Cardiac Flashcards
1
Q
Inflow/Outflow of blood from the heart
A
Inflow
- > sup/infer. vena cava
Outflow
- > aortic arch
2
Q
What are auricles
A
Their purpose is to increase the capacity of the atrium, and so also increase the volume of blood that it is able to contain
3
Q
myocardium
A
muscle/tissue of tje heart
4
Q
cardiac myocytes
A
cytes=mature cells
they’re individual cardiac muscle cells
5
Q
List the layers of the heart
A
endocardium = inner tissue layer of the heart
epicardium = outer tissue layers of the heart
pericardium = fibrous sac that surrounds the heart
6
Q
list all the heart chambers
A
right atrium; right ventricle; left atrium; left ventricle
7
Q
systole vs diastole
A
systole
- > contraction of the heart = ejection phase
diastole
- > relaxation of the heart = filling phase
8
Q
systolic pressure
A
pressure within the aorta during systole when blood volumes within the vessel are at their highest
- > usually determined using brachial artery
9
Q
diastolic pressure
A
pressure within the aorta during distole when blood volumes are at their lowest
10
Q
cardiac cycle
A
1 heartbeat = 1 systolic + 1 diastolic event (bump-bump)
11
Q
atria vs ventricle
A
Atria
- > resevoir for blood; low pressure chambers
ventricle
- > high pressure pumps for the ejection of blood from the heart
12
Q
list all major corornary arteries involved in the myocardial blood supply
A
13
Q
Which two major arteries branch from the root of the aorta and what do they supply?
A
- right coronary artery
- > supplies right atrium, right ventricle, part of left ventricle - left coronary artery
- > supplies left atrium and ventricle
14
Q
how does blood return from the myocardium to the right atrium
A
- > the great cardiac vein drains into the coronary sinus and then into the right atrium
- > the middle cardiac vein
15
Q
explain coronary blood to the left side heart/ how it can be affected
A
during ventricular systole(contraction) extravascular compression(closure of the coronary artery) of the coronary circulation occurs
- > this causes BF to be left coronary artery to be briefly reverse
16
Q
Where is the left ventricular myocardial pressure the greatest and lowest
A
Greatest
- > near the endocardium
Lowest
- > near the epicardium
17
Q
When does maximal left and right coronal inflow occur
A
Max left inflow occurs in early diastole, when the ventricle relaxes
max right coronary inflow still occurs during diastole
18
Q
explain the cornary blood supply to the right side of the heart
A
- > lower pressures here during systole because it requires less force for contraction to move the blood a shorter distance
- > blood flow reversa does not occur, therefore more coronary inflow during systole than for the left side of the heart
19
Q
S1 and S2 are caused by what?
A
Sound 1
- > closure of AV valves
Sound 2
- > closure of semilunar valves
both S1 and S2 cna be heard sometimes as “split” sound as the AV and semilunar valves don’t close at the same time
20
Q
Which two structures transport blood to the lungs and which two structures transport blood to the rest of the body
A
Blood - > lungs
right atria + right ventricle
Blood - > rest of body
left atria + left ventricle
21
Q
What is action potential
A
AP = a brief reversal of membrane potential
AP = a brief reversal in the overall charge inside vs the overall charge ouside the cell
22
Q
how are action potentials transported
A
through gap junctions
23
Q
SA nodes vs AV nodes
A
SA Nodes
- > primary pacemaker that sets the rate for tansmission of the action potentials
AV Nodes
- > the pacemaker (rate setters) for heart activity
24
Q
Explain how AV and SA nodes work together to set heart rate
A
- > electrical signal travels from SA node, through the atrial tissue to the AV node down the AV/His bundle and is split between the right and left bundle branches to the Purkinje fibres
- > the small Purkinje bibres will then send the electrical signals to all the cells of the ventricular myocardium
