Summary Nsg 322- Pharmacology Exam 1 Study guide

Exam 1 Drug List

CV I: INTRODUCTION TO THE CV SYSTEM

Concepts:

Heart: Anatomy
● The heart is a muscular organ with a closed system to keep pressure differences
to let the blood flow in a proper, singular direction
○ VEINS: carry blood towards the heart, deoxygenated- blue color
○ ARTERIES: carry blood away from the heart, oxygenated- red color
● RIGHT SIDE: deoxygenated blood from body via superior/inferior vena cava ->
right atrium -> through AV “node” -> right ventricle (contracts) -> through SA
“node” -> to pulmonary artery -> lungs oxygenate the blood (CO2 is removed)
○ Atrioventricular valve: tricuspid valve
■ Separates and controls blood flow from the right atrium and right
ventricle
○ Semilunar valve: pulmonary valve
■ Separates and controls blood flow from the right ventricle and the
pulmonary artery
● LEFT SIDE: reoxygenated blood from lungs -> pulmonary vein -> left atrium ->
through AV “node” -> left ventricle (contracts) -> through SA “node” -> to aorta ->
into systemic circulation
○ Atrioventricular valve: bicuspid (mitral) valve
■ Separates and controls blood flow from the left atrium and left
ventricle
○ Semilunar valve: aortic valve
■ Separates and controls blood flow from the left ventricle and the
aorta
Cardiac Cycle
● SYSTOLE: contraction of the heart- blood flows out
○ AV node gets a signal from SA node -> conducts signal to bundle of his ->
signals Purkinje fibers to contract ventricles -> AV nodes close -> SA
nodes open -> blood flows through pulmonary artery and aorta
○ “LUB”
● DIASTOLE: relaxation of the heart- blood flows in
○ SA nodes fire -> stimulates atrial contraction -> AV nodes open -> blood
flows from atria to ventricles -> SA nodes close
○ “DUB”
Starling’s Law
● “Rubber-band”
○ More blood in the ventricles (preload) = greater stretching of the
ventricular walls (SV) = more forceful contraction during systole
Circulation

, HR: the more the heart needs to pump, the faster it needs to pump = more O2 needed
Preload: stretching of the ventricle walls that the amount of blood in them is causing
● the amount of blood left after diastole
● Vaso-constriction = increased preload
● Vaso-dilation = decreased preload
Afterload: the resistance the heart has to beat against to eject the blood
● Vaso-constriction = increased afterload
● Vaso-dilation = decreased afterload

BP= CO x PR
● BP (blood pressure): the amount of pressure exerted on the walls of the arteries
as the blood flows through them
○ Vaso-constriction: increases BP
○ Vaso-dilation: decreases BP
● PR (peripheral resistance): resistance of the arteries to the blood being pumped
through them
○ Vaso-constriction = increased PR
○ Vaso-dilation = decreased PR
● CO (cardiac output): the amount of blood leaving the left ventricle per minute
○ Vaso-constriction = increases CO
○ Vaso-dilation = decreases CO
● CO= HR x SV
○ HR (heart rate): the number of times the heart pumps (beats)
■ Vaso-constriction = increases HR
■ Vaso-dilation = decreases HR
■ the more the heart needs to pump, the faster it needs to pump =
more O2 needed
○ SV (stroke volume): amount or volume of blood that is pumped from the
left ventricle each time the heart contracts
■ SV increases/decreases as a response to the increase/decrease
in blood volume
Hypertension
Risk factors:
● High BP, smoking, obesity, high salt intake, minimal exercise
● African Americans are at higher risk
Complications:
● Can damage the fragile inner lining of blood vessels
● Increases myocardial oxygen consumption- puts the heart as a muscle at risk
● Cardiac death, stroke, renal failure, loss of vision
Lifestyle modifications:
● Weight loss, exercise
● Decreasing salt intake, alcohol, smoking
HTN Crisis:
● Systolic: 180, Diastolic: 110-120

, ● In danger of rapidly developing damage to vital organs- brain, heart, and kidneys
○ Can lead to a stroke
● Priority: lowering BP

BP Regulation
Baroreceptors:
● Pressure receptors found in the arch of the aorta and in the carotid artery
Renin-Angiotensin-Aldosterone System (RAAS):
● Low BP causes kidneys to release renin
○ Renin -> liver releases angiotensinogen -> renin and angiotensinogen
combine -> into angiotensin 1 -> angiotensin 1 -> lungs -> uses ACE ->
converts to angiotensin 2
■ Angiotensin 2: very potent vaso-constrictor
● Stimulates aldosterone release
● Increases sympathetic nervous system activity

Drugs:

Diuretics: Brief overview:
● Exert their effects on different areas of the renal tubules
○ Excretion of Na+ and H2O - decreases CO and BP
● Used to decrease fluid volume when the body can’t regulate the fluid volume
○ Ex: heart failure, hypertension, pulmonary edema, kidney failure
● Adverse effect: electrolyte imbalance

RAAS
ACE-Inhibitors (-PRIL): captopril: acts in the lungs by preventing ACE from
converting angiotensin 1 to angiotensin 2
● Captopril inactivates ACE, blocking the breakdown of bradykinin, which
results in an increase of bradykinin levels and slight dilation. Stimulates
the dry cough.
● Contraindications: allergy, angioedema, pregnancy
● Decreases PR and BP
● Enalaprilat: only given through IV
○ Name: Captopril
○ Use: hypertension and heart failure
■ Beneficial for patients with chronic kidney disease and
diabetes- reduces proteinuria
○ Side effects: hypotension, chronic cough
■ 2 life-threatening effects: angioedema and neutropenia
● Angioedema: swelling of lips/pharynx
● Neutropenia: decrease in white blood cells
○ Black Box Warning: can cause injury or death to fetuses in the
2nd/3rd trimester