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Flashcards in Physiology Deck (155):


Heart is capable of beating rhythmically in the absence of external stimuli, or nervous stimuli


Specific location of the SA node

SA node is located in the upper right atrium close to where the Superior Vena Cava enters the right atrium


Spontaneous pacemaker potential

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


Which ion channels are behind the spontaneous pacemaker potential ie. reaching threshold in pacemaker cells?

Decrease in K+ efflux superimposed on a slow Na+ influx (the funny current)


Which ion channels are responsible for the rising phase of the action potential in pacemaker cells?

Voltage-gated Ca++ channels resulting in Ca++ influx


Which ion channels are responsible for the falling phase of the action potential in pacemaker cells?

Activation of K+ channels resulting in K+ efflux (which had been decreased previously)


What is the pathway of the spread of excitation?

1) SA node 2) AV node and RA (via Bachmann's bundle) 3) Bundle of His (R &L) 4) Purkinje fibres


How does the excitation spread between cardiac cells?

Via gap junctions


What is the only point of electrical contact between the atria and ventricles?

AV node


What important role does the AV node play?

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


What is the resting membrane potential of ventricular cells?

-90 MV


Which ion channels are responsible for the rising phase (Phase 0) of action potentials in the ventricular cells?

Fast Na+ influx (reverses the membrane potential to +30mV)


Which ion channels are responsible for the initial falling phase (Phase 1) of action potentials in the ventricular cells?

Closure of Na+ channels and Transient K+ efflux


Which ion channels are responsible for the plateau phase (Phase 2) of action potentials in the ventricular cells?

Mainly Ca2+ influx though voltage gated Ca2+ channels


Which ion channels are responsible for the final falling phase (Phase 3) of action potentials in the ventricular cells?

Closure of Ca2+ channels and K+ efflux


Vagal tone of the heart

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)


What effect does vagal stimulation have on the heart?

Negative chronotropic: Lowers intrinsic firing in the SA node (decreases slope of pacemaker potential to threshold) and prolongs the ventricular delay/plateau


Which neurotransmitter is responsible for the parasympathetic supply of the heart, and which receptors does it act on?

Acetylcholine through M2 receptors


How does atropine increase HR?

Acts as a competitive inhibitor of acetylcholine


Which areas does the parasympathetic system supply in the heart?

SA node and AV node


Which areas does the sympathetic system supply in the heart?

SA node, AV node and myocardium


**What effect does sympathetic stimulation have on the heart?

Increases HR (increases the slope of the pacemaker potential), decreases AV nodal delay AND increases the force of contraction


Which neurotransmitter is responsible for the sympathetic supply of the heart, and which receptors does it act on?

Noradrenaline acting through β1 adrenoceptors


All or None Law of the Heart

Gap junctions form low resistance communication pathways which ensures that each electrical excitation reaches all of the cardiac myocytes


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


What are the contractile units of the heart?

Sarcomeres of the myofibrils


Sliding filament theory

Muscle tension is produced by sliding of actin filaments on myosin filaments past each other to generate tension


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


What roles do Ca2+ play in muscle contraction?

Required to switch on cross bridge formation. Need it to form the Actin-myosin complex


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.


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


Why is the refractory period important in ventricular contraction?

Delay protects the heart from generating tetanic contractions (prolonged contraction)


Stroke volume

Volume of blood ejected by each ventricle per heartbeat (End diastolic volume - end systolic volume)


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


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



End diastolic volume - how much we load/stretch the heart with blood before it contracts


What is the main determinant of the preload?

Venous return


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)


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)


Length-dependent activation of the muscle fibre

Stretch also increases the affinity of troponin for Ca2+


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.


After load

The resistance into which the heart is pumping, which is imposed after heart contraction


What happens if there is a contuniusly raised after load e.g. hypertension?

Ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance


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


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


What is a normal healthy SV and CO?

70ml stroke volume and 5 litres a minute for CO


Cardiac cycle

Refers to all events that occur from the beginning of one heart beat to the beginning of the next


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)


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


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


What happens during the atrial contraction stage of cardiac cycle?

Atria contact, completing the final 20% of ventricular filling so the EDV of ~130ml


On the ECG, where does atrial depolarisation and then contraction occur?

Depolarisation = P wave, atrial contraction occurs between P wave and QRS


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


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)


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


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


What signals the starts of systole?



What signals the starts of diastole?



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


Blood pressure

The outwards (hydrostatic) pressure exerted by the blood on blood vessel walls


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


True or False: Laminar flow is audible through a stethoscope

False, normal blood flow is inaudible


When does blood flow stop in terms of taking BP?

When external pressure exceeds systolic pressure


When does blood flow become turbulent and audible in terms of taking BP?

When the external pressure is between systolic and diastolic pressure


When does blood flow become laminar and inaudible in terms of taking BP?

When the external pressure is below diastolic


Fifth Korotkoff

Point at which the sound disappears - where diastolic pressure is recorded


Where does the pressure gradient of the mean arterial pressure lie?

