Module 3 Cardiovascular Flashcards
Contents of superior mediastinum:
Organs: Thymus, trachea, oesophagus, and ligamentum arteriosum.
Arteries: Aortic arch with branches-brachiocephalic trunk, left common carotid artery, left subclavian artery.
Veins and lymphatics: SVC, brachiocephalic veins, arch of azygos, thoracic duct. Nerves – Phrenic, vagus.
Contents of anterior mediastinum:
Sternopericardial ligaments, fat, some lymphatic vessels, lymph nodes and branches of the internal thoracic vessels, and the thymus (in the infants).
Contents of middle mediastinum:
Heart, pericardium, great vessels, trachea, bronchi, oesophagus, and lymph nodes.
Contents of posterior mediastinum:
Descending thoracic aorta, the azygos and the two hemiazygos veins, the vagus and splanchnic nerves, the oesophagus, the thoracic duct, and some lymph glands.
Name some mediastinal tumours
Anterior mediastinum: substernal thyroid goiters, lymphoma, thymoma, and teratoma.
Middle mediastinum: lymphadenopathy, metastatic disease from small cell carcinoma of lungs.
Posterior mediastinum: Neurogenic tumors.
Mediastinitis
inflammation of the tissues in the mediastinum, due to rupture of the organs
Pneumomediastinum
presence of air in the mediastinum, which might lead to pneumothorax, pneumoperitoneum, and pneumopericardium.
What can widened mediastinum indicate?
indicative of several pathologies: Aortic aneurysm or dissection or rupture, hilar lymphadenopathy, oesophageal rupture, cardiac tamponade, mediastinal mass, pericardial effusion.
Pericardial layers
Fibrous outer
parietal layer
serous lining
visceral layer (epicardium)
myocardium
endocardium
pericardial sac attachments
attached to the central tendon of the diaphragm, the sternum, the mediastinal pleurae, and the tunica adventitia (outer layer) of the great vessels (SVC & pulmonary vessels).
Innervation of the pericardium
Nerves supplying the pericardium arise from the vagus nerve [X], the sympathetic trunks, and the phrenic nerves. The phrenic nerve (C3-C5) is responsible for the somatic innervation of the pericardium, as well as providing motor and sensory innervation to the diaphragm.
Blood supply of the pericardium
The pericardium is supplied by branches from the internal thoracic, pericardiacophrenic, musculophrenic, and superior phrenic arteries, and the thoracic aorta. The veins from the pericardium enter the azygos system of veins and the internal thoracic and superior phrenic veins.
What anatomical feature is useful for surgeons in heart surgery
The transverse pericardial sinus separates the heart’s arterial outflow (aorta & pulmonary trunk) from its venous inflow (SVC & pulmonary veins).
Location: Posterior to ascending aorta & pulmonary trunk; anterior to the SVC; superior to left atrium.
Applied anatomy: The transverse pericardial sinus can be used to ligate the arteries of the heart during coronary artery bypass grafting.
Pericarditis
Pericarditis: It is an inflammatory condition of the pericardium. Common causes are viral and bacterial infections, systemic illnesses (e.g., chronic renal failure), and after myocardial infarction.
Pericardial effusion
Pericardial effusion: Usually, only a tiny amount of fluid is present between visceral and parietal layers of the serous pericardium. In certain situations, this space can be filled with excess fluid.
Cardiac tamponade
As fibrous pericardium is a relatively fixed structure that cannot expand easily, a rapid accumulation of fluid within pericardial sac may compress heart, resulting in biventricular failure.
Constrictive pericarditis
Abnormal thickening of the pericardial sac, which usually involves only the parietal pericardium, can compress the heart, impairing heart function and resulting in heart failure
Heart surfaces
The base of the heart is quadrilateral and directed posteriorly. It consists of the left atrium, a small portion of the right atrium, and the proximal parts of the great veins
The right margin is the small section of the right atrium that extends between the superior and inferior vena cavae. The left margin is formed by the left ventricle and left auricle. The superior margin is formed by both the atria and their auricles. The Inferior margin is marked by the right ventricle.
The anterior surface faces anteriorly and consists mostly of the right ventricle, with some of the right atrium on the right and some of the left ventricle on the left.
The heart in the anatomical position rests on the diaphragmatic surface, which consists of the left ventricle and a small portion of the right ventricle
What is the cardiac skeleton
The cardiac skeleton is a collection of dense, fibrous connective tissue in the form of four rings (anulus fibrosus) between the atria and the ventricles, which surround the two atrioventricular orifices, the aortic orifice and opening of the pulmonary trunk.
