NURS 5315 UTA Exam 3 Skeletal Outlines + Practice Questions | Updated
1. How does blood flow through the heart chambers/valves?: Superior cava to inferior vena cave. Blood then enters the right atrium and passes t the tricuspid valve to the right ventricle. The right ventricle pumps the blood...
1. How does blood flow through the heart chambers/valves?: Superior cava to inferior
vena cave. Blood then enters the right atrium and passes t the tricuspid valve to the right
ventricle. The right ventricle pumps the blood lungs through the pulmonary valve to the
pulmonary arteries where it bec oxygenated. The oxygenated blood is brought back to the
heart by the pul veins which enter the left atrium. From the left atrium blood flows through the
(mitral) valve into the left ventricle.
2. Which coronary arteries provide blood to which part of the heart?: a. ) Left coronary artery
i.) Left anterior descending artery:widow maker LV and
RV, intraventricular septum
ii. ) Circumflex: LA and left lateral wall of LV.
b. ) Right coronary artery
RV, intraventricular sulcus and small vessels of the RV and LV
3. What factors contribute to blood flow in a vessel?: Pressure difference be- tween two ends of a
vessel
Resistance: r/t diameter of a vessel
Viscosity (n) of the blood
Length (l) of the vessel
4. What does QP: QS mean and what factors alter a normal ratio?: Q=blood flow QP= blood flow
to the lungs (pulmonary) : QS= blood flow to the body (systemic)
i ) Vascular resistance =measures in woods units
ii) Pulmonary vascular resistance (PVR)
1. ) <8 weeks of age: 8-10 woods units/m2
2. ) >8 weeks of age: 1-3 woods units/m2
iii) Systemic vascular resistance
1. ) Infant 10-15 woods units/m2
2.) 1-2 years old: 15-20 woods units/m2 3.) Child
to adult: 15-30 woods units/m2
a) Factors affecting resistance
i.) Compliance-ease that blood travels through the arteries
1. Constriction and relaxation of smooth muscle of arteries and arterioles
a. ) Sympathetic nervous system b.)
Local tissue metabolism
c.) Hormone responses
d.) Changes in chemical environment
5. Explain the process of cardiac contraction and relaxation.
What are the roles of actin, myosin, and troponin in this process?: At rest, active sites on actin are
blocked by troponin and tropomyosin complexes. During action potential, troponin C binds with
calcium and moves the complexes off the actin active site. Actin and myosin interact (contract).
"Walk-along" theory:
Head of myosin cross-bridge attached to the actin filament at the active site.
Intra molecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin
filament with it (power stroke)
Myosin head breaks away and interacts with the next actin active site. Z disc pulls
filaments together at the sarcomeres= muscle contraction.
6. What is the effect of Epinephrine on the cardiovascular system?: Stronger Alpha 1 than Alpha 2.
Works on both, equally strong on Beta 1 (renin release), and Beta 2. Positive inotrope. Increases heart
rate, smooth muscle contraction, myocar- dial contractility, coronary flow, increase systolic blood
pressure, mild increase in diastolic blood pressure.
7. What is the effect of Norepinephrine on the cardiovascular system?: Slightly stronger Alpha 2
than Alpha 1. Some effect on Beta 1, none on Beta 2. Strong vasoconstriction (smooth muscle
contraction). Increase coronary flow, increase systolic and some diastolic BP.
8. What is the effect of Dopamine on the cardiovascular system?: Positive inotrope. Increases
HR, increases BP (vasoconstriction) Alpha 1, 2, beta 1 and dopamine receptors)
9. What is the process of generating a cardiac action potential? What
electrolytes are involved?: 0-Depolarization
1-Early repolarization
Rapid sodium entering the cell
2. Plateau (repolarization)
Slow sodium and calcium enters the cell
3. Potassium moves out of the cells
4. Return to resting potential
Sodium, Calcium, Potassium
10.What is the conduction pathway?: SA Node, AV Node, Bundle of His, Right & Left Bundle
Branches, Perkinje Fibers
11. How does conduction correlate with the EKG and activity in the heart?: -
P-wave: spread of depolarization through the atria followed by atrial contraction.
