Chapter 20 Flashcards
functions of heart & blood vessels (3)
transport water, gases (O2, CO2, N2), proteins & hormones throughout body
- regulate temperature & blood pH
facilitate functions of immune system
Location of the heart
in the mediastinum
extends from sternum anteriorly to vertebral column posteriorly & lies medially between lungs & pleural membranes that cover them
2/3 of heart’s mass is slightly left of midline
Base of heart
posterior surface - formed by atria
tipped up medially & posteriorly
Apex of heart
formed by tip of left ventricle
projects inferiorly & laterally to left
Pericardium`
membrane that surrounds & protect heart & retains its position in mediastinum
(2) main parts
composed of a tough outer fibrous layer lined by a delicate serous membrane
(2) main parts of Pericardium
1) fibrous pericardium
2) serous pericardium
1) fibrous pericardium
very dense irregular CT
helps anchor & protect heart
2) serous pericardium
deep to fibrous pericardium
thinner, more delicate membrane that forms double layer around heart
(2) layers of serous pericardium
1) parietal layer
2) visceral layer
1) parietal layer of serous pericardium
adheres to ourmost fibrous layer
2) visceral layer of serous pericardium
epicardium
- inner layer
one of the layers that adheres tightly to surface of heart
Pericardial Cavity
space between parietal & visceral layer of serous pericardium
- contains pericardial fluid that lubricates space (secretion of pericardial cells)
Layers of Heart Wall (3)
1) Epicardium
2) Myocardium
3) Endocardium
1) Epicardium
thin, transparent outer layer (visceral layer of serous pericardium) - composed of mesothelium
- fibroelastic & adipose tissue beneath
contains blood vessels, lymphatics, and vessels that supply the myocardium.
2) Myocardium
thick middle layer - composed of cardiac muscle
responsible for the pumping action of heart
- makes up 95% of heart wall
3) Endocardium
thin layer of endothelium (simple squamous epithelium of circulatory system) overlaying thin CT layer
- smooth lining for chambers & covers valves
Chambers of the Heart
upper → Right & Left Atria
lower → Right & Left Ventricles
Right Heart
right atrium & right ventricle
taking venous blood from body & pumping to lungs for oxygenation
**→ powerspulmonary circuit **
Left Heart
left atrium & left ventricle
taking freshly oxygenated pulmonary blood & pumping it systemically
→ powers **systemic circulation **
Top part of heart
weak pump → right & left atria
- loads ventricles by giving an atrial kick before ventricle contract
Bottom part of heart
a strong pump consisting of right & left ventricles
- main pump for pulmonary & systemic circuits
Atrial kick
force contributed by atrial contraction immediately before ventricular systole that contributes to 20% increase in blood ejected by ventricles
Chronic Atrial fibrillation
no atrial kick
flow of blood is dictated by?
pressure differences not muscle
flows from area of high pressure to area of low pressure.
Heart Valves (2)
1) Atrioventricular
2) Outflow (semilunar)
1) Atrioventricular
open to allow blood to flow from atria into ventricles
located at entrance of ventricles
2) Outflow (semilunar)
open to allow blood to flow from ventricles into outflow vessels
located at entrance to outflow vessels leading into pulmonary & systemic circulation
1) Atrioventricular (2)
1) tricuspid (right AV) valve
2) bicuspid/mitral (left AV) valve
2) Outflow (semilunar) (2)
1) pulmonary (right outflow) valve
2) aortic (left outflow) valve
1) tricuspid (right AV) valve
3 leaflets/cusps → opens into right ventricle
2) bicuspid/mitral (left AV) valve
opens into left ventricle
1) pulmonary (right outflow) valve
opens into pulmonary trunk
2) aortic (left outflow) valve
opens into aortic arch
**Operation of Atrioventricular Valves **
- ventricles relaxed
when ventricles relaxed, papillary muscles relaxed & chordae tendinae are slack
blood moves from higher pressure in atria to lower pressure in ventricles through open AV valves
when open, rounded ends of cusps
Operation of Atrioventricular Valves
- ventricles contracting
when ventricles contract, pressure of blood drives cusps upward until edges meet & close opening
papillary muscles contract at same time, pulls on & tightens chordae tendinae to prevent cusps from opening into atria in response to high ventricular pressure
Operation of Semilunar Valves
made up of 3 crescent moon-shaped cusps
- each attached to arterial wall (each = 1/3 of valve)
- allow ejection of blood from heart into arteries but prevents backflow into ventricles
Operation of Semilunar Valves
- ventricles contract
pressure builds up in chambers
SL valves open when ventricle pressure > artery pressure → ventricular ejection
ejects blood from ventricles into **pulmonary trunk/aorta **
Operation of Semilunar Valves
- ventricles relaxed
SL valves close
- when blood in aorta/pulmonary outflow tract **leaks back into ventricles **
- SL cusps act as sails, fill up & free edges contact & close opening
No valves guarding which (2) junctions
1) between venae cava & right atrium
2) between pulmonary veins & left atrium
Backflow of blood between:
venae cava & right atrium
pulmonary veins & left atrium
as atria contract, small amount of blood flows back into vessels but minimized by the way atria contract
- which compresses & **nearly collapses venous entry points **
Arteries
vessels that always conduct blood away from heart
- contain oygenated blood (few exceptions)
- thick-walled & exposed to high pressure & friction forces
Veins
vessels that always bring blood back to heart
contain de-oxygenated blood (few exceptions)
thin-walled & exposed to low pressures & minimal friction forces
Arteries carry oxygenated blood - Exceptions?
