1
Q
nodes
A
specialized regions where pacemaker cells are grouped together ➔ control rate & coordination of cardiac contractions
- sinoatrial (SA) node exhibits autorhythmicity of 70 AP/min = fastest
- located in wall of R atrium near opening of superior vena cava
- atrioventricular (AV) node exhibits autorhythmicity of 50 AP/min
* follows SA node
* can take over if SA is damaged- located near base of R atrium
- bundle of His = tract of pacemaker cells
- starts at AV node & divides into p L & R ventricles
- L & R ventricle need own conduction system: necessary for tuning
- purkinje fibers = specialized transmission cells ➔ have pacemaker cells but not as strong
- small terminal fibers from bundle of His & spread through ventricular myocardium
- exhibit autorhythmicity of 30 AP/min
- follow SA node (& AV node)
- interatrial pathway conducts pacemaker activity from R ➔ L atrium
- L atrium ≠ nodes
- both atria have pacemaker cels, only R has nodes
- internodal pathway conducts from SA ➔ AV
- AV nodal delay = slowed conduction of pacemaker activity through AV node
- delay ensures ventricles contract AFTER atrial depolarization & contraction
- critical for allowing proper feeling
- node pathway: SA node ➔ internodal pathway ➔ AV node ➔ AV bundle of His ➔ R & L bundle branches ➔ purjinke fibers
2
Q
arteries
A
large vessels that carry blood from heart to systemic circulation
- a lot of elastin fibers to stretch to hold pressure from heart
- little resistance to blood flow b/c of large radius
- conduit for low resistance flow & acts as a pressure reservoir b/c elasticity ➔ driving force during ventricular diastole (relaxing & filling)
- can expand & store pressure from contraction
- energy from stretch used to continue propulsion
- arterial walls recoil & maintain pressure during relaxation
3
Q
capillaries
A
smallest diameter vessels that branch from arterioles
- most SA:V ratio
- majority of gas exchange ➔ “action”
- no elastin, SM, or collagen, only thin layer of endothelium
- ↓ thickness = ↑ ROD
4
Q
veins
A
= blood reservoir & channel for oxygen-poor blood flow back to heart
- large diameter vessels when venules merge
- large veins have less elastin because does not have pressure from heart
5
Q
microcirculation
A
collection of arterioles, capillaries, & venules
6
Q
blood flow is determined by
A
- pressure gradient in vessels
- resistance caused by friction & viscosity
7
Q
blood flow
A
F = ∆P/R
- F = flow rate: V of blood passing through vessel per unit of time
- ∆P = pressure gradient: diff in pressure between beginning & end of vessel
- R = resistance to flow
8
Q
resistance to flow depends on:
A
- blood viscosity = friction in blood based on concentration of plasma proteins & # of circulating RBC
- vessel length: ↑ inner vessel SA in contact w/ blood = ↑ resistance to flow
- vessel radius: resistance is inversely proportional to the fourth power of the radius (multiplying the radius by itself four times)
- R ∝ 1/r4
- F ∝ r4
9
Q
pulse pressure
A
diff between systolic & diastolic pressure
10
Q
mean arterial pressure
A
MAP = diastolic pressure + 1/3 pulse pressure
- monitored & regulated by BP reflexes
- systolic = highest arterial pressure
- diastolic = lowest arterial pressure
11
Q
R valves
A
- R atrioventricular (AV) (tricuspid) valve
- R pulmonary semilunar valve
12
Q
valve btwn L atrium & L ventricle
A
L atrioventricular (AV) (bicuspid or mitral) valve
13
Q
electrical activity general overview
A
- heart is self-excitable: initiiates own rhythmic contractions
- contractile cells = 99% of cardiac muscle ➔ do all mechanical pumping work
- autorhythmic cells initiate & conduct own AP that promote muscle contraction
- display pacemaker activity: membrane potential slowly depolarizes btwn AP, drifting to threshold
- cyclically initiate AP tbat spread throughout heart to trigger rhythmic contractions
14
Q
cardiac muscle AP
A
- -90 mV = too negative ∴ cannot initiate own AP
- long refractory period during plateau phase prevents muscle summation & tetanus
- rapid depolarization: fast Na channels open ➔ Na in fast
- plateau phase:
- early, brief repolarization: T-K+ channels open & Na+ channels close ➔ K+ out fast