, NURS 5315 UTA Exam 3 Skeletal Outlines + Practice
Questions | Updated
P-R interval: pause in conduction at the A-V node
QRS complex: Depolarization of the ventricle, followed by ventricular contraction T wave:
depolarization of the ventricles, happens just before the end of ventricular contraction
12.Define preload.: Volume of blood returning to the heart from systemic circula- tions. RA
pressure or CVP
13.Define afterload.: Systemic pressure=the pressure the heart must pump against to circulate
blood=MAP
14.Define stroke volume.: Amount of blood ejected with each contraction of the heart
15.Define end-diastolic volume.: Amount of blood in the heart after filling, before systole (end of
diastole)
16.Define end-systolic volume.: Amount of blood that remains in the heart after systole
17.Define ejection faction.: Percentage of blood in the chamber that is ejected with each systole
18.Define cardiac output.: Amount of blood pumped into the aorta each minute
19.What are the causes, risk factors, pathophysiology and manifestations of atrial fibrillation?:
Risk factors/causes: Heart failure, ischemic heart disease, HTN, obesity, obstructive sleep apnea,
rheumatic heart disease, thyroid disease
Patho: Remodeling of the myocytes of the myocardium-atria does not fully contract to empty contents.
Estimated 25% loss of blood from the artia to ventricle.
Manifestations: Fatigue, dizziness, dyspnea, irregular pulse, palpitations. Untreated: at risk
for thrombus formation and stroke
20.What are the causes, risk factors, pathophysiology and manifestations of premature
ventricular contractions (PVCs)?: Risk factors/causes: Abnormal
electrolytes (hypokalemia, hypercalcemia), hypoxia, aging, induction of anesthesia, central line
placement, cardiac cath, caffeine intake, drug use, exercise.
Patho: Decreased cardiac output from lack of atrial contribution to ventricular preload Manifestations:
fluttering, pound, palpitations
21.What is the role of lipproteins?: Lipoproteins include lipids, phospholipids, cholesterol, and
triglycerides.
Manufacture and repair plasma membranes and cholesterol needed for bile salts and steroid
hormones.
22. How do the lipproteins inform your knowledge of a persons cardiovascular risk?
Very-low-density lipoproteins (triglycerides) Low-
density liporoteins (LDL)
High-densitity lipoproteins (HDL): Very-low-density lipoproteins (triglycerides): Elevated number
is a strong predictor of risk for future coronary events
Low-density lipoproteins (LDL): "lousy", indicator of coronary risk but in context of other factors: age,
DM, CKD
High-density lipoproteins (HDL): "protective" against atherosclerosis-want high level. Can remove
excess cholesterol from arterial walls
23.What are the risk factors for dyslipidemia?: Primary
1. Geneteitcs reult in abnormal lipid metabolism and/or abnormal cellular lipd recep- tors.
Secondary
1. Lifestyle: Smoking, obesity, sedentary lifestyle, diet
2. Health status: HTN, DM, hypothyroidism, pancreatitis, renal nephrosis, chronic inflammation
2. Medications: Diuretics, beta-blockers, steroids, anti-retrovirals
4. Environmental (not much known): air pollution, exposure to radiation, gut biome.
24. Describe the pathophysiology of atherosclerosis?: 1. ) Injury to the endothe- lium causes an
inflammatory response, monocytes and platelets move to the site of injury.
2. ) LDL enters the intimal layer of vessel, causing inflammation and oxidative stress and macrophage
activation. LDL is engulfed =foam cells. Foam cell accumulation = fatty streak.
3. ) Further inflmmatory process in response to fatty streak. Causes the smooth mucle cells to produce
collagen, which forms over the fatty streak making a plaque. This may calcify: Monckeburg
atheroloclerosis
4.) Complicated lesions (unstable plagues): plaque prone to rupture. (cause ongoing inflammation,
apoptosis, plaque hemorrhage). Once ruptured, clotting cascade is activated and local thrombus can
cause occlusion, leading to ischemia and infarc-
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