CARDIOVASCULAR &

RESPIRATORY DRUGS
BY: DR. MARY JOYCE D. VALERA
CARDIO
CARDIO
ANATOMY AND PHYSIOLOGY

responsible for delivering

oxygen and nutrients to all of
the cells of the body and for
removing waste products for
excretion.
ANATOMY AND PHYSIOLOGY
ANATOMY AND PHYSIOLOGY

Septum
- separates the right half
from the left half

Right half: deoxygenated

blood from VEINS → lungs

Left half: oxygenated blood

from the lungs → aorta
(ARTERIES)
ANATOMY AND PHYSIOLOGY

Atrioventricular Valves:
Tricuspid Valve
Mitral Valve

Semilunar Valves:
Pulmonic Valve
Aortic Valve
ANATOMY AND PHYSIOLOGY

Purpose of Valves:
prevent backflow

*increase volume in the

previous chamber
*decrease volume in the next
chamber
ANATOMY AND PHYSIOLOGY

Myocardium: cardiac muscle fiber

Simultaneous contraction is a
necessary property for a muscle that
acts as a pump. A hollow pumping
mechanism must also pause long
enough in the pumping cycle to allow
the chambers to fill with fluid.
ANATOMY AND PHYSIOLOGY

Starling’s low of the heart

Cardiac Cycle
Cardiac Conduction
Cardiac Conduction

SA Node
|
AV Node
|
Bundle of His
|
Bundle branches
|
Purkinje fibers
ANATOMY AND PHYSIOLOGY

Cardiac Conduction
● Automaticity
● Conductivity
● Autonomic Influences
● Myocardial Contraction
ELECTROCARDIOGRAPHY
Electrocardiography
ANATOMY AND PHYSIOLOGY

ECG
ECG Abnormality Findings

ARRYHTHMIAS
- Sinus Arrythmia
- Supraventricular Arrythmias
- AV Block
- Ventricular Arrythmias
CIRCULATION

CIRCULATION
- Pulmonary Circulation
- Systemic Circulation
- Coronary Circulation
Coronary Circulation
Systemic Arterial Pressure
HYPOTENSION

The pressure of the blood in the arteries needs to remain relatively high to
ensure that blood is delivered to every cell in the body and to keep the blood
flowing from high-pressure to low-pressure areas

The pressure can fall dramatically from:

Loss of blood volume
Excessive vasodilation
Failure of the heart muscle to pump effectively.

Severe hypotension can progress to shock and even death as cells are cut off
from their oxygen supply.
Systemic Arterial Pressure
HYPERTENSION

Constant, excessive high blood pressure can damage the fragile inner lining
of blood vessels and cause a disruption of blood flow to the tissues.

It also puts a tremendous strain on the heart muscle, increasing myocardial

oxygen consumption and putting the heart muscle at risk.

Caused by:
Neurostimulation of the blood vessels → constrict → raising blood pressure,
or by increased volume in the system
Systemic Arterial Pressure

VASOMOTOR TONE

The smooth muscles in the walls of the arteries receive constant input from
nerve fibers of the sympathetic nervous system.

These impulses work:

To dilate the vessels if more blood flow is needed in an area
To constrict vessels if increased pressure is needed in the system
To maintain muscle tone so that the vessel remains patent and responsive.

The coordination of these impulses is regulated through the medulla in an

area called the cardiovascular center.
Renin-Angiotensin-Aldosterone System
Renin-Angiotensin-Aldosterone System
Venous Pressure

Blood in the veins also exerts a pressure that may

sometimes rise above normal

This can happen if the heart is not pumping

effectively and is unable to pump out all of the blood
that is trying to return to it.

This results in a backup or congestion of blood waiting

to enter the heart. Pressure rises in the right atrium and
then in the veins that are trying to return blood to the
heart as they encounter resistance.

