Dr. Mahmoud Taleb University of Al - Azhar Gaza Palestine lama Khaled Al Banna

1. Cardiovascular DrugsCardiovascular Drugs
Dr. Mahmoud H.Taleb
Assistant Professor of Pharmacology andToxicology
Department of Pharmacology and Medical Sciences,
Faculty of Pharmacy- Al azhar University
Dr. Mahmoud H. Taleb 1

2. Functional ComponentsFunctional Components
of the Heartof the Heart
Myocardium: cardiac muscle fibers are arranged into
four chambers, 2 atria and 2 ventricles
Conduction system: specialized tissue that conducts
nerve impulses throughout the heart, SA and AV
node, bundle of His, bundle branches, and Purkinje
fibers
Nerve supply: nerve branches from both the
sympathetic and parasympathetic divisions of the
autonomic nervous system, regulate heart rate and
force of contraction
Dr. Mahmoud H. Taleb 2

3. Structure of the HeartStructure of the Heart
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4. Normal electrocardiogram at restNormal electrocardiogram at rest
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5. Main Diseases of theMain Diseases of the
Cardiovascular SystemCardiovascular System
Hypertension
Congestive heart failure
Coronary artery disease
Myocardial infarction
Cardiac arrhythmias
Dr. Mahmoud H. Taleb 5

6. Congestive Heart FailureCongestive Heart Failure
Contractile function is reduced below normal
by disease or life style
Cardiac output unable to maintain normal
blood pressure
Blood accumulates in heart (dilatation), lungs
(pulmonary congestion), abdomen (ascites), and
lower extremities (peripheral edema)
Patient is weak and has difficulty breathing
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7. Coronary Artery DiseaseCoronary Artery Disease
Due to arterio- and atherosclerosis of
the coronary arteries
Fatty plaques cause blockage and
decreased blood flow to the myocardium
Main symptom is angina pectoris or chest
pain, caused by lack of blood and oxygen
Myocardial infarction (MI) occurs when
an artery is totally blocked
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8. Myocardial InfarctionMyocardial Infarction
Caused by complete blockage of one of the
coronary arteries
Heart cells deprived of blood/oxygen become
ischemic, die, and form an infarct
MI may result in sudden death, or the infarct
undergoes a healing process and is replaced
with connective tissue
After an MI the heart may be weakened and
develop congestive failure or cardiac
arrhythmias
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9. Cardiac ArrhythmiasCardiac Arrhythmias
Arrhythmias are disturbances in the
normal electrical activity of conduction
system
The electrical disturbance interferes with
the ability of the heart to pump blood,
and may cause angina pectoris or
congestive heart failure
Severe arrhythmias can cause ventricular
fibrillation and sudden death
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10. Use of ECG for Diagnosis (STUse of ECG for Diagnosis (ST
depression)depression)
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11. HypertensionHypertension
Hypertension is the leading cause of
cardiovascular disease and mortality
Disease symptoms and organ damage
caused by hypertension are not evident
until 10–15 years after the disease has
started
Proper medication and patient
compliance will control most cases of
hypertension
Dr. Mahmoud H. Taleb 11