The fibrous skeleton of the heart separates the atria from the ventricles and gives attachment to the cusps of the atrio-ventricular valves (mitral and tricuspid) valves to the myocardium.
Describe the anatomy of the different AV valves in the heart
Right AV/tricuspid valve has three cusps: anterior, septal & posterior.
The left AV/bicuspid/mitral valve has two cusps: anterior/aortic and posterior/mural.
Backward prolapse of the cusps is prevented by the chordae tendineae that connect the papillary muscles of the ventricular wall to the AV valves, that cause tension to better hold the valve, and prevent backflow of the blood from the ventricles to the atria.
The papillary muscles & chordae tendineae together are known as subvalvular apparatus, that keeps the valves from prolapsing into the atria when they close. AV valves are formed by the flap-like cusps that are anchored to the ventricular wall by tendinous filaments.
What can cause heart tremors
Papillary muscles damage can lead to valve incompetence and cardiac murmurs.
Describe Aortic semilunar valves
left, posterior, right cusps with semilunar valves prevent backflow of blood from these arteries into the ventricles. Unlike the AV valves, these valves do not have chordae tendineae and are like the valves in the veins.
Right and left coronary arteries begin in the right and left aortic sinuses found in each cusp
Describe pulmonary semilunar valves
left, anterior, right cusps with semilunar valves prevent backflow of blood from these arteries into the ventricles. Unlike the AV valves, these valves do not have chordae tendineae and are like the valves in the veins.
How to auscultate the heart valves
Aortic - 2nd R ICS medial
Pulmonary - 2nd L ICS medial
Tricuspid - 4/5th L ICS medial
Mitral 5th L I CS mid clavicular line
Interior of the right atrium
Presence of R atrio-ventricular orifice.
Presence of crista terminalis.
Openings of SVC, IVC, coronary sinus.
Coronary sinus receives blood from the coronary veins, and it opens in between IVC and the right AV orifice.
Interatrial septum - a solid muscular wall that separates right and left atria.
Fossa ovalis in the septal wall with its prominent margin, limbus fossa ovalis.
Openings of the smallest cardiac veins
interior of the right ventricle
Presence of right atrio-ventricular orifice, guarded by tricuspid valve.
Presence of trabeculae carneae, papillary muscles, and the chordae tendineae in the right ventricle.
interior of left atrium and left ventricle
Presence of trabeculae carnae, anterior and posterior papillary muscles in LV.
Presence of the mitral valve guarding the left atrio-ventricular orifice.
Presence of the interatrial and IV septa.
What can occur at the Right auricular appendage
Site for thrombi - PE
Often excised in pulmonary bypass
Triangle of Koch
Landmark for AV node
Just above coronary sinus
sites of arrhythmia genesis
crista terminalis and atrial septum
What is the inferior vena caval opening used for?
sending catheters into
Right Coronary Artery anatomy and supplies
RCA arises from right aortic sinus; anastomoses with the left circumflex artery, a branch of LCA.
Branches: SA nodal branch supplies the SA node
Its right marginal branch supplies apex of heart.
A branch to AV node before giving off its final branch, the posterior interventricular branch.
RCA supplies the right atrium, majority of right ventricle, SA & AV nodes, interatrial septum, a portion of left atrium & left ventricle, postero inferior one third of interventricular septum.
Left Coronary artery anatomy
LCA arises from left aortic sinus, and branches into left anterior descending & left circumflex.
Being larger than RCA, the LCA supplies most of left atrium and left ventricle, most of the IV septum, the AV bundle and its branches.
What does right dominant coronary artery
The posterior descending branch arises from the RCA and supplies major portion of the diaphragmatic surface of the LV.
L Circumflex artery is relatively small
What does left dominant coronary artery mean?
The posterior descending branch arises from an enlarged circumflex branch
Clinical examples of pathology in the coronary arteries
Narrowing of coronary arteries is caused by atherosclerosis or arteriosclerosis. It results from plaques deposits of cholesterol, resulting in coronary artery disease or ischemic heart disease.
Stable angina is the chest pain on exertion that improves with rest. Unstable angina is chest pain that occurs at rest, feels more severe and last longer than stable angina.
A heart attack results from a sudden plaque rupture and formation of a thrombus that blocks blood flow to a portion of the heart leading to tissue necrosis and death (infarct).