pulmonary arteries (& umbilical)
→carry de-oxygenated blood to lungs (pulmonary capillaries)
Veins carry de-oxygenated blood - Exceptions?
pulmonary veins (& umbilical)
→ carry oxygenated blood to **left atrium **
Major arteries that attach to heart
1) arch of aorta (ascending &descending)
2) pulmonary trunk (left & right pulmonary arteries)
3) **coronary arteries **
Major veins that attach to heart
(4)
1) superior vena cava
2) inferior vena cava
3) pulmonary veins (4)
4) coronary sinus (on back of heart)
(2) circuits of blood flow
1) Systemic
2) Pulmonary
1) Systemic Circulation
ejects blood into aorta, systemic arteries & arterioles
- is powered by left side of heart.
1) Pulmonary Circulation
ejects blood into pulmonary trunk
- powered by **right side of heart **
starting with venous return to heart.. blood flow?
deoxygenated blood →right atrium from (3) sources →right side of heart → lungs
oxygenated blood → left side of heart to be pumped through outflow tract of systemic circulation
Right Atrium recieves blood from? (3)
1) superior vena cava
2) inferior vena cava
3) coronary sinus
left side of heart pumps…
oxygenated blood into systemic circulation to all tissues of body except the air sacs (alveoli) of lungs.
right side of heart pumps…
deoxygenated blood into the pulmonary circulation to air sacs (alveoli) of the lungs
Blood Flow - complete circle
RA → triscuspid valve → RV → pulmonary trunk & arteries → lungs (pulmonary capillaries) - blood loses CO2 & gains O2
Lungs → pulmonary veins → LA → bicuspid valve → LV → aortic valve →aorta & systemic arteries → body systemic capillaries ** **
Coronary Circulation
blood circulation in network of blood vessels in myocardium - supplies nutrients
Coronary Circulation
- HEART CONTRACT/RELAXED
coronary arteries branch from ascending aorta
- encircle heart
when heart contracts, little blood flow in coronary arteries (squeezed shut)
when heart relaxes, high pressure of blood in aorta propels blood through coronary arteries → capillaries → coronary veins
When does blood flow through coronary circulation?
only during relaxation phase of ventricular **diastole **
Blood flow through Coronary circulation
- Coronary **Arteries **
aorta → left & right coronary arteries
LCA → anterior interventricular + circumflex branches
RCA → marginal + posterior atrioventricular branches
Blood flow through Coronary circulation
- Coronary Veins
arteries of coronary circulation → capillaries → deliver nutrients & O2 to heart muscle → coronary **veins **
→ coronary sinus → right atrium (de-oxygenated blood joins with that of the rest of body)
Cardiac Muscle Tissue
striated
shorter fibers than skeletal muscle
- branch
- only 1 central nucleus
Cardiac Muscle Cell Communication
connect to & communicate with neighboring cells through gap junctions in intercalated discs
Which tissues of heart can derive oxygen from blood flowing through chambers?
innermost tissues
Formation → Autorhythmicity of Heart Muscle Cells
During embryonic development, about 1% of all cardiac muscle cells become autorhythmic fibers & form network/ pathway called **cardiac conduction system. **
cardiac conduction system
network of specialized cardiac muscle fibers that produce path for each cycle of cardiac excitation to progress through heart
specialized group of myocytes
have ability to spontaneously depolarize
Autorhythmicity
rhythmical electrical activity produced by autorhythmic fibers
vBecause heart muscle is autorhythmic, it does not…
rely on CNS to sustain lifelong heartbeat
cardiopulmonary bypass
heart and lung machine reoxygenates blood & pumps it through system
technique that temporarily takes over function of heart and lungs during surgery, maintaining circulation of blood and the oxygen content of body.