25
What happens if no signal travels from SA- \> AV nodes OR AV node to the ventrical
then some cells in the bundles of His or in the Perkinje network can become the pacemaker for the ventricle **(ectopic beats)** with a rate of around 25-45 beats/min
26
What are the two types of action potentials in the heart
1. Fast response action potential
2. Slow response action potentials
27
Describe the resting state of pacemaker activity
THERE IS NO RESTING STATE FOR PACEMAKER ACTIVITY
28
Explain each phase in a slow response pacemaker action potential
**Phase 4**
- \> Na+ channels (slow channels) open and K+ channels close, causing a depolarization event
**Phase 0**
- \> occurs with the opening of the L-type Ca2+ channels
**Phase 3**
- \> rapid repolarization, Ca2+ channels close and K+ channels open; loss of interior K+ repolarizes and returns cell to a more negative interior
29
explain the intrinsic automaticity of the depolarization events
- \> these events occur because of the mycaridums voltage and membrane potential are constanty changing
- \> the intrinsic automaticity of the SA nodes results in around 100-110 depolarizations/minute (sinus rate)
30
what is the sinus rate
the fastest rate of depolarization in the conduction system
- \> a HR lower than sinus rate requires imput from parasympathetic NS
- \> a higher HR than sinus rate requires imput from sympathetic NS
31
What is a normal heart rate
around 60-80 BPM
32
Explain each phase in a fast response non pacemaker action potential
**Phase 4**
- \> resting potential/ diastole; ALL ion channels are closed
**Phase 0**
- \> Na+ channels open through relay of signal from the pacemaker cells and adjacent cells resulting in a rapid upstroke, as rapid influx of Na+ occurs
**Phase 1**
- \> Peak depolarization (higher than 0)
- \> As voltages reach 0 mV, the voltage gated Na+ channels close and transient outward K+ channels open = partial repolarization
**Phase 2**
- \> plateau phase = L-type Ca2+ channels open at ~ -40 mV and remain open for a long period with a slow influx of Ca2+ occurring
**Phase 3**
- \> rapid depolarization; Ca2+ channels close and K+ channels open resulting in K+ efflux
33
how do we acheive full resting potential in a fast response non pacemaker action potential
- \> Na, K and Ca must be restored to their resting concentrations within and outside the cell
- \> this is acheived with ATP pumps which use energy to move Na out and K back in
- \> the Ca ATP pumps move Ca back out of the cytoplasm to reset the resting concentration gradient
34
What happens when ATP-Pumps are inactivated or inhibited
- \> when ATP-pumps are inactivated or inhibited, Na accumulates within the cell and intracellular K decreases; this causes depolarization
35
What are fast-sodium channel blockers used for
- \> they're used as Class 1 anti-arrhythmic drugs and work by blocking the sodium channels in the fast action potentials.
- \> these drugs are used to suppress abnormal rhythms of the heart (cardiac arrhythmias)
- \> blockages results in a decreased degree of depolarization and a decrease in conduction velocity within the ventricle (these drugs include quinidine and lidocain)
36
Why are high concentrations of K added to cardioplegic solutions during heart surgery
this solution is used during surgery to halt the activity of the heart by preventing the normal flux of K ions from the cells
37
How are action potentials generated by SA nodes spread through the atria
primarily through cell to cell contact
38
**How fast** do action potentials generated by the SA node spread throughout the body
0.5m/sec (relatively slow)
39
How many pathways for action potentials to enter the ventricles are there in a healthy heart
only one; they enter the ventricles through the AV node
40
Why is it important how the AV node slows the conduction velocity of the SA node (0.5-0.05m/s)
It is important because...
