UTA patho EXAM QUESTIONS AND
CORRECT DETAILED ANSWERS WITH
RATIONALES|ALREADY GRADED A+
||BRAND NEW!!!
Blood flow through the heart - Answers - ✔✔1-Superior & Inferior Vena Cava, 2-Rt
Atrium, 3-Tricuspid Valve, 4- Rt Ventricle, 5-Pulmonary Valve, 6-Pulmonary Artery, 7-
Lungs-pick up oxygen, 8-Pulmonary Veins, 9- Lt Atrium, 10- Mitral Valve (Bicuspid), 11-
Lt Ventricle, 12- Aortic Valve, 13-Aorta, 14- Body
endocardium - Answers - ✔✔inner lining of the heart; made of simple squamous cells
and connective tissue
myocardium - Answers - ✔✔muscular, middle layer of the heart; contains myocytes
responsible for muscle contraction
pericardium - Answers - ✔✔outermost layer; two layers: fibrous- connective tissue that
provides the heart with stability by connecting to the sternum anteriorly and the
diaphragm inferiorly serous- two layers: epicardium- visceral layer- directly over the
heart and contains coronary arteries; parietal- above the epicardium and underneath
fibrous pericardium
placenta - Answers - ✔✔oxygen exchange occurs and that removes waste products
and provides nutrients
cardiac fetal blood flow oxygenated - Answers - ✔✔60% of the blood; placenta->
umbilical vein ->hepatic circulation and connects to the inferior vena cava by the ductus
venosus -> right atrium -> oxygenated blood shunted through the foramen ovale to the
left atrium -> left ventricle and to the head and rest of the body
cardiac fetal blood flow mixed blood - Answers - ✔✔40% of the blood; mixed
oxygenated and deoxygenated blood; right atrium -> right ventricle -> pulmonary artery-
>patent ductus arterious -> aorta -> umbilical artery -> placenta to exchange gas, get rid
of waste and pick up nutrients
fetal pressure in the heart - Answers - ✔✔right side is higher in utero and left becomes
higher after birth
diastole - Answers - ✔✔relaxation; ventricles fill with blood
,systole - Answers - ✔✔ventricular contraction that pushes the blood from the right vent
to the pulm artery and from the left vent to the aorta
atrial kick - Answers - ✔✔blood pushed into the ventricles because of atrial contraction;
increases the amount of blood put into the left ventricular and is 20% of cardiac output
cardiac output - Answers - ✔✔amount of blood pushed from the left ventricle in 1 min;
HR x stroke volume; normal is 5L/min
stroke volume - Answers - ✔✔amount of blood ejected by the ventricle for each cardiac
cycle; dependent on the force of the contraction (contraction is dependent on the
amount of preload which stretches the ventricles and promote contraction, stimulation
by endogenous positive inotropic agents (epinephrine and norepi), presence of inotropic
agents (medications and cytokines), and the myocardial contraction
ejection fraction - Answers - ✔✔percentage of blood ejected from the vent w/ea
contraction; SV/end diastolic vol; normal is 55-65%; used as a parameter to measure
cardiac fxn; decreases in systolic heart failure
Preload - Answers - ✔✔end diastolic volume and end diastolic pressure; dependent on
amount of venous return to the heart & the amount of bl in the left vent at the end of
systole; increased preload= heart failure which causes a decline in SV & back up in
pulm circulation
afterload - Answers - ✔✔resistance that the vent pushes against to contract; aortic
press and systemic vascular resistance; high: increases the work of the vent resulting in
hypertrophy
mean arterial pressure - Answers - ✔✔average pressure in the arteries during a cardiac
cycle; dep on elasticity of the arterial walls & the mean vol of bl in the aterials; norm is
70-100
cardiac contraction - Answers - ✔✔depends on degree of tension of the left vent & the
amount of intracellular ca; greater the amount of ca, the greater the contraction
Diltiazem, verapamil - Answers - ✔✔calcium channel blockers; effect contractility by
blocking the influx of ca; neg inotropic effects; should be avoided in pts with systolic hrt
failure
increase contractility - Answers - ✔✔-catecholamines (increase ca)
-increase in intracellular ca
- decrease extracellular NA (decreases the activity of the NA/CA exchanger)
- digitalis (blocks the Na/K pump which increases intracellular NA, decreases the activity
of the Na/Ca exchanger, and increases intracellular Ca
,decrease contractility - Answers - ✔✔-beta blockers
- systolic heart failure
- acidosis
- hypoxia/hypercapnia
