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1. How does blood flow through the heart chambers/valves?: Superior vena cava to
inferior vena cave. Blood then enters the right atrium and passes through the tricuspid valve to the right ventricle. The
right ventricle pumps the blood to the lungs through the pulmonary valve to the pulmonary arteries where it becomes
oxygenated. The oxygenated blood is brought back to the heart by the pulmonary veins which enter the left atrium.
From the left atrium blood flows through the bicuspid (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 between 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
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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, myocardial 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
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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.
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 circulations. 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 (hy-
pokalemia, hypercalcemia), hypoxia, aging, induction of anesthesia, central line placement, cardiac cath, caffeine intake,
drug use, exercise.
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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 triglyc-
erides.
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 receptors.
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 endothelium 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