1. it allows sufficient time for complete atrial depolarization (initiation of contraction) and emptying og atrial blood into ventricles
2. slow conducting velocity helps limit the frequency of impulses traveling through the AV node and activating the ventricle (prevents random electrical signals)
41
List the rate of all the conduction pathways
Slowest: AV node
Fastest: Purkinje fibres
SA Node rate can be altered by the ANS
42
what are ECG's
non-invasive means to examine the **ELECTRICAL** activity of the heart
43
different types of ECG
**12 Lead ECG**
- \> uses 10 electrodes to obtain 12 different views of the heart in many plains
- \> frontal plane: front-back electrical activity
- \> horizontal plane: upper-lower electrical activity
**Single lead/rhythm of test strip ECG**
- \>
44
List all ECG waves and intervals and what they mean
**\*LOOK IN PACK FOR SUMMARY\***
**P wave**
- \> atrial depolarization (end of p wave = initial contraction of atria)
**PR Interval**
- \> represents the time from atrial to ventricular activation
**QRS Complex**
- \> ventricular depolarization
**ST interval**
- \> represents ventricular depol - \> repol
**T wave**
- \> represents ventricular repolarization
**QT Wave**
- \> measures the timing of the entire ventricular depolarization and repolarization events
- \> varries depending of HR
**U Wave**
- \> not seen on ECG; represents the recovery period of the perkinje/ventricular conduction fibres
45
What happens when the PR interval is shorter/ longer than normal
Shorter than 0.12s
- \> this means that there is less time for signal transmission from atria to ventricle which means possible abnormal routing of signals (also impacts time for ventricular filling)
Longer
- \> this means longer time for signal transmission, can indicate block
46
What happens when the QT interval is too long
the faster the HR, the shorter the QT interval
the slower the heartbeat, the longer the QT interval
- \> QT interval that is too long inhibits the proper filling of ventricles
47
cardiac output
the amount of blood ejected by the heart in one minute (left ventricle)
48
What is the eqution to solve for cardiac output
CO = HR x SV (stroke volume; volume ejectded in one beat)
49
What are the factors that impact on CO
**1. HR**
- \> an increase in HR (with no change to SV) will increase CO (to a point;)
- \> the faster the HR, the less time spent in filling/diastole which decreases the availibility of BV in the LV which decreases SV and therefore CO
**2. SV**
**3. Venous Return and Preload**
**4. Afterload**
**5. Contractility**
**6. Ejection fraction**
50
EDV vs ESV
end diastolic volume = EDV
- \> greatest BP in the LV
end systolic volume = ESV
- \> lowest BV in the LV
51
the vagus nerve releases what to decrease HR
acetylcholine
52
Explain how venous return and preload can impact CO
- \> the greater the venous return, the greater the preload since there will be an increase in BV (increased EDV) and and increased pressure (EDP) within the chamber as a result of the increased blood volume
- \> preload increases with increased venous return
- \> reflects how much the heart is "stretched" before contraction
- \> increased preload results in increased SV (up to a point; max stretch) and increased SV results in increased CO
53
Explain how afterload impact CO
Afterload (TPR) = the pressure against the heart must pump to eject blood
- \> afterload increases with increased BP and decreased aortic compliance
- \> increased afterload results in decreased SV and decreased SV results in decreased CO
54
Explain how contractility impacts CO
Contractility = the force the heart is capable of developing as it contracts
- \> increased contractility results in increased SV (and increased CO)
- \> compliance/elastic elements play a role in the contractility of the heart
55
factors that increase contractility
**positive inotropic factors** (intropy = related to contractility)
56
examples of positive and negative inotropic factors
Postive inotropic factors
- \> Beta 1- sympathetic stimulation, increased extracellular Ca2+ concentrations (**increase the strength of muscular contraction**.)
Negative inotropic factors
- \> beta blockers (Beta-blockers “block” the effects of adrenaline on your body's beta receptors. This slows the nerve impulses that travel through the heart)
- \> **decrease workload/force of the heart**
57
How do ejection fractions impact CO; what is EF
\*EF IS NOT A FACTOR FOR CO BUT RATHER A MEASURE OF CO \*
EF = (SV) / (LVESV)
- \> Ejection fraction is a measurement of the percentage of blood leaving your heart each time it contracts
- \> a more forceful contraction propels more blood into the arteries resulting in a smaller end-systolic volume (i.e. smaller volume of blood will be left in the left ventricular chamber at the end of systole)
- \> increasing contractility will increase EF
58
How can CO be calculated using MAP and TPR
CO = MAP/TPR
59
MAP
Mean Arterial Pressure
- \> average arterial pressure that is continuously changing throughout the cardiac cycle
- \> MAP is important as it is the pressure driving blood into the tissues averaged over the entire cardiac cycle
60
What is TPR and how is it regulated?
