2. Cardiovascular Flashcards
Are capillaries permeable
Exercise effect on capilaries
Diameter?
Ccapillaries permit the leakage of plasma through fenestrations.
The ability of blood to flow through these capillaries is closely controlled by arteriolar tone. They do not have smooth muscle themselves. Hence exercise can stimulate greater opening up of the capillary beds.
The diameter of a capillary is 5 - 10 microns. Erythrocyte diameter is 6 - 8 microns.
CarboxyHb
Avidity for Hb
CO vs O2
Affect on O2 dissoc curve
Affect on cytochrome oxidase - which then does what
Men or women better clearing?
Affect inotropy?
Rhythym disturbance?
Ischameic?
Haemoglobin (Hb) has 250 times more affinity for carbon monoxide than for oxygen, which reduces the total amount of Hb available for oxygen transport.
CO shifts the oxygen-haemoglobin dissociation curve to the left and down, reducing the ability of Hb to release oxygen.
CO inhibits cytochrome oxidase, which reduces mitochondrial ATP formation and worsens tissue hypoxia.
Clearance is decreased in men and during sleep.
CO is negatively inotropic.
Carboxyhaemoglobin (COHb) levels of 4.5 to 6% reduce the onset time of exercise induced angina and increase the incidence of ventricular dysfunction and dysrhythmias.
Myocardial ischaemia itself promotes the formation of carboxyhaemoglobin, which further reduces oxygen delivery to the ischaemic myocardium.
Hb reduction -
Compensatory mechanism
what happens to viscoisty
2 3 dpg
What is the reticulocyte count
Raised when
A reduction in haemoglobin results in reduced oxygen delivery to tissues. Compensatory mechanisms include increased oxygen extraction that may cause a decreased mixed venous oxygen saturation.
Blood viscosity is reduced and 2,3 DPG levels increase which reduces the affinity of haemoglobin for oxygen.
The reticulocyte count is a measure of the numbers of immature red blood cells derived from the marrow. Is is typically raised when there is high red cell turnover such as chronic haemorrhage and haemolytic anaemia. It is not a feature of iron deficiency anaemia but the reticulocyte count may increase following iron therapy.
Catecholamine
Syntehsis where
stored where
Secretion from -
Secretion induced by
Hypothermia increase or decreased
Cells in the adrenal medulla synthesise and secrete the catecholamines norepinephrine and epinephrine which are stored in electron-dense granules (that also contain ATP and several neuropeptides).
Secretion of these hormones is stimulated by acetylcholine release from preganglionic sympathetic fibres innervating the medulla. Many types of “stresses” stimulate such secretion, including exercise, hypoglycaemia, pain, hypoxaemia, hypercapnia and trauma.
The physiologic consequences of medullary catecholamine release are justifiably framed as responses which aid in dealing with stress.
During mild hypothermia the arterial concentrations of norepinephrine increase, which induces vasoconstriction
AV node is where in relation to cornary sinus
sympathetic nerve supple to heart from where
Borders heart formed by what
number of cusps on valves
The atrioventricular node is situated above (not below) the opening of the coronary sinus.
The sympathetic nerve supply to the heart is provided by the superficial and deep cardiac plexuses.
The superficial cardiac plexus is formed by branches from the left superior cervical sympathetic ganglion and the left vagus.
The deep cardiac plexus is formed by branches from both the left and right inferior and middle, cervical sympathetic ganglia, both vagi and the upper four thoracic sympathetic ganglia.
The right border of the heart is formed entirely by the right atrium; the left border is formed mainly by the left ventricle; and the inferior border by the right ventricle, the lower part of the right atrium and the apex of the left ventricle.
The tricuspid, pulmonary and aortic valves have three cusps, the mitral valve has two.
Stab wound - compensation mechanism
How much circulating volume in
veins
artery
Which act as a reesevoir
resting CO -
How much to liver
- can it help in haemorrhage
The veins of the body contain 70% of the circulating blood volume, in contrast to the 15% in the arterial system.
Veins act as a reservoir, and venous tone is important in maintaining the return of blood to the heart, for example in severe haemorrhage, when sympathetic stimulation causes venoconstriction.
The liver receives approximately 30% of resting cardiac output and is therefore a very vascular organ. The hepatic vascular system is dynamic, meaning that it has considerable ability both to store and release blood - it functions as a reservoir within the general circulation.
