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Dr. Haji Bahadar
Assistant Professor
Khyber Medical University-IPMS
Major diseases
 Hypertension
 Coronary heart disease
 Congestive heart failure/Heart failure
 Angina
 Heart Attack
Anti-hypertensive drugs
Blood pressure is the force exerted by blood against the
walls blood vessels.
Factors that determine the blood pressure:
1- Cardiac output (CO): Cardiac output is the volume of
blood the heart pumps per minute
2- Total peripheral resistance (PR).
3- Elasticity of the aorta and large arteries.
4- Blood volume and circulatory capacity.
BP = CO X PR
 What is afterload: Afterload is the
pressure against which the heart
works to eject blood during systole.
 What is preload: ??
Hypertension is defined as having a blood pressure higher than 140/ 90
mmHg
 Baroreceptors are pressure sensors. Their function
is to sense pressure changes.
 Baroreflex or baroreceptor reflex is a homeostatic
mechanisms that helps to maintain blood pressure at
nearly normal level.
 .
The renin-angiotensin system (RAS) plays an integral role in blood pressure
regulation
 1. Beta adrenergic blockers
 2. Diuretics
 3. Calcium channel blockers
 4. Angiotensin converting enzyme inhibitors
 5. Angiotensin receptor blockers
 7. Direct arterial vasodilators (self study)
 8. Drug used in hypertensive emergency
 Beta-blockers are drugs that bind to beta- receptors.
 These drugs block the binding of norepinephrine and
epinephrine to these receptors.
 Beta-blockers are sympatholytic drugs.
 β1-receptors are located commonly in the heart and
kidneys.
 β2- receptors are located mainly in the lungs,
gastrointestinal tract, liver, uterus, vascular smooth
muscle, and skeletal muscle.
 β3- adrenergic receptors are located in fat cells.
 Hypertension is associated with an increase
cardiac output. Beta-blockers decrease blood
pressure by reducing cardiac output.
• Hypertension in some patients is caused by
emotional stress, which causes enhanced
sympathetic activity. Beta-blockers can be very
effective in these patients.
↓ HR, ↓ Force of contraction, ↓ Cardiac Output
↓ β 1 mediated renin release from kidney
↓ sympathetic outflow
ISA:
selective (β1):
 Metoprolol
 Acebutolol
 Esmolol
 Atenolol
 Bisoprolol
 Betaxolol
 Non selective (β1 & β2):
Without ISA
 Propronolol,
 Sotalol ,
 Timolol
With ISA: Pindolol
With additional α
blocking property:
Labetolol
Carvedilol
 Bradycardia
 Hypotension
 atrioventicular (AV) nodal conduction
block. Beta-blockers are therefore
contraindicated in patients with sinus
bradycardia and partial AV block
 Bronchoconstriction can occur when non-selective
beta-blockers are given to asthmatic patients.
Therefore, non-selective beta-blockers are
contraindicated in patients with asthma or chronic
obstructive pulmonary disease.
 Bronchoconstriction occurs because sympathetic
nerves innervating the bronchioles normally activate
β2-adrenoceptors that promote bronchodilation.
 Beta-blockers can also mask the tachycardia that
serves as a warning sign for insulin-induced
hypoglycemia in diabetic patients; therefore, beta-
blockers should be used cautiously in diabetics.
 Heart: Blockade of beta1-receptors in the sino-
atrial node reduces heart rate (negative
chronotropic effect) and blockade of beta1-
receptors in the myocardium decrease cardiac
contractility (negative inotropic effect).
Cardiac Effects of beta blockers
Decrease contractility
(negative intropy)
Decrease heart rate
(negative chronotropy)
Decrease conduction velocity
(negative dromotropy)
 Kidney: Blockade of beta1-receptors inhibit the release of renin from
juxta-glomerular cells and thereby reduce the activity of the renin-
angiotensin-aldosterone system.
 Renin is a proteolytic enzyme that is released into
the circulation by the kidneys. Its release is
stimulated by:
 sympathetic nerve activation (acting through β1-
adrenoceptors)
 renal artery hypotension (caused by systemic
hypotension or renal artery stenosis)
 decreased sodium delivery to the distal tubules of
the kidney.
 The renin-angiotensin-aldosterone system (RAAS)
regulate blood volume and systemic vascular
resistance, which together influence cardiac
output and arterial pressure.
 There are three important components to this
system: 1) renin, 2) angiotensin, and 3)
aldosterone. Renin, which is released primarily by
the kidneys, stimulates the formation of
angiotensin in blood and tissues, which in turn
stimulates the release of aldosterone from the
adrenal cortex.
