2. Cardiovascular Flashcards

1
Q

Are capillaries permeable

Exercise effect on capilaries

Diameter?

A

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.

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2
Q

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?

A

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.

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3
Q

Hb reduction -

Compensatory mechanism
what happens to viscoisty
2 3 dpg

What is the reticulocyte count

Raised when

A

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.

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4
Q

Catecholamine

Syntehsis where
stored where

Secretion from -

Secretion induced by

Hypothermia increase or decreased

A

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

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5
Q

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

A

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.

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6
Q

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

A

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.

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7
Q

Valsalva manoeuvre

what is it

How many phases
Describe effects on HR/BP in each

A

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.

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8
Q

Vasiconstrictor or vasodilator

Prostacyclin

ANP

Indoramin

AngII

Epoprostenol

A

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

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9
Q

1 met = what

A

1 MET = consumption of 3.5 ml O2/kg/minute.

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10
Q

Explain + draw the CVP trace

A

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

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11
Q

Exercise change on blood flow

What does it do - how soon

Does if affect CBF? how

Lymph?

Viscera?

A

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.

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12
Q

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?

A

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.

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13
Q

describe the phases of cardiac myocyte action potential

A

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.

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14
Q

Synchronised dardioversion

A

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

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15
Q

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

A

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.

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16
Q

ANP - what does it inhibit

Levels rise with stretch

affect on
blood vessels -

AngII
Renin

A

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.

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17
Q

SVR calcuation

A

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

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18
Q

PVR calculation

A

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

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19
Q

Giant a waves are seent with what

why

A

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.

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20
Q

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

A

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.

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21
Q

What is endothelin 1

what are some other agents that are powerful at the same thing

GTN affect on circulation

Adenosine affect cor circ

A

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.

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22
Q

Sympathetic activation to the heart = what

affect on cor blood flow

A

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.

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23
Q

Increased sympatetic activity - affect on renin

hr

arterial tone

bronchial sm

A

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.

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24
Q

How many PV

what is pulmonary resistance

svr calulation

pvr calulation

pvri

what if the affect of pvr on increasing PAP

A

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.

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25
Q

Sa node - intrinsic rate

what happens in tplx heart

A

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.

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26
Q

What causes cardiogenic syncope

What is the input
what is the effect

A

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.

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27
Q

Pouiseuilles law

A

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.

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28
Q
Pressures
RA
RV
PA
LA
LV
A

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).

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29
Q

Dominanat R wave

indicates what

Seen what

A

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.

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30
Q

Spread of excitation in the heart what direction

Cartoid sinus masage leads to what

Exercise which shortens more

A

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.

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31
Q

What o2 consumption is 1 met

A

1 MET approximates to a consumption of 3.5 ml O2/kg/minute.

The calculation is (2100/100)/3.5 = 21/3.5 = 6 METs.

1 MET	
Eating
Dressing
Use toilet
Walking slowly on level ground at 2-3 mph

2 METs
Playing a musical instrument
Walking indoors around house
Light housework

4 METs
Climbing a flight of stairs
Walking up hill
Running a short distance
Heavy housework, scrubbing floors, moving heavy furniture
Walking on level ground at 4 mph
Recreational activity, e.g. golf, bowling, dancing, tennis

6 METs
Leisurely swimming
Leisurely cycling along the flat (8-10 mph)

8 METs
Cycling along the flat (10-14 mph)
Basketball game

10 METs
Moderate to hard swimming
Competitive football
Fast cycling (14-16 mph)

32
Q

What provides most of the energy to the myocardium

what is second

A

Fatty acids provide 50-70% of the total energy demands of the myocardium. Glucose is the metabolic substrate for the remaining 30% of requirements.
Explanation
Under normal conditions with adequate oxygen supply, fatty acids provide 50-70% of the total energy demands of the myocardium. Glucose is the metabolic substrate for the remaining 30% of requirements.

The myocardium is able to produce ATP from a variety of substrates - fatty acids, glucose, lactate, pyruvate and even amino acids. The particular source of substrate will depend on the concentration of that particular substrate both in the plasma and myocyte.

Lactate is used under conditions of increased muscular activity during which period lactate concentrations in plasma increase significantly.

Ketone bodies and amino acids may contribute by as much as 10% to total energy production in diabetic ketoacidosis.