In the normal situation, 10-15% of the total blood volume is in the liver, with roughly 60% of that in the sinusoids. When blood is lost, the liver dynamically adjusts its blood volume and can eject enough blood to compensate for a moderate amount of haemorrhage.
Increased albumin synthesis begins at approximately 48 hours.
Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Increased levels of antidiuretic hormone (ADH) further contribute to the retention of water.
Valsalva manoeuvre
what is it
How many phases
Describe effects on HR/BP in each
The Valsalva manoeuvre involves forced expiration against a closed glottis to generate an intrathoracic pressure of 40 mmHg for 10 seconds. The effects on the heart rate (HR) and blood pressure (BP) are then monitored and divided into four phases.
Phase I - An initial increase in venous return from intrathoracic vessels causes a transient decrease in HR and increase in BP.
Phase II - As the high intrathoracic pressure in maintained there is a decrease in the venous return which is sensed by baroreceptors. This causes an increase in HR and decrease in BP. The BP tends to return to normal by the end of phase II.
Phase III - Sudden release of forced expiration and/or glottal opening results in a return of the intrathoracic pressure to normal. This causes pooling of blood into intrathoracic vessels resulting in a decrease in BP, whilst the HR remains elevated.
Phase IV - During phase IV the intrathoracic pressure remains normal and the continued increase return of systemic venous blood produces a reflex bradycardia associated with an increase in BP to normal.
Vasiconstrictor or vasodilator
Prostacyclin
ANP
Indoramin
AngII
Epoprostenol
Prostacyclin is a potent vasodilator and has been used as an intravenous infusion for critically ischaemic limbs. It is provided commercially as sodium epoprostenol.
Atrial natriuretic peptide (ANP) is a hormone which has been isolated from the atria, kidneys and neural tissue. It is a vasodilator (renal vessels are more sensitive than others) and a natriuretic that increases the glomerular filtration rate and sodium and water excretion. Plasma renin activity and aldosterone release is also inhibited.
Indoramin is an alpha-1 receptor antagonist.
Angiotensin II causes vasoconstriction, increased thirst, increased antidiuretic hormone (ADH) secretion and increased aldosterone levels.
Epoprostenol - dilator
1 met = what
1 MET = consumption of 3.5 ml O2/kg/minute.
Explain + draw the CVP trace
The central venous pressure waveform consists of named waves and descents:
The “a” wave is due to atrial contraction
The “c” wave is thought to be due to transmitted pulsation from the carotid arteries or to the bulging of the tricuspid valve into the right atrium
The “v” wave is due to the rise in atrial pressure before tricuspid opening
The “x” descent is due to atrial relaxation
The “y” descent is due to atrial emptying as blood enters the ventricle.
End insp -5
end exp -3
Exercise change on blood flow
What does it do - how soon
Does if affect CBF? how
Lymph?
Viscera?
Exercise produces an increase in heart rate, blood pressure and muscle blood flow (after at least a minute).
Cerebral blood flow is however very closely controlled and is generally stable. It increases in response to increased CO2.
d-Capillary pressure and surface area are increased, therefore more fluid leaves the bloodstream.
Muscle action assists the movement of lymph.
Visceral blood flow decreases due to sympathetic increased activity with the diversion of blood to the exercising muscles.
Hameorrhage affect
CO
blood vesells
increases secretion of what
What happens in kidney
how long does it take to replace plasma proteins
Increase production RCC takes how long
does the spleen help?
Cardiac output is reduced.
Haemorrhage produces both venous and arteriolar contraction.
Hypovolaemia increases aldosterone and angiotensin secretion.
Renal reabsorption of sodium is increased and volume homeostasis is eventually achieved.
Replacement of plasma proteins by increased hepatic synthesis of proteins (completion in 24-48 hours)
Increased production of red blood cells (N.B. reticulocyte response) and other cellular components (e.g. platelets) (completion in 5 to 7 days
Unlike carnivores, the human spleen does not act as a significant reservoir of red blood cells and does not contract in response to blood loss.
describe the phases of cardiac myocyte action potential
Phases of the cardiac myocyte action potential are as follows:
Phase 4: transmembrane potential (TMP)
The resting membrane potential in a cardiac myocyte is approximately −90 mV due to a constant outward leak of K+ through inward rectifier channels.
Na+ and Ca2+ channels are closed and inactive at in this phase.
