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Essential
Hypertension
Raheef Alatassi
4th year medical student
Internal medicine
Objectives
 Definition & classifications
 Prevention & detection & importance
 Causes
 HTN in pregnancy
 Management
 Goals of treatment
 Classes of drugs & side effects
 Specific management in e.g. IHD,DM
 HTN emergency & urgency with
management
Definition
&
classifications
Definition of essential
hypertension
Essential, primary, or idiopathic hypertension
is defined as high BP in which secondary
causes such as Reno vascular disease, renal
failure, aldosteronism, or other causes of
secondary hypertension or mendelian forms
(monogenic) are not present.
 Essential hypertension accounts for 95% of all
cases of hypertension.
 Essential hypertension is a heterogeneous
disorder, with different patients having
different causal factors that lead to high BP.
 Essential hypertension needs to be separated
into various syndromes because the causes of
high BP in most patients presently classified as
having essential hypertension can be
recognized.
Detection
Hypertension is diagnosed when
 systolic blood pressure is consistently equal to or
more than 140 mm Hg,
 or diastolic blood pressure is equal to or more than
90 mm Hg;
a single elevated blood pressure reading is not
sufficient to establish the diagnosis of hypertension.
Detection
Detection
 Blood pressure should be measured with a well-
calibrated sphygmomanometer.
 The bladder length within the cuff should encircle
at least 80% of the arm circumference.
 Readings should be taken after the patient has
been resting comfortably, back supported in the
sitting or supine position, for at least 5 minutes and
at least 30 minutes after smoking or coffee
ingestion.
classification
Importance
 Sixty-six million Americans have elevated
blood pressure.
 The prevalence of hypertension increases
with age and is more common in blacks
than in whites.
 Cardiovascular morbidity and mortality
increase as both systolic and diastolic
blood pressures rise.
Importance
Prevention
-1 Maintaining a healthy diet
a. Reduction of dietery sodium (salt) intake.
b. Minimizing saturated fat and cholestrol
intake
c. Including fresh fruits and vegetables in
every day meals.
Prevention
-2 Maintaing a healthy weight.
Being overweight can raise BP and losing
weight can lower BP.
Prevention
-3 Physical activity.
An average of 2 hours and 30 minutes of
moderate-intensity exercise weekly is ideal
for preventing hypertension.
Prevention
-4 Cessation of smoking
Smoking decreases the elasticity of the
blood vessels and increase blood vessel
resistance which causes hypertension.
Prevention
-5 Limitation of alcohol intake .
Heavy drinkers who cut back to moderate
drinking can lower their systolic blood
pressure by 2 to 4 (mm Hg) and their
diastolic blood pressure (by 1 to 2( mm Hg.
Causes of
primary &
secondary
hypertension
PRIMARY (ESSENTIAL) HYPERTENSION
 95% of the cases
The cause is unknown
 Between the age of (25 – 50)
Precipitating Factors
Genetic factors
Obesity
Alcohol
Salt
Smoking
Low K intake
Sympathetic overactivity
Insulin resistance
NSAIDs
Polycythemia
SECONDARY ( IDENTIFIABLE )
HYPERTENSION
 5% of the cases
 The cause of hypertension can be
discovered
 Common in ages ( below 20 or after
50 )
Causes of
SECONDARY ( IDENTIFIABLE ) HYPERTENSION
SECONDARY
HTN
Endocrine
disease
Renal
disease
Drugs
Hypertension
and
pregnancy
Its classified into 4 categories:
1. Chronic hypertension.
2. Gestational hypertension.
3. Preeclampsia.
4. Preeclampsia superimposed on chronic
hypertension.
1)Chronic hypertension
Blood pressure is defined as BP exceeding 140/90
mm Hg before pregnancy or before 20 week’s
gestation.
 When hypertension is first identified during
pregnancy and she is at less than 20 weeks gestation,
blood pressure evaluation usually represent chronic
hypertension.
2)Gestational hypertension:
 Refers to hypertension onset in the latter part of
pregnancy >20 weeks without any other features of
preeclampsia and normalization of the BP
postpartum .
