Cardiovascular Physiology W7 Flashcards
What the difference between a nerve AP and a cardiac AP?
Cardiac AP: long depolarisation! Due to Ca2+ keeping cell depolarised = long absolute refractory period (cant tell to contract when already contracted)
Nerve AP: Tetnus can happen with AP summation.
Difference: Neuron AP + Ca2+
The cardiovascular system consists of the heart and blood vessels. Transports blood around the body. It is a two circuit system…
- Pulmonary circut - recieving blood from body and pumping to lungs for oxygenation
- Systemic circut - pumping oxygenated blood (from the lungs) around the body. O2 focused.
Cardiac muslce has a unique structure, what is the formation of muscle?
Two bands at the atria, figure 8 surrounding ventricles
Cardiac muslce has a unique artcitecture. Describe the role of intercalated dics, desmosomes and gap junctions.
Branched cells.
- Intercalated discs: part of the cardiac muscle sarcolemma, contain gap junctions for depolarization
- Gap junctions allow cardiac cells to communicate with each other using signaling molecules (ions). Allow electrical signal to pass through. ie. One has AP, the next one recieves it.
- Desmosomes prevent cells from separating during a contraction
Describe the phases of a AP of cardiac muscle
‘cardiac contractile muscle action’
0 - Fast Na+ channels open = quick depolarisation
1 - Na channels close, fast K+ channels open (not many) - causes slight repolarisation (depression) in AP
2 - More K+ channels open (leaves), Ca2+ open (enters) = counteract eachother: PLATEAU
3- Ca2+ channels close, Slow K+ channels open (more leaving) = rapid repolarisation
Back to resting potential (K+ channels close)
What is the term for when heart muscle contracts as one
Syncytium *contraction in sync*
What do cardiac pacemaker cells do
Sets the rhythm of the heat by stimulating AP’s from cardiac muscle cells
SA node generates signal fastest = pacemaker (master controller) - Passes signal across atria
What are the 5 different tissue types of the heart and how does electrical potential spread (sequence)?
SA node (pacemaker)
AV node
AV bundle (bundle of His)
Bundle branches
Endocardial network (purkinje fibres)
= Contraction (Atria -> Ventricles)
AP gets passed on very quickly!
Why is the sequence of contraction important, ie. sequence of AP through various types of cells
To slow transmission of AP so that the atria have time to contract and send blood to ventricles before ventricles contract
*ordered sequence for transmission of blood*
Why is the AV bundle important
AP (electrical signal) can’t get across band of C.T at atria-ventricle junction therefore the AP can only get across at AV bundle
- Only place for AP to pass! Provides electrical gap that allows signal to pass
Why do you have autorhymisity of cardiac muscle cells ie. Packmaker cell AP
Pacemaker cells have Na+ leak channels (open themselves) allowing Na+ to enter cell slowly and cause depolarisation when threshold is reached
Describe the AP of a pacemaker cell
Na+ leak channels = constantly open, slow entry of Na+
when membrane threshold reached…
fast Ca2+ voltage channels open = rapid depolarisation
K+ voltage channels open = repolarisation
Na+ -> Ca2+ -> K+
= Continuous generating of AP’s
What is the difference in AP of a pacemaker cell vs cardiac muscle cell
Same sequence of ion movement (Na+ -> Ca2+ -> K+) but channels differ…
Cardiac Muscle cell: Na2+ voltage gated
Pacemaker: Na2+ Leak channels (unstable resting membrane potential)
What is a electrocardiogram (simply)…
Currents from the heart detected with electrodes (Electrical activity detected not contraction)
- number of leads used determines sensitity (usually 3 leads used)
Depol and Repol of the cardiac muscle
The normal sequence of the heart detected by a three lead ECG is divided into 3 distinct waves…
- P Wave = Atrial depol
- QRS complex = Ventricle depol
- T wave = Ventricle repol
Atria repol is within QRS complex, small amount of tissue means you cant see ie. ventricle depol overrides
What does the ST segment on an ECG symbolise
Where ventricles depolarisation and contracting (where blood is being pushed out)
What does the T wave symbolise on an ECG
Ventricular repolarisation
What is cardiac output and how do we measure it?