Angiotensin2 functions:
 Constricts resistance vessels increasing systemic
vascular resistance and arterial pressure
 Stimulates reabsorption.
 increase the release aldosterone, which in turn acts
on the kidneys to increase sodium and fluid retention
 Stimulates the release of vasopressin (antidiuretic
hormone, ADH) from the posterior pituitary, which
increases fluid retention by the kidneys
 Stimulates thirst centers within the brain
 Enhancing sympathetic adrenergic function
 Stimulates cardiac hypertrophy and vascular
hypertrophy.
 Benazepril
 Captopril
 Enalapril
 Fosinopril
 Lisinopril
 Moexipril
 Quinapril
 Ramipril
ACE inhibitors have the following actions:
 Dilate arteries and veins by blocking angiotensin II
formation
 Down regulate sympathetic activity
 Promote renal excretion of sodium and water
(natriuretic and diuretic effects) by blocking the
effects of angiotensin II in the kidney and by
blocking angiotensin II stimulation
of aldosterone secretion. This reduces blood
volume, venous pressure and arterial pressure.
 Inhibit cardiac remodeling associated with
chronic hypertension, heart failure, and myocardial
infarction.
In cardiology, ventricular remodeling (or cardiac remodeling) refers to
changes in the size, shape, structure, and function of the heart.
Angioedema
 Hypertension
 Heart Failure
 Diabetic and Nondiabetic Nephropathy
.
 Dry cough
 First-dose hypotension (due to vasodilatation)
 Angioedema: it is a serious type of skin reaction
that affects the skin layer and also the tissues
 Increased blood-potassium level (hyperkalemia)
 Patients with bilateral renal artery stenosis may
experience renal failure if ACE inhibitors are
administered. The reason is that the elevated
circulating and intrarenal angiotensin II in this
condition constricts the efferent arteriole more
than the afferent arteriole within the kidney, which
helps to maintain glomerular capillary pressure
and filtration. Removing this constriction by
blocking circulating and intrarenal angiotensin II
formation can cause an abrupt fall in glomerular
filtration rate.
 Renal artery stenosis is a narrowing
of arteries that carry blood to one or both of the
kidneys.
 Patients with renal artery stenosis, the kidneys
release large amounts of renin.
 High angiotensin II serve to maintain glomerular
filtration by two mechanisms: elevation of blood
pressure and constriction of efferent glomerular
arterioles.
 When ACE is inhibited, causing angiotensin II
levels to fall, the mechanisms that had been
supporting glomerular filtration fail, causing urine
production to drop
 Diuretics. Diuretics may intensify first-dose
hypotension. To prevent this interaction, diuretics
should be withdrawn 1 week prior to initiating ACE
inhibitor treatment
 ACE inhibitors increase the risk of hyperkalemia
caused by potassium supplements and
potassium-sparing diuretics
 Candesartan
 Irbesartan
 Losartan
 Olmesartan
 Telmisartan
 Valsartan
 These drugs have very similar effects
to angiotensin converting enzyme (ACE)
inhibitors and are used for the same indications
(hypertension, heart failure, post- myocardial
infarction).
A diuretic is any substance that promotes diuresis
(increased production of urine).
DIURETICS
Diuretics enhance the removal of sodium and water from
body through kidneys.
Ginger. ...
Parsley. ...
Caffeine
Types of diuretics
Thiazides: Hydrochlorothiazide, Chlorthalidone, indapamide
MOA:
these drugs Inhibit sodium-chloride transporter in the
distal tubule. This transporter normally reabsorbs about
5% of filtered sodium.
Loop diuretics: Furosemide (lasix), Torsemide, Bumetanide
MOA: Loop diuretics inhibit the sodium-potassium-chloride
co-transporter in the thick ascending limb. This transporter
normally reabsorbs about 25% of the sodium load.
Potassium-sparing diuretics: spironolactone and eplerenone.
Osmotic diuretics: Mannitol
 Hypertension
 Heart failure
 Pulmonary and systemic edema
 Amlodipine (Norvasc)
 Nimodifine (Nimotop)
 Felodipine.
 Isradipine.
 Nicardipine.
 Nifedipine (Adalat CC) Extended Release Tablets
 Nisoldipine
 Verapamil
 Calcium channel blockers decrease the amount of
calcium entering cardiac and smooth muscle cells
by blocking voltage-gated calcium channels.
 This causes blood vessels to relax and widen
(vasodilate), improves oxygen supply to the heart
 Calcium-channel blockers bind to L-type calcium channels
located on the vascular smooth muscle, cardiac myocytes, and
cardiac nodal tissue (sinoatrial and atrioventricular nodes).
 These channels are responsible for regulating the influx of
calcium into muscle cells, which in turn stimulates smooth
muscle contraction and cardiac myocyte contraction.
 In cardiac nodal tissue, L-type calcium channels play an
important role in pacemaker currents.
