Cardiovascular System Flashcards
The conduction velocity of action potentials in the heart is reduced as they pass through which of the following structures?
the atrioventricular node
Most of the blood volume in the body is contained within which of the following?
Veins
The pressure in the heart when the ventricles are relaxed is known as which of the following?
diastolic pressure
Oxygenated blood passes through which of the following?
Pulmonary veins.
Pulmonary arteries.
Left atrium.
Pulmonary veins.
Left atrium.
Venous return to the heart is assisted by which of the following?
low resistance of veins
low pressure in the right atrium
valves in veins
the skeletal muscle pump
all
The second heart sound corresponds with which of the following mechanical events?
Closing of the aortic valve.
Closing of the tricuspid valve.
Closing of the pulmonary valve.
Closing of the aortic valve.
Closing of the pulmonary valve.
Which of the following best describes the function of the tricuspid valve?
it prevents backflow of blood between the right atrium and the pulmonary artery
it prevents backflow of blood between the left atrium and left ventricle
it prevents backflow of blood between the right atrium and right ventricle
it prevents backflow of blood between the right and left atria
it prevents backflow of blood in veins
it prevents backflow of blood between the right atrium and right ventricle
Which of the following statements about cardiac pacemaker cells is/are TRUE?
Their membrane potential does not plateau following depolarisation.
Their resting membrane potential is -90 mV.
Their resting membrane potential is not stable.
Their membrane potential does not plateau following depolarisation.
Their resting membrane potential is not stable.
The wave on the electrocardiogram that represents ventricular repolarisation alone is which of the following?
T
Which of the following will increase mean arterial blood pressure?
- Increased heart rate.
- Decreased stroke volume
- Increased vasoconstriction of the systemic arteries.
1 & 3
Why is haematocrit often low in patients with kidney disease?
because these patients do not produce sufficient erythropoietin
The stage of the cardiac cycle where the pressure is the greatest within the heart is which of the following?
the ventricular ejection phase
Which of the following is/are a function of arterioles?
The control mean arterial pressure.
The regulation of blood flow to different regions of the body.
The transport of blood to capillaries.
all
The first and second heart sounds represent which of the following (in order)?
closure of the atrioventricular valves and closure of the semilunar valves
What is the difference in resting membrane potential between cardiac muscle cells and pacemaker cells?
30mV
the functions of the cardiovascular system
Transport of materials around the body:
(i) Between external environment and cells
Oxygen from lungs to cells
Nutrients from digestive tract to cells
(ii) From cell to cell
Hormones from endocrine cells to target cells
Stored nutrients (e.g. liver) to cells
(iii) Between cells and external environment
Carbon dioxide from cells to lungs
Metabolic wastes from cells to kidneys
consequences of cardiovascular system failure
Loss of blood supply to brain:
5‐10 seconds – loss of consciousness
2‐3 minutes – brain damage
Know what the major component of the cardiovascular system are how they are related to each other.
(i) Blood Vessels (Vasculature)
System that transports the blood around the body.
(ii) Blood
Liquid tissue that carries all the substances being moved.
(iii) Heart
Two‐channelled pump responsible for the movement of the blood.
Right Pump – delivers deoxygenated blood to lungs
Left Pump – delivers oxygenated blood to rest of body
Understand what constitutes the pulmonary and systemic circulations.
(i) Pulmonary Circulation
Vessels that connect heart to lungs
- Takes deoxygenated blood from the right hand side of the heart and is transported through the pulmonary artery to the capillaries where we get gas exchange and the oxygenated blood is transported back through the pulmonary arteries and returned to the left hand side of the heart
(ii) Systemic Circulation
Vessels that connect heart to other tissues
- Made up of a large number of circuits
- Oxygenated blood leaves the left hand side of the heart, flows out through arterial system which branches extensively to form capillary networks which provide blood supply to individual cells and systems
- Blood is then collected from those capillaries and transported back to the right hand side of the heart
Be familiar with the macroscopic structure differences between the major types of blood vessels.