Autorhythmic cells spontaneously depolarize at a given rate, some groups faster, some groups slower
vOnce a group of autorhythmic cells reaches threshold …
starts an AP
→ all cells in that area of heart also depolarize
The self-excitable myocytes that “act like nerves” (autorhythmic fibers) have (2) important roles
forming conduction system of heart
acting as pacemakers within that system
What acts as the normal pacemaker of the heart?
Why?
Location?
Sinoatrial (SA) node
because it has fastest rate of depolarization
located in right atrial wall just below where superior vena cava enters chamber.
Spontaneous Depolarization of autorhythmic fibers in the SA node fire how often
about once every 0.8 seconds
or
75 APs/min
SA node - functions as Pacemaker
sets rhythm of electrical excitation that causes heart contraction
AP from SA node goes where?
reaches next pacemaker throughout wall of atria to AV node in interatrial septum
AP at AV node…
signal is slowed, allowing atrium to mechanically move blood into ventricles
From AV node, signal goes where?
passes through AV bundle to right & left bundle branches in interventricular septum towards apex of heart
from left & right bundle branches in interventricular septum.. where does signal go?
towards apex of heart to Purkinje fibers that rapidly conduct AP through ventricles
(0.2 secs after atrial contraction)
Natural rhythm of the heart by the SA node
100 bpm
Coordinating Contractions of Atria & Ventricles
atrial muscle syncytium contracts as single unit to force blood down into the ventricles
syncytium of ventricular muscle starts contracting at apex (inferiorly), squeezing blood upward to exit the outflow tract
Cardiac Muscle Action Potential
- start?
AP initiated by SA node travels through conduction system to excite contractile muscle fibers in atria & ventricles
contractile fibers
resting membrane potential?
-90 mV
AP propogates through heart by?
opening & closing Na+ & K+ channels
Refractory Period in Cardiac muscle
lasts longer than contraction itself
→ meaning another contraction cant begin until relaxation is well underway
(safety mechanism)
Tetanus in Cardiac Muscle
DOES NOT OCCUR
leaving sufficient time b/w contractions for chambers to fill with blood
Complications of tetanus in cardiac muscle
heart attack
Cardiac Muscle AP
(3) steps
1) Depolarization
2) Plateau
3) Repolarization
1) Depolarization
-90 mV
reaches threshold by AP from neighboring fibers
fast Na+ channels open → Na+ inflow → rapid depolarization
2) Plateau
period of maintained depolarization → 0.25 sec
partially due to opening of slow Ca2+ channels → Ca2+ inflow
→ causes more Ca2+ from SR → triggers contraction
Just before plateau phase, K+ channels open → K+ outflow
(maintaining depolarization bc Ca2+ inflow balances K+ outflow)
3) Repolarization
recovery of resting membrane potential
after delay, more K+ channels open → K+ outflow restores negative RMP to -90mV
At same time, Ca2+ channels in SR close
Epinephrine
- released by?
- effect?
release by sympathetic NS
increases contraction force by enhancing movement of Ca2+ into cytosol
Electrocardiogram
recording of electrical changes on surface of body resulting from depolarization & repolarization of myocardium
vECG recordings measure ….(3)
the presence or absence of certain waveforms (deflections)
the size of the waves
** time intervals** of the cardiac cycle
By measuring the ECG, we can … ?
quantify & correlate, electrically, the mechanical activities of the heart.