How much bloody pumped out per beat
= Stroke volume (ventricular ejection) x Heart rate
note. Determined by Venous return: heart pumps out what it gets back
Measured by…
Mean arterial pressure/total peripheral resistance
The amt of bloood pumped out depends on…
- heart rate
- quantity of blood in ventricles
- pressure in ventricles (contraction pressure)
- pressure in arteries
Define ‘venous return’
How much blood comes in through major veins (to heart - imptly left ventricle)
Impt determinant in stroke volume
What is the anatomical differences in the left and right side of the heart and how does this relate to pressure
Left side muscle tissue = thick and big as its working/generating at higher pressure
Right side = little and less muscular
chamber size (volume) = SAME
Describe the Frank Starling law of the heat
Preload
More blood = more muscle contracts (stronger) = more blood pumped out (ejected)
Stroke volume proportional to diastolic volume
What is EDV and ESV
EDV: End diastolic volume (relaxation of ventriles ie. when filled - highest volume)
ESV: End systolic volume (end of contraction of ventricles still a little blood left)
Difference = Stroke volume (amount of blood pumpted out of the ventricle/beat)
Define stroke volume
Amount of blood pumped out of the ventricle per beat
= EDV-ESV
How do you alter HR and contraction strength
Nervous input - Sympathetic stimulation (adrenaline)
Acts on Pacemaker cells - speeds up activity - rise threshold faster by more Na+ leakage channels opening
= more AP’s = higher HR
What receptors do noradrenaline/adrenaline work on in the heart
Work via B1 receptors
B1 receptors stimulate contraction
= increases cardiac output
How does the parasympathetic N.S effect the heart
parasympathetic stimulation via vagus
Slows heart down by hyperpolarising therefore making it harder to reach threshold, less AP’s generated, slows HR
Works by M2 Channels - relax muscle!
Pressure is the molecules of blood hitting the walls of the heart. When heart contracts it creates pressure to move blood around body.
How is blood volume related to blood pressure?
More blood = More pressure (more interaction between blood and vessel wall - resistance to flow)
Need pressure to overcome resistance and get flow
What is one of most important factors that effects blood pressure
Vessel diameter
Vessels create resistance to flow
Vessel wider = More area = blood is in bigger space, less resistance = pressure drops
Vessel narrow = more resistance to flow
What two things effect BP
Change volume of the blood vessel that the bloods in (vessel radius/size)
The amount of blood present
To increase pressure you increase resistance and flow into heart
Pouiseuille’s Law…
Defines flow according to the individual components
Very small change in vessel diamater = huge change in flow
What is the lowest pressure describe as
Diastolic pressure
(just before contraction/ejection) - RELAX
Determined by diameter of arteries coming off major arteries (smaller ones - peripheral ones) ie. total peripheral resistance
Define systolic pressure
When the heart is pumping blood - CONTRACTION
Sum of diastolic pressure and rise in pressure created by heart pushing abit of blood out
Highest pressure
What is pulse pressure and mean arterial pressure
pulse pressure…
Difference between systolic and diastolic
- Big pulse pressure = heart pumped alot of blood out in contraction
mean arterial pressure…
Diastolic+systolic/3
Average pressure
Define blood pressure
Pressure created by blood in arteries driving blood movement
To increase flow, what would you do to pressure and resistance?
Increase pressure, decrease resistance
Describe how typical flow is altered during exercise
Where the blood goes depends on the diameter of the arteries.
Flow can be redirected according to need.
- during exercise more goes to skeletal muscle due to dilation of arteries! = increased flow, less blood is sent to the abdomen
AND
Heart is contracting harder and faster = increase cardiac output = more blood pumped
Why do you think there is a larger volume of mitochondria in cardiac muscle compared to skeletal muscle?
There is a less capacity for anaerobic respiration 25-40% of volume.
What features of cardiac muscle allows depolarisation to travel from cell to cell and the heart to contract as a unit?
Gap junctions electrically connect myocytes
What ensures atrial contraction occurs before ventricular contraction?
Atria and ventricles electrically isolated; depolarisation not passed from atria to ventricles via gap junctions…
It travels via the Intrinsic Conduction System ie. SV node to AV node to AV bundle
How do cardiac cells work together and what is this called?
Functional syncytium: cells (held together by desmosomes) communicate electrically via action potentials passed from cell-to-cell via gap junctions (on intercalated discs)
Allow for coordinated contraction of ventricles.
What controls resistance in tissues?
Resistance in arterioles is controlled by sympathetic control - noradrenaline = vasoconstriction
Local control- acetylcholine (constriction)
What controls blood pressure and where is it located?
Baroreceptors- on aorta arch (vagus nerve) and common carotid artery (carotid sinus nerve)
Compare and contrast action potentials in cardiac pacemaker tissues versus cardiac muscle
Cardiac muscle:
Stable RMP
Plateau phase (Ca in K out) -> Slow Ca channels
Cardiac pacemaker cells: Unstable RMP (Na leakage channels) Fast Ca channels
Similarities:
Sequence of ion movements inevents similar:Sodium in,calcium in,potassium out
Explain the events occurring in the heart during the phases of an ECG recorded on Lead IIA.
The P wave -> The QRS complex -> The T wave
Explain what will happen to an ECG in the case of a non-functional SA node
Bradycardia - With no P wave (no atrial contraction)
AV node takes over as pacemaker, HR is slower - 40-60bpm
Explain what will happen to an ECG in the case where a second pacemaker in atrial tissue is present due to ectopic tissue
Atrial Flutter ie. more AP generated (not just by the SA node)- for more contraction.