 Therefore, by blocking calcium entry into the cell, there is,
vasodilation,
 Decreased myocardial force generation (negative inotropy),
decreased heart rate (negative chronotropy),
 Decreased conduction velocity within the heart (negative
dromotropy),
 Flushing, headache, hypotension, edema and
reflex tachycardia
 Hypertension
 Angina
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1. Anti hypertensive drugs.pptx what's hypertension

  • 1. Dr. Haji Bahadar Assistant Professor Khyber Medical University-IPMS
  • 2.
  • 3. Major diseases  Hypertension  Coronary heart disease  Congestive heart failure/Heart failure  Angina  Heart Attack
  • 5. Blood pressure is the force exerted by blood against the walls blood vessels. Factors that determine the blood pressure: 1- Cardiac output (CO): Cardiac output is the volume of blood the heart pumps per minute 2- Total peripheral resistance (PR). 3- Elasticity of the aorta and large arteries. 4- Blood volume and circulatory capacity. BP = CO X PR
  • 6.  What is afterload: Afterload is the pressure against which the heart works to eject blood during systole.  What is preload: ??
  • 7. Hypertension is defined as having a blood pressure higher than 140/ 90 mmHg
  • 8.
  • 9.
  • 10.  Baroreceptors are pressure sensors. Their function is to sense pressure changes.  Baroreflex or baroreceptor reflex is a homeostatic mechanisms that helps to maintain blood pressure at nearly normal level.
  • 11.
  • 12.
  • 13.  . The renin-angiotensin system (RAS) plays an integral role in blood pressure regulation
  • 14.  1. Beta adrenergic blockers  2. Diuretics  3. Calcium channel blockers  4. Angiotensin converting enzyme inhibitors  5. Angiotensin receptor blockers  7. Direct arterial vasodilators (self study)  8. Drug used in hypertensive emergency
  • 15.  Beta-blockers are drugs that bind to beta- receptors.  These drugs block the binding of norepinephrine and epinephrine to these receptors.  Beta-blockers are sympatholytic drugs.  β1-receptors are located commonly in the heart and kidneys.  β2- receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.  β3- adrenergic receptors are located in fat cells.
  • 16.
  • 17.  Hypertension is associated with an increase cardiac output. Beta-blockers decrease blood pressure by reducing cardiac output. • Hypertension in some patients is caused by emotional stress, which causes enhanced sympathetic activity. Beta-blockers can be very effective in these patients. ↓ HR, ↓ Force of contraction, ↓ Cardiac Output ↓ β 1 mediated renin release from kidney ↓ sympathetic outflow
  • 18. ISA: selective (β1):  Metoprolol  Acebutolol  Esmolol  Atenolol  Bisoprolol  Betaxolol  Non selective (β1 & β2): Without ISA  Propronolol,  Sotalol ,  Timolol With ISA: Pindolol With additional α blocking property: Labetolol Carvedilol
  • 19.  Bradycardia  Hypotension  atrioventicular (AV) nodal conduction block. Beta-blockers are therefore contraindicated in patients with sinus bradycardia and partial AV block
  • 20.
  • 21.  Bronchoconstriction can occur when non-selective beta-blockers are given to asthmatic patients. Therefore, non-selective beta-blockers are contraindicated in patients with asthma or chronic obstructive pulmonary disease.  Bronchoconstriction occurs because sympathetic nerves innervating the bronchioles normally activate β2-adrenoceptors that promote bronchodilation.  Beta-blockers can also mask the tachycardia that serves as a warning sign for insulin-induced hypoglycemia in diabetic patients; therefore, beta- blockers should be used cautiously in diabetics.
  • 22.
  • 23.  Heart: Blockade of beta1-receptors in the sino- atrial node reduces heart rate (negative chronotropic effect) and blockade of beta1- receptors in the myocardium decrease cardiac contractility (negative inotropic effect).
  • 24. Cardiac Effects of beta blockers Decrease contractility (negative intropy) Decrease heart rate (negative chronotropy) Decrease conduction velocity (negative dromotropy)
  • 25.
  • 26.  Kidney: Blockade of beta1-receptors inhibit the release of renin from juxta-glomerular cells and thereby reduce the activity of the renin- angiotensin-aldosterone system.
  • 27.  Renin is a proteolytic enzyme that is released into the circulation by the kidneys. Its release is stimulated by:  sympathetic nerve activation (acting through β1- adrenoceptors)  renal artery hypotension (caused by systemic hypotension or renal artery stenosis)  decreased sodium delivery to the distal tubules of the kidney.
  • 28.  The renin-angiotensin-aldosterone system (RAAS) regulate blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure.  There are three important components to this system: 1) renin, 2) angiotensin, and 3) aldosterone. Renin, which is released primarily by the kidneys, stimulates the formation of angiotensin in blood and tissues, which in turn stimulates the release of aldosterone from the adrenal cortex.