- slow repolarization: K channels close & slow L-type Ca channels open ➔ Ca in slow
- rapid repolarization: L-type Ca channels close & ordinary K-channels open ➔ K out fast
- RMP maintained by open leaky K+ channels
15
Q
end-diastolic volume (EDV)
A
V of blood in ventricle when relaxation & filling is complete
- = max blood capacity
16
Q
end-systolic volume (ESV)
A
V of blood remaining in ventricle after contraction/emptying
17
Q
stroke volume
A
amount of blood pumped every contraction
- by each ventricle per beat
- EDV − ESV
18
Q
systole
A
ventricular contraction & emptying
- ST segment of ECG wave
- rapid emptying due to pressure
19
Q
diastole
A
ventricular relaxation & filling
- takes longer to fill than empty
- TP segment of ECG wave
20
Q
heart sounds
A
normal sounds from valve closings
- first heart sound (S1) = “lub” ➔ closing of AV valves
- second heart sound (S2) = “dub” ➔ closing of aortic & pulmonary valves
defective valves produce turbulent flow
- heart murmur
- stenotic = not open completely ➔ whistle
- insufficient = not close completely ➔ swish
21
Q
cardiac output (CO)
A
- CO = HR x SV
- ↑ venous return = ↑ ventricular filling (↑ EDV)
- more blood pumped back to heart ➔ more blood fills ventricles ➔ more blood remaining in ventricles after diastole
- ↑ EDV = ↑ stroke volume
22
Q
frank-starling law
A
- describes length-tension relationship btwn EDV & SV
- more blood returned to the heart = more blood pumped out
- intrinsic control of CO
- main determinant of cardiac muscle fiber length = degree of diastolic filling
- more heart is stretched = longer fibers before contraction
- ↑ length ➔ ↑ force of contraction ∴ ↑ SV
23
Q
heart walls
A
- cells
- fibroblasts protect heart from foreign substances → immune system
- monocytes
- endothelial cells
- endocardium = thin layer of endothelial tissue lining interior of each chamber ➔ exchanges O2 & gases quickly
- myocardium = middle layer of heart wall composed of CM
- CM cells are connected end-to-end by intercalated discs
- 2 types of contact:
- desmosomes mechanically hold CC together → strength for beating
- gap junctions provide paths of low resistance for transmitting info: small mol & electrical signals ➔ enables functional syncytium
- epicardium = thin external membrane covering heart filled w/ small volume of pericardial fluid ➔ lubrication ↓ friction
24
Q
endocardium
A
thin layer of endothelial tissue lining interior of each heart chamber ➔ exchanges O2 & gases quickly
25
myocardium
middle layer of heart wall composed of CM
* CM cells are connected end-to-end by **intercalated discs**
* 2 types of contact:
1. **desmosomes** mechanically hold CC together → strength for beating
2. **gap junctions provide** paths of low resistance for transmitting info: small mol & electrical signals ➔ enables **functional syncytium**
26
pacemaker potential
1. **slow depolarization** until threshold
1. K+ channels close = **no K+ out** & **I channels** (funny = Na channels) **open** = **Na+ in ** (critical driver)
2. Na channels close & **T-type Ca channels** open ➔ **Ca in** = main driver (T = transient)
2. **depolarization at threshold**: rising phase
1. **L-type Ca channels open** ➔ **Ca in** (L = long-lasting)
2. T-type Ca channels close
3. **repolarization**: K+ channels open ➔ **K+ out**
27
difference btwn pacemaker potential & CM contractile AP
1. **RMP**
2. **plateau phase** in contractile: fisrt fast K channels (K out fast) then T-Ca chanels (Ca in slow)
3. **slow depolarization** in PMC vs rapid in contractile
4. **maximum depolarization**
5. 1st **funny (Na) channels** then T-Ca channels vs fast Na channels
28
excitation-contraction coupling in contractile CM
* **dihydropyridine receptors** = voltage-gated Ca channels that allow entry in cardiac cell (does not trigger foot proteins like in skeletal muscle)
* Ca from both SR & ECF
1. **dihydropyridine receptors in T-tubules act as voltage-gated Ca channels ➔ open to let Ca into cytosol**
2. **Ca entry triggers more Ca released by SR**
* **# of activated cross-bridges proportional to cytosolic Ca**
