NURS 5315 Patho Module 5 Study Guide Cardiovascular- University of Texas Arl
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NURS 5315
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NURS 5315
NURS 5315 Patho Module 5 Study Guide Cardiovascular- University of Texas Arlington/NURS 5315 Patho Module 5 Study Guide Cardiovascular- University of Texas Arlington/NURS 5315 Patho Module 5 Study Guide Cardiovascular- University of Texas Arlington/NURS 5315 Patho Module 5 Study Guide Cardiovascula...
nurs 5315 patho module 5 study guide cardiovascular university of texas arlingtonnurs 5315 patho module 5 study guide cardiovascular university of texas arlingtonnurs 5315 patho module 5 study gui
Examine the anatomy and physiology of the cardiovascular system.
Cardiovascular Anatomy and Physiology
1. Explain the cardiac structure and blood flow through the heart
chambers/valves.
- Heart wall: Pericardium- pericardial sac: prevents displacement of heart, barrier of protection
against infection/inflammation, contains pain receptors/mechanoreceptors (changes BP/HR);
- Parietal pericardium: outer layer; mesothelium/ connective tissue; Visceral (epicardium): inner
layer of pericardium/outer layer of heart; folds to allow vessels to enter/leave heart without
breaching pericardial layers; helps contraction/relaxation of heart with minimal friction of
pericardium;
- pericardial fluid: lubricates membranes to decrease friction with heart beats (approx. 20 mL)
- Myocardium: thickest layer; cardiac muscle/anchored to fibrous skeleton (enlarges with LVH);
internal lining of myocardium- endocardium: connective tissue/squamous cells; lines vessels as
well- creates continual closed circulatory system
- Heart chambers- Right heart- low-pressure pumping to lungs; Left heart- high-pressure
pumping to body
- Atria: smaller/thinner walls (1-2 mm thick) because lower pressure/resistance
- Ventricles: thicker myocardial layer (bulk of the heart- RV is 4-5 mm thick; LV is 12-15 mm
thick); made of muscle fibers from fibrous skeleton of base of heart; thicker because need to be
stronger to pump blood against greater resistance; RV pumps against mean pulmonary
capillary pressure (15 mmHg);
- LV pumps against mean arterial pressure (92 mmHg) which makes LV thicker; RV
crescent/triangle shaped to help propel blood through pulmonary valve to lungs;
- LV bullet shaped to help propel blood through aortic valve to body
- Inflow tract: receives blood from atrium
- Outflow tract: sends blood to circulation
- Blood should not flow between right and left sides of heart unless in utero before being born-
foramen ovale (closes right after birth, normally)
- Septum separates right and left heart
- Heart valves: blood should only flow one way through the heart, valves help maintain the
correct flow- valves open and close at appropriate times to prevent backflow
- Atrioventricular valves- open when ventricles relaxed: blood flows from atria to ventricles; when
ventricular pressure increases, valves shut; leaflets are attached to fibrous skeleton at upper
end and papillary muscles at lower end by chordae tendineae; papillary muscles prevent
prolapse
● Tricuspid- between right atrium and right ventricle; has 3 cusps; largest diameter of opening
1
,● Mitral- between left atrium and left ventricle; cone-shaped funnel
● Mitral and tricuspid complex- atrium, fibrous rings, valvular tissue, chordae tendineae, papillary
muscles, and ventricular walls; damage to any of the six can alter the function significantly
- Semilunar valves- open when ventricular pressure higher, blood flows to systemic and
pulmonary circulation; valves close after ventricular contraction to prevent backflow
● Pulmonic- between right ventricle and pulmonary artery
● Aortic- between left ventricle and aorta
- Superior vena cava/inferior vena cava- deoxygenated blood from veins flow through these to
to right atrium
- Pulmonary artery- transports deoxygenated blood from right ventricle to the pulmonary
circulation; branch into the pulmonary capillaries to obtain oxygen/release carbon dioxide
- Pulmonary vein- carries oxygenated blood from lungs to left atrium;
- Blood flow- diastole: relaxation; blood fills ventricles; systole: contraction; blood flows out of
ventricles to pulmonary/system circulation
- Systemic blood (deoxygenated) from veins enters superior/inferior vena cava -> right atrium ->
tricuspid valve -> right ventricle (diastole)-> pulmonary valve -> pulmonary artery -> lungs (picks
up oxygen and drops CO2) -> pulmonary vein -> left atrium -> mitral valve -> left ventricle
(systole) -> aortic valve -> aorta -> back to systemic circulation through arteries (oxygenated
blood)
- Deoxygenated blood travels from the body through the superior vena cava into the right
atrium. Blood goes from the RIGHT ATRIA through the TRICUSPID valve into the RIGHT
VENTRICLE. Blood is pumped through the PULMONARY ARTERY to the lugs where is picks
up oxygen. Then, back through the PULMONARY VEIN to the LEFT ATRIA. From the atrium,
through the MITRAL (BICUSPID) VALVE to the LEFT VENTRICLE. The oxygenated blood goes
through the aortic valve into the aorta then through the body.