12. Causes of HypertensionCauses of Hypertension
Most people have essential hypertension where
the exact cause is not known
Increased sympathetic activity and sodium
overload increase blood pressure (BP)
Renal disease and increased renin-angiotensin-
aldosterone activity raise BP and cause sodium
and fluid retention
Smoking, body overweight, and increased
sodium consumption contribute to
hypertension
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13. Drug Classes Used toTreatDrug Classes Used toTreat
HypertensionHypertension
Diuretics
Sympatholytic drugs
Vasodilator drugs
Calcium antagonist drugs
Angiotensin-converting enzyme inhibitor and
angiotensin receptor blocking drugs
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14. DiureticTherapyDiureticTherapy
Diuretics increase sodium excretion and relax
arterial blood vessels (vasodilation)
Thiazides are preferred in patients with
adequate renal function
Organic acid diuretics (loop diuretics) are used
in patients with reduced renal function
Diuretics can be used alone or in combination
with other antihypertensive drugs
Excessive loss of fluid, sodium, and potassium
are common adverse effects
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15. Sympathetic Blocking DrugsSympathetic Blocking Drugs
Alpha blockers lower BP by vasodilation
Beta blockers lower BP by decreasing
heart rate and cardiac output
Centrally acting sympatholytic drugs
decrease the activity of the cardiovascular
centers in the medulla oblongata
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16. Vasodilator DrugsVasodilator Drugs
Vasodilators decrease the muscular tone
and contractile function of blood vessels
Hydralazine and minoxidil are potent
vasodilators that must be used with
diuretics and sympathetic blocking drugs
Minoxidil causes hirsutism and is sold
topically for treatment of baldness
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17. Calcium AntagonistsCalcium Antagonists
Block the influx of calcium into the heart
and arterial blood vessels
Verapamil and diltiazem act on both the
heart and blood vessels to lower BP
Nifedipine and other calcium blockers
lower BP only by vasodilation
Calcium antagonists are also used to
treat angina pectoris and cardiac
arrhythmias
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18. 1- Angiotensin-Converting Enzyme1- Angiotensin-Converting Enzyme
Inhibitors (ACEIs)Inhibitors (ACEIs)
ACEIs inhibit the formation of angiotensin which is a
potent vasoconstrictor
ACEIs decrease the release of aldosterone which
retains sodium and water
The ACEIs can be used with thiazide and organic acid
diuretics, but not potassium-sparing diuretics
These drugs produce a low incidence of adverse
effects and do not interfere with mental activity or
renal function
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21. Actions on the heart:
ACE inhibitors decrease vascular resistance,
venous tone, and blood pressure, resulting in an
increased cardiac output
ACE inhibitors also blunt the usual angiotensin II
mediated increase in epinephrine and
aldosterone seen in HF.ACE inhibitors improve
clinical signs and symptoms in patients also
receiving thiazide or loop diuretics and/or digoxin.
The use of ACE inhibitors in the treatment of HF
has significantly decreased both morbidity and
mortality.The ACE inhibitor enalapril decreases
the cumulative mortality in patients with CHFDr. Mahmoud H. Taleb 21