 Pathophysiology is still unknown.
 Maternal and fetal outcome are usually normal.
Gestational hypertension can
develop either of on of these four :
Preeclampsia (gestation
hypertension + protein urea)
Acute fatty liver of pregnancy.
HELLP syndrome (hemolysis +
elevated liver enzymes + low
platelets )
eclampsia (gestation
hypertension + protein urea +
tonic-colonic seizure )
3) preeclampsia
 Preeclampsia is a disorder of widespread
vascular endothelial malfunction and
vasospasm that occurs after 20 weeks'
gestation and can present as late as 4-6
weeks’ postpartum. It is clinically defined
by hypertension and proteinuria, with or
without pathologic edema
Risk factors
 Maternal RF
1. Women first pregnancy
(primigravida)
2. Age younger than 18 or
above 35
3. History of preeclampsia
4. Family history
5. Obesity
 Maternal medical RF
1. Chronic hypertension
especially when its 2ndary
(hyperaldostronisim ,
hypercortisolism)
2. Preexisting diabetes (I or II)
3. History of migraine
4. Use of SSRI beyond 1st
trimester.
Symptoms of preeclampsia
1. Visual disturbance.
2. Headache (women describe it as throbbing)
3. Epigastric pain or RUQ (due to hepatic swelling ).
4. Retinal vasospasm (if severe)
5. Hyperactive reflexes (severe stage)
6. On auscultation the presence of S4 suggests LV
Hypertrophy or diastolic dysfunction.
New seizures in pregnancy suggest preeclampsia-
eclampsia .
Management
Management
 Current control rates (SBP <140 mmHg
and DBP <90 mmHg).
 In the majority of patients, reducing SBP
has been considerably more difficult than
lowering DBP.
 the majority will require two or more
antihypertensive drugs
Goals of treatment
 reduce cardiovascular and renal
morbidity and mortality.
 Treating SBP and DBP to targets that are
<140/90 mmHg is associated with a
decrease in CVD complications.
 In patients with hypertension and
diabetes or renal disease, the BP goal is
<130/80 mmHg
Management of HTN
 Adoption of healthy lifestyles by all
persons is critical for the prevention of
high BP.
 Two types of management:
1) Lifestyle modification.
2) Pharmacologic Treatment.
Lifestyle modification
NO Modification Approximate SBP
Reduction
(Range)
1 Weight reduction 5–20 mmHg
2 Adopt DASH eating plan 8–14 mmHg
3 Dietary sodium reduction 2–8 mmHg
4 Physical activity 4–9 mmHg
Classes of drugs
& side effects
Classes of drugs & side effects
 More than 2/3 of hypertensive individuals
cannot be controlled on one drug and
will require two or more antihypertensive
agents selected from different drug
classes.
 Mild Hypertension can be often controlled
with a single drug.
Classes of drugs & side effects
Cardiac output & peripheral resistance controlled by
two mechanism:
1) Baroreflexes.
2) Renin-angiotensin-aldosterone system.
Anti HTN
Diuretics
ACE I
ARBS
Ca Channel
Blockers
Beta
blockers
Alpha
blockers
Diuretics
 tx: mild to moderate HTN
 First drug of treatment
 Also tx. heart failure or kidney disease
 Used with other antihypertensives to
enhance effectiveness
 Reduce edema assos. with CHF
Diuretics Actions
Diuretics
Action
 Reduce blood volume
through urinary excretion of
water and electrolytes
 Electrolyte imbalances
can occur (mainly
hypokalemia)
 Also, Hyperglycemia,
Hyperuricemia,HyperCa
Side effects
 Orthostatic hypotension
 Dry mouth,irritation
 Disorientation
 Dehydration
HyperK: with K sparing
Gynecomastia
Angiotensin-Converting
Enzyme Inhibitors
 “ACE” inhibitors
 Mainstay of oral vasodilator therapy
 More effective when used with diuretics
 First line of therapy if the Diuretics or betaB
are contraindicated.
