The document discusses drugs used to treat cardiovascular conditions. It covers antihypertensive drugs including diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and ARBs. It also discusses drugs for angina pectoris and myocardial infarction, including antiplatelets, beta blockers, calcium channel blockers, nitroglycerin, and ACE inhibitors. Finally, it addresses antiarrhythmic drugs and the mechanisms of different types of arrhythmias.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Cresar-H (Generic Telmisartan and Hydrochlorothiazide Tablets) The Swiss Pharmacy
Cresar-H (Generic Telmisartan and Hydrochlorothiazide Tablets) is used for the treatment of hypertension, to lower blood pressure as second line therapy. This fixed dose combination is not indicated for initial therapy for the treatment of hypertension. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions.
Cresar H / Cresar 80 H should be taken in patients whose blood pressure is not adequately controlled by Telmisartan alone.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Cresar-H (Generic Telmisartan and Hydrochlorothiazide Tablets) The Swiss Pharmacy
Cresar-H (Generic Telmisartan and Hydrochlorothiazide Tablets) is used for the treatment of hypertension, to lower blood pressure as second line therapy. This fixed dose combination is not indicated for initial therapy for the treatment of hypertension. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions.
Cresar H / Cresar 80 H should be taken in patients whose blood pressure is not adequately controlled by Telmisartan alone.
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the detail study of diuretics which include their drugs, use,classification of diuretics, side effect, mechanism of action, metabolism, synthesis etc. this all things are cover in this presentation.
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Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
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the detail study of diuretics which include their drugs, use,classification of diuretics, side effect, mechanism of action, metabolism, synthesis etc. this all things are cover in this presentation.
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According to the M. Optom curriculum, we have prepared a concise presentation on Cholinergic or parasympathomimetic or cholinomimetic drugs
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1. DRUGS USED IN CVS
Dr. Saroj Suwal
For BN and BSc. Nursing
2. DRUGS GROUP
Drugs for Hypertension- Anti Hypertensives
Drugs Used For Angina Pectoris and MI Anti Anginal/MI Drugs
Drugs Used for Shock
Drugs Used for Arrythmias Anti arrhythmic drugs
CardioTonic Drugs
3. ANTI HYPERTENSIVE DRUGS
Normal limit of BP
Systolic 100-140 mmHg( 120+-20)
Diastolic 60-90 mmHg(75+-15)
4. Hypertension
Bp Systolic >140mmHg and
Diasystolic >90mmHg
Types
Primary Hypertension( Essential
HTN)
HTN with unKnow Cause
Secondarry Hypertension
HTN with KnownCause Disease
7. DIURETICS
First line of drugs for mild to moderate Hypertension
Used in patients with adequate renal function.
They do not lower BP in normotensives.
the drugs that cause increase urine frequency
Drugs that cause loss of sodium and water in urine.
11. THIAZIDE DIURETICS
Most Commonly Used
Beside diuretics cause mild vasodilation
MOA
Inhibit Reabsorption of Na+ and Cl-
ions for distal convoluted tubule
increased Na+ and Cl- excretion
13. MOA
Na+, Cl- and K+ Symporter in thick
ascending loop of henle
Inhibit Na+, Cl- and potassium
Reabsorption in loop of Henle
Retention ofWater
NOTransport to descending loop of
Henle
14. K+ SPARING DIURETICS
Spironolactone or Amiloride
Has Weak Diuretic actions
Work in distal tubule
lower B.P slightly
Not effective asThiazide so not used in initial
management
Used with ACE inhibitors or ARB coz they inscrease
K+
15. Inhibition of Na+ reabsorption and K+
Absorption in distal convoluted tubule
Act as aldosterone receptor
Combination with thiazide diuretics to prevent
K+ loss
16.
17. OTHER DIURETICS MANNITOL
Retains water in proximal tuble
Inhibits transporte process in thichk asecding loop of henle
Expands extracellular fluid volume
Inscrease renl blood flow
18. CARBONIC ANHYDRASE INHIBITOR DIURETICS
Inhibit carbonic
anhydrase enzyme
Reduction of H+ ion
secretion at renal
tubule
Inscrese renal
excretion of Na+,
K+, HCO- and
water
• Acts on proximal tubule
19. SYMPATHOLYTIC( CENTRALLY ACTING)
Centrally acting
Methyl Dolpa decrease sympathetic tone
Clonidine( a2 adrenoceptor agonits
Peripherally Acting
Reserpine
Gluthedine for severe HTN
Alpha one adergenic blockers
parazosin
Beta blockers antiarrhythmic, angina, MI as well
Propranolol, Metopropol, esmolol
20. CALCIUM CHANNEL BLOCKERS
Calcium function as
Cardiac contraction
Smooth muscle
contraction
Propagation of cardiac
impulse
Drugs
• Nefidipine
• Amlodipine
• Verapamil
• diltiazem
25. VASODILATORS
Nitroprusside, Minoxidil
Not a first choice drug
Primary use:
emergency situations where immediate ↓ in BP is needed
Relaxes
smooth muscle
in arterioles
Decrease PVR Decrease BP
26. Highly effective but many side effects (some
serious)
Reflex tachycardia
Sodium/water retention
27. ACE INHIBITORS
Captopril, enalapril, ramipril
Also used in heart failure, scleroderma
and migraines.