The venous system begins to back up or become

congested with blood.
Summary of Cardiac Problems
Physiology Pathology Management
Systemic Arterial Pressure Hypotension Vasopressors (Sympathetic
*components of blood Adrenergic Agonists)
pressure BP-Raising Agents
Hypertension Anti-hypertensive
medication:
ACE
ARBS
CCB
Vasodilators
Diuretics, SNS
Venous Pressure Heart Failure Cardiotonic Agents
Cardiac Glycosides
Phosphodiesterase
Inhibitors
Summary of Cardiac Problems
Physiology Pathology Management
Cardiac Conduction Arrhythmias Antiarrhythmic Agents

Coronary Circulation Angina Antianginal Agents

Cholesterol levels Atherosclerosis Lipid-Lowering Agents

Blood Coagulation Blood Coagulation Anticoagulant

Blood Pressure
Blood Pressure

The pressure in the CV system is

determined by three elements:
Heart rate

Stroke volume, or the amount of

blood that is pumped out of the
ventricle with each heartbeat
(primarily determined by the volume
of
blood in the system)

Total peripheral resistance, or the

resistance of the muscular arteries to
the blood being pumped through
Blood Pressure
Blood Pressure
Blood Pressure
Blood Pressure
Renin-Angiotensin-Aldosterone System
Blood Pressure
Hypertension
ANTI-HYPERTENSIVE AGENTS
ANTI-HYPERTENSIVE AGENTS
ANTI-HYPERTENSIVE AGENTS
ANTI-HYPERTENSIVE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Affects the RAAS ACE Inhibitors (“-pril”) Captopril
Enalapril
Affects the RAAS ARBs (“-sartan”) Losartan
Telmisartan
Valsartan
Prevents calcium influx → Calcium-Channel Blockers Diltiazem
prevent smooth muscle (“-dipine”) Amlodipine
contraction Nicardipine
Nifedipine
Directly acts on vascular Vasodilators Nitroprusside
smooth muscle → muscle Hydralazine
Relaxation → vasodilation
and drop in BP
ACE Inhibitors (-pril)

MOA:

prevent ACE from converting

angiotensin I (AT I) to AT II
|
decrease in BP and in
aldosterone secretion

with a resultant slight increase

in serum potassium and a loss
of serum sodium and fluid.
ACE Inhibitors (-pril)

PK:
● detected in breast milk
● known to cross the
placenta
● associated with serious
fetal abnormalities

So, they should not be used

during pregnancy
ACE Inhibitors (-pril)

A/E:
related to the effects of vasodilation and
alterations in blood flow.

Taken on empty stomach

1 hour AC or 2 hours PC

ACE inhibitors are generally well

tolerated but can cause an unrelenting
nonproductive cough, possibly related
to effects in the lungs where the ACE is
inhibited, that may lead patients to
discontinue the drug.
ACE Inhibitors (-pril)
ARBs (-sartan)

MOA:

selectively bind with the AT II

receptors in vascular
smooth muscle and in the
adrenal cortex
|
block vasoconstriction and
the release of aldosterone

block the BP-raising effects of

the RAAS and lower BP
ARBs (-sartan)

A/E:
● Headache, dizziness, syncope, and weakness (drops in BP)
● Hypotension; GI complaints
● Symptoms of URTI and cough;
● Rash, dry skin, and alopecia

These drugs should not be used with ACE inhibitors or a renin inhibitor
because of the potential for serious adverse effects.

Administer without regard to meals; give with food to decrease GI distress if

needed.