Between the aorta (start of systemic) and RA (end of pulmonary)


Pressure gradient =

Mean arterial pressure (MAP) - central venous pressure (RA pressure)


Mean arterial pressure

The average arterial blood pressure during a single cardiac cycle (including systole and diastole). Normally around 7-105mmHg


Mean Arterial Pressure =

(2x diastolic pressure + systolic pressure) / 3 OR DBP + 1/3rd pulse pressyre


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)


What is the relationship of MAP with CO and TPR?

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance


Total peripheral resistance

Is the sum of resistance of all peripheral vasculature in the systemic circulation


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


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


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


True or False: Baroreceptors are responsible for blood pressure at all time durations

False, only short term


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


What causes postural hypotension?

Results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position


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


True or False: decreased BP causes decreased baroreceptor discharge



What makes up the total body fluid?

Intracellular fluid (2/3rd) + Extracellular Fluid (1/3rd)


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).


What are the 2 main factors affecting the ECF?

Water excess/deficit and Na+ excess/deficit


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


Which hormones regulate the extracellular fluid volume?

• Renin-Angiotensin- Aldosterone System hormones: Renin, Angiotensin and Aldosterone • Atrial Natriuretic Peptide - ANP • Antidiuretic Hormone (Vasopressin) - ADH


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


Where is renin released from?

Juxtaglomerular apparatus in the kidney


What is Anti-diuretic hormone?

Peptide hormone derived from a pre-hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary


What stimulates the secretion of ADH?

Secretion stimulated by (1) reduced extracellular fluid volume or (2) increased extracellular fluid osmolarity (main stimulus)


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


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


Which systems and hormones promote reabsorption of water?



Which systems and hormones promote excretion of water?



What are the main sites of TPR?



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


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


True or False: Intrinsic control of vascular smooth muscles can over-ride extrinsic control

True, they include local chemical and physical factors


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)


What are examples of local humeral agents that can cause relaxation of arteriolar smooth muscle?

• Histamine • Bradykinin • Nitric Oxide (NO


What are examples of local humeral agents that can cause constriction of arteriolar smooth muscle?

• Serotonin • Thromboxane A2 • Leukotrienes • Endothelin


What are examples of physical factors that can affect arteriolar smooth muscle?

Temperature, myogenic response to stretch and shear stress


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


Metabolic hyperaemia

Increase in blood flow that occurs when tissue is active eg. exercise


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



An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation


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


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


Cariogenic shock

Sustained hypotension caused by decreased cardiac contractility


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


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


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


Neurogenic shock

Occurs with damage to spinal cord


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


Vasoactive shock

Septic shock - which is a body-wide inflammatory response to infection, leads to dangerously low blood pressure


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


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


Up until what proportion of blood volume loss, can compensatory mechanisms maintain blood pressure?



What are the signs of hypovolaemic shock?

Tachycardia, higher resp rate and decrease in BP and pulse pressure


Pulse pressure

Difference between systolic and diastolic pressure (usually around 40mmHg)


What are 3 main special adaptation of coronary circulations?

High capillary density, high basal blood flow and high oxygen extraction


What intrinsic mechanisms act on coronary blood flow?

↓ Po2, metabolic hyperaemia and adenosine (product of breakdown from ATP) are all potent vasodilators


Why is left coronary blood flow almost 0 during isovolumetric ventricular contractions?

Because the muscle constricts the arteries (doesn't affect right coronary flow)


Auto regulation of cerebral blood flow

Guards against changes in cerebral blood flow if mean arterial blood pressure changes within a range (~ 60 - 160mmHg)


True or False: ↑ PCO2 causes cerebral vasoconstriction

False, increased PCO2 causes vasodilation


Cerebral Perfusion Pressure =

Mean Arterial Pressure (MAP) - ICP


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.


Net filtration pressure (NFP) is proportional to..

Forces favouring filtration - forces opposing filtration


Filtration co-efficient (Kf)

How permeable the capillaries are


Which forces favour filtration (movement of fluid out of capillaries)?

Pc - capillary hydrostatic pressure

πi - Interstitial fluid osmotic pressure


Which forces oppose filtration (movement of fluid into capillaries)?

πc - Capillary osmotic pressure

Pi - Interstitial fluid hydrostatic pressure


True or False: Starling forces favour filtration at arteriolar end, reabsorption at venular end




Accumulation of fluid in interstitial space


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.


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


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


What are the normal ranges for blood pressure?

108-132/75-83 mmHg


What are the normal values for total cholesterol?

5 mmol/L or less


What are the normal values for HDL cholesterol?

4 mmol/L or less


What are the normal values for blood glucose?

4.0-5.9 mmol/L before a meal and under 7.8 mmol/L after


What does a molar rash indicate?

Mitral stenosis


What angle should a patient be sitting at for a precordial and chest exam?

45 degrees


What do parasternal heaves indicate?

Right ventricular hypertrophy


What grade of murmur is palpable?

Grade 4


Which murmur radiates to the carotids?

Aortic stenosis


Which murmur radiates to the axilla?

Mitral regurgitation


What is a normal BMI range?

18-25 kg2/m


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.


What are the branches of the left coronary arteries?

LAD and circumflex


What are the branches of the right coronary arteries?

Posterior and marginal branches


What are the vessels that supply the tunica adventitia of the vessels?

Vaso vasorum


What system is used to grade murmurs?

Levine's scale


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


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

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