MSN 377: Exam 1 Questions and Correct Answers,
With Complete Solution, Updated 2024. 205 Questions
and Correct Answers.
body --> IVC/SVC --> RA --> Tricupsid valve --> RV --> Pulmonary Arteries -->
Lungs --> Pulmonary Veins --> LA --> Bi/Mitral Valve --> LV --> Aortic Valve -->
Aorta --> Body
Blood flow of the heart
55-65%
normal ejection fraction
preload
volume of blood in ventricles at end of diastole (rest)
afterload
The force or resistance against which the heart pumps.
anterior
front of the body
posterior
back of body
lateral
Away from the midline of the body; to the side
medial
Toward the midline of the body
proximal
Nearer to the trunk of the body
distal
Farther from the trunk of the body
chromotrope
heart rate
dronotrope
conduction rate (speed of electricity)
ionotrope
contraction of heart (strength of heart)
CO (L/min) = SV (cc/beat; preload, contractility, and afterload) x HR
How to calculate CO
SA node --> Bachman's bundle --> AV node --> Bundle of His --> Right/Left Bundle
Branch --> Purkinje fibers
Conduction pathway of the heart
4-8 L/min
Normal Cardiac Output
VS, inspection, palpitation, auscultation (Heart sounds-S3 and S4, murmurs,
bruits, friction rubs), observation (how does the patient look?)
What should be included in the CV Physical Assessment?
baroreceptors
, detect changes in blood pressure by sensing the MAP; a low MAP can trigger ADH and
RAAS
chemoreceptors
senses and responds to chemicals within the body such as O2, blood pH, CO2)
ADH (antidiuretic hormone)
Produced by Posterior lobe of Pituitary Gland. Targets kidneys for water conservation
by turning on the SNS to increase the HR
RAAS (renin-angiotensin-aldosterone system)
Renin is released by kidneys in response to decreased blood volume; causes
angiotensinogen to split & produce angiotensin I; lungs convert angiotensin I to
angiotensin II; angiotensin II stimulates adrenal gland to release aldosterone & causes
an increase in peripheral vasoconstriction
ANP (atrial natriuretic peptide)
Atrium secretes this to shut off the RAAS system
BNP
Works harder than ANP; the ventricles secrete this to shut down the RAAS system. This
is the unit of measure that will be utilized with HF
goes to the adrenal glands to produce aldosterone (hold Na2+ and H2O), goes to
pituitary to release ADH (hold onto H2O), potent vasoconstrictor, remodels heart
(LV hypertrophy)
4 functions of angiotensin II
aortic area
the right second intercostal space, just lateral to the sternum
pulmonary area
the left second intercostal space, just lateral to the sternum
tricupsid area
inferior left sternal margin
mitral area
5th intercostal space, mid-clavicular line. This is where the apex beat is
hypertensive crisis
BP >180 and/or >120
hypertensive urgency
BP is very high but no evidence of immediate or progressive target organ damage
hypertensive emergency
BP >180/120 and must be lowered immediately to prevent damage to target organs.
There is evidence of end-organ damage
Cardiac Output (cardiac-heart rate, contractility, conductivity;Renal fluid volume-
RAAS, NPs), systemic vascular resistance (SNS system w/ vasoconstriction vs
vasodilation, neurohormonal with vasoconstrictors- angiotensin or
norepinephrine, local regulation-prostaglandins/nitric oxide, endothelin)
Factors influencing Blood Pressure
eyes (arteriovenous nicking, narrowing of retinal arterioles, hemorrhages,
double/cloudy vision, HA), kidney (microalbuminuria, proteinuria, serum
creatinine >1.5), brain (stroke, TIAs), Heart (CAD, HF, LV hypertrophy), abdominal
(aneurysm, aortic dissection), penis (erectile dysfunction), peripheral vascular
(intermittent claudication, faint or absent peripheral pulses)
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