Multiple P waves
What causes ventricular tachycardia
Ventricular wavestake over due to a second pacemaker in ventricles from ectopic tissue
What are the phases of the cardiac cycle:
Passive ventricular filling
Atrial contraction
Isovolumetric ventricular contraction
Ventricular ejection
Isovolumetric ventricular relaxation
What happens during Phase 1 passive ventricular filling (in terms of pressures)
Pulmonary vein pressure = highest
Atria pressure: lower than Pulmonary vein, higher than ventricle
Ventricular pressure very low (lower than atria)
Aorta: high but decreasing (higher than othervessels/chambers)
What happens during Atrial contraction (in terms of pressures)
Pulmonary vein pressure: lower than atria
Atria pressure: higher than ventricle (and pulmonary vein)
Ventricular pressure very low (lower than atria)
Aorta: high but decreasing (higher than othervessels/chambers)
What happens during Isovolumetric contraction (in terms of pressures)
Pulmonary vein pressure: lower than atria
Atria pressure: lower than ventricle (and pulmonary vein)
Ventricular pressure rising (higher than atria, lower than aorta)
Aorta: high but decreasing (higher than other vessels/chambers)
What happens during ventricular ejection phase (in terms of pressures)
Pulmonary vein pressure: lower than atria
Atria pressure: lower than ventricle (and pul vein)
Ventricular pressure high (higher than atria and aorta)
Aorta: increasing but lower than ventricle
What happens in the Isovolumetric relaxation phase (in terms of pressures)
Pulmonary vein pressure:lower than atria
Atria pressure: lower than ventricle (and pul vein)
Ventricular decreasing (higher than atria lower than aorta)
Aorta: higher than ventricle
Why doesnt Blood doesn’t flow from the left ventricle back into atria during isovolumetric ventricular contraction
AV valves closed
Why can Blood flow from the left ventricle into the aorta during ventricular ejection
SL valves open
Why doesnt Blood flow into the left ventricle from the left atrium or the aorta during isovolumetric ventricular relaxation
Both SL and AV valves closed
Explain the what will happen to stroke volume if the following occur: End diastolic volume increases. End systolic volume increases. Preload increases. Afterload increases
Increases Decreases Increases Decreases
Why does the T-wave have a positive inversion?
Recording from the left-
the last cells to depolarize in the ventricles are the first to repolarize.
What is happening on the ECG here?
Ectopic tissue sending a second action potential- in the ventricles
Ventricular Tachycardia- heart doesn’t have time to fill but still pumps.
What is the difference between ventricular tachycardia vs ventricular flutter?
Ventricular Tachycardia- heart doesn’t have time to fill but still pumps. Because of passive ventricular filling- where pulmonary veins pressure is high and fills atria and ventricles (up to 80%) because AV VALVES ARE OPEN.
Whereas ventricular flutter- won’t pump affects cardiac output
Ventricular ejection occurs at which phase of the ECG?
S-T segment
If the Mean aortic pressure is 100mmHg, mean renal artery pressure is 80mmHg, mean hepatic artery pressure is 70mmHg, mean subclavian artery pressure is 90mm Hg
How would the body increase blood flow all over body?
Increase it to the liver?
and decrease it to the kidneys?
For body= increase cardiac output
For liver = vasodilation in hepatic arteries (raises blood pressure)
For kidneys = vasoconstriction in renal arteries (decreases blood pressure)
What is happening when receptors on the aortic arch detect a marked increase in blood pressure
Feedback to brainstem causing
Increased output from cardio inhibitory centre – decrease heart rate
Decrease cardiac output from vasomotor centre - vasodilation
Decreases sympathetic impulses, resistance and contraction
What happens when receptors on the carotid bodies detect a marked decrease in blood pressure?
Feedback to brainstem causing
Decreased output from cardio inhibitory centre –increase HR
Increased output from cardio accelerator centre - increase HR
Increased output from vasomotor centre - vasoconstriction
Increases cardiac output, tissue resistance, contractibility
What happens to SV if pulse pressure decreases?
Stroke volume decreases
If mean arterial pressure increases, blood pressure?
increases
What marks the end of the isovolumetric contraction?
Blood won’t pass through the Semi lunar valves until the ventricular pressure exceeds aortic/pulmonary pressure
What marks isovolumetric relaxation
SL valve closes due to:
Ventricular pressure decrease, blood in arteries flow back to heart
What are the two heart sounds we hear?
1: AV valves close and start of isovolumetric contraction phase (systole)
2: SL valves close after ejection at start of isovolumetric relaxation (diastole)
What causes the AV valves to open/close?
When ventricles relax - mid diastole- and atrial pressure is higher than ventricles = pressure gradient and AV valves open.
When ventricles contract- systole- and ventricular pressure exceeds atrial pressure AV valves close.
What is the dicrotic notch?
A small plateau in the pressure wave caused by the closure of AV valves WHEN ventricles relax and pressure drops below aortic pressure
What is the term for the volume that remains in the ventricles?
ESV around 50ml.
