Karteikarten
Cardiovascular System
Karten in diesem Stapel (50)
- 1How are systemic capillary beds arranged?In // (few exceptions where in series: portal system)
- 2What is the most important portal system?Hepatic portal system (blood drained from gut flows initially to liver)
- 3Why is the // arrangement important?1. each capillary bed receives arterial blood directly from LV
2. flow to different capillary beds can be altered selectively as situations demand - 4How is blood flow regulated?Flow determined by R that precedes each capillary bed:
-vasoconstriction (increased R)
-vasodilation (decreased R) - 5Where is cross-sectional A of blood vessels greatest? Why?Capillaries because large surface A maximizes efficiency of exchange of nutrients & tissue waste products
- 6How can you have smooth blood flow despite P variations between diastolic & systolic values?Arteries dampen this difference (pulse P) allowing smooth blood flow
- 7Where is blood flow regulated? Why?Arterioles (largest P drop => max R)
- 8Where is mean v of blood lowest? Why?Capillaries (maximizes efficiency of nutrient exchange along with large surface A)
- 9How do you calculate MABP?MABP=diastolic P+1/3PP
PP=systolic P-diastolic P - 10How much is 1kPa in mm Hg & cm H2O?1 kPa = 7.50 mm Hg = 10.2 cm H2O
- 11What is v & Q & how are they related?v: d/t (speed particle fluid moves)
Q: V/t(quantity fluid moving through vessel)
Q=v*A (if Q const, v varies opposite A)
In CVS, cardiac output (Q) units L/min - 12How are P gradient and Q related?dP=Q*R
- 13What is P gradient in systemic circulation? And pulmonary circulation?Systemic circulation: dP=MABP-RAP
Pulmonary circulation: dP=MpABP-LAP - 14How is Q in pulmonary & systemic circulations related? How to calculate 2 R?Q is equal (cardiac output)
R=dP/Q
Total peripheral R=(MABP-RAP)/Q
Pulmonary vascular R=(MpABP-LAP)/Q - 15What factor in the circulation determine particular value of vascular R?R depends on properties of vessels & fluid
Poiseuille´s law: Q=dP/R=(dP*π*r^4)/(8n*l)
R=(8*n*l)/(π*r^4) (R ↑ as n ↑ & R ↓ as r ↑)
Systemic circulation: R mainly in arterioles =>changing r (contraction/relaxation SM) regulates vascular R (and thus blood flow) - 16If r ↓ 50%, how much Q ↓? & if r ↑ 100%, how much Q ↑?1. ~5 times
2. 16 times - 17Which main factor affects n? Which conditions can ↑ n? Why can this be bad?Ht (blood of normal Ht n~3 relative to H2O)
n ↑ sharply as Ht ↑
main factor ↑ Ht is hypoxia but other disorders like sickle cell anemia also ↑ n
Effect: heart does + W 2 maintain same Q - 18Conducting system of heartAP originates at natural heart PM: SA node
AP propagates uniformly across A walls
AP delayed at AV node
AP propagates rapidly along bundle of Hiss & Purkinje fibers to activate rapidly V - 19What is the normal V calibration and t scale in the ECG for 1 heart cycle?1mV
several 100ms - 20What are the characteristic waves in the ECG and what do they represent?P-wave: A depolarization
QRS complex: V depolarization
T-wave: V repolarization - 21What are the characteristic intervals in the ECG and what do they represent? How are they affected by heart conditions?PR interval (0.12-0.2s): AP delay at AV node (longer t => heart block)
QRS complex t (0.08s): t 4 AP to activate V (longer t=>impaired Purkinje conduction)
QT interval (025-0.4s): avg duration of V AP (affected by many physiological & pathological factors)
ST segment: isoelectric region on ECG indicating no net current flow in heart (characteristic changes during certain cardiac diseases) - 22What is the function of heart valves? What are the valves on L&R sides of heart?Valves ensure unidirectional flow in heart
R: superior&inferior vena cavae=>RA=> tricuspid valve=>RV=>pulmonary valve=> pulmonary artery=>lungs
L: pulmonary vein=>LA=> mitral valve=> LV=>aortic valve=>aorta=>body - 23How is cardiac cycle related to: 1. ECG waves 2. P, V V and aortic flow 3. Heart sounds 4. Venous pulses1. ECG precedes contractile events: P-wave=>A contraction; QRS complex=>V contraction; T-wave=>V relaxation
2a. V contraction=>mitral valve closes=>P ↑until=arterial P=> aortic valve opens=> ejection
2b.V relaxation=>aortic valve closes=>V P ↓until=A P=>mitral valve opens=>V filling
3. 1st sound start V contraction (AV valve closes), 2nd sound end V contraction (semilunar valve closes)
