Physiology Flashcards
The heart can beat rhythmically in the absence of external stimuli. what is this called?
autorhythmicity
What is the heart?
an electrically controlled muscular pump which sucks and pumps blood.
Where are the electrical signals which control the heart generated?
within the heart.
Where does excitation of the heart normally originate?
in the pacemaker cells in the Sino-atrial (SA) node
Where is the SA node located?
upper right atrium close to where the superior vena cave enters the right atrium.
what does the cluster of specialised pacemaker cells in the SA node do?
initiate the heart beat.
What does the SA node normally do?
sets the pace for the entire heart.
a heart controlled by the sino-atrial node is said to be in?
sinus rhythm
what do the cells in the SA Node not have?
no stable resting membrane potential.
what do the cells in the SA node generate?
regular spontaneous pacemaker potentials
where does the cardiac impulse originate?
Sino-atrial (SA) node
what do the spontaneous pacemaker potential in the SA node do?
slowly depolarises the membrane to a threshold to generate an action potential.
how is the action potential spread?
by cell-to-cell conduction from the SA node to the atrio-ventricular (AV) node where it is delayed. From the AV node it is then spread to the ventricles via Bundle of his and its branches and the purkinje fibres and by cell-to-cell conduction within the ventricles.
The AV node is the only point of what?
point of electrical contact between the atria and the ventricles.
what is the pacemaker potential (slow depolarisation of membrane potential to a threshold) due to?
- decrease in K+ efflux
- Na+ and K+ influx (the funny current)
- transient Ca++ influx (T-type Ca++ channels)
What is the rising phase of action potential caused by? what does it result in?
activation of long lasting L-type Ca++ channels and results in Ca++ influx.
what is the falling phase of action potential caused by? what does it result in?
inactivation of L-type Ca++ channels and activation of K+ channels resulting in K+ efflux.
Cell-to-cell spread of excitation is spread via?
gap junctions
what is the AV node?
small bundle of specialised cardiac cells.
where is the AV node located?
at the base of the right atrium - just above the junction of atria and ventricles.
why is the conduction delayed in the AV node?
allows atrial systole (contraction) to precede ventricular systole.
what is the resting membrane potential of cardiac muscle cells?
-90mV
what is the rising phase of action potential in cardiac muscle cells caused by? what happens to membrane potential when this happens? what is this known as?
fast Na+ influx
rapidly reverses it to +20mV
phase 0 of action potential in contractile cardiac muscle cells.
what are the phases of ventricular muscle action potential?
phase 0 (rapid depolarisation) - fast Na+ influx phase 1 (early repolarisation)- closure of Na+ channels and transient K+ efflux phase 2 (plateau)- slow Ca2+ influx phase 3 (final repolarisation) - closure of Ca2+ channels and K+ efflux phase 4 - resting membrane potential returned by Na/K+ ATPase.
the membrane potential is maintained near peak of action potential for a few hundred milliseconds, what is this called?
plateau phase of action potential
what is the plateau phase mainly due to? what kind of cells is it unique to?
influx of Ca++ through L-type Ca++ channels
unique to contractile cardiac muscle cells.
what is the falling phase of action potential in ventricular muscle action potential due to?
inactivation of Ca++ channels and activation of K+ channels - results in K+ efflux.
what does sympathetic/parasympathetic simulation do to heart rate?
sympathetic - increases
parasympathetic - decreases
what is the parasympathetic supply to the heart?
Vagus nerve
what dominates under normal resting conditions?
Vagal tone
what does the vagal tone do?
slows the intrinsic heart rate from approx 100bpm to normal resting heart rate of 70bpm.
what is a normal heart rate?
between 60-100 bpm.
what is the name for a resting heart rate that is less than 60bpm?
bradycardia
what is the name of a resting heart rate of more than 100bpm?
tachycardia
what does the vagus nerve supply?
SA and AV node
what does vagal stimulation do?
slows heart rate and increases AV delay. decreases the slope of pacemaker potential.
what is the neurotransmitter for parasympathetic supply to the heart?
acetyl choline acting through muscarinic M2 receptors.
what is an inhibitor of acetyl choline and what is it used for?
atropine
used in extreme bradycardia to speed up heart
what do the cardiac sympathetic nerves supply?
