VTPP 435 EXAM QUESTIONS AND ANSWERS LATEST UPDATE 100%
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cardiac tamponade
excess fluid in pericardial space-- collapses ventricle
pericarditis
inflammation of pericardial sac
pericardium
thin membrane surrounding heart-- fluid-filled to lubricate heart
right atrium
receive deoxygenated blood from rest of body through superior/inferior vena cava
vena cava
a large vein carrying deoxygenated blood from systemic circulation into the heart
right ventricle
pumps deoxygenated blood to the lungs through pulmonary artery
left atrium
receives oxygenated blood from the lungs through pulmonary veins
left ventricle
pumps blood to the systemic circulation through the aorta
which side of the heart has thicker muscle and more pressure
LEFT-- pumps blood to whole body... need more pressure
coronary artery
supplies blood to heart muscle
cordae tendineae
heart string-- keep valves from prolapsing
Cardiac Output (L/min) =
Stroke volume (L/beat) x HR (beat/min)
semilunar valves
pulmonary valve and aortic valve
AV valves
tricuspid (right) and bicuspid (left/mitral)
stenosis
narrowing of a valve
intercalated discs of cardiac muscle
where myocytes come together- contain tight junctions to hold fibers together and gap
junctions to join cells into a FUNCTIONAL SYNCYTIUM
contractile cells
do NOT initiate their own APs
Autorhythmic cells
pacemaker cells, do not contract, DO initiate APs
AV node
causes electrical delay to allow atria and ventricles to contract at diff times- routes
electrical signals so heart contracts from apex to base
SA node
, sets pace of heartbeat-- AV node and purkinje fibers can pick up if SA fails
why does heart have a long refractory period
- allows ventricles time to refill
- prevents tetanus
P wave
atrial depolarization
PR segment
AV nodal delay
QRS complex
ventricular depolarization and atrial repolarization (start of systole)
ST segment
Time when ventricles are contracting and emptying
T wave
ventricular repolarization (beginning of diastole)
TP segment
ventricles are relaxing and filling
heart sound 1
closing of AV valves
heart sound 2
closing of semilunar valves
Stroke Volume =
EDV - ESV (avg 70 mL)
Frank-Starling law
stroke volume increases as EDV increases -- more heart stretches, the more it pumps
out
ejection fraction =
SV/EDV
Tachycardia
Fast heart rate
bradycardia
slow heart rate
Premature ventricular contractions (PVC)
-Foci in ventricles make AP before SA node
- wide and bizarre looking QRS complex w/ no p wave
Heart Block
problem conducting signal to ventricles-- dropped QRS complex
Myocardial infarction (heart attack)
- coronary blockage
-cell death
-anormal QRS complexes
Atrial fibrillation
-rapid, irregular, uncontrolled depol. of atria
- no definite P waves
- normal/sporadic QRS complexes
ventricular fibrillation
CORRECT A+ GRADED. Buy Quality Materials!
cardiac tamponade
excess fluid in pericardial space-- collapses ventricle
pericarditis
inflammation of pericardial sac
pericardium
thin membrane surrounding heart-- fluid-filled to lubricate heart
right atrium
receive deoxygenated blood from rest of body through superior/inferior vena cava
vena cava
a large vein carrying deoxygenated blood from systemic circulation into the heart
right ventricle
pumps deoxygenated blood to the lungs through pulmonary artery
left atrium
receives oxygenated blood from the lungs through pulmonary veins
left ventricle
pumps blood to the systemic circulation through the aorta
which side of the heart has thicker muscle and more pressure
LEFT-- pumps blood to whole body... need more pressure
coronary artery
supplies blood to heart muscle
cordae tendineae
heart string-- keep valves from prolapsing
Cardiac Output (L/min) =
Stroke volume (L/beat) x HR (beat/min)
semilunar valves
pulmonary valve and aortic valve
AV valves
tricuspid (right) and bicuspid (left/mitral)
stenosis
narrowing of a valve
intercalated discs of cardiac muscle
where myocytes come together- contain tight junctions to hold fibers together and gap
junctions to join cells into a FUNCTIONAL SYNCYTIUM
contractile cells
do NOT initiate their own APs
Autorhythmic cells
pacemaker cells, do not contract, DO initiate APs
AV node
causes electrical delay to allow atria and ventricles to contract at diff times- routes
electrical signals so heart contracts from apex to base
SA node
, sets pace of heartbeat-- AV node and purkinje fibers can pick up if SA fails
why does heart have a long refractory period
- allows ventricles time to refill
- prevents tetanus
P wave
atrial depolarization
PR segment
AV nodal delay
QRS complex
ventricular depolarization and atrial repolarization (start of systole)
ST segment
Time when ventricles are contracting and emptying
T wave
ventricular repolarization (beginning of diastole)
TP segment
ventricles are relaxing and filling
heart sound 1
closing of AV valves
heart sound 2
closing of semilunar valves
Stroke Volume =
EDV - ESV (avg 70 mL)
Frank-Starling law
stroke volume increases as EDV increases -- more heart stretches, the more it pumps
out
ejection fraction =
SV/EDV
Tachycardia
Fast heart rate
bradycardia
slow heart rate
Premature ventricular contractions (PVC)
-Foci in ventricles make AP before SA node
- wide and bizarre looking QRS complex w/ no p wave
Heart Block
problem conducting signal to ventricles-- dropped QRS complex
Myocardial infarction (heart attack)
- coronary blockage
-cell death
-anormal QRS complexes
Atrial fibrillation
-rapid, irregular, uncontrolled depol. of atria
- no definite P waves
- normal/sporadic QRS complexes
ventricular fibrillation