33
Q

Fick principle states
what

VO2 calculate how used calc CO

A

The Fick principle states that the uptake or release of a substance from peripheral tissues is equal to the product of blood flow to those tissues and the arterio-venous concentration difference of that substance. It can be used to measure the cardiac output or total blood flow through an individual organ.

The Fick principle states that the uptake or release of a substance from peripheral tissues is equal to the product of blood flow to those tissues and the arterio-venous concentration difference of that substance. It can be used to measure the cardiac output or total blood flow through an individual organ.

The oxygen extraction (VO2) can be determined by the following equation:

VO2 = (CO x Cv) - (CO x Ca)

Where CO = cardiac output, Ca = pulmonary arterial oxygen concentration and Cv = pulmonary venous oxygen concentration

Rearranging the equation;

CO = VO2/(Cv- Ca)

Substituting the values:

CO = 500mL/300-250 = 500/50 = 10 L/minute.

34
Q

What causes an anterior stemi

mortaility incidence

What does the LAD supply

A

Anterior ST elevation myocardial infarction (STEMI) results from the occlusion of the left anterior descending (LAD) coronary artery. Because of a larger infarct size it carries the worst prognosis of all the infarct locations. Compared with an inferior myocardial infarction it carries a higher incidence of total mortality (27% versus 11%), heart failure (41% versus 15%) and lower ejection fraction on admission (38% versus 55%).

The LAD artery supplies most of the interventricular septum; the anterior, lateral, and apical wall of the left ventricle, most of the right and left bundle branches, and the anterior papillary muscle of the bicuspid valve (left ventricle).

35
Q

What is the edv

how much

A

The end-diastolic volume (EDV) of the left or right ventricle is the volume of blood in each chamber at the end of diastole prior to systole. The EDV is synonymous with preload.

A typical left ventricular EDV is 120 mL (range 65-240 mL). A typical range of right ventricular EDV is (100-160 mL).

The patient is likely to be experiencing systolic dysfunction with a reduced ejection fraction (EF) <45%. With a reduced EF, the ventricles are likely to be inadequately emptied with increases in right and left ventricular end-diastolic pressures and volumes. The increased pressures on the left side of the heart are transmitted to the left atrium and the pulmonary vasculature.

The raised hydrostatic pressure in the pulmonary circulation favours the development of pulmonary oedema by causing an imbalance of the Starling forces acting across the capillaries. The capillary permeability, per se with cardiogenic pulmonary oedema, is likely to be unchanged.

The pressure changes will further be transmitted to the right side of the circulation resulting in biventricular failure. The systemic vascular resistance is also likely to be raised but is not the single most likely cause of this patient’s observations. The patient has cardiogenic shock secondary to biventricular failure. The patient is hypotensive and has a low cardiac output. The right-sided filling pressures are high suggesting right ventricular dysfunction.

36
Q

Most imrotant factor determining SVR

What is normal for them

A

The most important factor that determines the systemic vascular resistance (SVR) is the tone of the small arterioles.

These are otherwise known as resistance arterioles. Their diameter ranges between 100 and 450 µm. Smaller resistance vessels, less than 100 µm in diameter (pre-capillary arterioles), play a less significant role in determining SVR. They are subject to autoregulation.

Any change in the viscosity of blood and therefore flow (such as due to a change in haematocrit) might also have a small effect on the measured vascular resistance.

Changes of blood temperature can also affect blood rheology and therefore flow through resistance vessels.

Systemic vascular resistance (SVR) is measured in dynes·s·cm-5

It can be calculated from the following equation:

SVR = (mean arterial pressure − mean right atrial pressure) × 80
cardiac output

37
Q

Action potential in PM cells

What does PS stime

Describe the phases
How does it differ from non pacemaker cells

A

Pacemaker cell action potentials are made up of phase 4 (spontaneous slow diastolic depolarisation by ‘funny’ currents and calcium influx through T-type channels), phase 0 (depolarisation by calcium influx through L-type channels) and phase 3 (repolarisation by potassium efflux).

Parasympathetic stimulation causes hyperpolarisation of the cell through increased potassium permeability whereas sympathetic stimulation increases excitability by opening calcium channels.

Phase 0 (depolarisation) in pacemaker cardiac cells differs from that in non-pacemaker cells and muscle and nerve cells - it is primarily mediated by inward calcium influx rather than sodium influx as in the other cell types.

Phase 4 is indeed the spontaneous depolarisation from maximum diastolic potential of −45 to −55 mV, to the threshold potential of approximately −40 mV.