ACE INHIBITORS
ACE INHIBITORS
Angiotensin
Converting
Enzyme (ends in PRIL)
captopril enalapril benzapril
(Capoten) (Vasotec) (Lotensin)
ACE INHIBITORS
ACTION
 peripheral vascular resistanse without
Ø cardiac output
Ø cardiac rate
Ø cardiac contractility
Side effects
 Headache
 Orthostatic hypotension-infrequent
 dry Cough
 Hyperkalemia
 AKF
 Skin rash
Are fetotoxic & should not be used in pregnancy.
Drug interactions
 Diuretics specially K sparing
 Alcohol
 Beta-blockers
 All the above enhance the effects
 It’s standerd in the care of patient
following a myocardial infarction
Angiotensin 2 Receptor
antagonists
 Alternative of ACE I .
 Same effect to ACE I .
 Produce arteriole and venous dilatation .
 Inhibit aldosterone secretion.
ARBS
Don’t increase Bradykinin levels.
Decrease Nephrotoxixty of
Diabetes.
Decrease Dry cough
Don’t use it in pregnancy
Calcium Channel Blockers
 Emerged as major drug to tx. HTN when the
preferred first line are contraindicated.
 Used for arrythmias also
 Alternative to B-blocker (hx. Asthma)
 Avoid High dose of SA. CCB because of inc.
risk of Myocardial infarction.
Calcium Channel Blockers
Examples
 Verapamil Very
 Procardia (nifedipine)-HTN Nice
 Cardizem (diltiazem)-arrythmias Drugs
Calcium Channel Blockers
Calcium Channel Blockers
Action
blocks ca+ access to muscle cells
contractility +
conductivity of the
______________________
demand for oxygen
PVR (relaxing arterioles)
Calcium Channel Blockers
SIDE EFFECTS
 BP
 Bradycardia
 vertigo
 Headache
 constipation
 Peripheral edema
 A-V block (due to –ve Inotopic&
dromotropic)
Adrenergic Receptors
Review of ANS
 Sympathetic Nervous System
 Alpha 1 = vasoconstriction
 Alpha 2 = vasodilation
 Beta 1 = increases heart rate
 Beta 2 = bronchodilation
Beta Adrenergic Blocking
Agents
 Known as Beta-blockers
 Axn: Inhibit cardiac response to
sympathetic nerve stimulation by
blocking Beta receptors
 Decreases heart rate and C.O.
 Decreases blood pressure
 First line of therapy in HF
Beta Adrenergic Blocking
Agents
Examples – “olol” names
 Beta 1: Atenolol & Metoprolol
 Beta 1 and 2: Propranolol
Implications
 Can not be abruptly discontinued
 Check baseline b.p.
 Check hx. of resp. condition-aggravates
bronchoconstriction
Side effects
 Bradycardia
 Bronchospasm, wheezing
 Diabetic: hypoglycemia
 Insomnia
 Sexual Dysfunction
Alpha-1 adrenergic
blockers
 Alternative if B-blockers and diuretics do
not work
 Also used to tx. mild to mod. urinary
obstructive dx.
 Also used for treat of benign prostate
hyperplasia
Alpha-1 Adrenergic Blocking
Agents
Action
 Block postsynaptic alpha-1 adrenergic
receptors to produce arteriolar and
venous vasodilation
 Reduces peripheral-vascular resistance
Examples of Apha-1 blockers
 Cardura (doxizosin)
 Minipress (prazosin)
 Hytrin (terazosin)
Examples – “ZOSIN” names
Side effects
 Drowsiness
 Headache
 Weakness,lethargy
Centrally Acting Alpha-2
Agonists
 Stimulate Alpha-2 receptors in brainstem
 Decreases HR, SBP and DBP
 More frequent side effects – drowsiness,
dry mouth, dizziness
 Never suddenly DC = rebound HTN
 Clonidine – Catapres
 Methyldopa – (used in Pregnancy)
Direct Acting Vasodilators
 Action: direct arteriolar smooth muscle
relaxation, decreasing PVR
 Uses: HTN, renal dx.,
 Ex: Hydralazine, Minoxidel
 SE: tachycardia, orthostatic
hypotension,dizziness, palpitations,
nausea, nasal congestion
Hypertension
and ischemic
heart disease
Case study
55 year old man known case of IHD and he
now diagnosed with HT what is the drug of
choose to treat him?