Arteries
Arterioles
Capillaries
Venules
Veins
Be familiar with the microscopic structure differences of the major types of blood vessels.
(i) Tunica Intima
Endothelium - single layer flat epithelial cells
Internal Elastic Lamina - connective tissue with elastic fibre
(ii) Tunica Media
Smooth Muscle
External Elastic Lamina
(iii) Tunica Externa
Connective Tissue
Vaso vasorum - small blood supply to walls of arteries and veins
Relative thickness of these layers varies
Be able to describe the different functions of blood.
(i) Distribution
Gases
Metabolic Wastes
Hormones
(ii) Regulation
Body temperature
pH
Fluid Volume
(iii) Protection
Preventing blood loss
Fighting infection
Understand that blood is made up of both plasma and formed elements and know the components of each of these.
Viscous, opaque, liquid
~5.5 litres
~ 8% body weight
Liquid tissue so contains both cells and fluid components:
(i) Plasma
~3 litres liquid:
Water
Ions, proteins, nutrients, wastes, gases
(ii) Formed elements
~2.5 litres cells and cell fragments:
Erythrocytes
Leucocytes
Platelets
Haematocrit (or packed cell volume (PCV)):
% blood volume made up of red blood cells
45% males
42% females
Understand how vessel length, vessel radius and blood viscosity impact on blood flow and why.
Vessel length:
longer vessel - greater resistance
Vessel radius:
- because of laminar flow & cell - wall collisions: flow slower near vessel wall and faster near centre
- smaller vessel (vasoconstriction)- greater resistance - slower flow
- larger vessel (vasodilation)- less resistance - faster flow
- small changes in radius -> large change in flow
- vessels get smaller as they get further away from the heart
Viscosity:
- blood is 5 x more viscous than water
- caused by friction between: formed elements, proteins and liquid
- flow rate :
increase viscosity -> increase resistance -> decrease flow
decrease viscosity -> decrease resistance -> increase flow
- haematocrit affects viscosity:
increase erythrocytes -> increase haematocrit -> decrease flow
decrease plasma -> increase haematocrit -> decrease flow
how is haematocrit altered
(a) Erythropoietin (EPO)
Hormone secreted by kidney
In response to hypoxia
Stimulates erythrocyte production
(b) Recombinant EPO
Dramatically ↑ erythrocyte production
Improves athletic performance
↑ erythrocyte + ↓ plasma → ↑ haematocrit (Ht)
Stroke or heart failure
In 2003‐2004 ‐ 8 young elite cyclists died in 13 months
(c) Blood Doping
Collect own blood and store
Retranfuse when needed
2006 Tour De France ‘Operation Puerto’
(d) Polycythaemia vera
Red blood cell disease
Excessive red blood cells
Know who Jean Léonard Marie Poiseuille was, where and when he died as well as the equation that he is famous for.
French physician who died in 1869.
Equation allows calculation of flow rate (assuming laminar flow):
F = pressure gradient x (pie x radius cubed)/ (8 x viscosity x length of vessel)
Be familiar with the macroscopic structure of the heart, its chambers, valves and blood supply.
Chambers:
Atria Ventricles - left ventricle wall thicker than right
Valves:
Atrioventricular valves - left AV value (Bicuspid or Mitral) and right AV valve (Tricuspid)
Semilunar valves - pulmonary (towards lungs) & aorta
Understand the relationship between the two main heart sounds and the heart valves.
S1 - atrioventricular valves
S2 - semilunar valves
Be able to describe the microscopic features of cardiomyocytes and how these are connected to form a functional syncytium.
Involuntary
Autorhythmicity
Striated
Branched cells with single nucleus
Held together by intercalated discs (Desmosomes & Gap Junctions)
Sarcolemma
Sarcoplasm
Myofibrils
Forms functional syncytium
Understand the functional properties of the conducting‐system cells and how these are responsible for the initiation and spread of electrical activity in the heart.