The depolarisation of cardiac pacemaker and non-pacemaker cells lasts for approximately 200-400 milliseconds, as distinct from the much shorter nerve action potentials lasting approximately 1 millisecond.

The depolarisation plateau (phase 2) involves the opening slow calcium channels in non-pacemaker cardiac cells. However, there is no plateau phase in the SA node action potential, which consists of phases 4, 0 and 3 only.

38
Q

What is EDRF - what is it released from

what does it do to platletels

what type cells found

how does it act

How is its released increased by

A

Endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which is released from the vascular endothelium and causes vascular smooth muscle relaxation.

It is antiatherogenic and inhibits platelet aggregation but does not cause disaggregation.

It is found in many cell types including macrophages.

It acts by causing an increase in cyclic guanosine monophosphate or cGMP (not cAMP) from guanosine triphosphate.

The release of EDRF is increased by increased levels of intracellular calcium ions, which is caused by bradykinin, histamine and adenosine triphosophate (ATP). Thus, bradykinin, histamine and ATP stimulate the release of EDRF.

39
Q

Laminar flow

A

Assuming laminar flow, vascular resistance is inversely proportional to r4

Resistance (R) to the flow of blood is a function its viscosity (η), the radius to the power of 4 of the vessel (r) and vessel length (L). It is derived from the Hagen-Poiseuille formula assuming that the blood flow is laminar in nature:

(Q) = ΔPΠr4
8Lη
Where ΔP is the pressure difference.

Using a variation of Ohm’s law:

R = V/I
R = ΔP/Q

Substituting the variables:

R = ΔP8Lη
ΔPΠr4
The numerator and denominator, ΔP cancel each other out leaving:

R = 8Lη
Πr4
Assuming laminar flow, vascular resistance is:

Directly proportional to length of the vessel
Directly proportional to the viscosity of blood
Inversely proportional to r4

40
Q

ACXCY

Constrictive pericartidits

A

Deep x and y desenct

restic filling as diastole progress

41
Q

ACVXY

Afib

A

absent a wave

42
Q

Complete heart block

acvxy

A

cannon a
no corod
atria contract vs closed TR/MV

43
Q

ACVXY tricuspid steno

A

Enlarge a wave -
atria contract stenotic
generate higher pressure

44
Q

ACVCY Tricuspide regurg

A

enlarge v wave - v wave passive atrail filling vs close tricuspid
leaking - reduce back pressure - v gets deeper
may lead to loss of x descent

45
Q

BP =

A

CO x TPR

46
Q

CO -

A

SV x HR

47
Q

TPR

A

Contolled vcon - a1

stim NT Norad

48
Q

Block Beta -

A

HR SV fall - hypotension

49
Q

IABP

A

SynchECG
Inflate 50ml He - diastole

Increased diastolic press
improve CPP
Myo oxy deliver
deflation - prior systole decrease afterload/work

50
Q

COX enxymes

where express
general + most often

PGE+I2 effects

Whats a soruce of pgi2 synth

how is plip made

A

plipid = plip a2 => arachidonic acid
in cell membrane

express most cell
predom endothel, plt, renal tubular

Affect on gastric acid secretion is reduction
pge2 +pgi2
also vasodil mucosa + incr mucous production

cox2 major source pgi2 synth

51
Q

A2 adrenoreceptor stimulation leads to

A

Inhib Norad
Central mediaton of pain + sedation

stim plt aggregation
decreased insulin resistance

52
Q

Ventricular action potential

A

4- all perm normal
RMP -90 d/t K perm NOTE LOWER THAN NERVE

0 - fast Na open, decr K conductance

1 early repol - fast na close - k leak out

2 ca in k out - balance na decrease

3 ca close - k rectifier out

4 return normal permeability K, Ca, Na

53
Q

Blood flow to organs

brain

COronary

kidney

abdo organ

A

750

250

1100

1400

54
Q

blood fow to

skin

skin skel muslce - rest

skel muscle active

A

500

1200

20000

55
Q

Normal response to valsalva

map 87->98->85

A

Sinusoidal

Square wave response
map rises - main without vary pp
relase - map falls back
1 pulm circ olaod - vol mainta left filling despite change intratho pressure
2 failing heart - horixont stalring = ccf, mitral stenp LR shunt tamponade

