Physiology Flashcards
1
Q
Autorhythmicity
A
Heart is capable of beating rhythmically in the absence of external stimuli, or nervous stimuli
2
Q
Specific location of the SA node
A
SA node is located in the upper right atrium close to where the Superior Vena Cava enters the right atrium
3
Q
Spontaneous pacemaker potential
A
This gradual drift towards threshold. The cells in the SA node do not have a stable resting membrane potential. The spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential in the SA nodal cells
4
Q
Which ion channels are behind the spontaneous pacemaker potential ie. reaching threshold in pacemaker cells?
A
Decrease in K+ efflux superimposed on a slow Na+ influx (the funny current)
5
Q
Which ion channels are responsible for the rising phase of the action potential in pacemaker cells?
A
Voltage-gated Ca++ channels resulting in Ca++ influx
6
Q
Which ion channels are responsible for the falling phase of the action potential in pacemaker cells?
A
Activation of K+ channels resulting in K+ efflux (which had been decreased previously)
7
Q
What is the pathway of the spread of excitation?
A
1) SA node 2) AV node and RA (via Bachmann’s bundle) 3) Bundle of His (R &L) 4) Purkinje fibres
8
Q
How does the excitation spread between cardiac cells?
A
Via gap junctions
9
Q
What is the only point of electrical contact between the atria and ventricles?
A
AV node
10
Q
What important role does the AV node play?
A
Causes a delay in the spread of excitation to allow the ventricles time to fill. It does this as it is composed of slow conducting fibres
11
Q
What is the resting membrane potential of ventricular cells?
A
-90 MV
12
Q
Which ion channels are responsible for the rising phase (Phase 0) of action potentials in the ventricular cells?
A
Fast Na+ influx (reverses the membrane potential to +30mV)
13
Q
Which ion channels are responsible for the initial falling phase (Phase 1) of action potentials in the ventricular cells?
A
Closure of Na+ channels and Transient K+ efflux
14
Q
Which ion channels are responsible for the plateau phase (Phase 2) of action potentials in the ventricular cells?
A
Mainly Ca2+ influx though voltage gated Ca2+ channels
15
Q
Which ion channels are responsible for the final falling phase (Phase 3) of action potentials in the ventricular cells?
A
Closure of Ca2+ channels and K+ efflux
16
Q
Vagal tone of the heart
A
The vagus nerve (parasympathetic supply to the heart) exerts a continuous influence on the SA node under resting conditions (from 100 bpm to 70 bpm)
17
Q
What effect does vagal stimulation have on the heart?
A
Negative chronotropic: Lowers intrinsic firing in the SA node (decreases slope of pacemaker potential to threshold) and prolongs the ventricular delay/plateau
18
Q
Which neurotransmitter is responsible for the parasympathetic supply of the heart, and which receptors does it act on?
A
Acetylcholine through M2 receptors
19
Q
How does atropine increase HR?
A
Acts as a competitive inhibitor of acetylcholine
20
Q
Which areas does the parasympathetic system supply in the heart?
A
SA node and AV node
21
Q
Which areas does the sympathetic system supply in the heart?
A
SA node, AV node and myocardium
22
Q
**What effect does sympathetic stimulation have on the heart?
A
Increases HR (increases the slope of the pacemaker potential), decreases AV nodal delay AND increases the force of contraction
23
Q
Which neurotransmitter is responsible for the sympathetic supply of the heart, and which receptors does it act on?
A
Noradrenaline acting through β1 adrenoceptors
24
Q
All or None Law of the Heart
A
Gap junctions form low resistance communication pathways which ensures that each electrical excitation reaches all of the cardiac myocytes
25
What is the role of the desmosomes in the intercalated discs of the cardiac muscle?
Provide mechanical adhesion between adjacent cardiac cells. They ensure that the tension developed by one cell is transmitted to the next
26
What are the contractile units of the heart?
Sarcomeres of the myofibrils
27
Sliding filament theory
Muscle tension is produced by sliding of actin filaments on myosin filaments past each other to generate tension
28
What roles do ATP play in muscle contraction?
