CVS Physiology Flashcards
What is the CVS system made up of
Heart
Vessels
Blood
What is the function of the CVS system
Transport 02 and C02
Transport nutrients and metabolites
Hormones
Heat
What is the cardiac output of the heart
5l / minute
CO = SV x HR
What is 02 consumption compared to cardiac output
Organs use similar %02 to cardiac output
Kidney’s get more cardiac output
Heart gets 4% CO but uses 10% of the 02 so more prone to disease
What is flow through vessels determined by
Pressure difference (MAP - central venous pressure)
High in artery to low in venous system
Resistance of vessels
How is the heart and vascular system wired
R+L in series so both outputs equal
Vascular beds parallel so flow at same time
Hypothalamus + pituitary, gut + liver = series as need blood flow after each other
How should flow through CVS system be
At any point should be the same
Vary throughout day / clinical situation as arteries constrict and alter resistance
What is the aorta
Elastic artery
Very low resistance
High pressure blood to pump through higher pressure of arterioles
Dampens pressure variation in between systole + diastole as energy stored in wells so blood keeps coming out
What are arteries made up like
Muscular and non elastic
Wide lumen
Low resistance
What are arterioles made up like
Muscular wall with narrow lumen
Constrict to control total peripheral resistance and blood flow to organs
Pressure falls as goes through vascular tree
Small drop through artery but large drop through arterioles as high resistance
What are capillaries made up like
Exchange vessels
Very narrow lumen and thin wall
BP very low
What are veins made up like
Low resistance so blood can get back to the heart
Wide lumen
2/3 of blood stored in veins = capacitance vessels
What is MAP determined by
Cardiac output and total peripheral resistance
How is arteriolar resistance controlled
Extrinsic neural control
Extrinsic hormonal control
Intrinsic control - individual tissue
What is extrinsic control
Sympathetic release noradrenaline which binds to A1 receptors on smooth muscle
Cause contraction
Para has no effect
What is arteriolar resistance at rest
Largely high as tissue don’t require as much 02
What is hormonal control of resistance
Epinephrine binds to A1 receptor = constriction
Can also bind to B2 receptor = dilation if tissue needs 02
Angiotensin II = constriction
Vasopressin = constriction
ANP + BNP = dilatation
What is intrinsic control measures of controlling resistance
Active hyperaemia
Pressure auto regulation
Reactive hyperaemia
Injury response
What is active hyperaemia
When activity increase metabolites released from tissue - H, Co2, K, lactate etc.
EDRF released causing dilatation to match needs
When metabolites decrease tone goes back to normal
What is pressure autoregulation
If pressure goes down flow will decrease and metabolites will increase
Cause dilatation to maintain blood supply despite changes in MAP
Body can do to certain extent but if drops too low will fail
What is reactive hyperaemia
Occlusion of blood = metabolites increase
Extreme form of auto regulation
What is the injury response
C fibres release action potential stimulates substance P
Acts on mast cells = histamine + dilatation
What are special circulations
Coronary
Cerebral
Pulmonary
Renal
What happens in coronary
Blood is interrupted by systole
Has excellent active hyperaemia with B2 receptors
What is special about cerebral
Excellent pressure auto regulation so perfusion maintained if pressure drops
What is special about pulmonary
If 02 decreased = constriction so blood will go to well ventilated area
What happens win renal circulation
Filtration is dependent on MAP
Arterioles constrict and dilate depending on how much absorption is needed
What is Raynaud’s an example of
Reactive hyperaemia
Blood flow decreased so increase in metabolites
Dilate to wash out metabolites
When blood flow returns resistance is very low
Cardiac output
SV X HR
How is HR controlled and what achieves tonic control
The Autonomic Nervous System
Parasympathetic - sit at 60bpm
How do you increase your HR