4. Veins changes mirror A changes: a wave-A systole, c wave-start V systole, v wave-end of systole - 24If resting HR=70bpm&SV=70ml, what is CO?CO=HR*SV
Resting CO~70bpm*70ml~5L/min - 25Using Fick principle, calculate CO if [in]= 150ml O2/L blood & [out]=200ml O2/L blood & O2 consumption=250ml/min. What assumptions are you making?CO=O2 consumption/([out]-[in])
CO=250/(200-150)=5L/min
Fick principle measures flow through lungs & assumes entire CO passes through lungs - 26How does the body regulate CO?Change of either HR or SV. HR driven by f SA node APs (primary PM). SA node innervated by ANS. Parasympathetic NS (vagus nerve)=>ACh=>↓HR (bradycardia). Sympathetic NS (cardiac nerves)=>NA=> ↑HR (tachycardia)
- 27Which 4 factors determine CO?HR+myocardial contractility (characteristics of myocardium, regulated by neural& hormonal factors) & preload+afterload (depend on heart+vascular system)
- 28When venous return to heart (preload) ↑ (lie down), heart must pump+ blood out. How can it do this?Starling's law: End-diastolic V P/V↑=>F next contraction/SV↑
At cellular level-manifestation L-T relation: stretching muscle at rest ↑ contraction F up to limit (sliding filament hypothesis) - 29What are 2 important consequences of Starling's law?1. input to heart=output from V
2. output RV=output LV
(if we↑R heart filling (lie down)=>↑R heart output=>↑L heart filling=>↑L heart output) - 30How does heart maintain const CO/SV despite ↑R/afterload (vasoconstriction)?When afterload↑=>SV↓=>end-diastolic V↑=> SV↑ (Starling's law)
Thus, despite altered load, SV const – just transient change when load initially altered - 31How is myocardial contractility regulated?Positive inotropic effect: sympathetic stimulation=>↑cardiac contractility (↑cardiac W independent of preload)
(myocytes contract+effectively at=stretch) - 32CV shockFailure to ensure tissues receive adequate blood flow to meet nutritive demands
- 33What is the controlled variable in the CVS?What happens when is too high or too low?ABP
Too low=>inadequate perfusion of tissues, impaired metabolism, tissue necrosis
Too high=>capillary damage, fluid exudation into extravascular space - 34How is ABP regulated in long & short term?Long term: vascular V=>kidney controls Na+ reabsorption by renin-angiotensin system (e.g. ↓blood V-hypovolaemia=> ↓preload on heart=>↓CO =>↓MABP)
Short term (s/min): baroreceptor reflex
Both processes negative feedback loops - 35How can you manipulate ABP?MABP-RAP=CO*TPR
Assuming RAP~const, MABP regulated by changing myocardial contractility & HR (CO) or TPR (vasoconstriction/vasodilation) - 36The baroR reflex is a negative feedback process. How does a negative feedback process work?5 stages of negative feedback process:
1. value of controlled variable may be influenced by external factors
2. actual value measured by sensor
3. ‘feedback’ info relayed to comparator, upon which exerts inhibitory influence
4. comparator determines difference between set pt value & actual value
5. efferent arm determines activity of target organs to restore variable to set pt
Variable↑=>feedback↑inhibition=> efferent arm↓=>return variable to normal
Variable↓=>feedback↓inhibition=> efferent arm↑=>return variable to normal - 37Where are sensors that respond to ABP?Principal baroRs located in neck at bifurcation of common carotid artery into external&internal branches. These respond to blood P changes in normal physiological range. BaroRs also exists in aortic arch but respond to higher P
- 38How is afferent info conveyed by baroRs?Afferent info conveyed from carotid sinus by branches of sinus nerve (a branch of
glossopharyngeal nerve/CN IX). Aortic arch info conveyed by vagal nerve (CN X). - 39What/where is the comparator of the baroR reflex?Afferent info terminates in CV centers (nuclei in medulla oblongata). CV centers also receive info from other parts of brain that can change value of set-pt blood P (e.g. during exercise blood P can be set to higher value by cortex info)
- 40What are the target organs of the efferent activity (via the ANS)?1. SA node (HR): vagus (parasympathetic) ↓HR whereas sympathetic fibres↑HR
2. myocardium (SV): sympathetic fibres =>positive inotropic effect (↑SV)