Needed for both contraction and relaxation. ATP is needed to energise the myosin head to actually form the cross bridge Also need ATP to help break down the crossbridge
29
What roles do Ca2+ play in muscle contraction?
Required to switch on cross bridge formation. Need it to form the Actin-myosin complex
30
How do action potentials cause ventricular systole?
* Pacemaker cells of the SA node depolarise, which causes voltage-gated calcium channels to open.
* Ca2+ moves into sarcoplasm which bind on to ryanodine receptors, this causes another flux of calcium to the sarcoplasm.
* Ca2+ bind to troponin C, causing conformational change in the troponin-tropomyosin complex, and thus allowing myosin head binding sites on F-Actin to be exposed.
* This transition allows cross bridge cycling to occur.
31
According to the sliding filament theory, how does contraction occur?
* ATP binds to myosin head, causing it to change position and move up and out where it can bind to actin forming a cross-bridge.
* Then when the ATP becomes ADP and unbinds the myosin moves down again causing a power stroke, pulling the filaments past each other.
* The cross-bridge then dissociates and the cycle repeats
32
Why is the refractory period important in ventricular contraction?
Delay protects the heart from generating tetanic contractions (prolonged contraction)
33
Stroke volume
Volume of blood ejected by each ventricle per heartbeat (End diastolic volume - end systolic volume)
34
True or False: At rest, the cardiac fibres are at their optimum length for contraction
False, they aren't, because they need room to get greater contraction in exercise etc
35
What brings around the changes in stroke volume?
Diastolic length of myocardial fibres which is determined by the volume of blood within the ventricle at the end of diastole/filling - preload
36
Preload
End diastolic volume - how much we load/stretch the heart with blood before it contracts
37
What is the main determinant of the preload?
Venous return
38
Starling's Law
The greater the venous return, the greater the stretch and therefore the greater contractility and SV (The volume of blood leaving the ventricles should match the volume entering it)
39
Length-tension relationship
The changes in active tension caused by changes in preload are related to changes in the number of actin and myosin cross bridges formed, which depends on the sarcomere length (when tension (stretch) increases, length increases)
40
Length-dependent activation of the muscle fibre
Stretch also increases the affinity of troponin for Ca2+
41
Why doesnt cardiac muscle show a decrease in contraction when the stretch becomes too great and there is less overlap for cross bridges, like in skeletal muscle?
Because the greater stiffness of cardiac muscle normally prevents its sarcomeres from being stretched beyond its optimal length of 2.2 microns.
42
After load
The resistance into which the heart is pumping, which is imposed after heart contraction
43
What happens if there is a contuniusly raised after load e.g. hypertension?
Ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
44
What part of the ANS is responsible for extrinsic control of stroke volume, and through what neurotransmitters?
Sympathetic system has a positive inotropic effect via noradrenaline
45
What effects does the sympathetic system have on the stroke volume?
Positive inotropic by increasing the force of contraction (increase peak ventricular pressure via cAMP) and also increases the rate of pressure change and also rate of ventricular relaxation
46
What is a normal healthy SV and CO?
70ml stroke volume and 5 litres a minute for CO
47
Cardiac cycle
Refers to all events that occur from the beginning of one heart beat to the beginning of the next
48
At a HR of 75 beats/min, what is the duration of ventricular diastole and systole?
Diastole = 0.5sec and systole 0.3sec (total duration of cardiac cycle is 0.8s)
49
What are the 5 events of the cardiac cycle?
1) Passive filling
2) Atrial contraction
3) Isovolumetric ventricular contraction
4) Ventricular ejection and repolarisation
5) Isovolumetric ventricular relaxation
50
What happens during the passive filling stage of cardiac cycle?
Pressure in atria and ventricles are close to zero so when AV valves open, blood flows into ventricles down pressure gradient (80% of filling is passive). Pressure in the sort is 80mmHg so aortic valve remains closed
51
What happens during the atrial contraction stage of cardiac cycle?