* long refractory period prevents tentanus of CM
29
electrocardiogram
graphic record of electrical activity that reaches surface as result of depolarization/repolarization
* AP of heart generates electrical currents ➔ can reach body surface & be detected as voltage differences between 2 points
* **P wave** = atrial depolarization
* SA node fires to AV & internodal pathway
* **PR segment** = AV nodal delay: slower conduction through AV nodea
* ensures ventricles contract AFTER atrial depolarization & contraction
* **QRS wave** = ventricular depolarization
* simultaneous atrial repolarization, but cannot be detected because masked by ventricles)
* **ST segment** = systole = ventricular contracting & emptying
* **T wave** = ventricular repolarization
* **TP segment** = diastole = ventricular relaxation & filling
30
HR & rhythms
normal ≈ 60-100 bpm
* > 100 = **tachycardia**
* **ventricular fibrillation** = no conduction of purkinje fibers
* heart attack caused by **blockages**
31
mechanical events of the heart
cycle = alternating periods of systole & diastole
* **end-diastolic volume** = V of blood after relaxation (max blood capacity)
* **isovolumetric ventricular contraction** = closed valves ↑ pressure ➔ ventricular volume stays the same before systole while pressure builds
* **end-systolic volume** = blood left over after contraction/emptying
* **stroke volume** = amount of blood pumped each contraction
* **isovolumetric ventricular relaxation** = closed valves ↓ pressure ➔ volume in ventricles remains the same before diastole during atrial filling
* pressure from A carries on to B
32
stenotic valves
**won't open** completely ➔ **whistle**
33
insufficient valves
**not close** completely ➔ **swish**
34
1. lub-whistle-dub
2. lub-dub-whistle
3. lub-swish-dub
4. lub-dub-swish
1. stenotic + systolic
2. stenotic + diastolic
3. insufficient + systolic
4. insufficient + diastolic
35
parasympathetic regulation of HR
* **ACh** through muscarinic receptors
* **vagus nerve** to SA & AV nodes & atrial contractile cells
* little ventricular innervation
* **SA node**: **ACh** delays closing K+ channels ➔ **↑ K+ permeability** ➔ more K+ out ➔ **greater hyperpolarization = stronger depolarization required** (longer time) ➔ **slowing contractions**
* **AV node**: ACh ↑ **K+ permeability** ➔ ↓ excitability ➔ delays response
* **atrial contractile cells**: ACh ↓ Ca permeability during plateau phase ➔ less Ca enters cell ➔ ↓ contraction strength
36
sympathetic regulation of HR
* **NE** through beta-adrenergic receptors
* nerves innervate atria & ventricles
* **SA node**: NE ↓ K+ permeability: closes K+ channels faster after AP ➔ less hyperpolarization = faster depolarization
* **AV node**: NE ↑ Ca permeability ➔ shorter AV nodal delay
* **bundle of His** & **Purkinje fibers** = similar to AV node
* **atrial & ventricular contractile cells**: NE ↑ Ca permeability during plateau phase ➔ more Ca enters = ↑ contraction & stronger
37
regulation of stroke volume
**intrinsically** by **venous blood return**
* **Frank-Starling law**: heart normally pumps out during systole same V of blood returned to it during diastole
* **increased venous return results in increased SV**
* more blood returned = more blood pumped out
* main determinant of cardiac muscle fiber length = degree of diastolic filling
* more heart is stretched = longer fibers before contraction
* ↑ length ➔ ↑ force of contraction ∴ ↑ SV
* dependent on lengt-tension relationship
**extrinsically** by **SNS**
* shifts Frank-Starling curve L: ↑ Ca ➔ ↑ contractile force & SV of the heart
* extrinsic control enhances heart’s contractility ➔ contracts more forcefully and squeezes out a greater percentage of the blood it contains, leading to more complete ejection
38
heart failure
* ↑ BP ➔ ↑ heart workload
* CO cannot meet demands of body
* can happen in 1 or both ventricles ➔ congestion of blood in veins back to heart
* ventricle must generate more pressure to eject blood
1. ↑ BP
2. exit valve is stenotic
* ↓ in CO that shifts frank-starling curve ↓ & right
* SNS stimulation shifts curve ↑ & L
* heart compensates with:
* hypertrophy: ↑ thickness of cardiac muscle fibers (enlarged heart)