CAD can also result in heart failure or arrhythmias. Heart failure is caused by chronic oxygen deprivation due to reduced blood flow. Arrhythmias are caused by inadequate blood supply to the heart that interferes with heart’s electric impulse.
Spontaneous coronary artery dissection is a rare condition, in which the wall of one of the coronary arteries tears, causing severe pain. Unlike CAD, it tends to occur in younger individuals.
Coronary venous routes
Great: apex - anterior IV sulcus - coronary sulcus - sinus
middle: apex - posterior interventricular sulcus - sinus
Small: Coronary sulcus - sinus
Posterior: posterior surface of LV - sinus or great cardiac vein
Cardiac conduction route
SA node - AV node - bundle of his - L and R bundle - purkinje fibres
Intrinsic HR?
100bpm
Cardiac innervation
The heart is autorhythmic – without any neural input the heart will still beat.
Stimulation of the parasympathetic system decreases the heart rate, reduces force of contraction, & constricts coronary arteries.
.
Preganglionic parasympathetic fibers reach heart as cardiac branches from right and left vagus CNX.
Stimulation of the sympathetic system increases heart rate and increases the force of contraction.
Sympathetic fibers reach cardiac plexus through the cardiac nerves from the sympathetic trunk.
Preganglionic sympathetic fibers from the upper four or five segments of the thoracic spinal cord enter and move through the sympathetic trunk.
They synapse in the cervical and upper thoracic sympathetic ganglia, and postganglionic fibers proceed as bilateral branches from sympathetic trunk to the cardiac plexus.
Describe cardiac plexus anatomy
This plexus consists of a superficial part, inferior to the aortic arch and between it and the pulmonary trunk, and a deep part , between the aortic arch and the tracheal bifurcation. From the cardiac plexus, small branches that are mixed nerves containing both sympathetic and parasympathetic fibers supply the heart. These branches affect nodal tissue and other components of the conduction system, coronary blood vessels, and atrial and ventricular musculature.
From medial to lateral, list the main vessels
Common carotid artery, internal jugular vein, subclavian artery, subclavian vein
Five dilations appear during the growth of heart tube
Truncus arteriosus
Bulbus cordis
Primitive (left) ventricle
Primitive atrium
Left and right horns of sinus venosus
What do the components of the primitive heart tube become?
Sinus venosus horns: become the posterior walls of the true atria
Primitive atrium: forms the anterior walls and muscular parts of both atria (auricles)
Primitive ventricle: forms most of the left ventricle
Inferior end of the bulbus cordis (conus arteriosus) forms the right ventricle
Truncus arteriosus forms the ventricular outflow tracts (aorta and pulmonary trunk)
Folding of the primitive heart tube
Heart tube simultaneously elongates and begins to loop at end of week 3
Primitive atrium moves posteriorly & superiorly
Primitive ventricle moves to the left
Bulbus cordis (right ventricle) moves inferiorly, anteriorly and towards the right side
Folding is complete by end of week 4
Process of atria septation
Septation begins at the end of week 4 with a crescent-shaped outgrowth from the posterior wall – septum primum
Septum primum grows anteriorly and shrinks the opening between the left and right sides of the primitive atrium - the foramen (ostium) primum
Endocardial cushions develop around the periphery of the atrioventricular canal
Dorsal and ventral cushions fuse to form the septum intermedium (dividing the atrioventricular canal into right and left)
Septum primum fuses with the septum intermedium (closing the foramen primum)
Before the foramen primum closes, a new foramen opens near the superior edge of the septum primum due to cell death – foramen secundum
While septum primum is growing the septum secundum appears on ceiling of right atrium (next to the septum primum)
Grows posteroinferiorly and stops before reaching the septum intermedium
Leaves an opening near the floor of the right atrium – the foramen ovale
Septation of the ventricles
Heart undergoes remodelling to bring the future atria and ventricles into their correct positions
Ventricles align with their respective outflow tracts
Muscular interventricular septum forms at the end of week 4 and grows toward the endocardial cushion, leaving interventricular foramen