Atria contact, completing the final 20% of ventricular filling so the EDV of ~130ml
52
On the ECG, where does atrial depolarisation and then contraction occur?
Depolarisation = P wave, atrial contraction occurs between P wave and QRS
53
What happens during the isovolumetric ventricular contraction stage of cardiac cycle?
Ventricular contraction starts after the QRS and pressure rises, when it exceeds atrial pressure the AV valves close (first heart sound) indicating start of systole. The aortic valve is still closed however so the tension rises around a closed volume
54
What happens during the ventricular ejection stage of cardiac cycle?
When the ventricular pressure exceeds aorta/pulmonary artery pressure the aortic/pulmonary semilunar valve open and the stroke volume is ejected, leaving the end systolic volume (~60-70ml)
55
What happens during the ventricular repolarisation stage of cardiac cycle?
The T-wave in the ECG signals ventricular repolarisation. The ventricles relax and the ventricular pressure start to fall. When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut - the second heart sound (dub) signalling the start of diastole
56
What happens during the isovolumetric ventricular relaxation stage of cardiac cycle?
Ventricle is again a closed box, as the AV valve is shut so the tension falls around a closed volume “Isovolumetric Relaxation”. When the ventricular pressure falls below atrial pressure, AV valves open, and the heart starts a new cycle
57
What signals the starts of systole?
S1
58
What signals the starts of diastole?
S2
59
Why doesnt the arterial pressure not fall to zero during diastole?
Aorta has a lot of elastic tissue, so when blood is ejected it stretches. Then when it relaxes, it recoils back and keeps driving the blood forward
60
Blood pressure
The outwards (hydrostatic) pressure exerted by the blood on blood vessel walls
61
What is the normal condition for blood flow throughout most of the circulatory system?
Laminar flow - characterized by concentric layers of blood moving in parallel down the length of a blood vessel
62
True or False: Laminar flow is audible through a stethoscope
False, normal blood flow is inaudible
63
When does blood flow stop in terms of taking BP?
When external pressure exceeds systolic pressure
64
When does blood flow become turbulent and audible in terms of taking BP?
When the external pressure is between systolic and diastolic pressure
65
When does blood flow become laminar and inaudible in terms of taking BP?
When the external pressure is below diastolic
66
Fifth Korotkoff
Point at which the sound disappears - where diastolic pressure is recorded
67
Where does the pressure gradient of the mean arterial pressure lie?
Between the aorta (start of systemic) and RA (end of pulmonary)
68
Pressure gradient =
Mean arterial pressure (MAP) - central venous pressure (RA pressure)
69
Mean arterial pressure
The average arterial blood pressure during a single cardiac cycle (including systole and diastole). Normally around 7-105mmHg
70
Mean Arterial Pressure =
(2x diastolic pressure + systolic pressure) / 3 OR DBP + 1/3rd pulse pressyre
71
What is the minimum MAP needed to perfuse the coronary arteries, brain, and kidneys?
60mmHg (needs to be high enough to perfuse organs but not too high as to cause damage to the blood vessels)
72
What is the relationship of MAP with CO and TPR?
Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance
73
Total peripheral resistance
Is the sum of resistance of all peripheral vasculature in the systemic circulation
74
Where are the 2 groups of baroreceptors, what do they do and where do they singal?
Aortic arch and carotid sinus. They measure blood pressure by degree of stretch and then signal to medulla via CN IX and CN X
75
What is responsible for the sympathetic tone in the heart and where?
Sympathetic fibres releasing noradrenaline onto beta-receptors - vasomotor tone. Fibres in the atria SA and AV node, and also in the ventricles
76
What is responsible for the parasympathetic tone in the heart and where?
Parasympathetic fibres via acetylcholine. Fibres only in the atria, so can't affect contractility
77
True or False: Baroreceptors are responsible for blood pressure at all time durations
False, only short term
78
What happens when a normal person suddenly stands up from lying down?