Decrease para and increase sympathetic
Sympathetic - noradrenaline on B1 on SA node + AVN
Spreads up depolarisation
Also increase contractility (inotropic affect)
How do you decrease HR
Increase parasympathetic input
Vagus nerve release Act acts on muscarinic 2 receptor on SA + AVN
Hyperpolaries cell
What causes a tachycardia
Anxiety Infection Hypoglycaemia Hypovolaemia Hyperthyroidism Problems with conductance in the heart
What type of conductance issues can you get
Wide Complex Tachy - broad QRS
- Ventricular tachy
- Wolff parkinson white
Narrow complex tachy
- Sinus tachy
- AF and flutter
How do you treat wide complex and narrow complex
Wide
- Amiodarone
- DC conversion if unstable
Narrow
- Vagal manouvere
- IV adenosine
- DC conversion if unstable
- AF = BB to control rate + anti-coagulant
What is the stroke volume
The amount of blood expelled by the heart in a cardiac cycle
Determined by filling of heart in diastole and how easy it is to be expelled in systole
EDV + ESV
Contractility and inotropy
In HF these compensatory mechanism fail so can’t maintain CO
What affects stroke volume
Central venous pressure - if increases then increases filling of ventricles in diastole
Total peripheral resistance - decreases so easier for blood to be expelled
ESV
Contractility
Afterload
What affects contractility of heart
Para little effect
Sympathetic - Na on B1 of mycoytes
What does sympathetic do to calcium
More calcium from ECF = more forceful contraction
Also increases Ca-ATPase on sarcoplasmic retinaculum
Ca removed faster so shorter contraction
What else affects contractility
Inotropes - epinephrine,
Hypercalcaemia
Thyoid hormones
Glucagon
What decreases contractility
Ach by vagus nerve on m2 Hypocalcaemia Ischaemia - hypoxia Hyperkalaemia Barbituarates
What is Starling’s Law
The more the heart fills e.g. EDV, the harder it will contract and the larger the SV
Therefore a rise in central venous pressure will increase SV
This only occurs up to a certain point
What is pre-load
The degree of myocardial stretch (due to venous filling) before contraction
What determines preload
The end diastolic volume - the volume of blood in the heart at the end of diastole
Venous return and filling time
Sum this up
Increased venous return Increased EDV Increases Preload Increased SV Increased CO Self regulating mechanism summing up Starling's law
What factors affect venous return
Skeletal muscle pump - exercise
Respiratory pump - inspiration decrease pressure so more blood drawn in
Sympathetic - contract veins and increase return (venomotor tone)
Systemic filling pressure from ventricle
Gravity - orthostatic hypotension as decreased EDV when lying flat
What decreases preload
Decreased thyroid Decreased calcium High or low K / Na Low body temp Hypoxia Abnormal pH Drugs - CCB
What is after load
The load against which myocardial cells have to contract
If TPR increases then aorta at higher pressure so ventricle needs to work harder
SV decreases
SO
Resistance vessels affect after load
Capacitance veins affect pre-load
What happens in exercise
CO increases 4-6x
HR and contractility increases due to sympa
Venous return increases to maintain preload by sympa causing contraction
TPR falls due to dilatation so decreased after load
How does the heart compensate for reduced pumping ability
Works with increases EDV
Results in lower ejection fraction and reduced exercise capacity
What is the ejection fraction
Stroke volume / EDV
How do capillaries work
Allow gas exchange
One cell thick so quick diffusion
Individual high resistance but in parallel so reduces
What are the types of capillaries
Continuous - no clefts or channels e.g. in brain so anything polar is stuck inside
Fenetrated - contains cleft and channels e.g. intestine
Discontinous - cleft and massive channels e.g. in liver
02 nd C02 able to freely diffuse across
What affects diffusion rate
Concentration gradient
Distance
SA of area receiving
What forces control movement across capillaries
Blood hydrostatic - forces fluid out
Blood osmotic - pressure exerted by proteins which can’t get out so pulls fluid in