SA and AV node as well as myocardium
what does sympathetic stimulation do?
increases heart rate and decreases AV node delay. increases force of contraction. increases the slope of pacemaker potential.
what is the sympathetic neurotransmitter?
noradrenaline acting through beta1 adrenoceptors.
what does ECG stand for?
electrocardiogram
what does the ECG record?
depolarisation and depolarisation cycle of cardiac muscle obtained from skin surface.
where do lead I, II and III go for a ECG?
lead I - right arm-left arm
lead II - right arm - left leg
lead III - left arm - left leg
what does positive/negative chronotropic effect mean?
increase/decrease in heart rate.
why is cardiac muscle straited?
caused by regular arrangement of contractile protein.
how are cardiac myocytes coupled?
electrically by gap junctions.
what do desmosomes in the intercalated discs do?
provide mechanical adhesion between adjacent cardiac cells. ensure the tension developed by one cell is transmitted to the next.
what does each muscle fibre contain?
myofibrils
what is the thick filament in myofibrils called? what does it look like?
myosin - has a darker appearance.
what is the thin filament in myofibrils called? what does it look like?
actin - has a lighter appearance.
how are actin and myosin arranged in each myofibril?
into sarcomeres
how is muscle tension produced?
by sliding of actin filaments on myosin filaments.
what does the sliding filament theory explain?
how muscle shorten and produce force.
what is force generation dependant on?
ATP-dependant interaction between thick (myosin) and thin (actin) filaments.
what is required to switch on cross bridge formation?
Ca2+
where is Ca2+ released from?
sarcoplasmic reticulum (SR)
in cardiac muscle what is the release of Ca2+ from SR dependant on?
the presence of extra-cellular Ca2+
what does diastole mean?
it is when ventricles are relaxed and fill with blood.
what does systole mean?
when the heart ventricles contract and pump blood into the aorta and pulmonary artery.
what does ventricular muscle action potential trigger?
contraction
what does the long refractory period prevent?
generation of tetanic contraction
what is the refractory period?
a period following an action potential in which it is not possible to produce another action potential.
what is the stroke volume?
the volume of blood ejected by each ventricle per heart beat.
how is stroke volume calculated?
end diastolic (EDV) - end systolic volume
what is stroke volume regulated by?
intrinsic (within the heart) and extrinsic (nervous and hormonal control) mechanisms
what changes are brought about in stroke volume from intrinsic control?
brought about by changes in the diastolic length/diastolic stretch of myocardial fibres.
what is the diastolic length/diastolic stretch determined by?
end diastolic volume
what is the end diastolic volume?
the volume of blood within each ventricle at the end of diastole.
what is cardiac preload?
diastolic length/ diastolic stretch of myocardial fibres.
how is end diastolic volume determined?
by the venous return to the heart
what does starling’s law of the heart describe?
the relationship between venous return, end diastolic volume and stroke volume.
what does starling’s law of the heart state?
“the more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)”
how is the optimal length for cardiac muscle achieved?
by stretching the muscle.
what does afterload mean?
resistance into which heart is pumping into.
what happens if afterload continues to exist? example of a time it would continue to exist?
muscle mass would increase (ventricular hypertrophy) to overcome resistance. e.g. untreated hypertension.
stimulation of sympathetic nerves increases force of contraction, what is this known as?
positive inotropic effect
what is the effect of sympathetic stimulation on ventricular contraction?
force of contraction increases (activation of Ca2+ channels - greater Ca2+ influx). the effect is cAMP mediated. the peak ventricular pressure rises. rate of change during systole increases. this reduces the duration of systole. rate of ventricular relaxation increases which results in reduction of duration of diastole.
what is cardiac output (CO)?
the volume of blood pumped by each ventricle per minute.
how is Cardiac output calculated?
SV x HR
Define the cardiac cycle.
all events that occur from the beginning of one heart beat to the beginning of the next.
what are the 5 events during the cardiac cycle?