1) Venous return to the heart decreases due to gravity
2) Mean arterial pressure transiently decreases which reduced firing of baroreceptors
3) Vagal tone to the heart decreases, sympathetic tone increases
4) Sympathetic constrictor tone increases as well as HR and SV, increasing TPR
5) This increases the venous return to the heart
79
What causes postural hypotension?
Results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position
80
What happens to baroreceptors if high BP is sustained?
Firing decreases and they re-set, only firing again if there is an acute change in MAP
81
True or False: decreased BP causes decreased baroreceptor discharge
True
82
What makes up the total body fluid?
Intracellular fluid (2/3rd) + Extracellular Fluid (1/3rd)
83
What is extracellular fluid volume and what makes it up?
This is the fluid which bathes the cells and acts as the go- between the blood and body cells. Plasma Volume (PV) + Interstitial Fluid Volume (IFV).
84
What are the 2 main factors affecting the ECF?
Water excess/deficit and Na+ excess/deficit
85
What happens if the plasma volume falls?
Compensatory mechanisms shifts fluid from the interstitial compartment to the plasma compartment (part of the ECF) which would increase CO
86
Which hormones regulate the extracellular fluid volume?
• Renin-Angiotensin- Aldosterone System hormones: Renin, Angiotensin and Aldosterone • Atrial Natriuretic Peptide - ANP • Antidiuretic Hormone (Vasopressin) - ADH
87
Describe the RAAS system
* 1. Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)
* 2. Angiotensin I is converted to angiotensin II by Angiotensin converting enzyme - ACE (produced by pulmonary vascular endothelium)
* 3. Angiotensin II:
* stimulates the release of Aldosterone from the adrenal cortex
* Causes systemic vasoconstriction which increases TPR
* Also stimulates thirst and ADH release
* 4. Aldosterone (a steroid hormone) acts on the kidneys to increase sodium and water retention – increases plasma volume
88
Where is renin released from?
Juxtaglomerular apparatus in the kidney
89
What is Anti-diuretic hormone?
Peptide hormone derived from a pre-hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary
90
What stimulates the secretion of ADH?
Secretion stimulated by (1) reduced extracellular fluid volume or (2) increased extracellular fluid osmolarity (main stimulus)
91
What is the action of ADH?
ADH acts in the kidney tubules to increase the reabsorption of water (conserve water) - i.e. causing the production concentrate urine (antidiuresis). This would increase extracellular and plasma volume and hence cardiac output and blood pressure. It also vasoconstrictor blood vessels to increase TPR and BP
92
What is the action of Atrial Natriuretic Peptide (ANP) systemm?
Causes excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure. Acts as a vasodilator - decreases blood pressure. Essentially acts as a counter-regulatory mechanism for the RAAS
93
Which systems and hormones promote reabsorption of water?
RAAS and ADH
94
Which systems and hormones promote excretion of water?
ANP
95
What are the main sites of TPR?
Arterioles
96
What is resistance of blood flow proportional to and inversely proportional to?
Proportional to blood viscosity and length of blood vessel; and inversely proportional to radius of blood vessel to the power of 4 (meaning a small change in radius has a large effect on resistance): R ∝ η.L/r4
97
Which receptors does adrenaline act on to cause vasoconstriction and vasodilation?
Adrenaline acting on α receptors causes vasoconstriction predominant in skin, gut and kidneys , and acting on β receptors in cardiac and skeletal muscles causes vasodilation
98
True or False: Intrinsic control of vascular smooth muscles can over-ride extrinsic control
True, they include local chemical and physical factors
99
What are examples of local metabolites that can cause relaxation of arteriolar smooth muscle?
• Decreased local PO2 • Increased local PCO2 • Increased local [H+] (decreased pH) • Increased extra-cellular [K+] • Increased osmolality of ECF • Adenosine release (from ATP)
100
What are examples of local humeral agents that can cause relaxation of arteriolar smooth muscle?
• Histamine • Bradykinin • Nitric Oxide (NO
101
What are examples of local humeral agents that can cause constriction of arteriolar smooth muscle?
• Serotonin • Thromboxane A2 • Leukotrienes • Endothelin
102
What are examples of physical factors that can affect arteriolar smooth muscle?
