Nurs 5315: Adv Patho Exam 3 Set 1
Afterload definition - ANS-resistance that the ventricle must overcome during systole to eject
blood into circulation, aortic pressure and systemic vascular resistance
Increased aortic pressure/SVR > increased afterload > ventricular hypertrophy
decreased afterload enables heart to contract faster
Increased afterload slows contractions
\Alterations in anatomy and physiology with aging - ANS-blood vessel stiffening/decreased
elasticity
LV hypertrophy and fibrosis > valvular heart disease
\Anterior wall MI (LAD) - ANS-ST-elevation or Q waves, or ST depression in V1-V4
\Anterolateral MI (LAD or LCX) - ANS-ST elevations, Q waves or ST depression in V4-6
\Anteroseptal MI (LAD) - ANS-ST elevations, Q waves or ST depression in V1-V2
\antiarrhythmic drug classes - ANS-Class 1 = Na channel blockers
Class 2 = Beta blockers
Class 3 = K+ channel blockers (prolongs action potential duration)
Class 4 = Ca channel blockers
'No Bears Kiss Cats'
\Antiarrhythmic drugs - ANS-target cardiac action potentials
\arterial blood pressure - ANS-cardiac output x peripheral resistance
\arteriosclerosis: definition and three types - ANS-abnormal thickening and loss of elasticity
of the walls of an artery or arteries
monckeberg - calcification of medium sized arteries
arteriolosclerosis - hyaline thickening of small arteries
atherosclerosis - accumulation of fat, WBC, platelets in the vessel wall and forms a plaque in
the intima of the artery
\atrial septal defect (ASD): Risk factors, Etiology, clinical manifestations, pathophysiology -
ANS-E: flaw in the septum that divides the two atria of the heart
RF: age > 40, previous child w/ CHD, SLE, diabetes, ETOH, infection, aspirin, phenytoin
CM: crescendo-decrescendo systolic murmur
Patho:
Complications: increased risk of embolus
\Beta Blockers: effect on myocardial contraction - ANS-decrease heart rate and dilate
arteries by blocking beta receptors
Decreases contractions
They do this by blocking beta-adrenergic receptors
Clinical Implications: used for chest pain and hypertension
\Calcium imbalance affect on myocardial action potentials - ANS-Hypocalcemia-decreased
contractility
Hypercalcemia-increased contractility>ST and PJCs, vasoconstriction
\Cardiac action potential: phase 0 - ANS-rapid depolarization
Sodium influx d/t voltage-gated sodium channels opening
\Cardiac action potential: phase 1 - ANS-initial repolarization of cells
voltage gated sodium channels closed
voltage gated potassium channels open
, Potassium leaves cell slowly
\Cardiac action potential: phase 2 - ANS-plateau phase
voltage gated calcium channels open
influx of calcium into the cell
balances potassium efflux
calcium influx triggers more calcium from sarcoplasmic reticulum > myocardial contraction
\Cardiac action potential: phase 3 - ANS-Rapid Repolarization w/ potassium efflux
voltage gated potassium channels open
voltage gated calcium channels close
\Cardiac action potential: phase 4 - ANS-resting membrane potential, -85 mV
High potassium permeability from the potassium channels
\Cardiac Anatomy - ANS-The heart is the size of a closed fist
2/3 of the heart is to the left of the midline
1/3 under the sternum
\Cardiac Blood Flow - ANS-o From body
o Through:
♣ Vena cavas
♣ Right atrium
♣ Tricuspid valve
♣ Right ventricle
♣ Pulmonic valve
♣ Pulmonary artery
o To lungs
♣ Pulmonary vein
♣ Left atrium
♣ Mitral valve
♣ Left ventricle
♣ Aortic valve
o Back to body
\Cardiac Cycle: Diastole - ANS-Ventricles relaxed
Blood entering atria
Blood flows through AV valves into ventricles
Semilunar valves are closed
\Cardiac Cycle: Systole - ANS-Ventricles contract
Blood pushes against AV valves and they shut
Blood pushes through semilunar valves into aorta and pulmonary trunk
\Cardiac Output (CO) - ANS-Amount of blood pumped in 1 minute (~5 L)
HR x Stroke volume
\Cardiovascular disease - ANS-Most common cause of disease/death in the elderly
#1 HTN
#2 atherosclerosis
