Heart and Circulation (26-29) Flashcards
What is the function of the heart and circulation system?
To deliver nutrients and remove waste
→ delivers O2 and sugar to respiring tissues
→ removes CO2 and products of metabolism
→ delivers hormones to site of action
→ central to homeostasis (e.g. body temperature - blushing when hot as blood pushed to surface to remove excess heat)
How big is a human heart?
Size of your fist
→ 200 - 425g
→ beats ~100,000/day, pumps ~7,000 litres of blood/day
Does heart beat depend on size?
Yes
→ smaller size = faster heart rate
→ smaller size means bigger SA:V ratio, therefore more heat loss, higher metabolic rate and heart beats faster
mouse 450/min, man 70/min, elephant 28/min
(chicken and rabbit excretion due to different body temps)
Where does the heart sit in the human body?
Centrally
→ apex is situated on the left in the 5th intercostal space
What is the vena cava?
The major vein that returns blood back to the heart
Superior → from shoulders, arms, head
Inferior → from rest of body
What is the function of the pulmonary artery?
Takes blood away from heart to the lungs
→ only artery that carried deoxygenated blood
What is the function of heart valves?
Control blood flow - ensure its stays in one direction, prevent backward flow
→ tricuspid & bicuspid: shut in systole, open in diastole
→ pulmonary & aortic: open in systole, shut in diastole
Why is the wall of the right ventricle thinner?
Has to pump blood around a very short circuit (heart and lungs are close)
→ so requires less pressure
Is the duration of diastole of systole longer?
Diastole
→ the heart spends 300ms in systole (ventricular contraction) and 550ms in diastole (relaxation)
mean arterial pressure = 1/3 systole + 2/3 diastole
What gives rise to heart sounds?
Closing of valves (lub dub bub)
→ caused by changes in pressure
→ left side much louder
What does cardiac output depend on?
The number of beats and their volume
→ cardiac output = stroke volume x heart rate
→ amount of blood you pump per minute
e.g. 70 beats min^-1 x 70ml beats^-1 ~ 5L min^-1
What is stroke volume?
The volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction
What is Starling’s Law of the Heart?
Energy of contraction is a function of the length of the cardiac muscle fibres
→ link between length of myocardial fibres and force generated by contraction
→ stroke volume is governed by filling and stretching of muscle
→ due to an increased sensitivity of the contractile proteins to Ca2+
What type of activity does the heart show?
Myogenic → initiated within the heart itself, generates its own beat
How is heart contraction co-ordinated?
Electrical impulse starts at the sinoatrial node (found in RA, pacemaker)
→ travels to the atrioventricular node
→ trails to the ventricles through Purkinje fibres, bundle of His
→ spreads throughout myocardium
SA node → AV node → P fibres & His → myocardium
Where is there a pause in the heart conduction pathway?
At the AV node
→ inserts delay to wait for atrial contraction and insure maximal filling of ventricles
What does ionic pacemaker potential depend on?
Calcium
→ generated by reduced K+ and increased Na+ permeability
→ depolarisation mostly produced by increased Ca2+ permeability
What does the sinoatrial node pacemaker potential depend on?
Sodium
→ slow leak of Na+, constant move towards action potential threshold
→ no need for stimulus
What does the long refractory period of ventricular myocytes prevent?
Ventricles don’t have rapid depolarisation due to calcium (entry via L-type channels)
→ prevents repeated action potential, tetanus in cardiac muscle
→ if the heart stays constantly contracted - can’t fill with blood
What are myocytes?
Branches muscle cells with a single nucleus
→ striated appearance under microscope
How are myocytes electrically coupled?
Through intercalated disks
→ connected through tight junctions, coupled through connexins
→ contraction activated by entry of Ca2+
What do ECG recordings detect?
Change in ionic charge
→ the spread of the heart beat
→ can be used to diagnose cardiac disease
Why does the circulatory system have different vessels?
To accommodate different pressures
high partial pressure ~ 100mmHg
→ elastic/muscular arteries - more muscular
low venous pressure ~ 0-8mmHg
→ veins - valves
What is the common structure of blood vessels?