ECG recording can help determine?
normal from abnrmal cardiac activity
Abnormal ECGs show ?
problems within conduction pathways
whether or not heart is enlarged
if cerain regions are damaged
Major deflections & intervals in normal ECG include? (4)
P wave
P-Q interval
QRS wave
S-T segment
P wave
atrial depolarization
spreads from SA node through contractile fibers in both atria
P-Q interval
time from beginning of P wave to beginning of QRS complex
represents conduction time from beginning of atrial excitation to beginning of ventricular excitation
time it takes for atrial kick to fill ventricles
QRS wave
ventricular depolarization & atrial repolarization
as AP spreads through ventricular contractile fibers
S-T segment
- from end of S wave to beginning of T wave*
- time when ventricular contractile fibers depolarized during plateau*
time it takes to empty ventricles before they repolarize
T wave
ventricular repolarization
occurs just as ventricles start to relax
Correlation of ECG Waves with Atrial and Ventricular Systole
steps (6)
1) Depolarization of atrial contrctile fibers → P wave
2) Atrial systole (contraction)
3) Depolarization of ventricular contractile fibers → QRS wave
4) Ventricular systole (contraction)
5) Repolarization of ventricular contractile fibers → T wave
6) Ventricular diastole (relaxation)
1) Depolarization of atrial contrctile fibers → P wave
AP in SA node → through atrial muscle → AV node
(0.03 sec)
2) Atrial systole (contraction)
conduction of AP slows at AV node bc fibers have small diameter & gap junctions
result is 0.1-sec delay giving atria time to contract
3) Depolarization of ventricular contractile fibers → QRS wave
AP enters AV bundle →bundle branches → Purkinje fibers → ventricular myocardium
depolarization
4) Ventricular systole (contraction)
after QRS complex, continues during S-T segment
As contraction proceeds from apex toward base of heart, blood is squeezed upward toward SL valves.
5) Repolarization of ventricular contractile fibers → T wave
repolarization of ventricular contractile fibers begins at apex & spreads throughout ventricular myocardium
T wave 0.4 sec after onset of P wave
6) Ventricular diastole (relaxation)
after T wave begins, ventricles start to relax
By 0.6 sec, ventricular repolarization = complete
Although heart does not rely on outside nerves for its basic rhythm, there is …?
abundant sympathetic & parasympathetic innervation which alters rate and force of heart contractions.
Role of ANS input
regulate changes in:
BP
blood flow
blood volume to maintain enough cardiac output to provide for all organs 24/7
Input to CV center
FROM:
higher brain centers → cerebral cortex, limbic system, hypothalamus
sensory receptors →, proprio, chemo, baroreceptors
Output to heart
CV center
- cardiac accelerator nerves (sympathetic)
- vagus (cranial nerve X, parasympathetic)
cardioacceleratory center
- location
- recieves info from?
in medulla
sensory info from baroreceptors in carotid body & in arch of aorta relay info about BP & blood flow to cardioacceleratory center
Nervous system regulation of heart
originates in CV center in medulla
Sympathetic nerves of heart
present throughout atria (especially in SA node) & ventricles
Effect of Sympathetic activity
increases heart rate & strength of myocardiac contraction to increase blood flow out of heart (ejection fraction)
cardioinhibitory center
- made up of?
- input?
made up of cell bodies of neurons in medula
same sensory info coming in from peripheral baroreceptors goes here
Vagus Nerves (Parasympathetic & Cranial X Nerves)
- effect?
decreases heart rate (but not contractility bc few PS nerves innervate ventricles)
slows heart from its native rate of 100 bpm to about 70-80 in avg adult
Proprioreceptors
monitors movement
Chemoreceptors
monitor blood chemistry
Baroreceptors
monitor blood pressure
Hypocapnia
state of reduced carbon dioxide in the blood
Mechanism of contraction in Cardiac muscle
electrical activity → Ca2+ release from SR → actin & myosin filaments go through contraction cycle → tension develops as filaments slide past one another
Epinephrine & Cardiac contraction
- released by?
- effect?
released by sympathetic NS
increases contraction force by enhancing movement of Ca2+ into cytosol
Pacemaker potential
spontaneous depolarization is a pacemaker potential
Blood Pressure
- measured in?
large conducting arteries where high & low pulsations of heart can be detected
(usually brachial artery)
Systolic BP
higher pressure measured during left ventricular systole when aortic valve is open
Diastolic BP
lower pressure measured during left ventricular diastole when valve is closed
systole
contraction
diastole
relaxation
Normal BP
varies by age but ~120 mmHg over 80 mmHg in healthy young adult
(in females, pressures are often 8-10 mmHg less)
People have low BP if…? (2)
in good physical condition
favorable genetic predisposition
Best way to refer to BP
as a single number → mean arterial pressure (MAP)
mean arterial pressure (MAP) = ?
roughly 1/3 of way between diastolic & systolic BP
1/3(systolic BP - diastolic BP) + diastolic BP
gives us an idea of average pressure experienced by blood vessels during a cardiac cycle
Where are BP pulsations not detectable?