Alert the surgeon and mark the patient’s chart prominently if the patient is to undergo
surgery to notify medical personnel that the blockage of compensatory angiotensin II →
result in hypotension after surgery
ANTI-HYPERTENSIVE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Affects the RAAS ACE Inhibitors (“-pril”) Captopril
Enalapril
Affects the RAAS ARBs (“-sartan”) Losartan
Telmisartan
Valsartan
Prevents calcium influx → Calcium-Channel Blockers Diltiazem
prevent smooth muscle (“-dipine”) Amlodipine
contraction Nicardipine
Nifedipine
Directly acts on vascular Vasodilators Nitroprusside
smooth muscle → muscle Hydralazine
Relaxation → vasodilation
and drop in BP
CCB (-dipine)

MOA
● Alters action
potential and
block muscle
cell contraction
● Relaxation and
dilation

Fall in BP and
decrease in
venous return
CCB (-dipine)

CI
● Should not be used in pregnancy

A/E
CNS effects: dizziness, lightheadedness, headache
GI effects: nausea, hepatic injury
CV effects: hypotension, bradycardia, peripheral edema

Avoid grapefruit juice (may increase drug level in blood → toxicity)

Vasodilators
ANTI-HYPERTENSIVE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Affects the RAAS ACE Inhibitors (“-pril”) Captopril
Enalapril
Affects the RAAS ARBs (“-sartan”) Losartan
Telmisartan
Valsartan
Prevents calcium influx → Calcium-Channel Blockers Diltiazem
prevent smooth muscle (“-dipine”) Amlodipine
contraction Nicardipine
Nifedipine
Directly acts on vascular Vasodilators Nitroprusside
smooth muscle → muscle Hydralazine
Relaxation → vasodilation
and drop in BP
ANTI-HYPERTENSIVE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Sympathetic Nervous Beta-blockers (“-olol”) Metoprolol
System Drugs Propranolol
(blocks = sympatholytic) Atenolol
Blocks all the receptors in Alpha- and Beta-blockers Carvedilol
the SNS Labetalol
Block the postsynaptic Alpha1-Blockers (“-zosin”) Prazosin
alpha1-receptor sites Doxazosin
Terazosin
stimulate the alpha2- Alpha2-Agonist Clonidine
receptors in the Methyldopa
CNS and inhibit the CV
centers
Beta-Blockers (-olol)
Beta-Blockers (-olol)

● abcs
Beta-Blockers (-olol)
Alpha- and Beta-Blockers (-lol)
Alpha1- (-zosin) and Alpha2-Blockers
Alpha1- (-zosin) and Alpha2-Blockers

● abcs
Alpha1- (-zosin) and Alpha2-Blockers

● abcs
Alpha1- (-zosin) and Alpha2-Blockers

● abcs
Hypotension

If BP becomes too low, the vital centers in the brain, as well as the rest of the
tissues of the body, may not receive enough oxygenated blood to continue
Functioning

Hypotension can progress to shock, in which the body is in serious jeopardy

as waste products accumulate and cells die from lack of oxygen.

Hypotensive states can occur in the following situations:

(1) When the heart muscle is damaged and unable to pump effectively
(2) With severe blood or fluid loss, when volume drops dramatically
(3) When there is extreme stress and the body’s levels of norepinephrine are
depleted, leaving the body unable to respond to stimuli to raise BP
ANTI-HYPOTENSIVE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Sympathetic Adrenergic Sympathomimetic drugs Epinephrine
Agonists or Vasopressors Norepinephrine
Dobutamine
Dopamine
Ephedrine
Droxidopa
 ACEI, ARBS
HTN BB
BP Elements: CCB
HR, SV, TPR
Diuretics
WHITE COAT
HEART FAILURE
Heart Failure

RIGHT-SIDED LEFT-SIDED
Heart Failure

RIGHT-SIDED LEFT-SIDED
Heart Failure

RIGHT-SIDED LEFT-SIDED
Compensatory Mechanism
HF Drugs
HEART FAILURE AGENTS

MECHANISM CLASSIFICATION DRUG LIST

Increase intracellular Ca+ Cardiac Glycoside Digoxin

Blocks phosphodiesterase Phosphodiesterase Milrinone

→ increase cAMP → Inhibitor
increase Ca+
Cardiac Glycosides
Phosphodiesterase
Inhibitors
ANTIARRHYTHMIC
Arrhythmias

involve changes to the automaticity or

conductivity of the heart cells.