22. Pharmacokinetics:
All ACE inhibitors are adequately but incompletely
absorbed following. oral administration.
The presence of food may decrease absorption, so they
should be taken on an empty stomach. Except for
captopril ,ACE inhibitors are prodrugs that require
activation by hydrolysis via hepatic enzymes.
Renal elimination of the active moiety is important for
most ACE inhibitors, an exception being fosinopril
.Plasma half-lives of active compounds vary from 2 to
12 hours, although the inhibition of ACE may be much
longer.The newer compounds such as ramipril and
fosinopril require only once-a-day dosing.
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23. Adverse effects:
These include postural hypotension, renal
insufficiency, hyperkalemia, angioedema, and
a persistent dry cough.
The potential for symptomatic hypotension
with ACE inhibitor therapy requires careful
monitoring.
ACE inhibitors should not be used in
pregnant women, because they are fetotoxic.
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24. B.Angiotensin-receptor blockersB.Angiotensin-receptor blockers
Angiotensin-receptor blockers (ARBs) are
nonpeptide, orally active compounds that are
extremely potent competitive antagonists of the
angiotensin type 1 receptor. Losartan is the
prototype drug.ARBs have the advantage of more
complete blockade of angiotensin action, because
ACE inhibitors inhibit only one enzyme
responsible for the production of angiotensin II.
Further, the ARBs do not affect bradykinin levels.
Although ARBs have actions similar to those of
ACE inhibitors, they are not therapeutically
identical. Even so,ARBs are a substitute for ACE
inhibitors in those patients who cannot tolerate
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25. Actions on the cardiovascular system:
All the ARBs are approved for treatment of
hypertension based on their
clinical efficacy in lowering blood pressure
and reducing the morbidity and mortality
associated with hypertension.As indicated
above, their use in HF is as a substitute for
ACE inhibitors in those patients with severe
cough or angioedema.
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26. Pharmacokinetics:
All the drugs are orally active and require only
once-a-day dosing. Losartan, the first approved
member of the class, differs from the others in that
it undergoes extensive first-pass hepatic metabolism,
including conversion to its active metabolite.The
other drugs have inactive metabolites. Elimination of
metabolites and parent compounds occurs in the
urine and feces; the proportion is dependent on the
individual drug.
All are highly plasma protein bound (greater than
90 percent) and, except for candesartan have large
volumes of distribution.
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27. Adverse effects:
ARBs have an adverse effect profile
similar to that of ACE inhibitors. However,
ARBs do not produce cough.ARBs are
contraindicated in pregnancy.
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28. Nitrites and NitratesNitrites and Nitrates
Drugs stimulate the formation of nitric oxide, a
potent vasodilator of blood vessels
Vasodilation of veins and arteries decreases
cardiac work and cardiac oxygen consumption
to relieve the pain of myocardial ischemia
Nitrites and nitrates may cause a drop in blood
pressure and reflex tachycardia
These drugs can be used to treat acute attacks
of angina or to prevent anginal attacks
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29. Adverse Effects of Nitrites andAdverse Effects of Nitrites and
NitratesNitrates
Vasomotor flushing, dizziness, and
headache are common due to vasodilation
When administered for acute angina, the
sudden onset of vasodilation may cause
hypotension, fainting, and tachycardia
Patients should be seated when inhaling or
taking these drugs sublingually
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30. Beta Adrenergic BlockersBeta Adrenergic Blockers
Sympathetic beta receptor stimulation of the
heart increases heart rate, force of contraction,
and oxygen consumption
Blockade of beta receptors decreases cardiac
work and cardiac oxygen demand
Beta blockers are used prophylactically to
prevent angina and can be combined with other
antianginal drugs
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31. 2-2-ββ2-2-BlockersBlockers
Although it may seem counterintuitive to
administer drugs with negative inotropic activity
to a patient with HF, several clinical studies have
clearly demonstrated improved systolic
functioning and reverse cardiac remodeling in
patients receiving β2 -blockers.These benefits
arise in spite of occasional initial exacerbation of
symptoms.The benefit of β2 -blockers is
attributed, in part, to their ability to prevent the
changes that occur because of the chronic
activation of the sympathetic nervous system,
including decreasing the heart rate and inhibiting
the release of renin.
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32. In addition, β2 -blockers also prevent the
direct deleterious effects of norepinephrine
on the cardiac muscle fibers, decreasing
remodeling, hypertrophy and cell death.Two
β2 -blockers have been approved for use in
HF: carvedilol ,and Bisoprolol
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34. V. DiureticsV. Diuretics
 Diuretics relieve pulmonary congestion and peripheral
edema.These agents are also useful in reducing the
 symptoms of volume overload, including orthopnea and
paroxysmal nocturnal dyspnea. Diuretics decrease
plasma volume and, subsequently, decrease venous
return to the heart (preload).This decreases the cardiac
workload and the oxygen demand. Diuretics may also
decrease afterload by reducing plasma volume, thus
decreasing blood pressure.Thiazide diuretics are
relatively mild diuretics and lose efficacy if patient
creatinine clearance is less than 50 mL/min. Loop
diuretics are used for patients who require extensive
diuresis and those with renal insufficiency.
 [Note: Overdoses of loop diuretics can lead to
profound hypovolemia.]
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35. VI. DirectVasodilatorsVI. DirectVasodilators
Dilation of venous blood vessels leads to a
decrease in cardiac preload by increasing the
venous capacitance; arterial dilators reduce
systemic arteriolar resistance and decrease
afterload. Nitrates are commonly employed
venous dilators for patients with congestive
HF. If the patient is intolerant of ACE
inhibitors or B2-blockers, the combination of
hydralazine and isosorbide dinitrate is most
commonly used. [Note: Calcium-
channelshould be avoided in patients with HF.]
blockers Dr. Mahmoud H. Taleb 35