(outside - in)
Tunica adventitia (externa) → principally collagen
Tunica media → elastic tissue, smooth muscle
Tunica intima (interna) → endothelium, supporting connective tissue, release of paracrine signals
Lumen
Do elastic arteries store energy?
Yes
→ elastic parties store energy during systole (contraction) and release it in diastole - maintaining blood flow at this time and smoothing it
What is the Windkessel effect?
As blood is pumped into the aorta and major arteries they stretch
→ in systole more floor flows in than out
The walls of the aorta and elastic arteries recoil in diastole maintaining blood flow
How is blood flow pulsatile?
Elastic parties convert the intermittent pressure into pulsatile flow
→ follows the pressure of the chambers bit never reaches 0
What is resistance determined by?
Length of blood vessels
→ longer = greater resistance, each vessel remains constant
Viscosity of blood
→ more solute = greater resistance, in normal conditions solutes don’t change
Radius of blood vessels → can be changed
What does blood flow depend on?
Radius of blood vessels - muscular arteries control flow
Ohms law: Q = (P1-P2)/R
→ Q = flow
→ (P1-P2) pressure difference between two ends
→ R = resistance
resistance will rise if the vessel is narrower, flow will be reduced, the pressure will be increased
Is blood flow laminar?
Yes → blood flow is layered
Flow is fastest at the centre (provision of blood to organs/tissues)
Flow is slowest on the outside - friction (necessary to provide nutrients to blood vessels)
What happens to flow at high velocity?
It becomes turbulent - laminar flow disrupted
→ can’t deliver nutrients - tissues start to die
→ leads to endothelial damage, arterial disease
What are capillaries?
Smallest vessels comprised of only tunica intima
→ site of exchange
What are precapillary sphincters?
Segments of smooth muscle that control access to microcirculation
→ help direct blood flow into capillaries via path of least resistance
How do capillaries optimise diffusion?
Thin walled - single layer of endothelial cells
→ minimises resistance to diffusion
→ maximum amount of SA contact between blood and capillary wall
the exchange of blood gases and metabolites generates an equilibrium between plasma and interstitial fluid
How is permeability of molecules in capillaries determined?
By the nature of the molecules itself
→ lipid soluble molecules (O2, CO2) - diffuse easily through capillary cell membranes
→ hydrophilic molecules - travel through pores, via a paracellular route
→ molecules > 60kd - not transferred, retained in circulation important to the equilibrium between plasma and the ecf
What is Starling’s forces?
Extracellular fluid movements between blood and tissues is determined by differences between hydrostatic pressure and colloid osmotic (oncotic) pressure
→ loss of fluid from plasma - hydrostatic pressure (tries to move solution out)
→ reabsorption of fluid into plasma - colloid osmotic pressure (tries to pull solution in)
What determines the equilibrium between plasma and interstitial fluid?
Hydrostatic pressure
→ e.g. 35mmHg at arteriolar end and 15mmHg at venular end
Oncotic pressure
→ large molecules (>60kd) don’t cross capillary walls, their osmotic pressure draws fluid back into capillaries (constant 25mmHg)
What does filtration/reabsorption depend on?
The difference between hydrostatic and oncotic pressure
→ filtration pressure = hydrostatic pressure - oncotic pressure
e.g. hydrostatic pressure > 25mm Hg, push fluid out
hydrostatic pressure < 25mm Hg, draw fluid in
Where does excess fluid from capillaries go?
Taken up into lymphatic and returned to the circulation system
→ capillary beds are associated with lymphatic capillaries
What are veins?
Veins are capacitance blood vessels
→ provide a reservoir of blood
How do muscle pumps enhance venous return?
Contraction and relaxation of skeletal muscles opens and closes valves in veins enhancing venous return
What part of the nervous system innervates the heart?
Both arms of the autonomic nervous system innervate the heart
→ parasympathetic (response during rest) and sympathetic (fight or flight)
→ pacemakers and atrial muscle are innervated by the parasympathetic/sympathetic nerves
Blood vessels are only innervated by the sympathetic
What chronotropic (change heart rate) effects does the autonomic nervous system have n the heart?