Work in RENIN ANGIOTENSIN
ALDOSTERONE SYSTEM (RAAS)
29. ACE INHIBITORS-MOA
inhibit the enzyme ACE.
So these drugs decreases the
activity of RAAS and
also potentiate the
vasodilatory action of
bradykinin.
ACE Drugs
Blocks the
formation of
angiotensin
Relaxation of
Arteries
Decrease
Blood
pressure
30. ADVERSE EFFECTS
Cough – persistent brassy cough in 20% cases
(inhibition of bradykinin and substanceP breakdown in lungs )
Hyperkalemia in renal failure patients with K+ sparing diuretics,
NSAID and beta blockers (routine check of K+ level)
▪Hypotension (in hypovolemic states) – sharp fall may occur – 1st
dose
Acute renal failure- CHF and bilateral renal artery stenosis
▪Angioedema - swelling of lips, mouth, nose etc.
▪Rashes, urticaria etc
32. PHARMACOKINETICS
All are well absorbed orally
Food reduces absorption of captopril •
DOA of captopril is 8-12 hrs rest others > 24 hrs
All are excreted through the kidneys
33. ARBS
Angiontension Receptor Blockers
“-sartans”
losartan
valsartan
Frequently a second line
treatment for patients who do not
tolerate ACE-I
34. MECHANISM OF ACTION
: Blocks binding of Angiotensin II to its receptor sites
Angiotenin Receptor>constrict blood vessel Hypertension
36. ADVERSE EFFECTS
Most common is headache
Dizziness , lightheadedness, or faintness upon rising,
Diarrhea, muscle cramps or weakness, back or leg pain,
insomnia (difficulty sleeping), irregular heartbeat,
Interactions:
Other antihypertensives and diuretics (increased hypotensive
effects)
37. NURSING CONSIDERATIONS
• BP, I/O, daily weight, side effects
• Monitor Potassium levels and Monitor renal function
• Reinforce patient education •
Contraindicated to pregnant women
• Can be taken without regard to food
• Orthostatic BP checks
• Monitor renal, hepatic, and electrolyte level
38. . ANGINA PECTORIS
occurs when the heart muscle is
not getting enough blood.
39. MYOCARDIAL INFARCTION (MI)
commonly known as a heart attack,
The most common symptom is chest pain
or discomfort which may travel into the
shoulder, arm, back, neck, or jaw.
blood flow
decreases or stops
to a part of the
heart
Damage to Heart
Muscle
(Myocardium)
Myocardial
Infraction or Heart
Attack
40. DRUGS USED FOR ANGINA PECTORIS AND MI
Antiplatelet agents
Beta-adrenergic blocking agents
Calcium channel blockers
nitroglycerin
Angiotensin-converting enzyme inhibitors
41. ANTI PLATELETS
Aspirin
Prevents platelet aggregation by cyclooxygenase inhibition
subsequent suppression of thromboxane A2.
Low Dose use for the antiplatelet function
42. CLOPIDOGREL
Anti Platelet Actions
Also prevents MI and Stroke
inhibits ADP binding to platelet receptor
inhibiting platelet aggregation.
Used for patients with contraindication to
aspirin.
43. BETA-ADRENERGIC BLOCKING AGENTS
Beta blocker drugs drugs with “-olol”
blocking the effects of the hormone epinephrine, also known as
adrenaline.
beta blockers,
heart beats
more slowly and
with less force,
reducing blood
pressure.
44. ADRENERGIC OR SYMPATHETIC RECEPTORS
alpha, beta 1 and beta 2
Alpha-receptors are located on the
arteries.
50. Metoprolol
Selective beta1-adrenergic
receptor blocker that decreases
automaticity of contractions
Lipophilic –penetrates CNS
Atenolol
Selectively blocks beta-1
receptors with little or no effect
on beta-2 receptors.
Is hydrophilic and does not
penetrate CNS.
Propranolol (Inderal)
Nonselective beta-blocker that is
lipophilic (penetrates CNS).
Although generally short-acting
agent, long-acting preparations
also available.