Phase 0: Depolarization
An action potential triggered in a neighbouring cardiomyocyte or pacemaker cell causes the TMP to rise above −90 mV.
Fast Na+ channels open and there is Na+ influx, further raising the TMP.
TMP approaches −70mV, the threshold potential in cardiomyocytes
A sustained Na+ influx rapidly depolarizes the TMP to 0 mV and slightly above 0 mV for a transient period of time called the overshoot and at this point the fast Na+ channels close.
L-type (“long-opening”) Ca2+ channels subsequently open when the TMP is greater than −40 mV and cause a small but steady influx of Ca2+ down its concentration gradient.
Phase 1: Early repolarization
The TMP at this point is marginally positive.
K+ channels open briefly and an outward flow of K+ returns the TMP to approximately 0 mV.
Phase 2: The plateau phase
L-type Ca2+ channels are still open where there is a small, constant influx of Ca2+ ions.
K+ continues to leaks down its concentration gradient through delayed rectifier K+ channels. These two countercurrents are electrically balanced, and the TMP is maintained at a plateau just belowq 0 mV throughout phase 2.
Phase 3: Repolarization phase
Ca2+ channels become gradually inactivated.
Continuing efflux of K+ eventually exceeds Ca2+ influx, bringing the TMP back towards the resting value of −90 mV to prepare the cell for a new cycle of depolarization.
Normal transmembrane ionic concentration gradients are restored by returning Na+ and Ca2+ ions extracellularly, and K+ ions intracellularly. The pumps involved include the sarcolemmal active transport Na+-Ca2+ exchangers.
Slowing of phase 3 increases the QT interval.
Synchronised dardioversion
A synchronised direct current (DC) cardioversion involves the delivery of a predetermined shock of electric energy that corresponds to a specific point of the ECG complex. The peak of the first upstroke (R-wave) is the safest point for synchronisation. The QRS complex corresponds to the electrical activity associated with ventricular depolarisation during an effective refractory period.
This synchronized shock is delivered at this precise moment to avoid inducing more serious arrhythmias such as ventricular fibrillation.
The T-wave is the vulnerable period where this is most likely, especially the middle and second half of the T-wav
Carotid sinus barorectpors
what type of receptors are they
Where are they located exactly
Where are there similar receptors
What inerrvates it
what is a branche off
receives afferent fromt what
Wjat happens as arterial pressure increase in terms of discharge
which stimulates what
leading to
What happens to the baseline in hypertension
The carotid sinus baroreceptors are stretch receptors (not pressure) that control blood pressure and heart rate by a feedback mechanism.
They are located in the internal carotid artery
distal to the carotid bifurcation and carotid body
(the latter lies at the bifurcation).
Similar baroreceptors are found in the aortic arch, atria and left ventricle.
The carotid sinus nerve, which is a branch of the ninth cranial nerve, receives afferent fibres from the carotid sinus and carotid body and ascends to the vasomotor centre.
As the distending pressure in the artery increases, the discharge rate from the baroreceptors increases, which stimulates the cardioinhibitory centre, causing a fall in blood pressure, heart rate and cardiac output.
In chronic hypertension, in order to maintain an elevated blood pressure, the reflex mechanism is reversibly reset.
ANP - what does it inhibit
Levels rise with stretch
affect on
blood vessels -
AngII
Renin
Atrial natriuretic peptide (ANP) inhibits sodium reabsorption in the distal convoluted tubule (not loop of Henle).
Levels rise with stretching of the atrial wall as occurs in severe congestive cardiac failure.
It is a vasodilator and acts by preventing angiotensin II mediated vasoconstriction and inhibition of renin release.
SVR calcuation
Systemic vascular resistance (SVR) is a derived value based on the following:
The analogy is Ohm's law: Potential difference (V) = Flow of current (I) x Resistance (Ω) Therefore R = V/I
SVR = (MAP-CVP)/CO x 80
= (60 -10)/CO x 80 = 800 dynes.s.cm-5
Note: A correction factor of 80 is used to convert mmHg to dynes.s.cm-5
Normal values range between 700 -1600 dynes.s.cm-5
PVR calculation
Pulmonary resistance (PVR) similarly = (MPAP-PCWP)/80 x 80
= (10 - 5)/5 x 80 = 80 dynes.s.cm-5
To account for body size, instead of the denominator being CO, cardiac index (CI) can be used. CO/body surface area (m2) or mL/minute/m2.
