cardiovascular physiology Flashcards
1
Q
what are the parts of the cardiac physiology
A
- heart - dual pump with valves
- conduction system
- non-contractile cardiac muscle cells modified to initiate and distribute impulses throughout the heart
2
Q
parts of conduction system
A
- sinoatrial (SA) node - in right atrium
- atrioventricular (AV) node - in right atrium
- bundle of His (AV bundle)
- originates at AV node
- only route for electrical activity to go from atria to ventricles - purkinje fibres
- terminal fibers - stimulate contraction of the ventricular myocardium
- 30 APs/min
3
Q
what are the phases of pacemaker activity
A
- pacemaker potential
- low K+ permeability
- slows inwards leak of Na
- causes slow depolarization toward threshold (-40mV) - AP depolarization
- at threshold - AP
- Ca++ voltage open - Ca moves in depol gates close at threshold - AP repolarization
- K voltages gates open at peak lets K out - repolarization
- K gates close below threshold - Na channels open at -50mV
- starts pacemaker potential again once K+ gates close (continuous cycle)
4
Q
APs in ventricular myocardium
A
- cells=contractile
- purkinje fibre AP = ventricular myocardial AP (spread cell to cell by gap junction)
- resting MP= -90mV
5
Q
absolute refractory period
A
-long - Na + channels inactivated until MP closes to -70mV
6
Q
excitation-contraction coupling in myocardial cells
A
- open voltage-gated Ca channels of AP
- opens chemically-gated Ca channels on SR making the cytosolic Ca+ increase
- contraction
- sliding filament mechanism
- begins a few msec after AP begins
- duration of AP
- result: no summation
7
Q
what are the 3 components of the cardiac cycle
A
- electrical activity (ECG)
- small currents due to depol/repol of heart
- seen as waves - mechanical activity
a. systole - contraction, emptying
b. diastole - relaxation, filling
- both initated by electrical activity - blood flow through heart
8
Q
ECG waves
A
a. P wave = atrial depol. - followed by contraction
b. QRS wave = ventricular depol - contraction. aslo atrial repol. (relaxation)
c. T wave = ventricular repol - followed by relaxation
9
Q
ECG intervals
A
a. P-Q = atria contracted, signals passing through AV node
b. S-T = ventricles contracted, atria relaxed
c. T-P heart at rest
10
Q
abnormalities of heart beat
A
- tachycardia - resting HR more than 100 bpm
- bradycardia - resting HR less than 60 bpm
- heart block - when conduction through the AV node slowed
- ventricles may not contraction after each atrial contraction
11
Q
what is the timing of mechanical events
A
- average resting heart rate =75beats/min
12
Q
blood flow through heart is due to
A
a. pressure changes
b. valves
c myocardial contraction (raises P)
- in diast. ventricles have lowest P blow flows into them
- in syst - ventricles have highest P blood flows out of them
13
Q
during ventricular systole
A
a. high P in ventricles than atria forces AV valves shut causing turbulence of blood gives first heart sound
b. P rises - higher P in ventricle than aorta/pulm trunk pushes semilunar valves open - blood enters vessels
14
Q
during ventricular diastole
A
a. P drops - higher P in aorta/pulm trunk than ventricles forces semilunar valves shut making 2nd heart sound
b. AV valves open when P in ventricles drop below P in atria
15
Q
turbulent flow
A
noisy due to blood turbulence when valves shut
16
Q
laminar flow
A
no sounds
17
Q
what are the sounds of korokoff
A
turbulence heard in brachial artery during blood pressure measurements
- begin=systolic pressure
- stop = diastolic pressure
- due to cardiac cycle events
18
Q
cardiac output (CO)
A
volume of blood ejected by each ventricle in 1 min.
19
Q
stroke volume
A
volume ejected by each ventricle per beat
20
Q
end diastolic volume (EDV)
A
volume of blood in each ventricle at end of ventricular diastole
120ml
21
Q
end systolic volume (ESV)
A
volume of blood in each ventricle at the end of ventricular systole
50ml
22
Q
what are the controls of CO
A
- control of heart rate
2. stroke volume
23
Q
control of heart rate
A
- basic rate set by SA node (intrinsic control)
- modifiers of HR
24
Q
types of entrinsic control
A
- neural
- SNS: Na channels open wider
- PSNS : keeps resting HR lower than pace set by SA node - hormonal
-epinephrine, NE
- thyroid hormone - direct effect to increase HR - other factors
I. ions e.g. high K in ISF
ii) fever
-higher temp = higher HR
iii)age
- newborn =high
iv) fitness
- higher fitness lower HR
25
control of stroke volume: intrinsic control
a. intrinsic control: ( hearts build-in ability to vary SV - adjust to demands)
- increase venous return leads to increased EDV which leads to increase hear muscle stretch and increased force of contraction. increasing SV.
