Midterm 3 Flashcards
1
Q
functions of the heart (4)
A
- generate blood pressure
- route blood - right side of heart brings blood to the lungs, left side to the rest of the body
- ensure one-way flow of blood - valves to prevent back flow
- regulate blood supply
2
Q
pathway of blood through heart
A
enter right atrium from body through superior vena cava -> goes through tricuspid (AV) valve -> moves into right ventricle -> goes through pulmonary semilunar valve -> pushed into pulmonary arteries -> travels through lungs to be oxygenated -> enter into pulmonary veins -> enters into left atrium -> goes through bicuspid valve -> moves into left ventricle -> goes through aortic semilunar valve -> out to body tissues through aorta
3
Q
conducting system of the heart
A
- autorhythmicity: heart can contract on its own without any neural or hormonal input
- achieved by the cardiac conduction system
- sinoatrial node (SA) node: group of conduction cells found in right atrium, distributes energy to network using conducting cells
- atrioventricular node (AV): group of conduction cells located in right atrium, sends signal from atrium to ventricle
- conducting cells: wires throughout the heart, responsible for sending signal from one place to another
internal pathways: pathways between SA and AV node - Purkinje fibres act as conduction pathway of signal along ventricles
- Bundle of His conducts signal to left atrium and ventricle
- maximum conduction rate at the AV node = 230 bpm
- pumping efficiency decreases at 180 bpm
- rates over 230 bpm can occur when the conduction system is damaged
- max limit is about 300-400 bpm
4
Q
sinoatrial (SA) node
A
- located in right atrium
- contains pacemaker cells that maintain rhythm of heart beat
- connected to the AV node via the internal pathways in the atrial wall
- determines resting heart rate
- changes in membrane potential of pacemaker cells in the SA node affect the heart rate, faster heart beat causes it to reach threshold (-40 mV) faster, prepotential is steeper
5
Q
atrioventricular (AV) node
A
- located in right atrium, take rhythm from SA node and sends it to ventricles
- slows impulse down, can’t have atria and ventricles contracting at the same time, giving atria time to finish contraction and blood to flow into ventricles before contracting them
- moves impulse to the atrioventricular (AV) bundle
6
Q
pathway of conduction in the heart
A
- SA node activity and atrial activation begin, time 0ms
- stimulus spreads across the atrial surfaces and reaches the AV node, top of atria squeeze first, time 50ms
- there is a 100ms delay at the AV node, atrial contraction begins, time 150ms
- impulse travels along the inter ventricular septum within the AV bundle and the bundle branches of the Purkinje fibres and, by the moderator band, to the papillary muscles of the right ventricle, time 175ms
- impulse is distributed by Purkinje fibres and relayed throughout the ventricular myocardium, atrial contraction is completed, and ventricular contraction begins, time 225ms
7
Q
AV bundle, bundle branches and Purkinje fibres
A
- AV bundle = bundle of His
- right and left bundle branches feed into left and right ventricles
- Purkinje fibres connect with muscle cells of ventricles
8
Q
electrocardiogram main waves
A
- P wave: atrial depolarization caused by SA node
- atrial repolarization but QRS complex covers it
- QRS complex: ventricular depolarization caused by AV node
- T wave: ventricular repolarization
- PR interval: time between onset of P wave and QRS complex
9
Q
arrhythmias
A
- abnormal heart rhythm
- SA node develops abnormal rhythm
- conduction pathway interrupted
- ectopic pacemaker
10
Q
atrial fibrillation (AF)
A
- the impulses move over the atrial surface at rates of up to 500 bpm, the atrial wall quivers instead of producing an organized contraction
- the ventricular rate cannot follow the atrial rate and may remain within normal limits, even though the atria are now non-functional, their contribution to ventricular end-diastolic volume is so small the condition may go unnoticed in older individuals
- blood may start to clot in atria if it stays stationary for too long, clot then falls into ventricle and is pumped into lungs or to the body
11
Q
ventricular tachycardia (VT)
A
- defined as four or more premature ventricular contractions (PVCs), arising from an ectopic source, without intervening normal beats
12
Q
ventricular fibrillation (VF)
A
- responsible for the condition known as cardiac arrest
- VF is rapidly fatal because the ventricle quiver and stop pumping blood
13
Q
heart block
A
- related to the P-R interval, measures performance of AV node
- first degree: P-R interval is extended
- second degree: P-R interval is skipped, dropped heart beat
- third degree: no AV node function, ventricles rendered useless
14
Q
the cardiac cycle
A
- beginning of one heartbeat to the beginning of the next heartbeat
- contraction (systole) phase and relaxation (diastole) phase
- blood will move from high pressure to low pressure
- pressure increases during contraction phase
- valves open and close due to pressure
1. atrial systole
2. atrial diastole