* ↑ sympathetic activity
* ↑ blood volume from retention of salt & water by kidneys
39
sphygmomanometer
measures BP (systolic & diastolic arterial pressure) (i.e. 120/80)
* BP expressed as systolic over diastolic
* cuff pressure > BP: no blood flows = no sound
* cuff pressure between systolic & diastolic pressure
1. artery transiently opens a bit when BP reaches peak
2. blood escapes through partially occluded artery for brief interval before arterial pressure < cuff pressure & artery collapses again
* cuff pressure < systolic & diastolic: blood flows smoothly ➔ no sound
40
pressure graph from ventricle ➔ venules & veins
* **L ventricular pressure** swings between 0 during diastole & 120 during systole
* **arterial pressure** fluctuates between systolic & diastolic
* **arteriolar pressure** drops dramatically across length of arteriole
41
arteriolar radius factors
arterioles = major resistance vessels b/c of small radius regulated by:
* excercise
* temp
* stretch
intrinsic (local) control
1. local metabolic changes cause dilation: SM tone is controlled by release of mediators (NO) from endothelial cells lining interior walls of arterioles
* ↓ **O2** during demand
* ↑ **CO2** during demand
* ↑CO2 &/or lactic acid = ↓ blood **pH**
* ↑neuronal activity outpaces Na/K ATPases ➔ ↑ **extracellular K**
* ↑[solute] = ↑ **osmolarity**
* ↑ **adenosine** from cardiac muscles
* ↑ **histamine release** from damaged tissues ➔ vasodilation during inflammatory response
2. local physical control:
* ateriolar SM tone = **inversely proportional to temp**
* **myogenic response**: arteriolar SM responds to stretch by contracting
extrinsically:
* **vasopressin & angiotensin II**
* **EP/NE** influence on SNS
* **vasoconstriction** from sympathetic activity
42
capillary exchange
* exchange occurs btwn blood & **interstitial fluid**
* occurs by diffusion & **bulk flow**
* **pores** in capillary walls allow plasma to pass by not proteins or RBC
* **ultrafiltration** = bulk flow **out** of capillaries (+ net pressure)
1. **capillary BP (P_c)** = forces fluid out of capillaries into IF
4. **interstitial fluid-colloid osmotic pressure (πIF)** forces capillary water to IF
* **reabsorption** = bulk flow **into** capillaries ( − net pressure)
2. **plasma-colloid pressure (πp)** forces **IF to capillaries** controlled by [plasma proteins]
3. **interstitial fluid hydrostatic pressure (P_IF)** forces **IF to capillaries**
* **net pressure = (Pc + πIF) - (PIF + πP)** (out-in)
* inward pressure stays same throughout length
* outward pressure slowly declines
43
ultrafiltration
bulk flow **out of capillaries** (+ net pressure)
44
reabsorption
bulk flow **into capillaries** (− net pressure)
45
capillary BP (P_c)
forces fluid out of **capillaries into IF**
46
plasma-colloid pressure (πp)
forces **IF to capillaries**
* controlled by [plasma proteins]
47
interstitial fluid hydrostatic pressure (P_IF)
forces **IF to capillaries**
48
interstitial fluid-colloid osmotic pressure (πIF)
forces capillary water to IF
49
net pressure =
**(Pc + πIF) - (PIF + πP)** (out-in)
50
venous capacity
V of blood veins can hold
51
venous return
V of blood entering each atrium per minute
* influenced by:
* **sympathetic activity** produces vasoconstriction to ↑ venous pressure & ↑ venous return
* **skeletal muscle activity**: contraction compresses veins & ↑ venous pressure ➔ counteracts effects of gravity
* **venous valves** prevent backflow (located w/in lumen of large veins)
* **respiratory activity**: brief ↓ in pressure w/in chest cavity ↑ pressure gradient between veins & lower extremities ↑ chest
* **cardiac suction**: arterial pressure briefly falls below 0 mmHg during ventricular contraction ➔ ↑ venous pressure gradient & sucks venous blood into atria
52
sympathetic activity's influence on venous return
produces vasoconstriction to ↑ venous pressure & ↑ venous return
53
skeletal muscle's influence on venous return
contraction compresses veins & ↑ venous pressure ➔ counteracts effects of gravity
54
venous valves' influence on venous return
prevent backflow (located w/in lumen of large veins)