Temperature, myogenic response to stretch and shear stress
103
Which 4 factors influence venous return?
1) Increased sympathetic venomotor tone 2) Increased skeletal muscle pump from large veins in between muscles 3) Increased blood volume 4) Increases respiratory pump
104
Metabolic hyperaemia
Increase in blood flow that occurs when tissue is active eg. exercise
105
What are some of the chronic CVS responses to regular exercise?
* Reduces BP
* Reduction in sympathetic tone and noradrenaline levels
* Increased parasympathetic tone to the heart
* Cardiac remodelling
* Reduction in plasma renin levels
* Improved endothelial function: vasodilators vasoconstrictors
* Arterial stiffening
106
Shock
An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation
107
What is the pathway of shock to cellular failure?
1) Shock
2) Inadequate tissue perfusion
3) Inadequate tissue oxygenation
4) Anaerobic metabolism
5) Accumulation of metabolic waste products
6) Cellular failure
108
What is the pathway of hypovolaemic shock to inadequate tissue perfusion?
1) Loss of blood volume
2) Decreased venous return
3) Decreased EDV
4) Decreased SV
5) Decreases CO and BP
6) Inadequate tissue perfusion
109
Cariogenic shock
Sustained hypotension caused by decreased cardiac contractility
110
What is the pathway of caridogenic shock to inadequate tissue perfusion?
1) Decreased cardiac contractility
2) Decreased SV
3) Decreased CO and BP
4) Inadequate tissue perfusion
111
Obstructive shock
Occurs with tension pneumothorax, the intrathroacic pressure/transmural pressure is important for lung inflation, but also the venous return as the negative pressure gradient is needed to draw blood from the rest of the body into the venous system in the RA of the heart, since the MAP is generally low in the venous system
112
What is the pathway of obstructive shock to inadequate tissue perfusion?
1) Increased intrathoracic pressure
2) Decreased venous return and EDV
3) Decreased SV, CO and BP
4) Inadequate tissue perfusion
113
Neurogenic shock
Occurs with damage to spinal cord
114
What is the pathway of neurogenic shock to inadequate tissue perfusion?
1) Loss of sympathetic tone
2) Massive venous and arterial vasodilation
3) Decreased venous retune and TPR
4) Decreased CO and BP
5) Inadequate tissue perfusion
115
Vasoactive shock
Septic shock - which is a body-wide inflammatory response to infection, leads to dangerously low blood pressure
116
What is the pathway of vasoactive shock to inadequate tissue perfusion?
1) Release of vasoactive mediators
2) Massive venous and arterial vasodilation and capillary permeability
3) Decreased venous return and TPR
4) Decreased CO and BP
5) Inadequate tissue perfusion
117
What is the management of shock?
* 1) ABCDE
* 2) High flow oxygen
* 3) Specific management:
* Volume replacement if hypovolaemic
* Inotropes for cariogenic
* Chest drain for tension pneumo
* Adrenaline for anaphylactic
* Vasopressors for septic shock
118
Up until what proportion of blood volume loss, can compensatory mechanisms maintain blood pressure?
\>30%
119
What are the signs of hypovolaemic shock?
Tachycardia, higher resp rate and decrease in BP and pulse pressure
120
Pulse pressure
Difference between systolic and diastolic pressure (usually around 40mmHg)
121
What are 3 main special adaptation of coronary circulations?
High capillary density, high basal blood flow and high oxygen extraction
122
What intrinsic mechanisms act on coronary blood flow?
↓ Po2, metabolic hyperaemia and adenosine (product of breakdown from ATP) are all potent vasodilators
123
Why is left coronary blood flow almost 0 during isovolumetric ventricular contractions?
Because the muscle constricts the arteries (doesn't affect right coronary flow)
124
Auto regulation of cerebral blood flow
Guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~ 60 - 160mmHg)
125
True or False: ↑ PCO2 causes cerebral vasoconstriction
False, increased PCO2 causes vasodilation
126
Cerebral Perfusion Pressure =
Mean Arterial Pressure (MAP) - ICP
127
What is special about the pulmonary circulation?