Total Peripheral Resistance
- \> TPR is mostly controlled by arterioles where smooth muscle tone of arterioles is regulated by:
1. ANS (sympathetics)
2. Bloodborne agents
3. Autoregulation (primarily through secretion of local factors from epithelium)
61
Explain how MAP is calculated at normal vs HIGH heart rates
Normal, resting heart rate
- \> MAP is **NOT** the value halfway between systolic and diastolic pressure since time spent in diastole is 2x as long as the time spent in systole
HIGH heart rate
- \> MAP can be calculated as the average of the systolic and diastolic pressures since time spent in systole is approx. equal to time in diastole
62
formula to estimate MAP
MAP = DP +1/3 (SP-DP)
DP - \> diastolic pressure
SP - \> systolic pressure
(SP-DP) - \> pulse pressure
63
Pulse pressure; when can you notice it
the pulsation/ throb in the arteries of the wrist or neck felt with each heart beat
- \> PP should not be felt during diastole (filling), but can be felt during systole as the artery wall is pushed out by the rush of blood entering the arterial system from the left ventricle
64
What affects the magnitude of PP
1. Increased SV (increases CO which increases force of contractions)
2. Increased speed of ejection (contraction time)
3. Decreased arterial compliance
- \> "stiffer" walls builds higher presssures with low BV
65
Why does arterial compliance have no effect on MAP
- \> as arterial compliance changes, SP and DP change but in OPPOSITE directions such that SP will increase but DP will decrease
for example...
- \> a person with low arterial compliance, may have a large PP with increased SP and decreased DP, but MAP is close to normal
66
What happens when MAP is decreased
a decrease in MAP can result in loss of pressure gradients across the vasculature which decreases perfusion levels
- \> MAP is the key to perfusion pressure for the peripheral tissues
67
What happens to your blood/blood pressure when you're standing upright
- \> in the standing position, gravity influences the effective circulating blood volume with effects on peripheral blood pressure that **could add and extra 80mmHg to the average capilaries**
- \> when standing, **blood collects in the peripheral leg veins**, due to large venous compliance, **pooling blood can expand the vein walls without returning blood to the heart**
- \> increased venous pressure with pooling blood will laso increase capillary pressures, pushing fluid out of the circulation and into the tissues (this can result in a decrease in overall blood volume and a drop in BP)
68
Hemodynamics
hemo = blood
dynamics = movement
- \> the relationship between pressure and flow
69
The rate of blood flow through a blood vessel depends on what?
1. pressure gradients (P)
- \> maintenance of pressure gradients from arterial venules gives you **bloodflow(Q)**
2. resistance to flow (R)
70
what is a pressure gradent
P: blood flows from an area of high pressure to an area of low pressure
71
Starling's hypothesis
1. maintenance of plasma oncotic pressure = helps more H2O from the interstitium into the blood
2. increased pressures within the arteries (high inflow pressures = hydrostatic pressures) = \> force H2O out of the plasma and into the interstitium (edema)
3. increased pressures within the veins (high outflow pressures) = lose the pressure gradient from capillaries to veins, which causes high backpressure in the capillaries and pushes H2O out of the plasma
72
what is pressure in vessels
**hydrostatic** pressure
i.e. force exerted by the blood on the vessel walls
73
reduced resitance equation
**1/r4**
we can get rid of...
n (fluid viscosity)
L (vessel length)
8/pi
**because they're all contants**
74
what happens to **R and Q** if vessel diameter (vasocontriction/vasodilation) occurs
Vasocontriction
- \> when radius of a vessel decreases, **R increases and therefore Q decreases**
Vasodilation
- \> if the radius of the vessel increases, **R decreases and increases Q**
**THE MAIN CONTROLLER OF CHANGES TO R ARE THE ARTERIOLES**
75
Terminology of Cardiovascular functions
**\*POSITIVE INCREASES ACTIVITY, NEGATIVE INHIBITS ACTIVITY\***
inotropy = contractility of the cardiac muscle
dromotropy = velocity of conduction of the electrical signals
chronotropy = rate of heart beats
lusitropy = relaxation functions of the cardiac muscle and chambers
76
What is the role of the sympathetic nervous system in the regulation of cardiovascular functions
Sympathetics:
- \> major transmitter is norepinephrine (NE; major role in cardiac activity)
**- \> release of NE results in: increased HR(SA node stim.), increased contractility (atrial and ventricular), increased CO, and increased rate of conductance**
- \> when the symp. division is stimulated, symp. neurons will release NE in the adrenal glands and stimulate the release of epinephrine into circulation
77
what is the role of the parasympathetic nervous system in the regulation of cardiovascular functions
- \> innervation occurs via the vegus nerve
- \> transmitter is acetylcholine
the release of acetylcholine causes...