Factors:
(1) Electrolyte imbalances that alter the
action potential

(2) Decreased oxygen delivery to cells

that changes their action potential,

(3) Structural damage that changes the

conduction pathway

(4) Acidosis or waste product

accumulation that alters the action
potential.
Arrhythmias
Antiarrhythmics

MECHANISM CLASSIFICATION DRUG LIST

block the Na+ channels Class I Lidocaine
in the cell membrane during
an action potential
beta-receptor sites in the Class II Propranolol
heart and kidneys
block potassium channels Class III Amiodarone
and slow the outward
movement of potassium
block the movement of Class IV (Two CCBs) Diltiazem
calcium ions across the Verapamil
cell membrane
Arrhythmias

Whichever type of antiarrhythmic is used, the patient receiving

an antiarrhythmic drug needs to be constantly monitored while
being stabilized and throughout the course of therapy to detect
the development of arrhythmias or other adverse effects
associated with alteration of the action potentials of other
muscles or nerves
ANTIANGINAL
CORONARY ARTERY DISEASE

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANGINA PECTORIS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ACUTE MI
ANTIANGINAL AGENTS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Mechanism Class Drug List

relax and dilate veins, arteries, and capillaries, → Nitrates Nitroglycerin
increased blood flow through the vessels and Isosorbide dinitrate
lowering systemic BP Isosorbide mononitrate
block beta-adrenergic receptors in the heart and Beta-blockers Metoprolol
JG apparatus, decreasing the influence of the Propranolol
SNS on these tissue Atenolol
inhibit the movement of calcium ions across the Calcium channel Diltiazem
membranes of myocardial and arterial muscle blockers Amlodipine
cells, altering the action Nifedipine
potential and blocking muscle cell contraction Nicardipine
decrease myocardial workload, bringing the Piperazine Ranolazine
supply and demand for oxygen back into Acetamide
balance.
ANTIANGINAL AGENTS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Drug List
Nitrates Nitroglycerin
Isosorbide dinitrate
Isosorbide
mononitrate
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Drug List
RANOZALINE
Nitrates Nitroglycerin
Isosorbide dinitrate
first-line treatment for angina
Isosorbide
or for use in combination with nitrates,
mononitrate
beta-blockers, or amlodipine
Beta-blockers Metoprolol
Propranolol
Atenolol
Calcium Diltiazem
channel Amlodipine
blockers Nifedipine
Nicardipine
Piperazine Ranolazine
Acetamide
ANTIANGINAL AGENTS

Mechanism Class Drug List

relax and dilate veins, arteries, and capillaries, → Nitrates Nitroglycerin
increased blood flow through the vessels and Isosorbide dinitrate
lowering systemic BP Isosorbide mononitrate
block beta-adrenergic receptors in the heart and Beta-blockers Metoprolol
JG apparatus, decreasing the influence of the Propranolol
SNS on these tissue Atenolol
inhibit the movement of calcium ions across the Calcium channel Diltiazem
membranes of myocardial and arterial muscle blockers Amlodipine
cells, altering the action Nifedipine
potential and blocking muscle cell contraction Nicardipine
decrease myocardial workload, bringing the Piperazine Ranolazine
supply and demand for oxygen back into Acetamide
balance.
LIPID-LOWERING
Hyperlipidemia

When the levels of lipids in the blood increase, hyperlipidemia occurs

This can result from excessive dietary intake of fats or from genetic
alterations in fat metabolism → variety of elevated fats in the blood

Dietary modifications are often successful in treating hyperlipidemia that

is caused by excessive dietary intake of fats.

Drug therapy is needed if the cause is genetically linked alterations in lipid

levels or if dietary limits do not decrease the serum lipid levels to an acceptable
range.
CAD (Coronary Artery Disease)

CAD is associated with arterial atheromas or plaques, narrowed arterial

lumens, and hardening of the artery wall, all of which lead to impaired
contraction and vascular dilation.