51. USES FOR BETA BLOCKERS
High blood pressure
Irregular heart rhythm (arrhythmia)
Heart failure
Chest pain (angina)
Heart attacks
Migraine
Certain types of tremors
52. SIDE EFFECTS AND CAUTIONS
Common side effects of beta blockers
include:
Fatigue
Cold hands or feet
Weight gain
Less common side effects include:
Shortness of breath
Trouble sleeping
Depression
Beta
blockers
generally
aren't
used in
people
with
asthma
because
may
trigger
severe
asthma
attacks.
53. CALCIUM CHANNEL BLOCKERS
Calcium function as
Cardiac contraction
Smooth muscle
contraction
Propagation of cardiac
impulse
Drugs
• Nefidipine
• Amlodipine
• Verapamil
• diltiazem
54.
55. NITROGLYCERINS
prevent chest pain (angina
class of drugs known as nitrates.
relaxation of vascular smooth muscle.
Taken oral or sublinguial
63. ARRYTHMIA
Is problem with the rate or rhythm
of your heartbeat.
means that your heart beats too
quickly, too slowly, or with an
irregular pattern.
Tachycardia
Bradycardia
Fibrillation
Flutter
64. CAUSE
A variation in
site of impulse formation,
the rate of cardiac impulse formation or
sequence of cardiac impulse propagation.
Heart condition where disturbances in
Pacemaker impulse formation
Contraction impulse conduction
Combination of the two
Results in rate and/or timing of contraction of heart muscle that is insufficient to
maintain normal cardiac output (CO)
Bradycardia??
Tachycardia ???
65.
66. ELECTROPHYSIOLOGY
A transmembrane electrical gradient (potential) is maintained, with the
interior of the cell negative with respect to outside the cell
Caused by unequal distribution of ions inside vs. outside cell
Na+ higher outside than inside cell
Ca+ much higher “ “ “ “
K+ higher inside cell than outside
Maintenance by ion selective channels, active pumps and exchangers
67.
68. PHASES OF ACTION POTENTIAL
Divided into five phases (0,1,2,3,4)
Phase 4 - resting phase (resting membrane
potential)
Phase cardiac cells remain in until stimulated
Associated with diastole portion of heart cycle
Phase 0 – opening of fast Na channels and rapid
depolarization
Drives Na+ into cell (inward current), changing membrane
potential
Transient outward current due to movement of Cl- and K+
Phase 1 – initial rapid repolarization
Closure of the fast Na+ channels
Phase 0 and 1 together correspond to the R and S waves
of the ECG
69. Phase 2 - plateau phase
sustained by the balance between the inward
movement of Ca+ and outward movement of K +
Has a long duration compared to other nerve and
muscle tissue
Corresponds to ST segment of the ECG.
Phase 3 – repolarization
K+ channels remain open,
Allows K+ to build up outside the cell, causing the
cell to repolarize
K + channels finally close when membrane potential
reaches certain level
Corresponds toT wave on the ECG
72. NORMAL HEARTBEAT AND ATRIAL
ARRHYTHMIA
Normal rhythm Atrial arrhythmia
AV septum
73.
74.
75. Class I – blocker’s of fast Na+ channels
Subclass IA
Cause moderate Phase 0 depression
Prolong repolarization
Increased duration of action potential
Includes
Quinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias,
increases refractory period
Procainamide - increases refractory period but side effects
Disopyramide – extended duration of action, used only for treating ventricular
arrthymias
76. Quinidine
Quinidine is the prototype Class IA drug.
Also have property of class III
Because of the toxic potential of quinidine, calcium
antagonists, such as amiodarone and verapamil, are
increasingly replacing this drug in clinical use.
Quinidine binds to open and inactivate sodium
channels and prevents sodium influx, thus slowing
the rapid upstroke during Phase 0. it also
decreases the slope of Phase 4 spontaneous
depolarization and inhibits potassium channels.
77. EFFECTS AND ADVERSE EFFECTS OF
QUINIDINE
Quinidine is used in the treatment of a wide variety of
arrhythmias, including atrial, AV-junctional, and
ventricular tachyarrhythmias.
A potential adverse effect of quinidine (or of any
antiarrhythmic drug) is development of arrhythmia .
Quinidine may cause SA and AV block or asystole. At
toxic levels, the drug may induce ventricular
tachycardia. Nausea, vomiting, and diarrhea are
commonly observed. Large doses of quinidine may
induce the symptoms of cinchonism (for example,
blurred vision, tinnitus, headache, disorientation, and
psychosis).