 1-BB
 2-ACEI
 3-CCB
Hypertensive patients are at increased risk
for MI or other major coronary events Why?
1-increase in heart o2 demand
2- increase heart work (life ventricle
hypertrophy)
 If the patient have HT and IHD that even
increase the risk more
 Stable angina and silent ischemia
 BBs (propranolol) will lower BP; reduce
symptoms of angina; improve mortality; and
reduce cardiac output heart rate, and AV
conduction
 Treatment should also include smoking
cessation, management of diabetes, lipid
lowering, antiplatelet agents, exercise training
and weight reduction in obese patients.
 If angina and BP are not controlled by BB
therapy alone, or if BBs are contraindicated,
as in the presence of severe reactive airways
disease, severe peripheral arterial disease,
high-degree AV block,or the sick sinus
syndrome
 Use dihydropyridine or nondihydropyridine
type CCBs (amlodipine Verapamil)
 If angina or BP is still not controlled on this
two-drug regimen, nitrates can be
added, but these should be used with
caution in patients taking
phosphodiesterase-5 inhibitors such as
sildenafil. Short-acting dihydropyridine
CCBs should not be used because of their
potential to increase mortality,particularly
in the setting of acute MI.
Diabetes and HT
 The combined unadjusted prevalence of total
diabetes and impaired fasting glucose in those
over age 20 is 14.4 percent and is the leading
cause of blindness, ESRD, and nontraumatic
amputations
 The United Kingdom Prospective Diabetes Study
(UKPDS)174 demonstrated that each 10 mmHg
decrease in SBP was associated with average
reductions in rates of diabetes-related mortality
(15 percent), myocardial infarction (11 percent)
 American Diabetes Association
recommended that BP in diabetics be
controlled to levels of 130/80 mmHg or lower
 ACEIs(captopril), BBs(propranolol),
ARBs(valsartan), and calcium
antagonists(Verapamil) have a demonstrated
benefit in the treatment of hypertension in
both type 1 and type 2 diabetics
 The question of which class of agent is
superior for lowering BP is somewhat moot
because the majority of diabetic patients
will require two or more drugs to achieve
BP control
 The ADA has recommended ACEIs for diabetic
patients older than 55 years of age at high risk for
CVD, and BBs for those with known CAD
 showed a reduction in combined MI, stroke, and
CVD death of about 25 percent and a reduction
in stroke by about 33
 the ADA has recommended both ACEIs and
ARBs for use in type 2 diabetic patients with CKD
 BB is indicated in a diabetic with IHD but may be
less effective in preventing stroke than an ARB as
was found in the LIFE study
 CCBs may be useful to diabetics, particularly as
part of combination therapy to control BP
 The Appropriate Blood Pressure Control in
Diabetes (ABCD) Trial in diabetics was stopped
prematurely when it was found that the
dihydropyridine nitrendipine was inferior to lisinopril
in reducing the incidence of ischemic cardiac
events.
Hypertensive emergencies
 Hypertensive emergencies are characterized by
severe elevations in BP (>180/120 mmHg)
complicated by evidence of impending or
progressive target organ dysfunction
 Patients with hypertensive emergencies should be
admitted to an intensive care unit for continuous
monitoring of BP and parenteral administration of
an appropriate agent
 The initial goal of therapy reduce mean
arterial BP by no more than 25 percent
(within minutes to 1 hour)
 then if stable, to 160/100–110 mmHg
within the next 2–6 hours
 Excessive falls in pressure that may
precipitate renal, cerebral, or coronary
ischemia should be avoided. For this
reason, short-acting nifedipine is no longer
considered acceptable
 further gradual reductions toward a
normal BP can be implemented in the
next 24–48 hours
References
Essential Hypertension
Essential Hypertension

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Essential Hypertension

  • 1. Essential Hypertension Raheef Alatassi 4th year medical student Internal medicine
  • 2. Objectives  Definition & classifications  Prevention & detection & importance  Causes  HTN in pregnancy  Management  Goals of treatment  Classes of drugs & side effects  Specific management in e.g. IHD,DM  HTN emergency & urgency with management
  • 4. Definition of essential hypertension Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as Reno vascular disease, renal failure, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not present.