In smaller arterioles, capillaries & veins
→ only mean BP is measurable
Cardiac Cycle
all events of one heartbeat
including diastole (relaxation) & systole (contraction) of atria & ventricles
In each Cardiac Cycle..
atria & ventricles alternatively contract
all 3 heart valves open & close
Auscultation
listening (usually with stethoscope) to sound heart makes
“Lubb Dupp” sounds associated with Auscultation
produced by valve closure (valve opening usually silent)
During Atrial Systole…
(4)
- 1 sec → atria contracting while ventricles relaxed
1) Depolarization of SA node → atrial depolarization (P wave)
2) causes atrial systole → atria contract → exert pressure on blood within to force it through open AV valves into ventricles
3) contributes 25 ml to 105 ml of blood →130 mL at end of diastole (end-diastolic volume (EDV))
4) QRS complex marks onset of ventricular depolarization
During Ventricular Systole
(4)
- 3 sec - ventricles contracting
1) ventric. depolarization → ventric. systole → P increases → blood pushes against & closes AV valves →
Isovolumetric contraction - both SL & AV valves closed (isovolumetric)
→ cardiac muscle fibers contract & exert force but don’t shorten yet (isometric)
2) when ventric. P > aortic/pulm trunk. P → SL valves open → ventricular ejection (0.25 sec)
3) ventricles ejects 70 mL into aorta/pulm trunk
volume remaining in ventricle after systole (60 mL) = end-systolic volume
4) T wave marks onset of ventricular repolarization
During Relaxation Period
(2)
0.4 sec → both atria & ventricles are relaxed
1) ventric. repol. causes ventricular diastole
pressure falls → backflow from aorta/pulm trunk closes SL valves
dicrotic wave produced by rebounded blood of closed cusps of aortic valve
isovolumetric relaxation (all 4 valves closed)
2) when ventricular P < atrial P → AV valves open → ventricular filling
end‐diastolic volume (EDV)
~ 130 ml
volume of blood in ventricles at end of its relaxation period
Stroke Volume
volume ejected per bear from each ventricle
Dicrotic Wave
produced by blood rebounding of aortic valve cusps
End-Systolic Volume (ESV)
volume remaining in each ventricle at end of systole
~60 mL
Average time required to compled cardiac cycle
usually less than 1 second
(0.8 secs at heart rate of 75 BPM)
Stroke Volume = ?
End-diastolic volume (EDV) - End-systolic Volume (ESV)
EDV - ESV = SV
130 mL - 60 mL = 70 mL
Time for:
Atrial Systole
0.1 sec
Atria contract (atrial “kick”), ventricles relax
During Atrial Systole, __ are relaxed
ventricles
During Ventricular Systole, ___ are relaxed
atria
Time for:
Ventricular Systole
0.3 sec
atria relax, ventricles contract
Time for:
Relaxation Period
0.4 sec
allowing passive filing
atria & ventricles relaxed
Cardiac Output (CO)
volume of blood ejected from each ventricle into aorta/pulmonary trunk each minute
Cardiac Output (CO) = ?
Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)
CO (ml/min) = SV (mL/beat) x HR (beats/min)
On average, a person’s entire blood volume flows through pulmonary and systemic circuits each ____.
minute
cardiac reserve
difference between Cardiac Output (CO) at rest & maximum CO heart can generate
Average cardiac reserve = ?
4-5 times resting value
Exercise draws upon _ _ to meet __ ___ demands & maintain __
Exercise draws upon cardiac reserve to meet increased physiological demands & maintain homeostasis
The cardiac output is affected by changes in..? (3)
SV
heart rate
both
(3) important factors that affect SV
1) amount of ventricular filling before contraction
2) contractiliy of ventricle
3) resistance in blood vessels (aorta) or valves (aortic valve, when damaged) heart is pumpinh into (called afterload)
Starling’s Law of the Heart
the more heart msucle stretches (filed) before contraction (preload), the more forcefully heart will contract
*- SV increases with increase in EDV *
Stimulation of **sympathetic NS **during exercise…
**increases **venous return, stretches heart muscle & increases CO