Risk factors for CAD include increasing age, male gender, genetic
predisposition, high-fat diet, sedentary lifestyle, smoking, obesity, high
stress levels, bacterial infections, diabetes, hypertension, gout, and
menopause.

CAD prevention and treatment aim at decreasing risk factors to delay

disease or decrease its progress
Key Points

Bile acids act like detergents to break down or metabolize fats into
small molecules called micelles, which are absorbed into the intestinal
wall and combined with proteins to become chylomicrons to allow
transport throughout the circulatory system.

Cholesterol is a fat that is used to make bile acids; all cells can produce
cholesterol, which is the base for steroid hormones and cell membrane
structure.

The enzyme HMG–CoA reductase controls the early rate-limiting step

in the production of cellular cholesterol; HMG–CoA is active in every
cell.
LIPID-LOWERING

MECHANISM CLASSIFICATION DRUG LIST

Sympathetic Adrenergic HMG-CoA Reductase Atorvastatin
Agonists or Vasopressors Inhibitors (“-statin”) Rosuvastatin
Simvastatin
bind with bile acids in the Bile Acid Sequestrants Cholestyramine
intestine to form an (“c(h)ole-”) Colestipol
insoluble complex that is Colesevelam
then excreted in the feces
brush border of the small Cholesterol Absorption Ezetimibe
intestine to decrease the Inhibitors
absorption of dietary
cholesterol from the small
intestine
LIPID-LOWERING

MECHANISM CLASSIFICATION DRUG LIST

bind to the free PCSK9 Proprotein Convertase Alirocumab
enzyme and inhibit the Subtilisin/Kexin Type 9 Evolocumab
PCSK9 attachment to the
LDL receptors on the liver
(PCSK9) Inhibitors
cell
LIPID-LOWERING
HMG-CoA Reductase Inhibitors
COAGULATION
Coagulation

Coagulation: the process of blood changing from a fluid state to a solid

state to plug injuries to the vascular system
Anti-clot formation

MECHANISM CLASSIFICATION DRUG LIST

inhibit platelet adhesion and Antiplatelet Aspirin
aggregation by blocking Clopidogrel
receptor sites on the platelet
membrane
interfere with the normal Anticoagulants Heparin
cascade of events involved in Warfarin
the clotting process Fondaparinux
Antithrombin
Apixaban
activate the natural anticlotting Thrombolytic Urokinase
system — conversion of Alteplase
plasminogen to plasmin Tenecteplase
Antiplatelet
Anticoagulant
Thrombolytic
Anti-clot formation

MECHANISM CLASSIFICATION DRUG LIST

inhibit platelet adhesion and Antiplatelet Aspirin
aggregation by blocking Clopidogrel
receptor sites on the platelet
membrane
interfere with the normal Anticoagulants Heparin
cascade of events involved in Warfarin
the clotting process Fondaparinux
Antithrombin
Apixaban
activate the natural anticlotting Thrombolytic Urokinase
system — conversion of Alteplase
plasminogen to plasmin Tenecteplase
 BP: Hyper, Hypo
HF: left, right
CARDIO Arrhythmia
Angina
Hyperlipidemia
Coagulation
RESPI
ANATOMY AND PHYSIOLOGY

It brings oxygen into the

body, allows for the exchange
of gases, and leads to the
expulsion of carbon
dioxide and other waste
products
ANATOMY AND PHYSIOLOGY

responsible for delivering

oxygen and nutrients to all of
the cells of the body and for
removing waste products for
excretion.
UPPER RT
UPPER RESPIRATORY TRACT

The upper respiratory tract is

primarily involved in the
movement of air in
and out of the body, called
ventilation
UPPER RESPIRATORY TRACT

Cough Reflex
- air to be pushed through the
bronchial tree under
tremendous pressure, cleaning
out any foreign irritant