  • 5.  Essential hypertension accounts for 95% of all cases of hypertension.  Essential hypertension is a heterogeneous disorder, with different patients having different causal factors that lead to high BP.  Essential hypertension needs to be separated into various syndromes because the causes of high BP in most patients presently classified as having essential hypertension can be recognized.
  • 6. Detection Hypertension is diagnosed when  systolic blood pressure is consistently equal to or more than 140 mm Hg,  or diastolic blood pressure is equal to or more than 90 mm Hg; a single elevated blood pressure reading is not sufficient to establish the diagnosis of hypertension.
  • 8. Detection  Blood pressure should be measured with a well- calibrated sphygmomanometer.  The bladder length within the cuff should encircle at least 80% of the arm circumference.  Readings should be taken after the patient has been resting comfortably, back supported in the sitting or supine position, for at least 5 minutes and at least 30 minutes after smoking or coffee ingestion.
  • 10. Importance  Sixty-six million Americans have elevated blood pressure.  The prevalence of hypertension increases with age and is more common in blacks than in whites.  Cardiovascular morbidity and mortality increase as both systolic and diastolic blood pressures rise.
  • 12. Prevention -1 Maintaining a healthy diet a. Reduction of dietery sodium (salt) intake. b. Minimizing saturated fat and cholestrol intake c. Including fresh fruits and vegetables in every day meals.
  • 13. Prevention -2 Maintaing a healthy weight. Being overweight can raise BP and losing weight can lower BP.
  • 14. Prevention -3 Physical activity. An average of 2 hours and 30 minutes of moderate-intensity exercise weekly is ideal for preventing hypertension.
  • 15. Prevention -4 Cessation of smoking Smoking decreases the elasticity of the blood vessels and increase blood vessel resistance which causes hypertension.
  • 16. Prevention -5 Limitation of alcohol intake . Heavy drinkers who cut back to moderate drinking can lower their systolic blood pressure by 2 to 4 (mm Hg) and their diastolic blood pressure (by 1 to 2( mm Hg.
  • 18. PRIMARY (ESSENTIAL) HYPERTENSION  95% of the cases The cause is unknown  Between the age of (25 – 50)
  • 19. Precipitating Factors Genetic factors Obesity Alcohol Salt Smoking Low K intake Sympathetic overactivity Insulin resistance NSAIDs Polycythemia
  • 20. SECONDARY ( IDENTIFIABLE ) HYPERTENSION  5% of the cases  The cause of hypertension can be discovered  Common in ages ( below 20 or after 50 )
  • 21. Causes of SECONDARY ( IDENTIFIABLE ) HYPERTENSION SECONDARY HTN Endocrine disease Renal disease Drugs
  • 23. Its classified into 4 categories: 1. Chronic hypertension. 2. Gestational hypertension. 3. Preeclampsia. 4. Preeclampsia superimposed on chronic hypertension.
  • 24. 1)Chronic hypertension Blood pressure is defined as BP exceeding 140/90 mm Hg before pregnancy or before 20 week’s gestation.  When hypertension is first identified during pregnancy and she is at less than 20 weeks gestation, blood pressure evaluation usually represent chronic hypertension.
  • 25. 2)Gestational hypertension:  Refers to hypertension onset in the latter part of pregnancy >20 weeks without any other features of preeclampsia and normalization of the BP postpartum .  Pathophysiology is still unknown.  Maternal and fetal outcome are usually normal.