\Chronotropy - ANS-heart rate
Afterload definition - ANS-resistance that the ventricle must overcome during systole to eject
blood into circulation, aortic pressure and systemic vascular resistance
Increased aortic pressure/SVR > increased afterload > ventricular hypertrophy
decreased afterload enables heart to contract faster
Increased afterload slows contractions
\Alterations in anatomy and physiology with aging - ANS-blood vessel stiffening/decreased
elasticity
LV hypertrophy and fibrosis > valvular heart disease
\Anterior wall MI (LAD) - ANS-ST-elevation or Q waves, or ST depression in V1-V4
\Anterolateral MI (LAD or LCX) - ANS-ST elevations, Q waves or ST depression in V4-6
\Anteroseptal MI (LAD) - ANS-ST elevations, Q waves or ST depression in V1-V2
\antiarrhythmic drug classes - ANS-Class 1 = Na channel blockers
Class 2 = Beta blockers
Class 3 = K+ channel blockers (prolongs action potential duration)
Class 4 = Ca channel blockers
'No Bears Kiss Cats'
\Antiarrhythmic drugs - ANS-target cardiac action potentials
\arterial blood pressure - ANS-cardiac output x peripheral resistance
\arteriosclerosis: definition and three types - ANS-abnormal thickening and loss of elasticity
of the walls of an artery or arteries
monckeberg - calcification of medium sized arteries
arteriolosclerosis - hyaline thickening of small arteries
atherosclerosis - accumulation of fat, WBC, platelets in the vessel wall and forms a plaque in
the intima of the artery
\atrial septal defect (ASD): Risk factors, Etiology, clinical manifestations, pathophysiology -
ANS-E: flaw in the septum that divides the two atria of the heart
RF: age > 40, previous child w/ CHD, SLE, diabetes, ETOH, infection, aspirin, phenytoin
CM: crescendo-decrescendo systolic murmur
Patho:
Complications: increased risk of embolus
\Beta Blockers: effect on myocardial contraction - ANS-decrease heart rate and dilate
arteries by blocking beta receptors
Decreases contractions
They do this by blocking beta-adrenergic receptors
Clinical Implications: used for chest pain and hypertension
\Calcium imbalance affect on myocardial action potentials - ANS-Hypocalcemia-decreased
contractility
Hypercalcemia-increased contractility>ST and PJCs, vasoconstriction
\Cardiac action potential: phase 0 - ANS-rapid depolarization
Sodium influx d/t voltage-gated sodium channels opening
\Cardiac action potential: phase 1 - ANS-initial repolarization of cells
voltage gated sodium channels closed
voltage gated potassium channels open
, Potassium leaves cell slowly
\Cardiac action potential: phase 2 - ANS-plateau phase
voltage gated calcium channels open
influx of calcium into the cell
balances potassium efflux
calcium influx triggers more calcium from sarcoplasmic reticulum > myocardial contraction
\Cardiac action potential: phase 3 - ANS-Rapid Repolarization w/ potassium efflux
voltage gated potassium channels open
voltage gated calcium channels close
\Cardiac action potential: phase 4 - ANS-resting membrane potential, -85 mV
High potassium permeability from the potassium channels
\Cardiac Anatomy - ANS-The heart is the size of a closed fist
2/3 of the heart is to the left of the midline
1/3 under the sternum
\Cardiac Blood Flow - ANS-o From body
o Through:
♣ Vena cavas
♣ Right atrium
♣ Tricuspid valve
♣ Right ventricle
♣ Pulmonic valve
♣ Pulmonary artery
o To lungs
♣ Pulmonary vein
♣ Left atrium
♣ Mitral valve
♣ Left ventricle
♣ Aortic valve
o Back to body
\Cardiac Cycle: Diastole - ANS-Ventricles relaxed
Blood entering atria
Blood flows through AV valves into ventricles
Semilunar valves are closed
\Cardiac Cycle: Systole - ANS-Ventricles contract
Blood pushes against AV valves and they shut
Blood pushes through semilunar valves into aorta and pulmonary trunk
\Cardiac Output (CO) - ANS-Amount of blood pumped in 1 minute (~5 L)
HR x Stroke volume
\Cardiovascular disease - ANS-Most common cause of disease/death in the elderly
#1 HTN
#2 atherosclerosis
\Chronotropy - ANS-heart rate