Non‐contractile cells (few myofibrils)
Initiation & spread of electrical activity
Sinoatrial (SA) Node -> atria (contraction) ->
Atrioventricular (AV) Node ->
Bundle of His ->
Purkinje Fibres -> ventricles (contraction)
Be able to explain the ionic-basis of the action potential in atrial and ventricular cardiomyocytes.
Depolarising Phase:
Opening of Na+ channels
Na+ influx
Plateau Phase:
Closure of Na+ channels
Opening of L‐type Ca 2 + channels
Ca 2 + influx
Repolarising Phase:
Closure of L‐type Ca 2 + channels
Opening of K+ channels
Efflux of K+
N.B. Atrial & ventricular muscle fibres action potentials similar in shape
Know the features of cardiomyocyte action potentials.
Resting Membrane Potential (‐90 mV)
Depolarising Phase
Plateau Phase (0 mV)
Repolarising Phase
Know the features of pacemaker action potentials.
‘Resting’ Membrane Potential (‐60 mV)
Pacemaker Potential (slow depolarisation)
Depolarising Phase (0 mV)
Repolarising Phase
Be able to explain the ionic-basis of the pacemaker potential and action potential in pacemaker cells.
Pacemaker Potential:
Opening of F‐type channels
Net Na+ influx
Opening of T‐type Ca 2 + channels
Ca 2 + influx
Depolarising Phase:
Opening of L‐type Ca 2 + channels
Ca 2 + influx
Repolarising Phase:
Closure of L‐type Ca 2 + channels
Opening of K + channels
Efflux of K+
Understand why the basic rhythm of the heart is set by pacemaker cells in the sinoatrial node.
Pacemaker potential in SA Node is shortest:
SA Node = 100 beats/min (bpm)
AV Node = 50 bpm
Purkinje fibres = 30 bmp
Cardiac muscle fibres have an absolute refractory period:
250 ms long
Ion channel inactivation
Prevents ectopic excitation
Be able to explain how and why the sympathetic and parasympathetic divisions of the autonomic nervous system modify heart rate.
Parasympathetic Division:
Acetylcholine binds to muscarinic receptors
Responsible for ‘rest & digest’ behaviours
SA Node
Acetylcholine binds to muscarinic receptors
Increases duration of pacemaker potential
Decreases heart rate
Sympathetic Division: Noradrenaline binds to adrenergic receptors Responsible for ‘fight or flight’ behaviours Both spontaneously active Dual innervation of most organs Dynamically opposing effects Noradrenaline binds to β adrenergic receptors Decreases duration of pacemaker potential Increases heart rate Similar effect from adrenaline secreted by adrenal medulla At rest parasympathetic division predominates: Resting heart rate is ~70 bpm Block parasympathetic input (through vagus nerves) Heart rate increases to 100 bpm
Understand why conduction disorders affect heart rate and cardiac output.
Drugs or disease can result in abnormal rhythms.
E.G. AV conduction disorder: Affects transmission through AV Node Ventricles initiate their own rhythm (slow) Atria and ventricles contract asynchronously
Abnormal rhythms can be treated with artificial pacemaker
Be able to describe what an electrocardiogram is and the role that Willem Einthoven played in its history.
Electrical activity of heart recorded by electrodes in body surface
Synchronous activity
Conducting medium
Sum of all action potentials occurring in heart
Potential Difference (P.D.)
Electrodes are referred to as leads
Placed on chest wall or limbs
Willem Einthoven
Nobel Prize for Medicine – 1924
Standard leads are placed on wrists and left leg
Know what Einthoven’s triangle is and the different perspective provided by leads 1-3.
Lead I P.D. from RA to LA
Lead II: P.D. from RA to LL
Lead III: P.D. from LA to LL
Provides different views of heart
Understand how the electrocardiogram differs from normal in patients with an AV conduction disorder and long QT syndrome and the clinical consequences of these pathologies.
Idealised ECG
Waves separated by segments
P wave ‐ atrial depolarisation
QRS complex ‐ ventricular depolarisation.