- nondihydropyridine ca channel blockers
conduction system - Answers - ✔✔- SA node (right atrium) generates impulse of 60-100
which is transmitted to the AV node
- If the SA node fails then the AV node will generate an impulse of 40-60 and pass the
impulse down to the bundle of His
- if the AV node fails then the bundle of his will generate an impulse at less than 40 and
the impulse will travel to the purkinje fibers which travel up the wall of the vent and
cause contraction of the vent
Ventricular action potential - Answers - ✔✔occurs in the purkinje fibers and the bundle
of his
- phase 0: rapid depolarization: voltage gated Na channels open and Na comes in
- phase 1: initial repolarization of the cells: voltage gated Na channels are closed and
the voltage gated K channels open and K slowly leaves the cell
- phase 2: plateau phase: Ca channels open and Ca comes into the cell. Influx causes a
balance with K causing a temporary plateau in repolarization; influx of Ca triggers
release of more Ca from the sacroplasmic reticulum and causes myocardial contraction
- phase 3: rapid repolarization: massive K efflux; K channels open and Ca channels
close
- phase 4: resting membrane potential of -85 mV
SA/AV node action potential - Answers - ✔✔no phase 1 or 2; no stimulus needed to
generate an action potential
-phase 0: depolatization: Ca channels open; Na channels are inactivated; slow
conduction of the impulse used by the AV node to prolong transmission from the atria to
the vent
-phase 3: repolarization: Ca channels close and K channels open; K efflux
-phase 4: slow depolarization from the slow influx of Na
Anti-arrhythmic drugs - Answers - ✔✔class 1- Na channel blockers
class 2- beta blockers
class 3- prolong action potential duration by blocking K efflux
class 4- block the cardiac Ca current (Ca channel blockers)
P wave - Answers - ✔✔atrial depolarization
PR interval - Answers - ✔✔0.12-0.20; conduction delay through the AV node
QRS complex - Answers - ✔✔ventricular depolarization; <120 milliseconds
, QT interval - Answers - ✔✔mechanical contraction of the ventricles; prolonged QT can
be caused by meds such as fluoroquinolones, diflucan, zofran, psych meds, and mg
deficiency which can increase the risk of V tach, torsades, or V fib
T wave - Answers - ✔✔ventricular repolarization
ST segment - Answers - ✔✔ventricular depolarization
U wave - Answers - ✔✔present in someone with bradycardia or hypokalemia
T wave inversion - Answers - ✔✔myocardial ischemia
ST elevation - Answers - ✔✔indicates myocardial infarction or myocardial injury
newborn cardiac development - Answers - ✔✔-right vent dominance at birth w/ a
thickened wall but systemic vascular resistance increases after birth and the left vent
becomes thicker
- 1 month: vent are = in size
- changes include rise in arterial O2 tension, increased alveloar oxygenation which stim
vasodilation which causes decreased peripheral vascular resistance
- 2 month: pulmonary resistance is equal to the adult
- normal HR: 100-180 due to the oxygen consumption doubling and the increase
demand for O2
- minimal cardiac reserves & additional stressors which increase O2 demands and may
cause acute decomp of the newborn
Age related changes in cardiovascular system - Answers - ✔✔- most common cause of
morbidity and mortality in the elderly
- HTN leads to atherosclerosis
- bl vessels stiffening, left vent hypertrophy and fibrosis, loss of exercise capacity, &
increased incidence of Afib
- decreased elasticity of the arteries r/t changes in the intima media which include
changes in the cross linking of collagen, increase in the amount of collagen, arterial
calcification, changes in the nature of elastin, presence of inflammatory molecules, and
change sin endothelial cell fxn; leads to increase in afterload which causes increase
work for the left ventricle which can lead to hypertrophy
- baroreceptor activity decreases which slows how fast one adjusts to changes in bl
pressure and posture
- fibrosis and calcification
- valvular ds and hrt failure
- decrease in the cardiac index for women while at rest, decrease in CI with exercise for
both gendersd/t decrease in HR & SV
- SV increases
- afterload increases
- myocardial contraction increases while at rest but decreases w/ exercise
CORRECT DETAILED ANSWERS WITH
RATIONALES|ALREADY GRADED A+
||BRAND NEW!!!