Membranous part of interventricular septum grows inferiorly from the endocardial cushion to close the foramen
Septation of the ventricles and outflow tract
During weeks 7 and 8 the truncus arteriosus undergoes a process of septation & division to convert it into the ascending aorta and a separate pulmonary trunk
Conotruncal ridges divide truncus arteriosus into two channels and fuse with interventricular septum
Process occurs helically – right ventricle connects to pulmonary trunk and left ventricle to aorta as a result of spiral fusion process
During this process, swellings within the truncus arteriosus give rise to the semilunar valves of the aorta and pulmonary trunk
Key Pharyngeal arch arteries
3rd pharyngeal arch arteries form common carotid and internal carotid arteries
4th pharyngeal arch arteries form right subclavian artery and part of aortic arch on the left
Left 6th arch artery forms ductus arteriosus (fetal shunt)
Right 6th arch artery degenerates to allow passage of right recurrent laryngeal nerve
What is Coarctation of the aorta
Congenital constriction of aorta
Surgical repair needed soon after birth if severe
Ductus arteriosus may still be patent
Most common occurrence is distal to the left subclavian artery, directly opposite the opening for the ductus arteriosus
Circulatory changes after birth
Loss of umbilical circulation causes the ductus venosus to degenerate – forms ligamentum venosum in adult
More blood enters pulmonary arteries
Blood returning from the lungs increases pressure in left atrium and septum primum is pushed against septum secundum to close foramen ovale – fossa ovalis in adult
Constriction of the ductus arteriosus - ligamentum arteriosum in adult
Atrial septal defects (ASDs)
Incomplete septation of atrium
E.g. ostium secundum defect – defect in middle of septum
Patent foramen ovale
Not a true septal defect but similar
Incompetence of fossa ovalis valve, may be probe-patent
~25% of the population
Reverse flow from left to right atrium
Non-cyanotic – may not be identified until adulthood
Ventricular septal defects (VSDs)
Incomplete septation of ventricles
Most common congenital cardiac abnormality in children
Commonly due to incomplete closure of the membranous part of the interventricular septum (80% of VSDs)
Reverse flow from left to right ventricle
Non-cyanotic, but if large may lead to pulmonary hypertension and increased risk of arrhythmias
Patent ductus arteriosus
Ductus arteriosus connects pulmonary trunk to aorta
Blood bypasses lungs in fetal circulation
Normally closes after birth due to reversed flow and withdrawal of placental prostaglandins
Failure to close = blood flow from aorta to pulmonary circulation
Non-cyanotic, but lead to pulmonary hypertension long-term
Persistent truncus arteriosus
Incomplete septation of truncus arteriosus
Aorta and pulmonary trunk fail to develop separately, remaining as one single vessel
Ventricular septal defect present
Cyanotic
Transposition of the great arteries
Aorta arising from the right ventricle (dextro-transposition)
Pulmonary trunk arising from the left ventricle
Pulmonary and systemic circulations are not continuous, therefore oxygenated blood not pumped around body
Cyanotic
Dependent on ductus arteriosus to deliver oxygenated blood to the aorta – can be encouraged using prostaglandin E1
Tetralogy of Fallot
Four defining features:
Pulmonary valve stenosis
Ventricular septal defect
Over-riding aorta
Right ventricular hypertrophy
(also cyanosis – ‘tet spells’)
Is cardiac muscle striated?
Cardiac Muscle is STRIATED
Contraction of Striated Muscle:
The shortening of striated muscle is brought about by the thick filaments pulling the thin filaments towards the centre of the sarcomere, thereby making the H zone and I bands shorter
What is the contraction of cardiac muscle dependent on?
Contraction is calcium and ATP dependent
Describe cardio myocytes
Small cells with a single nucleus (usually)
T-tubule and sarcoplasmic recticulum systems less well developed than skeletal muscle (IC Ca+ increase (from SR release) facilitated by EC Ca+ entering through Ca+ channels)
Mitochondria take up 30-40% of cell volume (much higher than any skeletal muscle cells) as continued contraction required so no capacity for oxygen debt
Branched cells linked together by intercalated disks
Acts as a functional (but not structural) syncytium
What are intercaleted discs in cardiac muscle
Act as electrically boundaries between cardiac muscle cells with ‘leaky’ gap junctions
What are connexons?