  • 26. Gestational hypertension can develop either of on of these four : Preeclampsia (gestation hypertension + protein urea) Acute fatty liver of pregnancy. HELLP syndrome (hemolysis + elevated liver enzymes + low platelets ) eclampsia (gestation hypertension + protein urea + tonic-colonic seizure )
  • 27. 3) preeclampsia  Preeclampsia is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 weeks' gestation and can present as late as 4-6 weeks’ postpartum. It is clinically defined by hypertension and proteinuria, with or without pathologic edema
  • 28. Risk factors  Maternal RF 1. Women first pregnancy (primigravida) 2. Age younger than 18 or above 35 3. History of preeclampsia 4. Family history 5. Obesity  Maternal medical RF 1. Chronic hypertension especially when its 2ndary (hyperaldostronisim , hypercortisolism) 2. Preexisting diabetes (I or II) 3. History of migraine 4. Use of SSRI beyond 1st trimester.
  • 29. Symptoms of preeclampsia 1. Visual disturbance. 2. Headache (women describe it as throbbing) 3. Epigastric pain or RUQ (due to hepatic swelling ). 4. Retinal vasospasm (if severe) 5. Hyperactive reflexes (severe stage) 6. On auscultation the presence of S4 suggests LV Hypertrophy or diastolic dysfunction. New seizures in pregnancy suggest preeclampsia- eclampsia .
  • 31. Management  Current control rates (SBP <140 mmHg and DBP <90 mmHg).  In the majority of patients, reducing SBP has been considerably more difficult than lowering DBP.  the majority will require two or more antihypertensive drugs
  • 32. Goals of treatment  reduce cardiovascular and renal morbidity and mortality.  Treating SBP and DBP to targets that are <140/90 mmHg is associated with a decrease in CVD complications.  In patients with hypertension and diabetes or renal disease, the BP goal is <130/80 mmHg
  • 33. Management of HTN  Adoption of healthy lifestyles by all persons is critical for the prevention of high BP.  Two types of management: 1) Lifestyle modification. 2) Pharmacologic Treatment.
  • 34. Lifestyle modification NO Modification Approximate SBP Reduction (Range) 1 Weight reduction 5–20 mmHg 2 Adopt DASH eating plan 8–14 mmHg 3 Dietary sodium reduction 2–8 mmHg 4 Physical activity 4–9 mmHg
  • 35. Classes of drugs & side effects
  • 36. Classes of drugs & side effects  More than 2/3 of hypertensive individuals cannot be controlled on one drug and will require two or more antihypertensive agents selected from different drug classes.  Mild Hypertension can be often controlled with a single drug.
  • 37. Classes of drugs & side effects Cardiac output & peripheral resistance controlled by two mechanism: 1) Baroreflexes. 2) Renin-angiotensin-aldosterone system.
  • 38.
  • 39. Anti HTN Diuretics ACE I ARBS Ca Channel Blockers Beta blockers Alpha blockers
  • 40. Diuretics  tx: mild to moderate HTN  First drug of treatment  Also tx. heart failure or kidney disease  Used with other antihypertensives to enhance effectiveness  Reduce edema assos. with CHF
  • 41.
  • 43. Diuretics Action  Reduce blood volume through urinary excretion of water and electrolytes  Electrolyte imbalances can occur (mainly hypokalemia)  Also, Hyperglycemia, Hyperuricemia,HyperCa
  • 44. Side effects  Orthostatic hypotension  Dry mouth,irritation  Disorientation  Dehydration HyperK: with K sparing Gynecomastia
  • 45. Angiotensin-Converting Enzyme Inhibitors  “ACE” inhibitors  Mainstay of oral vasodilator therapy  More effective when used with diuretics  First line of therapy if the Diuretics or betaB are contraindicated.
  • 47. ACE INHIBITORS Angiotensin Converting Enzyme (ends in PRIL) captopril enalapril benzapril (Capoten) (Vasotec) (Lotensin)
  • 48. ACE INHIBITORS ACTION  peripheral vascular resistanse without Ø cardiac output Ø cardiac rate Ø cardiac contractility
  • 49. Side effects  Headache  Orthostatic hypotension-infrequent  dry Cough  Hyperkalemia  AKF  Skin rash Are fetotoxic & should not be used in pregnancy.