T wave – ventricular repolarisation
Clinically useful
Routine monitoring of heart rate
Detection of alterations in electrical signalling:
AV Conduction Disorder:
Action potential delayed or blocked in AV node
Long QT Syndrome (LQTS)
Congenital disorder
Mutation of K+ channels
Delayed repolarisation
Fainting, cardiac arrest, sudden death
Understand what is meant by sinus arrhythmia, how it appears in an electrocardiogram and what causes it.
When there is irregularity in the sinus rate in which the variation in the R-R interval is greater than 0.12 secs
Know what is meant by excitation‐contraction coupling in cardiomyocytes and be able to describe the molecular processes responsible.
Contraction:
Action Potential in T-tubule -> L-type Ca 2+ channels open, Ca 2+ influx -> opens ryanodine receptor -> large Ca 2+ release from SR -> Ca 2+ triggers shortening of myofibrils
Relaxation:
Ca 2+ pumped back into sarcoplasmic reticulum + Ca 2+ pumped out of fibre -> decrease in sarcoplasm (Ca 2+) -> lengthening of myofibrils
Know the six variables that are typically used to describe the changes in the heart that take place in the cardiac cycle.
Be able to describe the four major stages of a single cardiac cycle and the key steps involved in each.
Systole:
Ventricles relaxed & pressure low
a) Iosvolumetric Ventricular Contraction
Initiated by depolarisation of ventricle (–> QRS wave) -> contraction of ventricles -> closure of AV valve (1st heart sound) -> increase ventricular pressure (no change in volume)
b) ventricular ejection
ventricular pressure > aortic pressure -> aortic valve opens -> blood ejected (stroke volume) -> aortic pressure increase -> ventricular volume decrease -> ventricular relaxation (–> T wave) -> ventricular pressure decrease
Diastole:
a) isovolumetric ventricular relaxation
Ventricular pressure decreases -> aortic valve closes (–> 2nd heart sound) -> no changes in volume
b) Ventricular filling
Artial pressure > ventricular pressure -> Av valve opens -> blood flows into ventricle -> increase ventricular volume (80%) -> artial systole (–> P wave) -> completes ventricular filling (20%)
Understand what stroke volume is and the three factors that can modify its magnitude.
Stroke volume is volume of blood ejected from ventricle during each contraction
Controlled by three factors:
- End-Diastolic Volume
- Sympathetic Nervous System
- Afterload
- End-Diastolic Volume
Volume of blood in ventricle after filling is complete
The greater EDV the greater the stroke volume
Otto Frank & Ernest Starling
Frank‐Starling Law of the Heart
Mechanism:
increase venous return -> increase end-diastolic volume -> stretches myofibrils -> increase force of contraction -> increase stroke volume
- Sympathetic nervous system
Sympathetic neurones innervate ventricles
Noradrenaline increases force of cardiac muscle fibre contraction
Mechanism:
Noradrenaline -> B adrenergic receptors -> increase Ca 2+ release or increase Ca 2+ influx -> increase sarcoplasmic Ca 2+ -> increase force of contraction -> increase stroke volume
- Afterload
Heart has to move blood against arterial pressure
If ↑ arterial pressure then ↓ stroke volume
Usually only a consideration in chronic hypertension
Know what venous return is, why it is important and the factors that can modify it.
Venous return = volume of blood entering right atrium/min
Venous pressure low
venules = 18 mmHg
right atrium = 2 mmHg
Little resistance to flow
Very compliant
↑ volume with littlechange in pressure
Veins can ‘store’ large volumes of blood
Venous return affected by a number of variables:
(i) Muscular Pump and Valves
Contraction of skeletal muscle compresses vein
Pumps blood towards heart
Valves prevent backflow
Significantly increases venous return
(ii) Respiratory Pump
Heart located in thoracic cavity
During inspiration ‐ intrapleural pressure ↓
Decreases pressure in atria
Increases pressure gradient
Increases venous return
(iii) Sympathetic Tone
Smooth muscle of veins innervated by sympathetic neurones
Noradrenaline binds to α receptors
Venous constriction
Returns blood to heart
Increases venous return
Be able to define cardiac output, be able to calculate it and understand how it can change with exercise.