* w/out: contracted skeletal muscle would squeeze blood both towards & away from heart
55
respiratory's influence on venous return
inhaling ↓ pressure in chest ➔ blood flows fown pressure
56
cardiac suction's influence on venous return
arterial pressure briefly falls below 0 mmHg during ventricular contraction ➔ ↑ venous pressure gradient & sucks venous blood into atria
57
extrinsic
attached partly to an organ or limb and partly to some other part said of certain groups of muscles
58
intrinsic
coming from within, from the inside
59
intrinsic
coming from within, from the inside
60
regulation of MAP
**CO**
* **HR**
* **parasympathetic**:: ACh via muscarinic receptors
* SA & AV: ↑K permeability = more K out = greater hyperpolarization = stronger depolarization required = delayed response = slower contractions
* contractile cells: ACh ↓ Ca permeability during plateau phase = less Ca in = ↓contraction strength
* **sympathetic**: NE via beta-adrenergic receptors
* SA: ↓ K permeability closes K channels faster = less hyperpolarization = faster depolarization
* AV: ↑ Ca permeability = shorter AV nodal delay
* bundle of His & purkinje fibers = similar to AV node
* contractile cells: ↑ Ca permeability during plateau phase
* **SV**
* **NE/EP** ↑ Ca = stronger contractions
* **venous return**:
* blood volume:
* passive bulk flow shifts btwn capillary & IF
* salt & water balance influenced by vasopressin & angiotensin II that affect vassopressin, renin-aldosterone system
* **respiratory activity:** inhalation ↓ chest pressure ➔ concentration gradient
* **skeletal muscle activity** counteracts gravity when contractions force blood through veins
* **cardiac suction** from pressure gradient when arterial pressure falls below 0 during ventricular contraction
**total peripheral resistance**
* blood viscocity: hydration & RBC
* arteriolar radius:
* local metabolic control: skeletal muscle activity
* ↓ **O2** during demand
* ↑ **CO2** during demand
* ↑CO2 &/or lactic acid = ↓ blood **pH**
* ↑neuronal activity outpaces Na/K ATPases ➔ ↑ **extracellular K**
* ↑[solute] = ↑ **osmolarity**
* ↑ **adenosine** from cardiac muscles
* ↑ **histamine release** from damaged tissues ➔ vasodilation during inflammatory response
* extrinsic vasoconstrictor control:
* vasopressin & angiotensin II
* sympathetic activity & EP/NE
**blood volume**
61
baroreceptor reflex
automatically regulates CO & total peripheral resistance
* responds to changes in arterial BP by ↑ or ↓ rate of firing via parasymp & symp neurons of **cardiovascular control centers**
1. carotid sinus baroreceptor
2. aortic arch baroreceptor
* **baroreceptors** = mechanoreceptors sensitive to changes in MAP & pulse pressure
62
BP anormalilties
* **hypertension** = BP above 140/90 mm Hg
* 1° = unknown cause (90%)
* 2° to others (10%)
* **orthostatic hypotension**: when a person moves from lying down to standing up, pooling of blood in the leg veins from gravity reduces venous return, decreasing stroke volume and thus lowering CO and blood pressure
63
compared to the resting state, the cardiac cycle during exercise:
both systole & diastole decrease, but greater decrease in diastole because the arterioles dilate due to local control
64
response to exercise
**diastole decreases**
intrinsic (local) control
1. local metabolic changes cause dilation: SM tone is controlled by release of mediators (NO) from endothelial cells lining interior walls of arterioles
* ↓ **O2** during demand
* ↑ **CO2** during demand
* ↑CO2 &/or lactic acid = ↓ blood **pH**
* ↑neuronal activity outpaces Na/K ATPases ➔ ↑ **extracellular K**
* ↑[solute] = ↑ **osmolarity**
* ↑ **adenosine** from cardiac muscles
* ↑ **histamine release** from damaged tissues ➔ vasodilation during inflammatory response
2. local physical control:
* ateriolar SM tone = **inversely proportional to temp**
* **myogenic response**: arteriolar SM responds to stretch by contracting
extrinsically:
* **vasopressin & angiotensin II**
* **EP/NE** influence on SNS
* **vasoconstriction** from sympathetic activity
65
3 phases of the cardiac cycle
1. mid-to-late diastole
2. ventricular systole
3. early diastole
