Cardiovascular Flashcards

1
Q

Primary function of the cardiovascular system (5)b

A
  • Respiratory gas exchange
  • Nutrient supply/waste removal
  • Hormone signalling
  • Fluid maintenance
  • Body temperature regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of capillary

3

A
  • Sinusoid (discontinuous) capillary
  • Continuous capillary
  • Fenestrated capillary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Locations of sinusoid capillary

3

A
  • Spleen
  • Liver
  • Marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Locations of continuous capillary

A

Capillaries of most tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Location of fenestrated capillary

A

Glomerular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Structure of large elastic arteries
  2. Function
  3. Example
A
  1. thick tunica media with lots of elastin
  2. Windkessel stretch to accommodate high blood pressure in systole
  3. Aorta, pulmonary artery, carotid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Structure of muscular arteries
  2. Function
  3. Example
A
  1. Media composed of smooth muscle
  2. Distributing vessels
  3. Radial, femoral, coronary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Structure of arterioles

2. function

A
  1. contain 1 - several layers of smooth muscle

2. Resistance vessels that act as the gateway for microcirculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. structure of capillaries

2. function

A
  1. Endothelial cell layer resting on basement membrane. no smooth muscle
  2. Exchange vessels, diffusion occurs here
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. structure of venules

2. function

A
  1. some smooth muscle present

2. collecting vessels. as blood leaves the capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. structure of veins
  2. purpose
  3. examples
A
  1. thinner walls than arteries, less elastic tissue. valves present in limbs
  2. transporting deoxygenated blood back to the heart
  3. Vena cava, jugular vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Valve between right atrium and right ventricle

A

Tricuspid valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Valve between the left atrium and left ventricle

A

Mitral valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Valve between left ventricle and aorta

A

Aortic semilunar valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Valve between Right ventricle and pulmonary arteries

A

Pulmonary semilunar valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Difference between cardiac and skeletal muscle

A

Presence of intercalated disks and gap junctions between the filaments in cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Calcium induced calcium release

  • definition
  • role of T tubule
  • AP
  • SR
A
  • Cardiac muscle requires an influx of Ca2+ ions through voltage-gated Ca2+ channels for contraction
  • T-tubule membranes act as voltage gated Ca2+ channels.
  • During AP these open, allowing Ca2+ to enter heart cell
  • triggering release of Ca2+ from SR for muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
Cardiac muscle 
-Excitation?
- Organisation?
- Action potential duration? 
- tetanus?
Dependance on Ca2+ influx?
A
  • Electronic spread from pacemaker region
  • striated, branching
  • long (350ms)
  • No
  • great
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
Skeletal muscle 
-Excitation?
- Organisation?
- Action potential duration? 
- tetanus?
Dependance on Ca2+ influx?
A
  • neuromuscular junction
  • striated, isolated motor unit cells
  • brief (5ms)
  • yes
  • little
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
Smooth muscle 
-Excitation?
- Organisation?
- Action potential duration? 
- tetanus?
Dependance on Ca2+ influx?
A
  • Neurohumoral/electrical
  • non-striated, electrically coupled
  • only exceptionally
  • slow tension development
  • great
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

From where does autonomic regulation of heart rate originate in the brain?

A

The medulla oblongata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  • How many days for the primordial heart to develop in a foetus?
  • What shape does it form?
  • What happens at 4-5 weeks
A
  • Primordial heart is developed by 23 days
  • Forms a tube which forms different bulbs, blood vessels begin to form and join
  • At 4-5 weeks the heart tube begins to fold in on itself, forming primitive L/R atria and ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Comparison of foetal and adult circulation (3)

  • Reliance?
  • Supportive organs?
  • UV?
A
  • The foetus is completely reliant on maternal circulation for oxygen and nutrients
  • These come from the placenta and are delivered by the umbilical cord and umbilical vein
  • Umbilical vein carries oxygenated blood into the liver and the inf. Vena Cava, via the ductus venosus, of the foetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Foramen ovale?