- passive filling
- atrial contraction
- isovolumetric ventricular contraction
- ventricular ejection
- isovolumetric ventricular relaxation.
what happens during passive filling in the cardiac cycle?
pressure in atria and ventricles is close to zero. AV valves open so venous return flows into the ventricles. aortic pressure is approx 80 mmHg and aortic valve is closed. similar events happen in the right side of heart but the pressures are lower. ventricles become approx. 80% full by passive filling.
what does the P-wave in the ECG signal?
atrial depolarisation.
when does the atria contract in a ECG?
between P-wave and the QRS.
when does ventricular contraction start after in an ECG?
QRS
What happens in isovolumetric ventricular contraction?
ventricular pressure rises. when it exceeds atrial pressure the AV valves shut. this means no blood can leave or enter the ventricle. tension rises around a closed volume ‘isovolumetric contraction’. the ventricular pressure rises very steeply.
what happens during ventricular ejection?
when the ventricular pressure exceeds aorta/pulmonary artery pressure, the aortic/pulmonary valve open. stroke volume is ejected by each ventricle leaving behind the end systolic volume. aortic pressure rises. the ventricles relax and pressure starts to fall. when the ventricular pressure falls below aortic/pulmonary pressure - the aortic/pulmonary valves shut.
what produces the first heart sound (S1)? what does it symbolise the start of?
AV (atrioventricular - tricuspid and mitral) valve shutting. start of systole.
what does the T-wave in a ECG signal?
ventricular repolarisation
what produces the second heart sound (S2)? what does it symbolise?
when the aortic/pulmonary valve shuts. end of systole and start of diastole.
what happens during isovolumetric ventricular relaxation?
ventricle is again a closed box, as the AV valve is shut. the tension falls around a closed volume. when the ventricular pressure falls below atrial pressure, AV valve open and the heart starts a new cycle.
what is a possible cause of a S3 heart sound? when would it be heard?
physiological, at the end of S2.
what is a possible cause of a S4 heart sound? when would it be heard?
pathological, before S1.
what is troponin?
a complex of three proteins involved in skeletal and cardiac muscle contraction.
what are the subunits of troponin? what do they bind to?
troponin C - binds to calcium ions.
troponin T - binds to tropomyosin, forming a troponin-tropomyosin complex.
troponin I - binds to Actin to hold the troponin-tropomyosin complex in place.
what is blood pressure?
the outwards pressure exerted by the blood on blood vessel walls.
what is systolic arterial blood pressure?
the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts
what is diastolic arterial blood pressure?
the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes.
what should the systolic/diastolic blood pressure not exceed?
systolic - 140 mmHg
diastolic - 90 mmHg
what is pulse pressure?
difference between systolic and diastolic blood pressure.
what is the normal range for pulse pressure?
between 30 and 50 mmHg.
Define mean arterial blood pressure (MAP)?
the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart.
how do you calculate MAP?
[(2x diastolic pressure) + systolic pressure]/3
or
DBP + 1/3rd of pulse pressure
what is the normal range of MAP?
70-105mmHg
what pressure does MAP need to be at least to perfuse coronary arteries, brain and kidneys.
at least 60 mm Hg
why must MAP be regulated?
needs to be high enough to perfuse internal organs such as brain, heart and kidneys.
can’t be too high to damage the blood vessels or place an extra strain on the heart.
what is the relationship between MAP, CO and SVR?
MAP = CO x SVR
what is systemic vascular resistance? what is another name for it?
total peripheral resistance
the sum of resistance of all vasculature in the systemic circulation.
what effect does sympathetic/para sympathetic stimulation have on MAP?
parasympathetic - decrease
sympathetic - increase
what is the control centre for negative feedback if their is any disturbance in MAP?
medulla
what are the pressure sensors for negative feedback if their is any disturbance in MAP?
baroreceptors
what does postural hypotension result from?
failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position.
how is a positive result in postural hypotension indicated?