Sympathetic → drives heart through noradrenaline, increased rate increased conduction
Parasympathetic → slows the heart through acetylcholine, decreased rate decreased conduction
How are chronotropic effects exerted?
By altering pacemaker potential
→ sympathetic and parasympathetic alter the steepness of Na+ influx - the point at which the threshold is hit changes
What innervates ventricular muscles?
Sympathetic nerves only
What part of the nervous system can alter contractility of the heart?
Only the sympathetic nervous system
→ increases contractility through NA enhancing Ca2+ release in myocytes
→ positive inotropic effect - greater force of contraction, increase stoke volume
(parasympathetic has no effect)
Do sympathetic nerves have vasoconstrictor action?
Yes, vasoconstriction causes:
→ increase in resistance in arteries
→ increase in venous return in veins
(causes higher blood pressure)
What neurotransmitter do sympathetic nerves release onto smooth muscle?
Noradrenaline - increasing causes vasoconstriction
→ sympathetic nerve in tunica media cause contraction from NA
→ controls resistance of systemic circulation
→ regulates flow to organs or tissues
How do sympathetic nerves cause vasodilation?
Decreasing noradrenaline release
→ dilation increases flow to capillaries
How does noradrenaline work on smooth muscle?
NA acts on α1 and α2 receptors to mobile Ca2+ in smooth muscle
→ it alters the activity of myosin light chain kinase: more phosphorylation - more contraction
→ and myosin light chain phosphatase
What is the baroreceptor reflex?
One of the body’s homeostatic mechanisms to help maintain blood pressure at a constant level, in spite of changing requirements
→ sensing of blood pressure
→ integration by the CNA
→ correction of error
Where are the baroreceptors?
Aorta → that’s where BP is the highest, don’t want to break the aorta
Carotid → ensure brain has enough pressure, skull can’t take too much
What determines mean arterial blood pressure (MAP)?
Cardiac output (CO) and peripheral resistance (TPR)
→ MAP = CO x TPR
Baroreceptor reflex alters CO and TPR
What is the long term adjustment of blood pressure?
Blood volume
→ secretion of renin by the kidney is an important factor in regulating blood volume
→ increased frequency of impulses from sympathetic nerve system to kidney (detects quantity of blood) - increased renin secretion
What does angiotensin II do that affect circulation?
Rapid: powerful vasoconstricter → increase in peripheral resistance and venous tone
Slow: secretion of aldosterone → retention of Na+, thirst
What part of the heart senses filling pressure?
Atrial stretch receptors
→ activation controls output of hormones
→ rescue ECF (and therefore blood) volume
What is the endocrine function of the atria?
Secreting atrial natriuretic peptide/factor (ANP)
→ atrial stretch receptors help regulate extracellular fluid volume
→ release of ANP: renal excretion of Na+ and reduction of ECF volume
→ sends information to hypothalamus to decrease secretion of anti-diuretic hormone (ADH) - reduces ECF volume, removes vasoconstrictor effect
How can blood flow to a particular tissue be modified?
Adjusting vasomotor tone
→ vasoconstriction will reduce blood flow
→ vasodilation will increase blood flow
What counters increased vasomotor tone?
Potassium and adenosine act as paracrine signals
→ metabolites oppose sympathetic innervation - vasoconstrictor sympathetic nerve fibres are opposed by paracrine effects of metabolites
→ vasodilator metabolites ensure flow meets metabolic requirements
Overall what controls vessel diameter regulation?
Vasoconstriction → sympathetic tone, angiotensin II, ADH
Vasodilation → adenosine, K+, NO, adrenaline
How do vessels in the pulmonary circulation differ?
They are thin walled (look like veins but arteries) and are highly compliant (always want blood flow to lungs)
→ pulmonary circulation under low resistance - short distance, large diameter - essential yo stop fluid build up in lungs
Is hydrostatic pressure lower of higher than oncotic pressure in pulmonary circulation?
Hydrostatic pressure is less than oncotic pressure in the pulmonary circulation
→ reabsorption throughout capillary bed rather than tissue fluid formation
→ don’t want to push fluid into lungs
How is vessel dilation in the pulmonary circuit governed?