3. ventricular systole
4. ventricular diastole
15
Q
atrial systole
A
- atria begin to contract due to SA node
- pressure increases
- atria push blood into ventricle, 30% of volume of ventricle
- “topping up” ventricle
16
Q
atrial diastole
A
- atria begin to relax
- continually filling while relaxed
17
Q
ventricular systole
A
- two phases: isovolumetric ventricular contraction and ventricular ejection
18
Q
isovolumetric ventricular contraction
A
- occurs during ventricular systole
- end-diastolic volume (EDV, 120 mL), amount of blood at end of diastole
- ventricular contraction
- heart valves remain closed, pressure increases
19
Q
ventricular ejection
A
- occurs during ventricular systole
- pressure in ventricle exceeds pressure in aorta or pulmonary trunk, causes aortic and pulmonary valves to open
- valve opens, this is when arterial pressure is measured
- ventricles continue to contract
- pressure continues to increase, peaks, then decreases
- volume of blood ejected = stroke volume (SV), typically 70-80 mL, around 60% of EDV at rest
- blood remaining in ventricle at end of contraction = end systolic volume (ESV, 40 mL)
20
Q
ventricular diastole
A
- all valves closed
- isovolumetric ventricular relaxation
- ventricular pressure decreases
- AV valves open and passive filling occurs (70%)
21
Q
Wiggers diagram
A
look at it and practice labelling
22
Q
heart sounds
A
- ausculation
- “Lubb” = start of ventricular contraction, AV valve closes
- “Dupp” = start of ventricular filling, semilunar (aortic and pulmonary) valve closes
23
Q
cardiac output
A
- cardiac function over time
- cardiac output = amount of blood pumped by the left ventricle per minute
- Q (mL/min) = HR (beats/min) x SV (mL/beat)
- at rest, average Q is 6 L/min
- normal range of Q during heavy exercise is 20 L/min
- maximum for trained athletes exercising at peak levels is 40 L/min
24
Q
factors affecting cardiac output
A
- heart rate (chronotropic factors): autonomic innervation and hormones
- stroke volume (inotropic factors): EDV -ESV
25
Q
autonomic innervation and Q
A
- sympathetic (increase HR) and parasympathetic ( decrease HR) divisions
- cardiac centre in medulla oblongata:
- cardioacceleratory centre (sympathetic)
- cardioinhibitory centre (parasympathetic)
- autonomic tone: how much parasympathetic and sympathetic system are activated
- effects on SA node: affect flow of Na+ into pacemaker cells, more permeability leads to increased HR
- atrial reflex: if heart pumps faster, more blood comes back to heart, atria fills more and stretches, stretch receptors send signal to SA node to beat faster, leading to more opening of Na+ channels in SA node
26
Q
hormones and Q
A
- epinephrine, norepinephrine and thyroid hormone all affect the SA node leading to increases in heart rate by encouraging Na+ to enter SA and depolarize more frequently
27
Q
end-diastolic volume (EDV) and Q
A
- EDV is the volume of blood in left ventricle at end of filling in diastole
- can increase EDV by increasing filling time, this occurs by slowing down HR
- slower the HR, the more time it has to fill
- can increases EDV by increasing venous return, the amount of blood returning to heart after travelling through the body, exercising increases venous return
- filling time and venous return affect preload, increasing either leads to increases in preload, the initial stretching of cardiac myocytes prior to contracting
28
Q
end-systolic volume (ESV) and Q
A
- ESV is the amount of blood left in left ventricle after contraction, want it to be as small as possible
- increasing preload, decreases ESV by pumping more blood out of left ventricle, uses Frank-Starling law to generate more elastic energy for more powerful contraction
- increasing contractility of heart decreases ESV, either via autonomic activity or hormones
- increasing afterload, amount of pressure heart needs to overcome to eject blood out of LV, increases ESV, if afterload is higher more pressure is required to open the valves for ejection of blood causing the heart to work harder, vasodilation and vasoconstriction can impact afterload
29
Q
enlarged heart
A
- can exist due to hypertension as it tries to compensate for the higher arterial pressure, leads to thickening of the walls of LV, causing SV to get smaller
- can also occur due to having a stronger heart from exercise and training
30
Q
factors affecting heart rate
A
- autonomic innervation
- hormones
- fitness levels
- age
31
Q
factors affecting stroke volume (7)
A
- heart size
- fitness levels
- gender
- contractility
- duration of contraction
- preload (EDV)
- afterload (resistance)
32
Q
path of blood through blood vessels
A
- arteries -> arterioles -> capillaries -> venules -> veins
33
Q
arteries
A
- relatively thick muscular walls (contractile and elastic properties), needs to withstand high pressure blood being ejected by heart
- elasticity allows for passive changes in diameter, expand when blood volume gets pumped out of LV and when returning back to resting diameter helps continue pushing blood forward
- contractility allows for active changes in diameter
- sympathetic activity -> vasoconstriction and vasodilation
34
Q
elastic arteries
