoil anything but it gets good guys, it gets really good. I started this series about two weeks ago and I am on Issue 25 and have invested at least fifty dollars into getting the comics. I have literally forgone food in order to afford another volume one time! It's that good.
Invincible is from the twisted mind of Robert Kirkman. That alone should make you want to buy it. The beautiful and downright disturbing artwork from Cory Walker and later Ryan Ottley is the icing on the cake. There are characters that are very easy to love, and some that are even easier to hate. Mark Grayson's tale is so awesome that I have tried for the past five minutes to use every possible adjective I can to describe it and it looks like garbage. Pick this one up guys. Seriously, it's worth it. Now if you'll excuse me I have more Invincible to read/