36. VII. Inotropic DrugsVII. Inotropic Drugs
Positive inotropic agents enhance cardiac
muscle contractility and, thus, increase
cardiac output.Although these
drugs act by different mechanisms, in each
case the inotropic action is the result of
an increased cytoplasmic
calcium concentration that enhances the
contractility of cardiac muscle.
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37. Calcium AntagonistsCalcium Antagonists
Drugs block influx of calcium ions into the heart and
blood vessels to vasodilate and lower blood
pressure, cardiac work, and oxygen demand
Verapamil and diltiazem act on both the heart and
blood vessels
Nifedipine and other calcium antagonists act mainly
to dilate arterial blood vessels
Calcium antagonists are used prophylactically to
prevent angina
Adverse effects include excessive vasodilation,
hypotension, cutaneous flushing, and headache
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38. Congestive Heart Failure (CHF)Congestive Heart Failure (CHF)
Heart failure (HF) is a complex, progressive disorder in
which the heart is unable to pump sufficient blood to
meet the needs of the body. Its cardinal symptoms are
dyspnea, fatigue, and fluid retention. HF is due to an
impaired ability of the heart to adequately fill with
and/or eject blood. It is often accompanied by abnormal
increases in blood volume and interstitial fluid, hence
the term congestive HF because symptoms include
dyspnea from pulmonary congestion in left HF, and
peripheral edema in right HF.
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39. Underlying causes of HF include
arteriosclerotic heart disease, myocardial
infarction, hypertensive heart disease, valvular
heart disease, dilated cardiomyopathy, and
congenital heart disease. Left systolic
dysfunction secondary to coronary artery
disease is the most common cause of HF,
accounting for nearly 70 percent of all cases.
The number of newly diagnosed patients with
HF is increasing, because more individuals
now survive acute myocardial infarction.
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Compensatory physiological response in CHF
The failing heart evokes three major compensatory mechanism to enhance cardiac
output
Increased sympathetic activity: Baroreceptor sense a decrease in blood pressure,
and trigger activation of β- adrenergic receptors in the heart. This results in an
increase in heart rate and a greater force of contraction of the heart muscle, in
addition, vasoconstriction enhances venous return and increases cardiac preload. and
therefore , can contribute to further decline in cardiac function.
2- Fluid retention: A fall in cardiac output decreases blood flow to the kidney,
prompting the release of rennin, with a resulting increase in the synthesis of
angiotensin II and aldosterone. This results in increased peripheral resistance and
retention of sodium and water. Blood volume increases, and more blood is returned to
the heart. If the heart is unable to pump this extra volume, venous pressure increases
and peripheral oedema and pulmonary oedema occur.
3- Myocardial hypertrophy:
The heart increases in size and the chambers dilate. Initially, stretching of the heart
muscle leads to a stronger contraction of the heart. However, excessive elongation of
the fibers results in a weaker contraction 4

41. B. Goals of pharmacologicB. Goals of pharmacologic
intervention in HFintervention in HF
The goals are to alleviate symptoms, slow disease
progression, and improve survival.Accordingly, six
classes of drugs
have been shown to be effective:
1) inhibitors of the renin-angiotensin system,
2) B-adrenoreceptor blockers,
 3) diuretics
, 4) inotropic agents,
5) direct vasodilators, and
6) aldosterone antagonists Dr. Mahmoud H. Taleb 41

42. Depending on the
severity of cardiac failure and individual
patient factors, one or more of these
classes of drugs are administered.
Beneficial effects of pharmacologic
intervention include reduction of the load
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43. Figure Action potential of a Purkinje fiber.
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44. Figure Ion movements during the contraction of cardiac muscle.
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45. Therapeutic strategies in HFTherapeutic strategies in HF
Chronic HF is typically managed by:
Reduction in physical activity
 low dietary intake of sodium (<1500 mg/day),
Treatment of comorbid conditions, and judicious use o
diuretics, inhibitors of the renin-angiotensin system, and
inotropic agents.
Drugs that may precipitate or exacerbate HF, such as
nonsteroidal anti-inflammatory drugs, alcohol, calcium-
channel blockers, and some antiarrhythmic drugs, shoul
be avoided if possible. Patients with HF complain of
dyspnea on exertion, orthopnea, paroxysmal nocturnal
dyspnea, fatigue, and dependent edema.
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48. Cardiac GlycosidesCardiac Glycosides
Drugs originally obtained from plant source,
Digitalis purpurea and Digitalis lanata
Digoxin and digitoxin are the only cardiac
glycosides currently available
Main pharmacologic effect of cardiac glycosides
is to increase the contractile force of
myocardial contraction
Cardiac glycosides also decrease heart rate and
atrioventricular conduction
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1- Cardiac glycosides ( Digoxin, Digitoxin, Quabin)
The cardiac glycosides exert their effects through actions both on the rate and
rhythm and on the force of contraction of the heart.
Inhibition of Na+- K+-ATP ase an enzyme responsible for transport of Na+ &
K+ in & out the cell. Na+ - input → ↑ Sodium concentration inside the cells →
increased transmembrane exchange of sodium & calcium increase the
intracellular Ca2+ →Increase contraction of cardiac muscle ( +ve inotropic
effect),. An increased myocardial contraction leads to decrease in end diastolic
volume, thus increasing the efficiency of contraction, resulting improved
circulation, leads to reduced sympathetic , which then reduced peripheral
resistance. Vagal tone is also enhanced so the heart rate decreases, and
myocardial oxygen demand is diminished (Positive inotropic effect).
Therapeutic uses:
Digoxin therapy is indicated in patients with severe left ventricular systolic
dysfunction after initiation of diuretic and vasodilator therapy.