  • 50. Drug interactions  Diuretics specially K sparing  Alcohol  Beta-blockers  All the above enhance the effects  It’s standerd in the care of patient following a myocardial infarction
  • 51. Angiotensin 2 Receptor antagonists  Alternative of ACE I .  Same effect to ACE I .  Produce arteriole and venous dilatation .  Inhibit aldosterone secretion.
  • 52. ARBS Don’t increase Bradykinin levels. Decrease Nephrotoxixty of Diabetes. Decrease Dry cough Don’t use it in pregnancy
  • 53. Calcium Channel Blockers  Emerged as major drug to tx. HTN when the preferred first line are contraindicated.  Used for arrythmias also  Alternative to B-blocker (hx. Asthma)  Avoid High dose of SA. CCB because of inc. risk of Myocardial infarction.
  • 54. Calcium Channel Blockers Examples  Verapamil Very  Procardia (nifedipine)-HTN Nice  Cardizem (diltiazem)-arrythmias Drugs
  • 56. Calcium Channel Blockers Action blocks ca+ access to muscle cells contractility + conductivity of the ______________________ demand for oxygen PVR (relaxing arterioles)
  • 57. Calcium Channel Blockers SIDE EFFECTS  BP  Bradycardia  vertigo  Headache  constipation  Peripheral edema  A-V block (due to –ve Inotopic& dromotropic)
  • 58. Adrenergic Receptors Review of ANS  Sympathetic Nervous System  Alpha 1 = vasoconstriction  Alpha 2 = vasodilation  Beta 1 = increases heart rate  Beta 2 = bronchodilation
  • 59. Beta Adrenergic Blocking Agents  Known as Beta-blockers  Axn: Inhibit cardiac response to sympathetic nerve stimulation by blocking Beta receptors  Decreases heart rate and C.O.  Decreases blood pressure  First line of therapy in HF
  • 60. Beta Adrenergic Blocking Agents Examples – “olol” names  Beta 1: Atenolol & Metoprolol  Beta 1 and 2: Propranolol
  • 61. Implications  Can not be abruptly discontinued  Check baseline b.p.  Check hx. of resp. condition-aggravates bronchoconstriction
  • 62. Side effects  Bradycardia  Bronchospasm, wheezing  Diabetic: hypoglycemia  Insomnia  Sexual Dysfunction
  • 63. Alpha-1 adrenergic blockers  Alternative if B-blockers and diuretics do not work  Also used to tx. mild to mod. urinary obstructive dx.  Also used for treat of benign prostate hyperplasia
  • 64. Alpha-1 Adrenergic Blocking Agents Action  Block postsynaptic alpha-1 adrenergic receptors to produce arteriolar and venous vasodilation  Reduces peripheral-vascular resistance
  • 65. Examples of Apha-1 blockers  Cardura (doxizosin)  Minipress (prazosin)  Hytrin (terazosin) Examples – “ZOSIN” names
  • 66. Side effects  Drowsiness  Headache  Weakness,lethargy
  • 67. Centrally Acting Alpha-2 Agonists  Stimulate Alpha-2 receptors in brainstem  Decreases HR, SBP and DBP  More frequent side effects – drowsiness, dry mouth, dizziness  Never suddenly DC = rebound HTN  Clonidine – Catapres  Methyldopa – (used in Pregnancy)
  • 68. Direct Acting Vasodilators  Action: direct arteriolar smooth muscle relaxation, decreasing PVR  Uses: HTN, renal dx.,  Ex: Hydralazine, Minoxidel  SE: tachycardia, orthostatic hypotension,dizziness, palpitations, nausea, nasal congestion
  • 70. Case study 55 year old man known case of IHD and he now diagnosed with HT what is the drug of choose to treat him?  1-BB  2-ACEI  3-CCB
  • 71. Hypertensive patients are at increased risk for MI or other major coronary events Why? 1-increase in heart o2 demand 2- increase heart work (life ventricle hypertrophy)  If the patient have HT and IHD that even increase the risk more
  • 72.  Stable angina and silent ischemia  BBs (propranolol) will lower BP; reduce symptoms of angina; improve mortality; and reduce cardiac output heart rate, and AV conduction  Treatment should also include smoking cessation, management of diabetes, lipid lowering, antiplatelet agents, exercise training and weight reduction in obese patients.