- more blood in = more blood out
26
Frank-starling's law of the heart
force of ejection is directly proportional to length of ventricular contractile fibres
27
getting an increase of venous return is due to
- exercise: venous return speeded up
| - lower HR: has longer to fill, less of an effect than exercise
28
extrinsic controls: ANS-SNS`
- increase force of contraction.
- increase SV but SNS also increases HR which is less time to fill. this leads to a decrease in EDV at higher HR. however, increase force increases ESV
- PSNS no significant eggect
- overall SNS increases, PSNS decreases
29
extrinsic controls: hormones
- epi, NE: same mechanism as SNS which increases force
| - thyroid hormone increases force
30
extrinsic controls: other factors
```
force is increased by:
- increased external Ca++
-digitalis (drug) - increases Ca++ inside
force is decreased by;
-acidosis
- increased external K+
- Ca++ channel blockers (drugs)
```
31
blood circulation
- blood flow: volume of blood flowing through any tissue and in a vessel is determined by pressure and resistance
32
what is the relationship of blood circulation
F= (triangle)(P)/ R
```
f= flow
(triangle)(P) = blood pressure gradient
R= resistance
- opposes flow
- depends on:
1. vessel length
2. viscosity of blood
3. radius of arterioles *most important*
```
33
blood flow to organs is controlled by
1. vasoconstriction
- radius decreases raising R and decreasing Flow
- P in artery increases
- P in organ decreases
2. vasodilation
- radius increases making the R decrease and flow increase
- P in artery decreases
- P in organ increases
34
if vasoconstriction is local what happens
no observable change in systemic (Arterial) BP
35
if vasoconstriction is systemic what happens
systemic BP will change
36
what is the vasoconstriction/dilation controlled by
1. intrinsic regulation
- allows organs to control it own blood flow
2. extrinsic regulation
- external control by NS and endocrine system
37
myogenic regulation
when smooth muscle is stretched it contracts. if systemic blood increases P arterioles constrict.
38
metabolic regulation
if blood levels of e.g. O2 decrease, CO2 increase, pH decreased - endothelial cells + hemoglobin release nitric oxide which increases blood flow to organs
39
neural regulation
- arteriolar vasocon
- vasodilation due to decrease in SNS signals
- also venoconstriction
40
hormonal regulation
I) epinephrine
- vasocon: skin, viscera
- vasodil: heart, skel muscle, liver opposes SNS
41
SNS causes release of epinephrine, what is the arteriolar response
- in skin, viscera: both vascon (blood shifts to where its needed)
- in heart skeletal muscles and liver has opposite effects, response mainly determined by metabolic regulation
42
systolic pressure
arterial bp produced by ventricular contraction
43
diastolic pressure
arterial bp due to recoil of elastic arteries (when ventricles are relaxed)
44
how do we measure blood pressure
- syst/diast.