a drop, within 3 minutes of standing from lying position in systolic blood pressure of at least 20mmHg (with or without symptoms)
or
a drop in diastolic blood pressure of at least 10mm Hg (with symptoms)
what are symptoms of postural hypotension?
lightheadedness
dizziness
blurred vision
faintness and falls.
what do baroreceptors only respond to?
acute changes in blood pressure
what can blood volume and MAP be controlled by?
extracellular fluid volume
how do you calculate total body fluid?
intracellular fluid (2/3rd) + extracellular fluid (ECF) (normally around a 1/3rd of total)
how do you calculate extracellular volume?
plasma volume (PV) + interstitial fluid volume (IFV)
what two main factors affect extracellular fluid volume?
water excess or deficit
Na+ excess or deficit
what three hormones regulate extracellular fluid volume?
- the renin-angiotensin-aldosterone system (RAAS)
- Natriuretic peptides (NPs)
- Antidiuretic hormone (arginine vasopressin) - ADH
what does RAAS play an important role in?
regulation of plasma volume and SVR and hence regulation of MAP.
where is renin released from? what does it do?
kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)
what is angiotensin I converted to angiotensin II by?
angiotensin converting enzyme - ACE (mainly produced by pulmonary vascular endothelium)
what does angiotensin II do?
(1) stimulates the release of aldosterone from the adrenal cortex.
(2) causes systemic vasoconstriction - increases SVR, also stimulates thirst and ADH release i.e. contributes to increasing plasma volume mainly brought about by aldosterone.
what does aldosterone do? what is it?
it is a steroid hormone. acts on the kidneys to increase sodium and water retention - increases plasma volume.
what is rate limiting step for RAAS?
renin secretion.
what regulates the release of renin?
- renal artery hypotension - caused by systemic hypotension (decrease blood pressure)
- stimulation of renal sympathetic nerves
- decreased concentration of Na+ in renal tubular fluid - sensed by macula densa
what are NPs released in response to?
cardiac distension or neurohormonal stimuli
what do NPs cause?
excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure.
what do NPs act as?
vasodilators - decrease SVR and blood pressure.
what do NPs provide?
a counter-regulatory system for RAAS.
what do NPs do in relation to renin?
decrease renin release - decrease blood pressure.
what are the two types of NPs released by the heart?
atrial natriuretic peptide (ANP) and brian-type natriuretic peptide (BNP)
what is ANP?
a 28 amino acid peptide synthesised and stored by atrial muscle cells (atrial myocytes)
what is ANP released in response to?
atrial distension (hypervolemic states)
what is BNP?
a 32 amino acid peptide synthesised by heart ventricles, brain and other organs.
what is BNP first synthesised as? what does it become?
prepro-BNP, which is then cleaved to pro-BNP (108 amino acids) and finally BNP.
what can be measured in patients with suspected heart failure?
serum BNP and N-terminal piece of pro-BNP (NT-pro-BNP)
where is ADH stored?
posterior pituitary
what is ADH derived from?
prehormone precursor synthesised by the hypothalamus.
what is secretion of ADH stimulated by?
(1) reduced extracellular fluid volume
or
(2) increased extracellular fluid osmolality (main stimulus)
what does plasma osmolality indicate?
relative solute-water balance
what is plasma osmolality monitored by?
osmoreceptors mainly in the brain in close proximity to hypothalamus.
what does ADH do?
acts in the kidney tubules to increase the reabsorption of water (conserve water) i.e. concentrate urine (antidiuresis)
what does increasing water reabsorption do?
increase extracellular and plasma volume and hence cardiac output and blood pressure.
what does ADH also do to blood vessels?
vasoconstriction - increase SVR and blood pressure
when is vasoconstriction by ADH important?
hypovolaemic shock (e.g. hamorrhage)
what is the conduction velocity of atrial conduction?
spreads along ordinary atrial myocardial fibres at 1m/sec
what is the conduction velocity of AV node conduction?
0.05m/sec
what is the conduction velocity of ventricular conduction?
purkinje fibres are of large diameter and achieve velocities of 2-4 m/sec (this allows a rapid and coordinated contraction of ventricles)