This will produce the parameters SVRI or PVR
Giant a waves are seent with what
why
Giant “a” waves occur in the jugular venous pressure (JVP) in pulmonary hypertension and tricuspid stenosis when there is a poorly compliant right ventricle which increases the impedence against which the right atrium has to eject blood.
In constrictive pericarditis the JVP is high with an abrupt fall in systole (x descent) and may rise with inspiration (Kussmaul’s sign).
Giant “a” waves are not seen in aortic regurgitation or thyrotoxicosis.
Adrenlaine - does what to skeletal muscles
and other vesells
norad does what
what is the affect of decreasing po2 on vessel calibre
serotonin - causes what
and what about in muscle arterioles
Epinephrine (adrenaline) produces vasodilatation of arterioles within skeletal muscles but constriction of other vessels.
Norepinephrine (noradrenaline) causes marked vasoconstriction.
A decreased PO2 produces vasodilatation, but serotonin (or 5HT) generally causes vasoconstriction except for vasodilatation within muscle arterioles.
What is endothelin 1
what are some other agents that are powerful at the same thing
GTN affect on circulation
Adenosine affect cor circ
Endothelin-1 is a very powerful coronary vasoconstrictor produced by the endothelium and acts to counter the effects of Nitric oxide (NO). Other powerful coronary vasoconstrictors include angiotensin1, neuropeptide-Y, nicotine, cocaine and vasopressin.
Adenosine is a naturally occurring purine nucleoside that is formed from the breakdown of adenosine triphosphate (ATP). In coronary vascular smooth muscle, adenosine binds to adenosine type 2A (A2A) receptors, which are coupled to the Gs protein. This leads to hyperpolarisation of smooth muscle cells causing them to relax and coronary blood flow increases.
GTN is both a veno and arteriolar dilator (including coronary arteries). It is a pro-drug with NO as the active metabolite.
Sympathetic activation to the heart = what
affect on cor blood flow
Activation of sympathetic nerve fibres to the heart results in chronotropy and inotropy, both of which contribute to an increase in myocardial oxygen consumption. This, in turn, results in an increase in coronary blood flow by a local metabolic mechanism. There is also a concomitant alpha-receptor-mediated coronary vasoconstrictor effect that competes with this metabolic vasodilation and limits the decrease in coronary vascular resistance. “Metabolic” dilators include CO2, lactic acid, potassium and hydrogen ions.
NO is formed by the action of endothelial NO synthase (eNOS) on L-arginine. This second messenger plays crucial roles in the regulation of coronary blood flow through vasodilatation, decreased vascular resistance and inhibition of platelet aggregation and adhesion.
Increased sympatetic activity - affect on renin
hr
arterial tone
bronchial sm
Increased sympathetic activity is inotropic.
Renin secretion is stimulated by decreased extracellular fluid volume and blood pressure or increased sympathetic output. This is via sympathetic innervation of the juxtaglomerular apparatus and catecholamine induced release of renin is part of the physiological response to to volume depletion and hypotension. This action leads to salt and water retention.
Increased sympathetic tone is also chronotropic via facilitated conduction through the AV node.
Increased sympathetic activity causes increased tone (vasoconstriction); think of the effects of a sympathectomy on the circulation in a lower limb. The situation is more complex, since circulating adrenaline causes vasodilatation in skeletal muscle. However the word ‘consistent’ makes it definitely true.
Beta 2 stimulation leads to bronchodilatation.
How many PV
what is pulmonary resistance
svr calulation
pvr calulation
pvri
what if the affect of pvr on increasing PAP
There are four pulmonary veins. On each side there is one vein coming from the hilum above and one from below the oblique fissure.
The pulmonary system is low pressure and low resistance. The ‘normal’ pressure in the pulmonary trunk is 24/9 mmHg, pulmonary artery 14 mmHg and 8 mmHg in the left atrium.
Systemic vascular resistance:
SVR = 80 × (MAP − RAP) / CO
Pulmonary vascular resistance (the PAWP equates to left atrial pressure):
PVR = 80 × (MPAP − PAWP) / CO
Pulmonary vascular resistance index is related to body surface area:
PVRI = 80 × (MPAP − PAWP) / CI
Cardiac index:
CI = CO / BSA
Pulmonary vascular resistance does not increase with an increase in pulmonary artery pressure as additional vascular beds open (having high compliance) thus maintaining PVR.