Blood flow through the heart - Answers - ✔✔1-Superior & Inferior Vena Cava, 2-Rt
Atrium, 3-Tricuspid Valve, 4- Rt Ventricle, 5-Pulmonary Valve, 6-Pulmonary Artery, 7-
Lungs-pick up oxygen, 8-Pulmonary Veins, 9- Lt Atrium, 10- Mitral Valve (Bicuspid), 11-
Lt Ventricle, 12- Aortic Valve, 13-Aorta, 14- Body
endocardium - Answers - ✔✔inner lining of the heart; made of simple squamous cells
and connective tissue
myocardium - Answers - ✔✔muscular, middle layer of the heart; contains myocytes
responsible for muscle contraction
pericardium - Answers - ✔✔outermost layer; two layers: fibrous- connective tissue that
provides the heart with stability by connecting to the sternum anteriorly and the
diaphragm inferiorly serous- two layers: epicardium- visceral layer- directly over the
heart and contains coronary arteries; parietal- above the epicardium and underneath
fibrous pericardium
placenta - Answers - ✔✔oxygen exchange occurs and that removes waste products
and provides nutrients
cardiac fetal blood flow oxygenated - Answers - ✔✔60% of the blood; placenta->
umbilical vein ->hepatic circulation and connects to the inferior vena cava by the ductus
venosus -> right atrium -> oxygenated blood shunted through the foramen ovale to the
left atrium -> left ventricle and to the head and rest of the body
cardiac fetal blood flow mixed blood - Answers - ✔✔40% of the blood; mixed
oxygenated and deoxygenated blood; right atrium -> right ventricle -> pulmonary artery-
>patent ductus arterious -> aorta -> umbilical artery -> placenta to exchange gas, get rid
of waste and pick up nutrients
fetal pressure in the heart - Answers - ✔✔right side is higher in utero and left becomes
higher after birth
diastole - Answers - ✔✔relaxation; ventricles fill with blood
,systole - Answers - ✔✔ventricular contraction that pushes the blood from the right vent
to the pulm artery and from the left vent to the aorta
atrial kick - Answers - ✔✔blood pushed into the ventricles because of atrial contraction;
increases the amount of blood put into the left ventricular and is 20% of cardiac output
cardiac output - Answers - ✔✔amount of blood pushed from the left ventricle in 1 min;
HR x stroke volume; normal is 5L/min
stroke volume - Answers - ✔✔amount of blood ejected by the ventricle for each cardiac
cycle; dependent on the force of the contraction (contraction is dependent on the
amount of preload which stretches the ventricles and promote contraction, stimulation
by endogenous positive inotropic agents (epinephrine and norepi), presence of inotropic
agents (medications and cytokines), and the myocardial contraction
ejection fraction - Answers - ✔✔percentage of blood ejected from the vent w/ea
contraction; SV/end diastolic vol; normal is 55-65%; used as a parameter to measure
cardiac fxn; decreases in systolic heart failure
Preload - Answers - ✔✔end diastolic volume and end diastolic pressure; dependent on
amount of venous return to the heart & the amount of bl in the left vent at the end of
systole; increased preload= heart failure which causes a decline in SV & back up in
pulm circulation
afterload - Answers - ✔✔resistance that the vent pushes against to contract; aortic
press and systemic vascular resistance; high: increases the work of the vent resulting in
hypertrophy
mean arterial pressure - Answers - ✔✔average pressure in the arteries during a cardiac
cycle; dep on elasticity of the arterial walls & the mean vol of bl in the aterials; norm is
70-100
cardiac contraction - Answers - ✔✔depends on degree of tension of the left vent & the
amount of intracellular ca; greater the amount of ca, the greater the contraction
Diltiazem, verapamil - Answers - ✔✔calcium channel blockers; effect contractility by
blocking the influx of ca; neg inotropic effects; should be avoided in pts with systolic hrt
failure
increase contractility - Answers - ✔✔-catecholamines (increase ca)
-increase in intracellular ca
- decrease extracellular NA (decreases the activity of the NA/CA exchanger)
- digitalis (blocks the Na/K pump which increases intracellular NA, decreases the activity
of the Na/Ca exchanger, and increases intracellular Ca
,decrease contractility - Answers - ✔✔-beta blockers
- systolic heart failure
- acidosis
- hypoxia/hypercapnia