Adjacent plasma membranes of neighbouring muscle cells communicate rapidly through transmembrane protein channels called connexons
These are charged aqueous pores which allow small ions to move freely from one cell to another changing the electrical activity of the neighbouring cell
Action potential in SA node vs other cardiac cells
SA NODE – Needed as trigger and not to generate contraction force
OTHER CELLS – Na+ initially then Ca+ induced plateau phase to maintain (200ms) depolarisation and contraction
Autonomic control of the heart
Higher centres > cardiac accelerator nerves (s) > NA on B1
> Vagus nerves (ps) > ACh on musc
The heart contains 2 types of specialized cardiac muscle cells:
- Contractile cells or Cardiomyocytes (99%) – Mechanical work
2. Autorhythmic or pacemaker cells – Initiate and conduct action potentials for contractile cells
Sinoatrial (SA) node
Small, specialized region in the right atrial wall near the opening of the superior vena cava
Atrioventricular (AV) node:
Small bundle of specialized cardiac muscle cells located at the base of the right atrium, near the septum, just above the atria-ventricular junction
Bundle of His (AV bundle):
Tract of specialized cells that originates at the AV node and enters the interventricular septum. At the septum, it divides to form the right and left bundle branches that travel down the septum, curve around the tip of the ventricles, and travel back toward the atria along the outer walls
Purkinje fibers
Small, terminal fibers that extend from the Bundle of His and spread throughout the ventricular myocardium, like twigs of a tree branch
Two areas of myocardium
SubENDOcardial section
Fibres run away from midwall towards the endocardial surface
SubEPIcardial section
Fibres run away from midwall towards the epicardial surface
How does an ECG relate to the areas of the myocardium
ECG = ENDO - EPI
ENDO cells are activated slightly quicker:
Phases of the cardiac cycle:
Atrial systole, Isovolumetric Contraction, Rapid Ejection, Reduced Ejection, Isovolumetric Relaxation, Rapid Ventricular Filling, Diastasis
Atrial systole:
Last phase of diastole
ECG P to R-wave.
Depolarisation of the atria leads to atrial contraction (see the ‘a’ wave on the atrial pressure curve).
A tiny amount of ‘topping off’ completely fills the ventricle.
Affected by AF (atrial stasis)
Rarely, a 4th heart sound (atrial “jet” or LV stiffness).
Isovolumetric Contraction:
First phase of systole.
Begins at the peak of the R-wave of the ECG.
No real change in the volume of the ventricles during this phase.
First heart sound (‘lub’) caused by closing of the A-V valves and associated blood turbulence when ventricular pressure exceeds atrial pressure.
Rapid Ejection:
During ST segment.
When ventricular pressure exceeds that in the aorta or the pulmonary artery, semilunar valves open and rapid ejection (2/3) from the ventricles starts.
‘c’ wave in the atrial pressure curve is caused by slight (due to papillary muscles) distension of the A-V valves into the atria (normally not measurable).
Reduced Ejection:
Final phase of systole.
Coincides with the T-wave of the ECG (ventricular repolarisation).
Blood flow out of the ventricles continues, but happens more slowly (reduced ejection).
Eventually, pressure in the ventricle falls below that in the arteries. Semilunar valves close.
Isovolumetric Relaxation
First phase of diastole.
Atria have been filling with blood (atop the closed A-V valves) and atrial pressure has been rising gradually.
Blood flow out of the ventricles stops (hopefully the ventricles are sufficiently empty).
The 2nd heart sound (‘dup’) occurs when the semilunar valves close.
Rapid Ventricular Filling:
When ventricular pressure falls below atrial pressure, the A-V valves open.
This allows blood to flow from the atria into the ventricles.
A third heart sound may be heard in children, who have thinner chest walls, but in adults this is usually a clear sign of cardiac problems, such as congestive heart failure (atrial press. too high
Diastasis
Filling of the ventricles continues more slowly, as atrial and ventricular pressures rise.
This continues until the ventricles are almost full (at 120mL), when the whole thing starts over again!
Mitral stenosis
Incomplete opening of the mitral (bicuspid, left AV) valve can lead to backup of blood into the left atrium and inadequate filling of the ventricle.
Aortic stenosis
Incomplete opening of the aortic valve – can lead to inadequate ventricular emptying.
Mitral regurgitation
Either the mitral valve closes, but cannot fully prevent backflow of blood into the left atrium during ventricular contraction, or it does not close properly.