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Figure Mechanism of action of cardiac glycosides

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Toxicity of cardiac glycoside
** Symptoms: 3 group of symptoms occur in digitalis toxicity:
GIT effects: Anorexia- nausea, vomiting, diarrhea and abdominal cramp.
CNS effects: headache, malaise, lethargy, fatigue, dizziness,
stupor, delusion , parasthesia ,various type of scotoma,
neurological pain, hallucination, yellow or green vision.
Cardiac effects: Bradycardia. Partial or complete heart block,
arrhythmias. Ventricular extrasytole, paroxysmal tachycardia and
ventricular tachycardia.
** The cardiotoxic effects of digitalis are probably due to an
excessive loss of K+ ( intracellular) , resulting from
inhibition of membrane Na+- ATP ase
** Treatment of cardiac arrthymia due to digitalis toxicity:
1- Stop administration of digitalis
2- Kcl
3- Ca2+-ion chelating agents e.g.EDTA
4- Atropine
5- Specific antiarrhythmic drugs
6- Digoxin –specific Fab fragments

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** Cardiac glycoside and pregnancy
Long- term digoxin treatment during pregnancy may shorten the
duration of pregnancy and retard intrauterine growth, resulting in low birth
weight and shorter labor. Nevertheless, digoxin is the drug of choice for
fetal supraventricular tachycardia, it is generally considered a safe drug
during pregnancy, with no risk of teratoginicity, but overdose cab be
detrimental to the mother and lethal to the fetus.
Drug interactions
Digitalis action may be enhanced by substances that
1- Slow GI motility and thereby increase gastrointestinal absorption
2- Disrupt body electrolytes by lowering plasma potassium levels, eliciting
hypokalemia and hypomagnesia and hypercalcemia e.g. diuretics,
amphotericin B, oral and parental glucose.
3-Change renal clearance and or alter plasma protein binding
4-Stimulate ß- adrenoreceoptor and cause cardiac dysrhythmias
Digitalis action may be reduced by substances that
Reduce gastrointestinal absorption e.g. kaolin-pectin, antihyperlipidemic
agents, antacids.
Increase gastrointestinal motility e.g. metoclopramide
Stimulate hepatic microsomal enzymes e.g. phenytoin, ASA, barbiturate.
Spironolactone, phenylbutazone

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Other positive inotropic agents
*** ß - adrenergic agonist :
ß - adrenergic stimulation improve cardiac performance by positive inotropic
effects and vasodilation. Bobutamine is the most commonoly used , where it leads
tob an increase in the intracellular concentration of cAMP. This results in an
increase in intracellular calcium, which results in the activation of protein kinase.
Slow calcium channels are one important site of phosphorylation by protein kinas.
When phosphorylated, the entry of calcium ions into the myocardium increases
thus enhances contraction. Dobutamine must be given by IV infusion.
** Phosphodiasteras inhibitors
Amrinone and milrinone are phosphodiasteras inhibitors that increase the
intracellular concentration of cAMP. This results in an increase in intracellular
calcium, and thus cardiac contractility and improvement of myocardial function.,
they increase mortality in heart failure.

58. Mechanism of ActionMechanism of Action
Cardiac glycosides inhibit Na/K adenosine
triphosphatase, the “sodium pump” which
causes more Na to remain inside myocardial
cells
Increased intracellular Na stimulates Na/Ca
exchange that brings more Ca inside heart cells
to increase the force of contraction
Cardiac glycosides also stimulate the vagus
nerve which decreases heart rate
Dr. Mahmoud H. Taleb 58