* Dual supply from RA and also bronchial circulation.
* Pulmonary capillary pressure is low (~ 8-11 mmHg) compared to systemic capillary pressure (~ 17-25 mmHg)
* Absorptive forces exceed filtration forces - protects against pulmonary oedema
* Hypoxia causes vasoconstriction of pulmonary arterioles.
* Completely opposite to effect of hypoxia on systemic arterioles, to help divert blood from poorly ventilated areas of lung to well ventilated ones.
128
Net filtration pressure (NFP) is proportional to..
Forces favouring filtration - forces opposing filtration
129
Filtration co-efficient (Kf)
How permeable the capillaries are
130
Which forces favour filtration (movement of fluid out of capillaries)?
Pc - capillary hydrostatic pressure
πi - Interstitial fluid osmotic pressure
131
Which forces oppose filtration (movement of fluid into capillaries)?
πc - Capillary osmotic pressure
Pi - Interstitial fluid hydrostatic pressure
132
True or False: Starling forces favour filtration at arteriolar end, reabsorption at venular end
True
133
Oedema
Accumulation of fluid in interstitial space
134
Why does pulmonary oedema cause breathlessness?
Diffusion distance increases as it has to pass through the fluid, so gas exchange is compromised. Compliance is also reduced as the fluid means that it is harder to stretch.
135
What are the causes of oedema?
1) Raised capillary pressure (from arterial dilation or raised venous pressure)
2) Reduced plasma osmotic pressure
3) Lymphatic insufficiency
4) Changes in capillary permeability
136
What causes pulmonary oedema in LHF?
Increased distribution of blood into the pulmonary circulation due to increased hydrostatic pressure, backing up from the systemic circulation
137
What are the normal ranges for blood pressure?
108-132/75-83 mmHg
138
What are the normal values for total cholesterol?
5 mmol/L or less
139
What are the normal values for HDL cholesterol?
4 mmol/L or less
140
What are the normal values for blood glucose?
4.0-5.9 mmol/L before a meal and under 7.8 mmol/L after
141
What does a molar rash indicate?
Mitral stenosis
142
What angle should a patient be sitting at for a precordial and chest exam?
45 degrees
143
What do parasternal heaves indicate?
Right ventricular hypertrophy
144
What grade of murmur is palpable?
Grade 4
145
Which murmur radiates to the carotids?
Aortic stenosis
146
Which murmur radiates to the axilla?
Mitral regurgitation
147
What is a normal BMI range?
18-25 kg2/m
148
Why is smoking a risk factor for heart disease?
* Damages the lining of your arteries, leading to atherosclerosis.
* The carbon monoxide in tobacco smoke reduces the amount of oxygen in your blood - meaning your heart has to pump harder to meet body's oxygen demand
* The nicotine in cigarettes stimulates your body to produce adrenaline, which makes your heart beat faster and raises your blood pressure, making your heart work harder.
* Your blood is more likely to clot, increases the risk of having a heart attack or stroke.
149
What are the branches of the left coronary arteries?
LAD and circumflex
150
What are the branches of the right coronary arteries?
Posterior and marginal branches
151
What are the vessels that supply the tunica adventitia of the vessels?
Vaso vasorum
152
What system is used to grade murmurs?
Levine's scale
153
Where do you place the chest leads for an ECG?
* V1 – 4th intercostal space – right sternal edge
* V2 – 4th intercostal space – left sternal edge
* V4 – 5th intercostal space – mid clavicular line
* V3 – midway between V2 & V4
* V5 – anterior axillary line – same horizontal level as V4
* V6 – mid-axillary – same horizontal level as V4
154
Where do you place the limb leads for an ECG?
* RED – Right arm – ulnar styloid process at the wrist
* YELLOW – Left arm – ulnar styloid process at the wrist
* GREEN – Left leg – at the ankle – medial / lateral malleolus
* BLACK – Right leg – at the ankle – medial / lateral malleolus
*"Ride Your Green Bike"*
155