2. Describe which coronary arteries provide blood to which part of the heart.
Right Coronary Artery (RCA): Branches into 3
● Conus: Blood to the upper right ventricle
● Right Marginal Branch: Traverses R ventricle to the apex; supplies smaller branches to both
surfaces of the R ventricle
● Posterior Descending Branch: Lies in the posterior interventricular sulcus and supplies smaller
branches to both ventricles
Left Coronary Artery (LCA): Branches into 2
● Left Anterior Descending Artery (LAD): Delivers blood to portions of left and right ventricles and
much of the interventricular septum
● Circumflex Artery: Travels in a groove called the Coronary Sulcus (separates the left atrium and
ventricle) Supplies blood to the left atrium and the lateral wall of the left ventricle
Collateral Arteries:
2
, ● Functional importance is that they protect the heart from ischemia; they supply blood and
oxygen to the myocardium that has been deprived of oxygen following narrowing of a major
coronary artery (Coronary Artery Disease)
3. Analyze the process of cardiac action potentials.
● Ventricular Action Potential generated from Bundle of His or Purkinji Fibers, 5 phases.
○ Resting membrane potential is ~-85mV.
○ Phase 0: Rapid depolarization (less negative) of the cell. Na+ influx as the result of voltage
gated Na+ channels opening
○ Phase 1: Initial repolarization (more negative) of the cells. Voltage gates Na+ channels are
closed, voltage gages K+ channels being to open and K+ leaves the cell.
○ Phase 2: Plateau change. Ca+ channels open, influx of Ca+ into the cells. This balances out K+
efflux thus causing a temporary plateau in repolarization. Influx of Ca+ triggers release of more
calcium from the sarcoplasmic reticulum and thus massive myocardial contraction.
○ Phase 3: Rapid repolarization with massive K+ efflux. Voltage gated K+ channels open, voltage
gated Ca+ close, causes rapid repolarization.
○ Phase 4: Resting membrane potential of -85mV. High potassium permeability from potassium
channels.
● SA & AV Node Generation
○ 3 Phases
○ Phase 0: Depolarization from the opening of voltage gated Ca+ channels. Voltage gated Na+
are inactivated. *Slow conduction of the impulse which is used by the AV node to prolong
transmission from the atria to the ventricles*
○ Phase 3: Repolarization, from the closure of the voltage gated Ca+ channels, opening of
voltage gated K+ channels.
○ Phase 4: Slow depolarization from the slow, spontaneous efflux of Na+. This gives the SA & AV
nodes the property of automaticity. Do not need stimulus, automatically generate action
potential.
● Acetylcholine and Adenosine cause a decrease in the rate of depolarization and decrease heart
rate.
● Catecholamines increase the rate of depolarization and increase heart rate.
4. Discuss how potassium and calcium imbalances affect myocardial action
potentials, contraction, and the clinical manifestations which result.
● Hypokalemia: Extracellular K+ is depleted, so K+ inside the cell can diffuse more easily. The
cell is HYPERpolarized (more negative) so the cell will need a larger than normal stimulus to
reach threshold potential.
○ Clinical manifestations: weakness, smooth muscle atony, paresthesias, U wave sometimes
present on EKG, and cardiac dysrhythmias
● Hyperkalemia: When extracellular K+ increases, with no change to intracellular K+, the
resting membrane potential becomes more positive. The cell is HYPOpolarized (more positive)
and is more excitable.
○ Clinical manifestations: Peak T waves of EKG, cardiac standstill, paralysis, paresthesias
● Hypocalcemia: Increase the cell permeability to sodium… causes threshold potential to be
more negative and closer to the resting potential. Can cause an action potential more often.
MORE excitability
○ Clinical manifestations: Tetany, hyperreflexia, circumoral paresthesia, seizures, and
3
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