Children gross motor skills milestones
Social smile 4-6 weeks
Holds head up when sat 3 months
Rolling over 5 months
Sitting without support 6-7 months
Crawling 8-9 months
Cruises 10 months
Fine motor skills children milestones
Holds small objects 3-4 months
Reaches for toys 5 months
Transfers from one hand to other 6-7 months
Grips with fingers 8-9 months
Pincer grip 10 months
Children speech and language milestones
Cooing 3 months
Dada-Mama 10 months
2-3 words 12 months
Name 3 body parts 18 months
2-3 word sentences 2 years
Full sentences 2.5 years
Children receptive language milestones
By 1 year
Pointing
Understands simple commands
By 18 months
Simple two step commands
By 2-3 years
Understands up to 300-900 words
Understands complex commands
Social skills in children
Social smile 4-6 weeks
Finger feeds 6-8 months
Peek-a-boo 6-9 monts
Waves bye-bye 10 months
Drinks from a cup 12 months
Helps undress 18 months
Warning signs to spot in child development
No smile by 8 weeks
No eye contact by 3 months
Not reaching for objects by 5 months
Not sitting at 9 months
Not walking at 18 months
No speech at 18 months
No 2-3 word sentences at 2½
Order for assessing children development
primitive reflexes, gross motor, vision, fine motor, hearing, speech and language.
What is the small blip in arterial pressure called and what causes it
There is a small ‘blip’ in the pressure profile when the aortic valve closes; this is known as the ‘incisure’ or the ‘dichrotic notch’
How is mean arterial pressure calculated?
MAP = DBP + ⅓PP
=DBP + ⅓ (SBP-DBP)
The Milieu Interieur:
homeostasis
What percentage of blood is found in venous circulation?
afferent vessels act as conduits and reservoirs. About 70% of blood volume is in the venous circulation (capacitance)
Four Parameters affecting arterial blood pressure:
Circulatory volume (and hence stroke volume)
Force of ventricular contraction
Elasticity of arteries
Peripheral resistance
Describe the factors affecting resistance to steady, streamlined flow through a rigid cylindrical tube
R = 8ηL/πr4
resistance R, viscosity η, length L, radius r
Baroreceptor reflex
Pressure receptors (baroreceptors) exist in the wall of the arch of the aorta and in the carotid sinus
These specialised nerve endings send information to the CNS about MAP
If MAP decreases, the receptors decrease input which results in activation of the SNS and inactivation of the PNS
The overall effect is to increase MAP by increasing HR and SV, and increasing TPR by constricting blood vessels
Aldosterone
Released from the adrenal cortex; increases salt and water retention by the kidneys
Antidiuretic hormone (vasopressin)
Released from the posterior pituitary; constricts blood vessels and increases water retention by the kidneys
Atrial natriuretic peptide
Released from the atria when stretched; increases salt and water excretion by the kidneys
Cortisol
Released from the adrenal cortex; increases the actions of the sympathetic nervous system on its target cells
Erythropoietin
released from the kidney; increases production of erythrocytes (increasing blood viscosity)
Describe how angiotensin II is formed (RAAS)
Renin is released from cells near the glomeruli in the kidney in response to lowered kidney perfusion pressures caused by (amongst other things) lowered BP
Renin acts on a protein called angiotensinogen (gen– erates angiotensin) and cleaves this precursor at specific sites to form angiotensin I (inactive)
Angiotensin I is converted to angiotensin II by the action of angiotensin converting enzyme (ACE; lung capillaries and endothelial cells of blood vessels). Angiotensin II is the active form of the peptide
Physiological Actions of Angiotensin II:
Angiotensin II constricts blood vessels; hence it can increase TPR and raise MAP
Angiotensin II also stimulates thirst and promotes the release of ADH; increasing circulating blood volume, CO and MAP
Angiotensin II also stimulates the release of aldosterone from the adrenal cortex; increasing circulating blood volume, CO and MAP by this route also (salt & water retention)
How does atrial stretch regulate MAP
When venous return is raised (e.g. in the case of increased circulatory volume):
Atrial myocytes release atrial natriuretic peptide (ANP), which is a vasodilator and:
Promotes Na+ excretion – H2O follows
Inhibits secretion of ADH (antidiuretic
hormone or “vasopressin”)
Cardiac accelerator nerves send signals to:
c. Increase heart rate and ventricular contractility
Sympathetic vasomotor nerves cause … in BP responses
vasoconstriction
Layers of blood vessel
Lumen
Tunica intima; Endothelial cells & basement membrane, Supporting connective tissue
Internal elastic lamina
Tunica media; Smooth muscle and elastin
External elastic lamina
Tunica adventitia; Supporting connective tissue (fibres with some vessels & nerves)
Tunica media in arteries and veins
Large tunica media in arteries for strength
Role of arterioles in resistance & blood pressure
Reduced blood flow leads to improper perfusion of tissues and lack of nutrients (ischaemia) which can lead to cell death
Too much flow damages delicate tissue structure.
Arterioles control this by varying their diameter