- \> decreased HR
- \> decreased **atrial** contraction (no ventricular control from parasymp. div.)
- \> decreased conduction velocity (AV node)
- \> decreased CO
78
what is the role of the CNS in the regulation of cardiovascular function
2 centres associated with the CNS and control of cardiovascular function
1. cardiopulmonary plexus which is part of the sympathetic response
2. the vegas nerve which is part of the parasympathetic response
- \> increased arterial pressures will inhibit the cardiopulmonary plexus response and excite the vegas response resulting in dialation of the arterioles and venules and a decrease in BP (also a decrease in HR through parasym. patheays)
79
what happens when there is an increase in sympathetic activity
- \> norepinephrine will be secreted by the symp. nerve fibres while epinephrine will be secreted by the adrenal glands
- \> both norepinephrine and epinephrine will result in dilation of blood vessels and increase HR and myocardial contractility
80
myocardial contractility
Myocardial contractility is the ability of the heart to increase force of contraction, determined by the strength of the actomyosin filament interaction
81
what happens with there is an increase in parasympathetic activity
- \> the vegas nerve will be stimulated and acetylcholine will be secreted from parasymp. fibres resulting primarily in decreased HR and CO
82
which major systems play a role in the regulation of cardiovascular function
1. ANS
2. CNS
3. CNS + sympathetics
4. CNS + parasympathetics
5. Baroreceptor reflexes
6. Bloodborne regulation
83
Which structures of the heart act as pressure receptors (baroreceptors)? How?
- \> the carotid sinus and the aortic arch
- \> afferent neurons travel from these baroreceptors to the CNS medullary cardiovascular center providing input regarding arterial pressure
- \> the rate of neural discharge is directly proportional to the MAP and PP ensuring that the CNE receives input from both
84
What are baroreceptors
they're either neurons, or specialized cells associated with a neuron that are stmulated with changes in pressure
85
what happens when arterial pressure decreases
- \> the discharge rate from baroreceptors decreases inducing the following at the medullary cardiovascular centre
1. increased HR due to increase symp. activity (and decreased symp activity)
2. increased ventricular contractility, again due to sympathetic activity
3. arteriolar contriction (again due to symp. activity)
4. Increased venous contriction
- \> all this results in increased cardiac output, increased total peripheral resistance and increased blood pressure
86
explain how sustained changes to blood pressure can impact baroreceptor reflexes/signals
- \> baroreceptor reflexes are very effective in regulating blood pressure over a short time frame, but sustained changes to blood pressure (such as chronic hypertension) will result in a decrease in signals to the CNS from the barorecptors and the CNS will maintain blood pressure at a higher set point
87
ADH
- \> antidiuretic hormone increases BP by vasocontriction and by action on the renal tubules (increase water retention)
released by the pituitary in response to...
- \> decreased BP
- \> dehydration (decreased plasma volumes)
- \> increased Na intake
88
ANP
atrial natiuretic peptide
- \> released by the myocardium in response to increased atrial pressures
- \> decreases BP by relaxation of vascular smooth muscle and stimulation of water loss through the renal system
89
Angiotensin II
is a potent vasoconstrictor with receptors in on vascuar smooth muscle (both atrial and venous)
- \> increases BP by:
1. direct action on vascular smooth muscle
2. increases sympathetic activity
3. stimulates the release ADH (not really)
4. stimulates the release of aldosterone
90
Kinins
- \> inflammatory mediator
- \> vasodilators
- \> decreases BP
**- \> increases venular permeability**
**- \> induces non-vascular smooth muscle contractions**
91
histamine
- \> inflammatory/immune mediator
- \> causes arteriolar dialation resulting in decreased BP
- \> increases venular permeability
- \> induces non vascular smooth muscle contractions
92
What are the valves found within the heart
1. Right atrioventricular (tricuspid)
2. Pulmonary semilunar
3. Left atrioventricular (bicuspid or mitral)
4. Aortic Semilunar