  • 29.
  • 30. Angiotensin2 functions:  Constricts resistance vessels increasing systemic vascular resistance and arterial pressure  Stimulates reabsorption.  increase the release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention  Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary, which increases fluid retention by the kidneys  Stimulates thirst centers within the brain  Enhancing sympathetic adrenergic function  Stimulates cardiac hypertrophy and vascular hypertrophy.
  • 31.  Benazepril  Captopril  Enalapril  Fosinopril  Lisinopril  Moexipril  Quinapril  Ramipril
  • 32. ACE inhibitors have the following actions:  Dilate arteries and veins by blocking angiotensin II formation  Down regulate sympathetic activity  Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion. This reduces blood volume, venous pressure and arterial pressure.  Inhibit cardiac remodeling associated with chronic hypertension, heart failure, and myocardial infarction. In cardiology, ventricular remodeling (or cardiac remodeling) refers to changes in the size, shape, structure, and function of the heart.
  • 34.  Hypertension  Heart Failure  Diabetic and Nondiabetic Nephropathy .
  • 35.  Dry cough  First-dose hypotension (due to vasodilatation)  Angioedema: it is a serious type of skin reaction that affects the skin layer and also the tissues  Increased blood-potassium level (hyperkalemia)
  • 36.
  • 37.  Patients with bilateral renal artery stenosis may experience renal failure if ACE inhibitors are administered. The reason is that the elevated circulating and intrarenal angiotensin II in this condition constricts the efferent arteriole more than the afferent arteriole within the kidney, which helps to maintain glomerular capillary pressure and filtration. Removing this constriction by blocking circulating and intrarenal angiotensin II formation can cause an abrupt fall in glomerular filtration rate.
  • 38.  Renal artery stenosis is a narrowing of arteries that carry blood to one or both of the kidneys.
  • 39.  Patients with renal artery stenosis, the kidneys release large amounts of renin.  High angiotensin II serve to maintain glomerular filtration by two mechanisms: elevation of blood pressure and constriction of efferent glomerular arterioles.  When ACE is inhibited, causing angiotensin II levels to fall, the mechanisms that had been supporting glomerular filtration fail, causing urine production to drop
  • 40.  Diuretics. Diuretics may intensify first-dose hypotension. To prevent this interaction, diuretics should be withdrawn 1 week prior to initiating ACE inhibitor treatment  ACE inhibitors increase the risk of hyperkalemia caused by potassium supplements and potassium-sparing diuretics
  • 41.  Candesartan  Irbesartan  Losartan  Olmesartan  Telmisartan  Valsartan  These drugs have very similar effects to angiotensin converting enzyme (ACE) inhibitors and are used for the same indications (hypertension, heart failure, post- myocardial infarction).
  • 42. A diuretic is any substance that promotes diuresis (increased production of urine). DIURETICS Diuretics enhance the removal of sodium and water from body through kidneys. Ginger. ... Parsley. ... Caffeine
  • 43.
  • 44. Types of diuretics Thiazides: Hydrochlorothiazide, Chlorthalidone, indapamide MOA: these drugs Inhibit sodium-chloride transporter in the distal tubule. This transporter normally reabsorbs about 5% of filtered sodium. Loop diuretics: Furosemide (lasix), Torsemide, Bumetanide MOA: Loop diuretics inhibit the sodium-potassium-chloride co-transporter in the thick ascending limb. This transporter normally reabsorbs about 25% of the sodium load. Potassium-sparing diuretics: spironolactone and eplerenone.
  • 46.
  • 47.
  • 48.  Hypertension  Heart failure  Pulmonary and systemic edema
  • 49.  Amlodipine (Norvasc)  Nimodifine (Nimotop)  Felodipine.  Isradipine.  Nicardipine.  Nifedipine (Adalat CC) Extended Release Tablets  Nisoldipine  Verapamil
  • 50.  Calcium channel blockers decrease the amount of calcium entering cardiac and smooth muscle cells by blocking voltage-gated calcium channels.  This causes blood vessels to relax and widen (vasodilate), improves oxygen supply to the heart
  • 51.  Calcium-channel blockers bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes).  These channels are responsible for regulating the influx of calcium into muscle cells, which in turn stimulates smooth muscle contraction and cardiac myocyte contraction.  In cardiac nodal tissue, L-type calcium channels play an important role in pacemaker currents.  Therefore, by blocking calcium entry into the cell, there is, vasodilation,  Decreased myocardial force generation (negative inotropy), decreased heart rate (negative chronotropy),  Decreased conduction velocity within the heart (negative dromotropy),
  • 52.
  • 53.  Flushing, headache, hypotension, edema and reflex tachycardia