78. Subclass IB
Weak Phase 0 depression
Shortened depolarization
Decreased action potential duration
Includes
Lidocane (also acts as local anesthetic) – blocks Na+
channels mostly in ventricular cells, also good for digitalis-
associated arrhythmias
Phenytoin – anticonvulsant that also works as
antiarrhythmic similar to lidocane
79. Subclass IC
Strong Phase 0 depression
No effect of depolarization
No effect on action potential duration
Includes
Flecainide
Propafenone
80. FLECAINIDE
suppresses Phase 0 upstroke in Purkinje and myocardial
fibers .
This causes marked slowing of conduction in all cardiac
tissue.
Flecainide can cause dizziness, blurred vision, headache, and
nausea
aggravate preexisting arrhythmias or induce life-threatening
tachycardia
Now days flecainide is substituted by
Propafenone, shows actions similar to those of
flecainide
81. Class II – β–adrenergic blockers
Based on two major actions
1) blockade of myocardial β–adrenergic receptors
2) Direct Na+ channel blockade
Includes
Propranolol
Metoprolol
Nadolol
Atenolol
Acebutolol
82. PROPANOLOL , METEPROLOL AND OTHER
CLASS II DRUGS
Class II agents are B-adrenergic antagonists.
These drugs diminish Phase 4 depolarization, thus depressing
automaticity, prolonging AV conduction, and decreasing heart
rate and contractility.
Class II agents are useful in treating tachyarrhythmias caused by
increased sympathetic activity.
83. Class III – K+ channel blockers
Developed because some patients negatively sensitive
to Na channel blockers (they died!)
Cause delay in repolarization and prolonged refractory
period
Includes
Amiodarone – prolongs action potential by delaying K+ efflux
but many other effects characteristic of other classes
Ibutilide – slows inward movement of Na+ in addition to
delaying K + influx.
Bretylium – first developed to treat hypertension but found to
also suppress ventricular fibrillation associated with myocardial
infarction
Dofetilide - prolongs action potential by delaying K+ efflux with
no other effects
84. AMIODARONE
Amiodarone (Class III agents) block potassium
channels and, thus, diminish the outward potassium
current during repolarization of cardiac cells.
is effective in the treatment of severe refractory
supraventricular and ventricular tachyarrhythmias
They work in almost all phases of action potential
generation
Pulmonary fibrosis, gastrointestinal tract intolerance,
tremor, ataxia, dizziness, hyper- or hypothyroidism,
liver toxicity, photosensitivity, neuropathy, muscle
weakness, and blue skin discoloration are common
ADR
85. Class IV – Ca2+ channel blockers
slow rate of AV-conduction
Includes
Verapamil – blocks Na+ channels in addition to Ca2+; also
slows SA node in tachycardia
Diltiazem
Amlodipine
86. VERAPAMIL, DILTIAZEM AND OTHER CA
CHANNEL BLOCKERS
Verapamil shows greater action on the heart than on
vascular smooth muscle
Whereas nifedipine, a calcium-channel blocker used to treat
hypertension, exerts a stronger effect on the vascular
smooth muscle than on the heart.
Diltiazem is intermediate in its actions.
verapamil and diltiazem, are more effective against the
voltage-sensitive channels, causing a decrease in the slow
inward current that triggers cardiac contraction
By decreasing the inward current carried by calcium,
verapamil and diltiazem slow conduction and prolong the
effective refractory period
87. ADR
Verapamil and diltiazem have negative inotropic properties and,
therefore, may be contraindicated in patients with preexisting
depressed cardiac function.
Both drugs can also produce a decrease in blood pressure
because of peripheral vasodilation
88. OTHER ANTIARRHYTHMIC DRUGS
A. Digoxin
Digoxin shortens the refractory period in atrial and ventricular
myocardial cells while prolonging the effective refractory period
and diminishing conduction velocity in the AV node.
Digoxin is used to control the ventricular response rate in atrial
fibrillation and flutter
89. B. Adenosine
Adenosine is a naturally occurring nucleoside, but at high doses,
the drug decreases conduction velocity, prolongs the refractory
period, and decreases automaticity in the AV node.
Intravenous adenosine is the drug of choice for abolishing acute
ventricular tachycardia. It has low toxicity but causes flushing,
chest pain, and hypotension. Adenosine has an extremely short
duration of action (approximately 15 seconds).
90. PACEMAKERS
Surgical implantation of electrical leads attached to
a pulse generator
1) Leads are inserted via subclavicle vein and advanced to the
chambers on the vena cava (right) side of the heart
2) Two leads used, one for right atrium, other for right ventricle
3) Pulse generator containing microcircuitry and battery are attached
to leads and placed into a “pocket” under the skin near the clavicle
4) Pulse generator sends signal down leads in programmed sequence
to contract atria, then ventricles
Pulse generator can sense electrical activity
generated by the heart and only deliver electrical
impulses when needed.
Pacemakers can only speed up a heart experiencing
bradycardia, they cannot alter a condition of
tachycardia