Interstitial hydrostatic - forces fluid back into capillary
Interstitial osmotic - pulls fluid out of capillary
Whats bulk flow mechanism
Hydrostatic pushes fluid out of capillary
Oncotic pressure builds up as protein conc increases
Draws fluid back in
Capillary hydrostatic vs ISF hydrostatic
Capillary oncotic vs ISG oncotic
What volumes of blood move in and out of the capillaries
20l
17l regained
3l picked up by lymphatics
What do lymph capillaries do
Same structure but no return valves so fluid goes to the heart
What causes oedema
Excess fluid caused by lymph obstruction, raised CVP, huypopoteinaemia (no oncotic to pull water in), increased capillary permeability
What is shock
Inadequate blood flow
What can cause shock
Cardiogenic - pump failure reduces CO so decreased MAP, CVP may be normal or raised,
Mechanical - pump doesn’t fill, e.g. cardiac tamponade, high CVP and low MAP
Hypovolaemic - loss of blood volume
Distibutive - uncontrollable fall in TPR
Toxic shock - endotoxins released in infection = vasodilation and drop in TPR
What are typical symptoms of shock
Tachycardia
Rapid and shallow breathing
Reduced BP
Fluid resus and treat cause
What is systolic blood pressure
The pressure during ventricular systole / heart contraction
What is diastolic BP
The pressure during ventricular diastole / after contraction but before the next
What is the mean arterial pressure MAP
CO x TPR
The driving force of blood through the circulation
Pulse pressure + 1/3 of your diastolic
What controls short term regulation of BP
Autonomic nervous system
What detects change in BP
Baroreceptor in aortic arch + carotid sinus
What happens when there is an increase in BP
Increased MAP = greater stretch which baroreceptor detect
Send AP to medullary CVS control centre
Parasympathetic acts to reduce BP
What does aortic arch baroreceptor stimulate and carotid sinus
Aortic arch = vagus
Carotid sinus = glossopharyngeal
What are other inputs to short term control
Cardiopulmonary - in low pressure areas of heart and lung which fire if high volume
Central chemoreceptors - if low O2
Muscle chemoreceptors - increased metabolites
Joint receptors - movement
What is the valsalva manouvre
Forced expiration against a closed glottis
What happens in the valsalva manoeuvre
Increase in thoracic pressure transported to vessel
Decreased venous return
Decreased EDV, SV, CO + MAP
Common when you strain and go to toilet
Decreased MAP detected by baroreceptors which work to increase BP
What is the reflex
Deceased vagal = increased HR + CO
Increased sympa = Increased HR, CO, contractility, venoconstriction so increased VR, arteriolar constriction so increased TPR
What is the long term control of BP
Renin-angiotensin system (RAAS)
Where is renin produced
JG of kidney
What triggers renin production
Activation of sympathetic ( reduced MAP post JG)
Decreased distention of afferent / blood flow
Decreased delivery of NACL detected by macula densa
What does renin do
Converts angiotensinogen to ANG 1
ANG1 - ANG2 by ACE
What does ANG2 do
Release of aldosterone from adrenal cortex
Na reabsorption in proximal tubule
Increased release of ADH from PP
Potent vasoconstrictor so increases TPR
What does aldosterone do
Increase NA reabsorption in distal tubule so increased volume
What does ADH do (Vasopressin)
Increased water permeability of collecting duct
Increased thirst
What else triggers ADH
Decrease in blood volume - cardiopulmonary
Increased osmolarity
What does ANP do
Released from myocardial cells when increased distension
Inhibits renin
Dilates afferent arterioles so increased GFR
Increases NA excretion
Decreases MAP
What is the link between respiratory system + CVS
If hypoxia / hypercapnia = often pulmonary hypertension (constrict) + R heart failure (due to hypertension as increased after load)
Initially compensate but won’t get enough 02 in vessels
Leads to L HF and further pulmonary hypertension
Increased hydrostatic pressure so fluid out = pulmonary oedema
Decreased gas exchange as increased distance
CO2 decreases respiratory drive
What do prostaglandins do
Local vasoconstrictor to increase GFR and reduce Na reabsorption