Sa node - intrinsic rate
what happens in tplx heart
The sinoatrial node has intrinsic automaticity (intrinsic pacemaker activity) at a rate of 100-110 beats per minute. The intrinsic rate is primarily influenced by a balance between the parasympathetic (vagal) tone and sympathetic (T1-T4 ganglia). Vagal influence is dominant at rest, producing a normal resting heart rate of 60-80 beats per minute.
A transplanted heart has no autonomic neural “hardwire” innervation therefore resorts to the intrinsic firing rate. The SA node will respond to endogenous and exogenous catecholamines.
An autonomic neuropathy affecting both sympathetic and parasympathetic nervous system will result in loss of R-R heart rate variability with respiration (abnormal valsalva). Mononeuropathy affecting the right vagus is most unlikely.
Hypokalaemia causes myocardial excitability and potential for ventricular ectopics and supraventricular arrhythmias.
Hyperthyroidism is unlikely. Tacrolimus (immunosuppressive agent) is associated with hypothyroidism.
SA node dysfunction can cause bradycardias or tachycardias.
What causes cardiogenic syncope
What is the input
what is the effect
Discharge from afferent vagal cardiac C fibres overcome the influence of sympathetic activity causing neurocardiogenic syncope.
The symptoms suggest this patient is experiencing neurocardiogenic or vasovagal syncope. This is usually a benign condition characterised by a self-limited episode of systemic hypotension and a transient loss of consciousness or “faint”.
Higher cortical centres in response to a triggering event (e.g. panic, fright or pain) stimulate adrenergic tone. This results in a tachycardia and increased myocardial contractility. Mechanoreceptors in the left ventricle are not only stimulated by stretch but also by changes in systolic contraction.
Stimulation of mechanosensitive afferent vagal cardiac C fibres results in vasodilatation and an increase in vagal tone with a reduction in cardiac filling and profound bradycardia. The receptors innervated by the vagus in the sinoatrial node are post-ganglionic muscarinic (M2) receptors.
The nucleus tractus solitarius (NTS) is a primary integrative centre for cardiovascular control and other autonomic functions within the central nervous system. Baroreceptor afferent messages are first integrated within the NTS and it is thought that an excitatory amino acid (glutamate) is the principal neurotransmitter of corresponding afferents fibres. Evidence points to the fact that 5-HT acts at 5-HT2A receptors, facilitates the baroreceptor reflex.
The nucleus accumbens is part of the mesolimbic region of the brain that receives dopaminergic projections from the brainstem and influences reward behaviour, and it is thought to be primarily involved in reinforcing addictive behaviour in response to drug use.
Pouiseuilles law
This question refers to Poiseuille’s Law.
R = P/Q = ΔP/ (ΔP r4/ I n)
Rearranging equation: R = 1/(ΔP r4/ I n), therefore R α I n/r4
ΔP is the pressure gradient along the vessel
Q is the volume flow rate
r is the radius of the vessel
n is the viscosity (haematocrit) of the blood
l is the length of the blood vessel.
Thickness of the vessel wall does not affect blood flow, but the stiffness of the vessel wall does affect blood flow.
Pressures RA RV PA LA LV
Right atrium = 2-6mmHg
Right ventricle = 28/4 mmHg (range 15-30/0-8)
Pulmonary artery = 25/12 mmHg
Left atrium = mean of 8 mmHg
Left ventricle = 125/8 mmHg (range 90-140/4-12).
Dominanat R wave
indicates what
Seen what
A rightward shift of axis acutely can produce a dominant R wave in lead V1 in a massive PE but ‘characteristic’ implies commonly seen, which it is not.
It is characteristic in Wolff-Parkinson-White (WPW) syndrome type A.
Posterior MI
In LBBB and hyperkalaemia a leftward shift is commonly seen.
Spread of excitation in the heart what direction
Cartoid sinus masage leads to what
Exercise which shortens more
The spread of the excitatory wave is from the endocardial surface outwards corresponding with the position of the neural network.
Carotid sinus massage (vagal stimulation) increases the force of ventricular contraction through improved preload. There is reduced rate, increased filling time and hence increased force of contraction.
During exercise it is diastole that shortens most.
De-innervation of the heart produces a significant increase in heart rate due to reduced vagal tone.