56
Q

Respective blood flows to areas as % CO

Brain

heart

Kidney

Liver

Skeletal

A

Brain
14%
700ml min

20ml/100g white
70ml 100g grey
50ml.100g - global

Heart
5%
250ml

kidney
20-25% 
1200ml
cortex 500ml
outer medulla 100ml inner 20

liver 30% 1800ml min
Portal vein - 2/3
Hepatic artery 1/3

Resting skel
20% co 1200

57
Q

Absolute refractory period

relative refractory

catecholamine act on what whats the msgr

A

200ms

50ms

b1
Gs -AC - increase Ca open
phospyrlate myosin + phospalamban - increase contraction and relax

58
Q

DIg

A

increase intracell Na

indir inrease Ca

59
Q

Bachmanns bundle

A

Action potential SA -> La

60
Q

Response to blood loss inital

A

Haemorrhage = fall circ vol

decrease MAp
Decrease vol - decrease intralum pressure in barreceptor - arch + sinus

Decrease firing baroc

Decrease inhibition of pressor area

promot sym activity + decreaseing vagal tone

Inotropy chronotrop and increase svr
aim restore map

subseq fdrop GFR later = RAAS Act = Aldo Na retent DCT, increase osmolar = adh = water retent

61
Q

MABP

A

Diastoilic + 1/3 (systolic - diastolic)

62
Q

What is the windkessel

A

Upon vent contraction - small proport blood propel artery / tissue

reamined - remins aort - distend elastic wall
shigh impedence to flow but produces continue flow blood

follow ejection 1/3 flows directly to tissue

63
Q

Arteries contain what & of circ BV

A

15%

64
Q

How calculate LV stroke work

A

SV x (MABP - PCWP) x 0.0136

65
Q

Supply heart commonest
av node
sa node

blood and nerve

A

L vagus av and
rca 60% SA node 90% av node

R vagus sa

66
Q

rest what % capil patent

relative velolcity art vein cap

A

25%

art 20cm/s

cap 0.5mm/s

vena c 12cm s

supie 75% blood is in syetmic
16% in pulm
8% heart

67
Q

Pressure volume loops

elastance

is cardiac pump energy efficient?

A

Elastance
Reflected slop of diastolic pressure volume curve

Inefficent (20% heat lost)

Triangle enclosed - end systolic p-v line
+ end diastolic pressure vol line + line repping relax - rep amt potent energy

p-v area = total mechanical work and heat generated

68
Q

Innervation

A

PS + SNS - originate cvs control medulla

Sym fibres - synapse stellate

R vagus - SA node
L vagus - av slows conduction

Effect SNS - slower + longer duration

Nodes rich cholinesterase - deact vagal act quickll

norepi slower onset action
not meatob - longer duration

69
Q

What muscarinic receptor responsible for HR

A

M2
Gi- brady cardia

m1 - autonomic ganglia, saliv, gastric, higher cog
gq

m3
Smooth muscle contract - bhcon
gi motility
increase asalvi gland stomach
miosis
cerbral vessel diln

m4 +m5 - cns

70
Q

fastest velocity in cardiac tissues

A

purkinje bibres
4 ms

bundle his 2ms

av node - slows for allowing ventric filling .05ms

71
Q

Refractpry VF with no amio around

How much Ca in 10ml 10%
gluc
chlroide

A

Lido 1mg/kg

Gluc 2.2mmol

Cl 6.8

72
Q

Smooth muscle reponse to rising pressure in wall

A

arterioles spontaneosuly contract

73
Q

Txa2 affect

A

vasoconstrictor and plt agregator

74
Q

Adrenl -action organ

A

a - vasocon

b2 - vdil
balance receptor stim - determ response

75
Q

killikrein

affect sm

A

activate inactive kinin -> active form = SM relax

ie inrdirect

76
Q

PV curve

What is the index of contractility

increase in preload does what to curve

area enclosed reps what

shape of rv

A

During ischaemia = rightward lean
- as fibres lengthen during isovol contract (instead of shorten)
bulge out and fibre shorten during relax

Shortening active / recpil = rleate ctricically to ischaemic vent

Gradient of ESPVL = index contractility

Shape RV - triangle

Area enclosed = stroke work done by lv

increase preload - singif increase area enclose

77
Q

Anrep effect

A

Method autoreg -
increased afterload causes increase contractility
related stretch at end systole

Intrinsic mechanism increase CO maint in denrvated
1 Strech via starling = increase preload

anrep - afterload increased contractily

bowditch effect
increase HR - increase contractiliy