A
  • A junction between atria in the foetal heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Foetal lung structure?
- Foetal lungs are collapsed and not functioning - Pulmonary arteries are constricted due to low oxygen levels in the lungs - causes lower left atrium pressure, so blood flows into the left ventricle from the right
26
What causes an acceleration in heart rate? (3) - Fibres? - Ligands? - Chronotropism??
- Sympathetic fibre activity - Noradrenaline binds to b1-adrenoreceptors, resulting in increased slope of the pacemaker potential - positive chronotropism
27
What causes the heart rate to slow? (3) - Fibres? - Ligand and receptor - Chronotropism
- Parasympathetic fibre activity slows the heart - Acetylcholine binds to muscarinic receptors causing a decrease in the slope of the P.P / slight hyperpolarisation - negative chronotropism
28
Cardiac cycle: atrial systole
corresponds to the P wave of the ECG, completes ventricular filling. mitral valve is open
29
Ventricular systole (1):
Q wave of the ECG, mitral valve closes, isovolumetric contraction (no volume change), aortic valve closed
30
Ventricular systole (II):
Ejection phase, blood is expelled into the aorta as aortic valve opens
31
Ventricular diastole (I):
Isovolumetric relaxation, the aortic valve closes and the ventricle relaxes
32
Ventricular diastole (II)
Passive filling as mitral valve reopens
33
Cardiac Output: defintion
= Volume of blood(L) / Minute
34
Stroke Volume (SV)
= Litres per beat
35
calculate CO using SV and HR
CO = SV X HR
36
Resting cardiac output =
4 - 7 L.min^-1
37
Exercise cardiac output =
16 - 42 L.min^1
38
Factors affecting cardiac output (3)
- Preload: filling pressure, starling's law of the heart - Afterload: Atrial pressure opposing ejection - Contractility: sympathetic nerves, circulating agents
39
Laplace's Law (P) = | T= tension, r=radius, S=stress, W=wall thickness P=pressure
P = 2T/r = 2Sw/r
40
Starling's law of the heart
The energy of contraction of a cardiac muscle fibre is proportional to the initial fibre length at rest
41
Preload:
- The wall stress in resting myocardium
42
Afterload:
- the wall stress opposing shortening of muscle fibres, atrial pressure
43
Autonomic control of the heart - influence from - Sympathetic innervation:
- influence from higher brain centres and cardiovascular receptors - Sympathetic innervation arrises at T1-T5
44
Contractility definition:
The energy of contraction independent of fibre length at rest
45
Positive inotropy: | Positive inotropes:
- increased contractility | - Noradrenaline, adrenaline, digoxin
46
Negative inotropes:
- decrease contractility | - Ca channel blockers, beta-blockers
47
Positive lusitropy:
- Increased rate of relaxation
47
Positive lusitropy:
- Increased rate of relaxation
48
``` Cardiac output (Q): MAP,CVP,TPR equation ```
``` Q = (MAP - CVP)/TPR MAP = Mean arterial pressure CVP = Central venous pressure TPR = Total peripheral resistance ```
48
Cardiac output (Q): - MAP - CVP - TPR
``` Q = MAP - CVP TPR MAP = Mean arterial pressure CVP = Central venous pressure TPR = Total peripheral resistance ```
49
Pulse Pressure (PP) =
``` PP = SBP - DBP SBP = Systolic blood pressure DBP = Diastolic blood pressure ```
50
Mean Arterial Blood Pressure (MABP) =
MABP = DBP + 1/3 PP | = 2/3 DBP + 1/3 SBP
51
Microcirculation
-Smooth muscle cells surrounding the arterioles control the entry of blood into the capillary network and the resistance to flow around the systemic circulation
52
Laminar flow:
Friction between the blood and the wall of the blood vessel slows flow at the edge of the vessel
53
Turbulent flow:
Eddies and swirls appear, determined by the Reynold's number (Re)
54
Reynolds number (Re):
Re = (v X D X p)/n | v: velocity,D: diameter, p=density, n=viscosity
55
Single-file flow:
the internal diameter of capillaries is 6 micrometers, less than the 7 micrometer diameter of red blood cells. Cells are squeezed through one by one
55
Single-file flow:
the internal diameter of capillaries is 6 micrometers, less than the 7 micrometer diameter of red blood cells. Cells are squeezed through one by one
56
Metabolic hyperaemia:
- Caused by a build up of metabolites, relaxation of smooth muscle in the medial layers of the arterioles supplying the tissue causes vasodilation , blood flow increases, metabolites get used up, returns to normal
57
Reactive hyperaemia:
An increase in blood flow after a period of arrested blood flow. Tissue in occluded limbs continue to metabolise, causing a build up of metabolites. when blood flow returns, the metabolites cause vasodilation, increasing blood flow
58
Orthostasis: (5)
- When lying down (supine) venous blood is evenly distributed - When standing venous blood pools in the legs - Central venous pressure drops, reducing SV - Reducing MABP - Causing transient hypotension
59
Vasovagal syncope:
- psychogenic reduction in blood pressure - Vagal bradycardia and vasodilation in response to psychological stress - (e.g. sight of blood)
60
White coat hypertension:
- Anxiety results in increase in blood pressure due to increased sympathetic output - Increasing HR and TPR
61
Capillary types: sinusoid (discontinuous capillary)
- Found in spleen, liver, bone marrow | - RBCs and large lipophobic molecules can pass through
62
Capillary types: fenestrated capillaries
- Glomerular capillaries | - Small lipophobic molecules can diffuse
63
Types of capillaries: continuos capillaries
