1. ventricles are not filling with blood because AV valves closed 2. ventricles are not ejecting blood because ventricular pressure is less than aortic pressure, so semilunar valves are still closed occurs during phase 2

CV Physiology Flashcards by Hannah P Erickson

Systemic circulation

path of oxygen rich blood from LV through aorta, pumped to all organ systems, back to heart (RA)

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Pulmonary circulation

path of partially oxygen-depleted blood from RV through lungs and back to the heart (LA)

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Semilunar valves

origin of pulmonary artery and aorta

one-way valves that open during systole to allow blood to enter pulmonary and systemic circulations

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Atrioventricular valves

atria and ventricles are separated into 2 functional units by connective tissue and by AV valves

tricuspid and mitral valves
one-way valves that open during diastole to allow blood into ventricles

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Valves…

prevent backflow of blood
what opens a valve is a difference in pressure

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Cardiac Cycle

repeating pattern of contraction and relaxation of the heart

includes all mechanical and electrical events of the heart

divided into 5 phases

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Systole

contraction phase

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Diastole

relaxation phase

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Phases of Cardiac Cycle

atrial systole
isovolumetric contraction
ejection
isovolumetric relaxation
rapid inflow and diastasis

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Phase 1 Cardiac Cycle

Atrial Systole

Mitral valve is already open, ventricle has been filling with blood before atrial contraction
P wave, atrial depolarization
Atrial contraction pushes 10-20% more blood into ventricle
S4 sound, always abnormal, vibration sound

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Phase 2 Cardiac Cycle

Isovolumetric ventricular contraction

QRS complex, ventricular depolarization
contraction of ventricles causes ventricular pressure to rise
S1 sound: LUB
Ventricular P > atrial P, so AV valves closes
EDV

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Isovolumetric

ventricles are not filling with blood because AV valves closed
ventricles are not ejecting blood because ventricular pressure is less than aortic pressure, so semilunar valves are still closed

occurs during phase 2

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End-diastolic volume

volume of blood in ventricle before ejection
about 120 mL

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Phase 3 of Cardiac Cycle

Ejection

Contraction of ventricles causes ventricular pressure to rise above aortic pressure
Ventricular pressure > atrial pressure, AV valves are closed
Ventricular repolarization (T wave)
Stroke volume is about 80 mL

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T wave

ventricular reploarization
LV pressure starts to fall

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Stroke volume

volume of blood ejected during one contraction
resting SV = 80 mL

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Phase 4 of Cardiac Cycle

Isovolumetric ventricular relaxation

ventricles are fully repolarized and relaxed
ventricular pressure falls below aortic pressure, AV closes
S2 sound–DUB
ESV–volume of blood in ventricles is constant
phase lasts until pressure in ventricles falls to pressure in atria

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Phase 5 Cardiac Cycle

Rapid inflow and diastasis

ventricular pressure < atrial pressure, which opens AV valves
ventricular pressure is low, chamber is relaxed
Rapid ventricular filling occurs (S3 sounds)
cycle returns to phase 1, with active rapid filling

longest phase of cardiac cycle

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Diastasis

reduced ventricular filling and longest phase of cardiac cycle

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S3 sound…

sometimes normal in <40 yrs
abnormal leads to heart failure

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Left ventricular pressure volume loop

1–> 2 Isovolumetric contraction
2–> 3 ventricular ejection
3–>4 isovolumetric relaxation
4–>1 ventricular filling

Isovolumetric contraction…

pressure increases
all valves closed
ventricular volume remains constant

Ventricular Ejection

aortic valve opens
pressure remains high
volume decreases to 70 mL

Isovolumetric relaxation

Ventricle relaxes
aortic valve closes
volume remains constant at 70 mL

Ventricular filling

pressure rises mitral valve opens volume increases

Preload

end-diastolic volume (EDV)

Ejection fraction

portion of blood pumped out of ventricle with each contraction (SV/EDV), often expressed as a percentage healthy/normal = 55-70% systolic heart failure <40%

Afterload

pressure against which the heart has to work to eject blood strictly speaking = aortic pressure more broadly = systemic BP

Contractility

intrinsic ability of myocardial cells to develop force

Increased preload

Increased afterload

Increased Contractility

S1 Sounds

Closing of AV valves when ventricles contract at systole LUB sounds mitral and tricuspid

S2 Sounds

Closing of semilunar valves when ventricles relax at diastole, sometimes can be split during breathing DUB sounds aortic and pulmonic

Heart murmurs

abnormal heart sounds produced by abnormal patters of blood flow in heart caused by turbulent blood flow--> defective heart valves and septal defects

Defective heart valves

causes murmur stenotic = valves do not open fully Regurgitant/insufficient/incompetent = valves do not close tightly

Causes of incompetent heart valves

Congenital Damage by antibodies (rheumatic endocarditis) damage to papillary muscles

Septal Defects

holes in the septum between left and right sides of heart 1. usually congenital 2. can occur in either septa, blood goes from left to right 3. result is increased blood and pressure on right side of heart, leading to pulmonary HTN and edema

Cardiac muscles

myocardial cells are striated, actin/myosin are arranged in sarcomeres, short, branched, interconnected cells. Have gap junctions cardiac muscle can produce action potentials spontaneously

Gap junctions

each cell is joined to adjacent cell by electrical synpase helps depolarization to spread quickly

Functional Synctium

adjacent cardiac muscle cells are all connected results in myocardium behaves like a single, large muscle cell no graded contractions like those in skeletal muscle, electrical impulses spreads to all cells

How can myocardial contractility be increased?

increased EDV/frank-starling mechanism epinephrine/norepinephrine (increases Ca)

Types of heart cells

Contractile cells conducting/automatic cells

Contractile cells

produce the force of contraction the pump

Conducting/automatic cells

contribute little to no force generation in heart include SA node, AV node, bundle of His, purkinje fibers

Depolarization

occurs when there is a net movement of positive ions into the cell (inward current)

Hyperpolarization

occurs when there is a net movement of positive ions out of the cell (outward current)

Mechanisms that can produce in membrane potential

change in driving force for a permeant ion opening and closing of ion channels

Automaticity

automatic nature of the heartbeat

Sinoatrial node

group of myocardial cells in RA demonstrate spontaneous depolarization functions as pacemaker, has fastest firing rate don't maintain stable resting membrane potential SA nodes initiate the SINUS rhythm