- nondihydropyridine ca channel blockers
conduction system - Answers - ✔✔- SA node (right atrium) generates impulse of 60-100
which is transmitted to the AV node
- If the SA node fails then the AV node will generate an impulse of 40-60 and pass the
impulse down to the bundle of His
- if the AV node fails then the bundle of his will generate an impulse at less than 40 and
the impulse will travel to the purkinje fibers which travel up the wall of the vent and
cause contraction of the vent
Ventricular action potential - Answers - ✔✔occurs in the purkinje fibers and the bundle
of his
- phase 0: rapid depolarization: voltage gated Na channels open and Na comes in
- phase 1: initial repolarization of the cells: voltage gated Na channels are closed and
the voltage gated K channels open and K slowly leaves the cell
- phase 2: plateau phase: Ca channels open and Ca comes into the cell. Influx causes a
balance with K causing a temporary plateau in repolarization; influx of Ca triggers
release of more Ca from the sacroplasmic reticulum and causes myocardial contraction
- phase 3: rapid repolarization: massive K efflux; K channels open and Ca channels
close
- phase 4: resting membrane potential of -85 mV
SA/AV node action potential - Answers - ✔✔no phase 1 or 2; no stimulus needed to
generate an action potential
-phase 0: depolatization: Ca channels open; Na channels are inactivated; slow
conduction of the impulse used by the AV node to prolong transmission from the atria to
the vent
-phase 3: repolarization: Ca channels close and K channels open; K efflux
-phase 4: slow depolarization from the slow influx of Na
Anti-arrhythmic drugs - Answers - ✔✔class 1- Na channel blockers
class 2- beta blockers
class 3- prolong action potential duration by blocking K efflux
class 4- block the cardiac Ca current (Ca channel blockers)
P wave - Answers - ✔✔atrial depolarization
PR interval - Answers - ✔✔0.12-0.20; conduction delay through the AV node
QRS complex - Answers - ✔✔ventricular depolarization; <120 milliseconds
, QT interval - Answers - ✔✔mechanical contraction of the ventricles; prolonged QT can
be caused by meds such as fluoroquinolones, diflucan, zofran, psych meds, and mg
deficiency which can increase the risk of V tach, torsades, or V fib
T wave - Answers - ✔✔ventricular repolarization
ST segment - Answers - ✔✔ventricular depolarization
U wave - Answers - ✔✔present in someone with bradycardia or hypokalemia
T wave inversion - Answers - ✔✔myocardial ischemia
ST elevation - Answers - ✔✔indicates myocardial infarction or myocardial injury
newborn cardiac development - Answers - ✔✔-right vent dominance at birth w/ a
thickened wall but systemic vascular resistance increases after birth and the left vent
becomes thicker
- 1 month: vent are = in size
- changes include rise in arterial O2 tension, increased alveloar oxygenation which stim
vasodilation which causes decreased peripheral vascular resistance
- 2 month: pulmonary resistance is equal to the adult
- normal HR: 100-180 due to the oxygen consumption doubling and the increase
demand for O2
- minimal cardiac reserves & additional stressors which increase O2 demands and may
cause acute decomp of the newborn
Age related changes in cardiovascular system - Answers - ✔✔- most common cause of
morbidity and mortality in the elderly
- HTN leads to atherosclerosis
- bl vessels stiffening, left vent hypertrophy and fibrosis, loss of exercise capacity, &
increased incidence of Afib
- decreased elasticity of the arteries r/t changes in the intima media which include
changes in the cross linking of collagen, increase in the amount of collagen, arterial
calcification, changes in the nature of elastin, presence of inflammatory molecules, and
change sin endothelial cell fxn; leads to increase in afterload which causes increase
work for the left ventricle which can lead to hypertrophy
- baroreceptor activity decreases which slows how fast one adjusts to changes in bl
pressure and posture
- fibrosis and calcification
- valvular ds and hrt failure
- decrease in the cardiac index for women while at rest, decrease in CI with exercise for
both gendersd/t decrease in HR & SV
- SV increases
- afterload increases
- myocardial contraction increases while at rest but decreases w/ exercise