- Fast diffusion: gases, lipophilic molecules - Slow diffusion: small lipophobic molecules - Very slow diffusion: large lipophobic molecules \ - E.g. most tissues
64
Ultrafiltration in capillaries: | - Interstitial fluid
- Pressure of interstitial (Pi) is slightly negative to Pressure inside the capillary (Pc) - H2O diffuses out of capillary, creating interstitial fluid
65
Oedema:
- Excess tissue fluid, leads to water-logged interstitium - Arises when: Fluid production by capillaries becomes greater than fluid removal by lymphatics
66
Excess fluid drainage:
- Drained by the lymphatic system
67
The red blood cell (erythrocyte): functional adaptations
- Bioconcave shape: maximises SA - Strong yet flexible - No internal organelles: maximises space for haemoglobin
68
Erythropoiesis:
- Production of red blood cells
69
Locations of erythropoiesis: - In utero - In children - In adults
- In utero: liver - In children: bones with red marrow, liver and spleen - In adults: ends of long bones, skull, vertebrae, ribs, sternum, pelvis (liver and spleen)
70
Erythropoiesis steps: (7) - HSC - Pro-E - Baso - Poly - Ortho - R - RBC
- Haematopoietic stem cell (1) - Pro-erythroblast (2) - Basophilicc (4) - Polychromatic (8) - Orthochromatic (16) - Reticulocyte (16) _ RBC (16)
71
Erythroid cell differentiation: Proerythroblast to orthochromatic
- Massive synthesis of erythroid specific proteins
72
Erythroid cell differentiation: | Whole cycle
- Increasing production of systolic proteins (haemoglobin)
73
Erythroid cell differentiation: polychromatic to erythrocyte
- Loss of organelles
74
What stimulates erythropoiesis:
- Erythropoietin (EPO) | - Secreted by the kidneys, increases RBC count
75
Where does erythropoiesis occur in the bone marrow: (3) - MI - Interactions - What is is produced/engulfed
- Macrophage islands - A central macrophage interacts with developing erythroid cells - Macrophage produces regulatory GHs and TFs and engulfs discarded nucleus's
76
Destruction and recycling of RBCs: - Phagocytosis - Globulin portion - Cell components
- Old and damaged erythrocytes are phagocytized by macrophages - The globulin (protein) portion of haemoglobin is metabolised into amino acids - Cell components also recycled
77
The fick principle: oxygen uptake rate (VO2)= - Q=flow rate - CA- Arterial O2conc. - CV- Venous O2conc.
``` - VO2 = Q.CA - Q.CV = Q(CA-CV) - Q = flow rate (CO) - CA = O2 conc. (oxygenated blood) - CV = O2 conc. (deoxygenated blood) - VO2 = rate of oxygen uptake (consumption) ```
78
Metabolic hyperaemia:
- Build up of metabolites causes vasodilation and local increase in blood flow
79
Cardiovascular responses to dynamic exercise: (5)
- Metabolic vasodilation - Coronary vasodilation - Pulmonary blood flow increases - SV increases - Splanchnic/renal vasoconstriction
80
Dynamic exercise: - Definition - Systolic BP - Diastolic BP
- Alternating contraction and reaction - Systolic BP increases as a result of increased cardiac output - Diastolic BP may decrease due to fall in TPR due to vasodilation (heat loss)
81
Static exercise: - Definition - Effect on BP - Moderation
- Sustained contraction - Both systolic and diastolic BP increase - Compression of muscles impairs blood flow - Muscle metaboloreceptors mediate a peripheral vasoconstriction
82
Cardiovascular response to exercise: - Anticipation - Central command hypothesis - Effects
- Anticipation of exercise causes HR and breathing increase - Cerebral cortex influences autonomic and respiratory neurones in the brainstem - This causes HR and blood pressure to increase
83
Effects of aerobic training: (5) - H - R B - B V - C - V
- Left ventricular enlargement: increases stroke volume - Resting bradycardia - 5-10% increase in blood volume - Increased myocardial contractility - Increased muscle vascularisation
84
Cardiac conduction system: (2)
- Excitation spreads from the Sinoatrial node (SAN) via internodal pathways to the Atrioventricular node (AVN) - from here it travels down the interventricular septum and across both ventricles via purkinje fibres
85
Action potential of a ventricular myocyte: (4) 4. K+ 0. Na+ 1. Na+ 2. Ca+ 3. K+
4. Resting membrane potential, determined by K+ permeability 0. Activation of voltage-gated Na+ channels, inward current, cell moves toward E(Na) 1. Early repolarisation due to slow inactivation of Ca channels 2. slow inward current of Na+ causes a plateau phase 3. Depolarisation phase bought by increased permeability to K+ and Ca inactivation
86
The refractory period:
- When sodium channels are inactivated, ensures each AP only generates a single twitch as tetany would be fatal
87
Pacemaker potential in the SA node:
- SA nodal cells show an unstable resting membrane potential due to slow inward Ca and Na currents
88
Effect of pacemaker potential:
- Slope of the pacemaker potential sets the heart rate
89
Positive chronotropism:
- Sympathetic fibre activity accelerates the heart | - Noradrenaline binds to B1-adrenoreceptors, increasing slope
90
Negative chronotropism:
- Parasympathetic fibre activity slows the heart | - Acetylcholine binds to muscarinic receptors, decreasing slope. Slowing the heart rate
91
The electrocardiogram:
- Conduction of the AP through the heart creates an electrical field that can be detected at the body surface as an ECG
92
P wave:
- Atrial depolarisation
93
PR interval:
- Atrial depolarisation, atrioventricular conduction, spread through purkinje fibres
94
QRS interval:
- Ventricular depolarisation
95
QT interval:
- Ventricular depolarisation and repolarisation