3. vascular SM (R): sympathetic fibres-↑activity=>vasoconstriction, ↓activity=> vasodilatation
Sympathetic fibres also innervate SM in veins&venules: ↑activity=>↓R=>↑venous return=>↑preload on heart - 41When you move from horizontal to vertical position, often you feel faint but a few s after you recover. Why does this happen and how does the body recover?Syncope (faintness) due 2 ↓blood flow 2 brain from ↓blood P (hypoT)=>baroR reflex=>recovery from postural hypoT:
1. on standing blood pools in lower extermeties=>↓venous return 2 heart
2. ↓filling P (preload)=>SV&CO↓
3. blood P↓ (postural hypoT)=>faintness
4. baroR activity↓=>afferent nerve firing↓
5. Inhibition CV center↓
6. Efferent arm activated 2 restore blood P 2 normal:
i) vasoconstriction ↑sympathetic
ii) ↑HR ↓parasympathetic (↑sympathetic)
iii) positive inotropy ↑sympathetic - 42Which feedback control system responsible 4 long term regulation of ABP? How?Long term: BP regulated by kidney regulation of circulating V through Na+ regulation at distal tubule by renin-angiotensin system+regulation of aldosterone secretion by adrenal cortex. Disrupting BF 2 kidney=>retain excess Na+&fluid. ANP released by A when circulating V large causing natriuresis (loss of Na+ in urine)=>↓ circulating fluid
- 43Can you name component parts of long term feedback control system of ABP?Variable: effective circulating V
Sensor: V sensors
Comparator: kidney
Efferent arm: adjustment to NaCl excretion - 44Which observations can you make regarding the distribution of CO to different capillary beds?(3) Some beds receive large faction of CO (kidney~1/4CO)
(3) Some beds change BF over very large ranges according to circumstances (SKM, skin) whereas others exhibit much less variation (brain, kidney)
(4) unit BF at rest very large some tissues (kidney, heart, brain): high metabolic rate
(6) high unit BF matches unit O2 consumption
(7) Some tissue extract O2 from blood very effectively (heart) - 45How, where and why regulate BF?BF 2 tissues regulated by altering R of pre-capillary vessels/arterioles. 2 reasons why arteriolar R should be varied:
1. Intrinsic mechanisms (match BF 2 metabolic rate)
2. Extrinsic mechanisms (homeostatic functions, like control of BP or body T) - 46How is intrinsic regulation carried out? How is it carried out in brain, heart, SKM and endothelium?Intrinsic regulation: metabolic rate↑=> waste products↑=>vasoldilation↑=>BF↑.
Different tissue beds use different waste products e.g. cerebral circulation=>CO2; coronary circulation (heart)=>adenosine; SKM=>↑CO2/↓O2/acidosis/↑[K+].
Endothelium releases vasodilator NO in response to shear stress (↑lumen P) or local release of chemicals like ACh, bradykinin, histamine, 5HT or ATP. - 47How is extrinsic regulation carried out?Extrinsic regulation: NS (mainly sympathetic)+hormones (adrenaline)
Postganglionic NA=>α-Rs on vascular SM =>vasoconstriction. Some capillary beds respond 2 adrenaline=>β-Rs (β2-subtype) =>vasodilation (e.g. SKM circulation responds 2 adrenaline release during exercise 2 accommodate large CO↑). Other circulating vasoactive compounds: angiotensin II (constriction), ANP (renal dilation), vasopressin, ADH (constriction) - 48How is BF re-directed to vital organs despite sympathetic NA release (e.g. during acute hypovolaemia)?Certain capillary beds extensive sympathetic control e.g. gut, liver, pancreas, spleen, skin, renal, SKM Others little functional control e.g. coronary&cerebral. Sympathetic drive to peripheral circulation=>α-regulated beds ↓BF (2 restore BP by ↑TPR). Heart&brain not affected=>don't participate in this homeostatic control=>blood re-directed to these vital organs
- 49How do adrenaline&NA affect heart?Adrenaline&NA=>β1-Rs=>positive inotropic effect (↑cardiac contraction F)+positive chronotropic effect (↑HR/tachycardia)
- 50What is autoregulation? Where does it happen? Why is it important?Autoregulation: tissue BF relatively const despite ABP changes e.g. renal&cerebral circulations. Very important 4 tissues requiring reasonably const&stable BF
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- Physiology Karteikarten am Cardiovascular System, erstellt von Francisco Sacadura am 28/01/2017.
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- Francisco Sacadura
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