Sneeze Reflex
- forces foreign materials directly
out of the system, opening it for
more efficient flow of gas.
URT PATHOPHYSIOLOGY

Common Cold
Seasonal Rhinitis
Sinusitis
Pharyngitis
Laryngitis
URT Meds

INDICATION CLASSIFICATION DRUG LIST

Nonproductive Cough Antitussive Codeine
Dextromethorphan
Productive Cough Mucolytic Acetylcysteine

Productive Cough Expectorant Guaifenesin

Colds, Rhinitis Decongestant Pseudoephedrine

Phenylephrine
Allergic Rhinitis Antihistamine Diphenhydramine
Cetirizine
Loratadine
URT Meds
URT Meds

MECHANISM CLASSIFICATION DRUG LIST

act directly on the medullary Antitussive Codeine
cough center ofthe brain to Dextromethorphan
depress the cough reflex
decrease in the tenacity and Mucolytic Acetylcysteine
viscosity of the secretions d/t
splitting of disulfide bonds
reducing the adhesiveness and Expectorant Guaifenesin
surface tension of these fluids
ANTITUSSIVE
MUCOLYTICS
EXPECTORANTS
URT Meds

MECHANISM CLASSIFICATION DRUG LIST

Sympathomimetics → Decongestant Pseudoephedrine
vasoconstriction → decreased Phenylephrine
edema and inflammation of the
nasal membranes
selectively block the effects of Antihistamine Diphenhydramine
histamine at the histamine-1 Cetirizine
receptor sites, decreasing the Loratadine
allergic response
DECONGESTANTS
ANTIHISTAMINE
URT Meds

INDICATION CLASSIFICATION DRUG LIST

Nonproductive Cough Antitussive Codeine
Dextromethorphan
Productive Cough Mucolytic Acetylcysteine

Productive Cough Expectorant Guaifenesin

Colds, Rhinitis Decongestant Pseudoephedrine

Phenylephrine
Allergic Rhinitis Antihistamine Diphenhydramine
Cetirizine
Loratadine
LOWER RT
LOWER RESPIRATORY TRACT

Gas exchange occurs across the respiratory

membrane in the alveolar sac.

The type II cells of the alveoli produce

surfactant, which reduces surface tension to
keep the alveoli open for gas exchange.

The medulla controls ventilation, which

depends on a functioning muscular system
and a balance between the sympathetic and
parasympathetic systems.
LRT PATHOPHYSIOLOGY

Atelectasis
Pneumonia
Bronchitis
Bronchiectasis
COPD
Asthma
RDS
LRT Meds

INDICATION CLASSIFICATION DRUG LIST

Asthma Bronchodilators/ Xanthine
Anti-asthmatics Sympathomimetics
Anticholinergics
Asthma Anti-Inflammation Inhaled steroids
Leukotriene receptor
antagonist
RDS: Respiratory Distress Lung Surfactants Beractant
Syndrome
ANTI-ASTHMATICS: Xanthine
ANTI-ASTHMATICS: Sympathomimetic
ANTI-ASTHMATICS: Anticholinergic
LRT Meds

INDICATION CLASSIFICATION DRUG LIST

Asthma Bronchodilators/ Xanthine
Anti-asthmatics Sympathomimetics
Anticholinergics
Asthma Anti-Inflammation Inhaled steroids
Leukotriene receptor
antagonist
RDS: Respiratory Distress Lung Surfactants Beractant
Syndrome
ANTI-INFLAMMATORY: Inhaled Steroids
ANTI-INFLAMMATORY: Leukotriene Antagonist
LRT Meds

INDICATION CLASSIFICATION DRUG LIST

Asthma Bronchodilators/ Xanthine
Anti-asthmatics Sympathomimetics
Anticholinergics
Asthma Anti-Inflammation Inhaled steroids
Leukotriene receptor
antagonist
RDS: Respiratory Distress Lung Surfactants Beractant
Syndrome
LUNG SURFACTANTS
- END -