| - normal bp is 120/80
45
how do we measure pulse pressure
systolic -diastolic
46
mean arterial pressure (MAP)
regulated by the body i.e. what the body measures
47
how does MAP regulate
1. cardiac output
2. TPR(Arteriolar radius)
3. blood volume
48
extrinsic regulation of MAP
1. neural control
a. baroreceptor reflexes: short term changes e.g. standing
b. chemoreceptor reflexes
- peripheral chemoreceptors responds to pH, CO2. found in the aortic arch
2. hormonal control
a. epinephrine
b. renin-angiotensin system
c. atrial natriuretic peptide (ANP)
- causes decrease in renin, aldosterone, ADH whiche increase urine production
49
how do stretch receptors monitor MAP
1. ceratoid sinus (brain bp)
| 2. aortic arch (systemic bp)
50
angiotensin II causes
- increase vasocon, increase venocon which increases MAP
| - increase aldosterone, ADH results in increase renal Na, h20 abs, increase thirst and blood volume
51
capillary exchange
- between blood and ISF
52
how do solutes enter and leave capillaries
1. diffusion - major route (except brain)
- CO2, O2, ions, glucose, hormones
2. vesicular transport
- large proteins
- occurs via transcytosis
3. mediated transport
- requires a membrane carrier protein. mainly in brain
53
fluid (water) enters or leave capillaries by
1. osmosis
| 2. bulk flow - due to P difference
54
what are the 4 pressures involved in bulk flow
a. blood hydrostatic P
b. . blood osmotic P
c. ISF hydrostatic P
d. ISF osmotic
55
Net filtration pressure
- sum of hydrostatic and osmotic pressures acting on the capillary
56
circulatory shock
inadequate blood flow (decrease oxygen, nutrients to cells)
57
hypovolemic shock
- decrease blood volume
| - due to: blood loss severe burns, diarrhea, vomiting
58
vascular shock
- blood volume normal, but vessels expanded
| - due to: systemic vasodilation of blood vessels
59
cardiogenic shock
- pump failure result in decrease CO
| - heart cannot sustain blood flow
60
stages of shock
1. compensatory
- mechanisms can restore homeostasis by themselves
- involves
a. baroreceptors
b. chemoreceptors
c. ischemia of medulla
2. progressive
- mechanisms inadequate to restore homeostasis
- decrease CO, BP, blood to brain
3. irreversible
- decrease CO - too little blood to heart
- self-perpetuating cycle - leads to death
61
what does the compensatory trigger
- increase HR, generalized vasocon
| - decrease blood flow to kidneys triggers renin release
62
what does blood contain
1. plasma (90.5% water
| 2. formed elements
63
what does plasma contain
a. H20
b. proteins
- albumins
- globulins
- fibrinogen
c. electrolytes (ions)
d. other solutes
64
what is the function of proteins in plasma
1. produce osmotic pressure
2. buffer pH
3. globulins: transport lipids, metal ions, hormones
4. y globulins = antibodies
5. clot formation
65
what is the function of electrolytes in plasma
1. membrane excitability
| 2. buffers (HCO3)
66
what other solutes does the plasma contain
nutrients, wastes, gases, hormones
67
what formed elements does blood contain
a. red blood cells (RBCs)
| b. White blood cells (WBCs)
68
what are the functions of RBCs
1, transport
2. buffer - globin binds to H reversibly
3. carbonic anhydrase
69
hemoglobin in RBCs
- Hb = 4 hemes + 4 globins (proteins)
70
how is hemoglobin broken down
by macrophages into:
1. heme
- iron is removed and stored
- bone marrow make heme
- non iron protein excreted by bile in liver
2. globin
- converted to amino acids : recycled
71
granulocytes WBCs
1. neutrophils
- phagocytic
2. eosinophils
- attack parasites
- break down chemical released in allergic reactions
3. basophils
- secret histamine
- secrete heparin `
72
agranulocytes WBCs
1. monocytes
- enter tissues, enlarge to become phagocytic marcophages
2. lymphocytes
73
T lymphocytes
- helper T + cytotociv lymphocytes
74
B lymphocytes
when activated give rise to plasma cells , secrete antibodies
- natural killer cells , attack foreign cells, abnormal cells
75
platelets
cell fragments from megakaryocytes in red marrow
76
functions of platelets
forms platelet plug which prevents excess blood loss
77
hemostasis
- process of stopping bleeding.
78
what does hemostasis involve
1. vascular spasm
- vasoconstriction of damaged arteries, arterioles, decreases blood flow
2. platelet plug formation
- platelets stick to damaged blood vessel, releasing chemicals
- healthy endothelial cells release chemicals to prevent spread of plug
3. clot formation
4. clot retraction + repair
- retraction - blood vessel edges pulled together
- repair - fibroblasts form new CT, new endothelial cells repair lining
5. fibrinolysis
- clot dissolution
- digesting enzymes = plasmin
79
what does the release of chemicals in platelet plug formation cause
a. cause more platelets to stick
b. promote clotting
c. begin healing
80
what are the three stages of clot formation
1. production of prothrombin
2. prothrombin converted to thrombin
3. fibrinogen converted to fibrin
- positive feedback to increase its formation, thrombin trapped in clot, inactivated, washed away
81
how is production of prothrombin activated
1. extrinsic pathway
- uses factors released by damaged tissues
2. intrinsic pathway
- uses factors contained in blood
- require Ca++, tissue, platelet and or plasma factors
82
hemophilia
clotting abnormal/absent
| - about 83% = type A lack clotting factor