  • 73.  If angina and BP are not controlled by BB therapy alone, or if BBs are contraindicated, as in the presence of severe reactive airways disease, severe peripheral arterial disease, high-degree AV block,or the sick sinus syndrome  Use dihydropyridine or nondihydropyridine type CCBs (amlodipine Verapamil)
  • 74.  If angina or BP is still not controlled on this two-drug regimen, nitrates can be added, but these should be used with caution in patients taking phosphodiesterase-5 inhibitors such as sildenafil. Short-acting dihydropyridine CCBs should not be used because of their potential to increase mortality,particularly in the setting of acute MI.
  • 75. Diabetes and HT  The combined unadjusted prevalence of total diabetes and impaired fasting glucose in those over age 20 is 14.4 percent and is the leading cause of blindness, ESRD, and nontraumatic amputations  The United Kingdom Prospective Diabetes Study (UKPDS)174 demonstrated that each 10 mmHg decrease in SBP was associated with average reductions in rates of diabetes-related mortality (15 percent), myocardial infarction (11 percent)
  • 76.  American Diabetes Association recommended that BP in diabetics be controlled to levels of 130/80 mmHg or lower  ACEIs(captopril), BBs(propranolol), ARBs(valsartan), and calcium antagonists(Verapamil) have a demonstrated benefit in the treatment of hypertension in both type 1 and type 2 diabetics
  • 77.  The question of which class of agent is superior for lowering BP is somewhat moot because the majority of diabetic patients will require two or more drugs to achieve BP control
  • 78.  The ADA has recommended ACEIs for diabetic patients older than 55 years of age at high risk for CVD, and BBs for those with known CAD  showed a reduction in combined MI, stroke, and CVD death of about 25 percent and a reduction in stroke by about 33  the ADA has recommended both ACEIs and ARBs for use in type 2 diabetic patients with CKD
  • 79.  BB is indicated in a diabetic with IHD but may be less effective in preventing stroke than an ARB as was found in the LIFE study  CCBs may be useful to diabetics, particularly as part of combination therapy to control BP  The Appropriate Blood Pressure Control in Diabetes (ABCD) Trial in diabetics was stopped prematurely when it was found that the dihydropyridine nitrendipine was inferior to lisinopril in reducing the incidence of ischemic cardiac events.
  • 80. Hypertensive emergencies  Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction  Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of BP and parenteral administration of an appropriate agent
  • 81.
  • 82.
  • 83.  The initial goal of therapy reduce mean arterial BP by no more than 25 percent (within minutes to 1 hour)  then if stable, to 160/100–110 mmHg within the next 2–6 hours
  • 84.  Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable  further gradual reductions toward a normal BP can be implemented in the next 24–48 hours

Hinweis der Redaktion

  1. Unknown before the age of 20
  2. renal diseases : renovascular disease glomerulonephritis Polycystic kidney disease Endocrine disease : Endocrine disease Pheochromocytoma Cushing syndrome Primary aldosteronism ( conn's syndrome ) Hyperparathyroidism Primary hypothyroidism Thyrotoxicosis Acromegaly …etc Drugs : oral contraceptive containing estrogen NSAIDs Corticosteroids …etc
  3. Weight reduction : (body mass index 18.5–24.9 kg/m2). Adopt Dietary Approaches to Stop Hypertensioneating plan : Consume a diet rich in fruits, vegetables, and lowfat dairy products with a reduced content of saturated and total fat. Dietary sodium reduction : reduce it to more than 100 mmol per day Physical activity : brisk walking (at least 30 min per day, most days of the week). Smoking and alchol.
  4. Factors influence HTN
  5. Myocardial infarction due to excessive vasodiltaion.
  6. nonDih: heart / Verapamil & Diltizam (used in angina ) Dih: Vessels : vascular smooth muscle to relax.
  7. Inotopic: contractility Dromotopic: conductivity
  8. Hydralazine (cause lupus like syndrome) Minoxidel ( treat baldness)