A
- aka conducting arteries
- first arteries that exit from heart, experience large changes in volume and pressure
- few smooth muscle fibres and a high density of elastic fibres
- expand during ventricular systole and recoil to original size during ventricular diastole, helps propel blood forward since heart isn’t contracting to generate pressure
- helps make blood flow continuous
35
Q
muscular arteries
A
- aka distribution arteries
- more smooth muscle fibres and fewer elastic fibres
- most arteries are muscular arteries
- distribute blood to skeletal muscle and internal organs
36
Q
arterioles
A
- aka resistance vessels
- smaller than arteries, thickness of wall smaller, thinner wall because blood pressure is much lower once it reaches arterioles
- capable of constriction and dilation
- no elastic component
- determine the pressure that is required to push blood through the vessels, creates a bottleneck to help direct blood to where it is needed
37
Q
capillaries
A
- “workhorses” of the cardiovascular system
- form network of vessel throughout the body
- thin walls allow gas exchange between blood and surrounding fluid
- blood travels slowly allowing for two-way exchange of gases
38
Q
venules
A
- collect blood from the capillary beds
39
Q
veins
A
- contain majority of blood in body at any one time (2/3)
- medium and large sized veins
- low-pressure system, important because when standing blood in legs pools and can’t get back to heart, assisted by venous valves for one way flow of blood
- venules and medium sized veins contain venous valves to prevent backflow, valve opens superior to contracting muscle and closes inferior to contracting muscle
- blood is moved up by contraction of gastrocnemius and soleus (muscular pump), once into abdomen, breathing helps return it to heart
40
Q
proportions of blood sitting in different blood vessels
A
- 64% of blood sitting in veins
- 7% in heart
9% in pulmonary circuit - 13% in arteries and arterioles
41
Q
pressure, resistance and flow
A
F = P/R
- flow is directly proportional to pressure, if pressure increases flow increases
- pressure drops dramatically once its exits arterial system, low pressure in capillaries and even lower in veins
- flow is inversely proportional to resistance, increasing resistance decreases flow
- to ensure flow, want pressure to be high and resistance to be low
- in veins, pressure is low but so is resistance
- in arteries, pressure is high but resistance is also high
42
Q
total peripheral resistance
A
- most important factor is friction between the blood and vessel walls
- friction depends on:
- vessel length: long = more resistance than if short, but length remained relatively constant, directly proportional to resistance
- vessel diameter: large has less resistance than smaller vessel, this is controlled by constriction and dilation, inversely proportional to resistant, significant effect on resistance
R = 1/r^4 - blood viscosity: thickness of a fluid, hematocrit is a measure of how many red blood cells are in blood, kidneys help maintain blood viscosity by controlling amount of fluid in blood
- blood doping increases the viscosity of blood by adding more RBCs
- turbulence: due to irregular surfaces and sudden changes in diameter, increases resistance, plaques lining vessels cause turbulence disrupting laminar flow affecting blood pressure and flow
43
Q
arterial blood pressure
A
- systolic pressure: during systole or contraction of LV, normal is 120 mmHg
- diastolic pressure: during diastole or relaxation, normal is 80 mmHg
- pulse pressure is the difference between systolic and diastolic pressure
- mean arterial pressure is the average arterial pressure throughout one cardiac cycle
44
Q
hypertension
A
- > 135/>85 mmHg
- increased workload on heart
- left ventricle gets larger
- greater demand for oxygen
- coronary ischemia when blockages occur
- stresses blood vessels, affects capillaries most, can cause them to burst
- promotes development of arteriosclerosis
- increased risk of aneurysms
45
Q
elastic rebound
A
- during diastole, continues to push blood away from heart and to arterioles
- maintains even blood flow
46
Q
venous return
A
- small pressure determines return
- posture can affect venous return via gravity
- two factors assist venous return:
- muscular compression: calf and leg muscles
- respiratory pump: once blood is in abdomen, respiratory system helps return it to heart
47
Q
arteriosclerosis
A
- thickening or toughening of the arterial wall
- focal calcification: accumulation of calcium in arterial walls, makes them stiffer and less flexible, can’t expand as well so BP increases
- atherosclerosis: when inner wall fill up with lipids and plaques, really unhealthy, tends to be linked to diet
48
Q
atherosclerosis
A
- tends to develop due to high levels of cholesterol
- changes in lining of artery leads to plaque
- can be reverse early with diet changes
- if not, plaque can grow and get more complex, some could even completely block an artery causing an occlusion
- more common in older men
- other factors: high cholesterol, hypertension, and cigarette smoking, diabetes, obesity and stress