By oxygen levels and adenosine
→ principle regulator is O2 - low O2 results in vasoconstriction
→ innervated by the sympathetic nervous system - plays little role in physiological control of resistance
What does hypoxia induce?
Adenosine release causes:
→ vasodilation in system circulation
→ vasoconstriction in pulmonary circulation - stops blood flow to areas of dead lung
What are the reflexes induced by haemorrhage?
(Rapid loss of blood)
→ respond to reduction in blood volume
→ maintain blood pressure and cardiac output
→ restore circulating fluid volume
(become counterproductive)
What does haemorrhage lead to?
Fall in blood volume → fall in venous return
→ decrease in venous and arterial pressure
→ decrease in cardiac output
During haemorrhage where do initial corrections come from?
Baroreceptors → vasomotor centres → ANS
→ increasing cardiac output: elevating heart rate, enhancing contractility - increases rate of haemorrhage
→ increasing drive to vasculature: raising TPR (arterioles constrict), arising venomotor tone (veins constrict to push reservoir of blood) - stops blood flow to tissues
Why is interstitial fluid recruited during haemorrhage?
Haemorrhage causes drop in hydrostatic pressure
→ oncotic pressur recruits interstitial fluid
→ reabsorption of fluid at the expense of viscosity
How is loss of blood volume corrected?
Secretion of renin from kidneys
→ release of angiotensin II
short term: constriction of arterioles → increase TP + constriction of veins → restoring filling pressure
longe term: secretion of aldosterone → fluid retention + thirst → restoring ECF
How is loss of red blood cells corrected?
Secretion of erythropoietin
→ hormone which induces production of red blood cells
What are the classes of haemorrhage?
Class I → 15% bv: no change in vital signs e.g. blood donation
Class II → 15-30% bv: tachycardia, blood pressure changes, peripheral vasoconstriction, pale, cool
Class III → 30-40% bv: heart rate increase, bp drops, peripheral hyperfusion (shock)
Class IV → >40% bv: limit of body’s compensation reached, resuscitation required to prevent death
What clinical intervention is used for haemorrhage?
- treat cause of blood loss → prevent further bleeding
- give fluids → preferably blood, saline with colloid to maintain oncotic pressure
- monitor oxygen saturation
- in server situationsm monitor filling pressure of the heart with catheter
What is needed for exercise?
Provide skeletal muscle with radically increased blood supply
→ rase cardiac output and balance changes in peripheral resistance
→ increase coronary blood flow
During exercise how is the blood supply redistributed to skeletal muscles?
Exercise induces sympathetic nervous system
→ vasoconstriction in peripheral tissue
→ vasodilation in muscle blood vessels
What is the effect of adrenaline during exercise?
Sympathetic drive increases adrenaline
alpha receptors → vasoconstriction
beta receptors → vasodilation in skeletal muscles
What local effects override any sympathetic vasoconstriction during exercise?
Electrical activity release K+ → plasma [K+] rises in exercise, K+ relaxes vascular smooth muscle
ATP converted to Adenosine - an important paracrine vasodilator
Anaerobic respiration → lactat production, acidification leads to vasodilation
→ vasodilator metabolites match blood flow to metabolic needs
What would occur if filling pressure increased during exercise?
Lead to overstitching cardiac muscle
→ high filling pressure also leads to oedema - fluid in lung if left atrial pressure too high
→ at high filling pressures stroke volume no longer increases with increasing filling pressure - hit elastic capacity
How is the heart protected from overfilling/stretching during exercise?
Reduction in diastole
→ cardiac output rises - cannot be sustained through an increase in stoke volume alone so increase in heart rate
→ increase in heart rate reduces filling time protecting from over filling
How is the increased blood pressure during exercise countered?
Reduced total peripheral resistance
How does cutaneous (skin) vasodilation contribute to thermoregulation during exercise?
Get rid of excess heat during exercise through sweating and cutaneous vasodilation
→ however, reduces peripheral resistance and will divert blood from muscles - initially thermoreg wins but if central venous pressure falls then thermoreg abandoned
(hot climates: heat stroke)
When does blood flow to myocardium occur?
Coronary circulation flows during diastole (ceases during systole - contraction)
→ heart very good at extracting O2 70% efficient