59. Pharmacokinetics and DosingPharmacokinetics and Dosing
Digoxin is water soluble and eliminated mostly
unmetabolized by the urinary tract
Digitoxin is more lipid soluble, requires
metabolism, and has a longer half-life
In acute CHF, initial “digitalization” doses are
administered to rapidly attain effective
therapeutic concentration
Lower daily maintenance doses are then given
to maintain desired therapeutic concentrations
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60. Electrolyte and Cardiac GlycosideElectrolyte and Cardiac Glycoside
InteractionsInteractions
Low serum potassium (K) levels “hypokalemia”
increase drug toxicity and can cause cardiac
arrhythmias
High serum potassium levels “hyperkalemia”
decrease the actions of the cardiac glycosides
Increased serum calcium levels “hypercalcemia”
can increase the actions and toxicity of the
cardiac glycosides
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61. Adverse EffectsAdverse Effects
Common complaints include headache,
dizziness, nausea, and vomiting
Visual disturbances “halo effect” around
lights often signals overdosage
Bradycardia, ectopic beats, and a variety
of other cardiac arrhythmias can occur
and can be life-threatening
Dr. Mahmoud H. Taleb 61

62. DiureticTherapy of CHFDiureticTherapy of CHF
Diuretic drugs are used to eliminate
excess sodium and fluid retention
Elimination of excess fluid allows the
heart to function more efficiently
Diuretics can be administered with
cardiac glycosides and other drugs used
to treat CHF
Dr. Mahmoud H. Taleb 62

63. VasodilatorTherapy of CHFVasodilatorTherapy of CHF
Vasodilator drugs relax and dilate blood
vessels
Vasodilation decreases peripheral
resistance, allows more efficient blood
flow, and usually increases cardiac output
Angiotensin-converting enzyme inhibitors
and angiotensin receptor blocking drugs
are particularly useful in CHF
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64. Dr. Mahmoud H. Taleb 64
Figure Treatment options for various stages of heart failure.

65. Cardiac ArrhythmiasCardiac Arrhythmias
Arrhythmias are disturbances in the normal
electrical activity of the heart
Arrhythmias can be detected on a recording of
the electrocardiogram (ECG)
Supraventricular arrhythmias occur above the
ventricles in the atria, SA node, and AV node
Ventricular arrhythmias occur in the ventricles
and Purkinje fibers and are usually more serious
and life-threatening
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66. Electrophysiological Properties ofElectrophysiological Properties of
the Heartthe Heart
Excitability – associated with membrane
depolarization and the influx of Na ions
Refractory period – associated with repolarization
and the efflux of K ions
Automaticity – ability of the SA and AV nodes to
initiate membrane depolarizations
Under conditions of hypoxia and excessive
sympathetic stimulation, the ventricles can also
demonstrate automaticity to cause ectopic beats or
PVCs
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67. Quinidine and ProcainamideQuinidine and Procainamide
Classified as class 1 antiarrhythmic drugs
Possess local anesthetic activity and block the
influx of Na ions during depolarization
Main effects are to decrease excitability, slow
conduction, and prolong the refractory period
ECG: prolong the PR, QRS, and QT intervals
Used for both supraventricular and ventricular
arrhythmias
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68. LidocaineLidocaine
Class 1 local anesthetic-type
antiarrhythmic used only for ventricular
arrhythmias
Must be administered IV by infusion
The drug of choice in acute and
emergency ventricular arrhythmias
Main effect is to decrease automaticity
Mexiletine and tocainide are similar to
lidocaine and can be administered orally
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69. PropranololPropranolol
Classified as a class 2 antiarrhythmic drug
Primarily blocks cardiac beta receptors to
slow heart rate,AV conduction, and
prolong the refractory period
ECG: mainly increases the PR interval
Used for both supraventricular and
ventricular arrhythmias
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70. AmiodaroneAmiodarone
Classified as a class 3 antiarrhythmic drug
Usually reserved for more serious
arrhythmias when other drugs have failed
Main effect is to prolong the refractory
period and increase the QT interval
Drug contains iodine and can interfere
with thyroid function
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71. Verapamil and DiltiazemVerapamil and Diltiazem
Classified as class 4 antiarrhythmic drugs
Act by blocking calcium ions
Main effects are to decrease heart rate
and AV conduction, increase the PR
interval
Mainly used to treat supraventricular
arrhythmias
May cause cardiac depression at higher
doses
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72. AdenosineAdenosine
Administered IV in emergency situations
Main action is to decrease AV conduction
and slow the heart rate
Used to treat acute supraventricular
tachycardia
Duration of action is 15–30 seconds
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