Volume of blood pumped by each ventricle in a minute:
Cardiac Output (CO) = Heart Rate x Stroke Volume
CO = 72 bpm x 70 ml
CO = 5040 ml/min (~ 5 litres/min)
Exercise: ↑ by 4‐5 times (20 – 25 litres/min)
Athlete: ↑ by 7 times (35 litres/min).
Understand how cardiac output can be modified by changes in heart rate, stroke volume, hormones and drugs.
(i) Changes in Heart Rate:
Referred to as chronotropic effects
ii) Changes in Stroke Volume:
Referred to as inotropic effects
(iii) Hormones:
(a) Adrenaline
↑ Heart rate
↑ Stroke volume
(b) Thyroxine
↑ Heart rate
↑ Stroke volume
(c) Glucagon
↑ Stroke volume
(iv) Drugs:
(a) Ivabradine
Acts on F‐type channels
Prolongs pacemaker potential
↓ heart rate
(b) Sympathomimetics
β adrenergic receptor agonists
↑ heart rate
↑ stroke volume
(c) Beta‐blockers
β adrenergic receptor antagonists
Reduce sympathetic tone
↓ heart rate
↓ stroke volume
Be familiar with the terms systolic pressure, diastolic pressure, pulse pressure and mean arterial pressure.
Systolic pressure (~120 mmHg)
Diastolic pressure (~80 mmHg) – maintained by elastic arteries
Pulse Pressure = systolic pressure ‐ diastolic pressure
Mean Arterial Blood Pressure = diastolic pressure + ⅓ of pulse pressure
Be able to demonstrate how to record systolic and diastolic pressure and calculate pulse pressure and mean arterial pressure.
Know what the Korotkoff sounds are and be able to explain what causes them.
Know what the Harvard step test is and how to administer one.
Understand the effects of exercise on heart rate, blood pressure and cardiac output.
Understand how blood volume, cardiac output, diameter of veins and the diameter of arterioles all modify blood pressure.
Blood volume:
increase in volume leads to an increase in pressure
Cardiac output:
An increase in cardiac output leads to an increase in blood pressure
Diameter of veins:
determines resistance of the system to blood flow
Diameter of arterioles:
When arterioles constrict, the resistance to blood flow increases, leading to an increase in blood pressure. Conversely, when arterioles dilate, resistance decreases, leading to a decrease in blood pressure.
Be able to describe how intrinsic and extrinsic controls modify blood flow through arterioles.
(a) Intrinsic (Local) Controls
Self‐regulation of arteriole resistance to control blood flow
Independent of neural or hormonal input
Ensure adequate blood supply to tissues
Metabolically active tissues
↓
Local vasodilation
↓
↓ arteriole resistance –> ↑ local blood flow
(b) Extrinsic Controls
Sympathetic division of autonomic nervous system:
noradrenaline
α adrenergic receptors
↑ sympathetic tone – vasoconstriction
↓ sympathetic tone – vasodilation
Changes regional (rather than local) blood flow
Example: During exercise:
↑ blood flow to skeletal muscles
↓ blood flow to digestive tract
Reinforced by adrenaline from adrenal medulla.
Be able to explain what orthostatic hypotension is and how the cardiovascular control systems react to restore normal blood pressure.
Orthostatic hypotension is a condition in which your blood pressure suddenly drops when you stand up from a seated or lying position.
Rapid & short term control
Ensure enough pressure to generate adequate blood flow
Especially to the brain and heart
Two important elements:
(i) Arterial Baroreceptors
Stretch sensitive nerve‐endings
Carotid arteries
Aortic Arch
Spontaneously active
Detect changes in blood pressure:
↑ BP ↑ actin potentials
↓ BP ↓ action potentials
Relay this information to brainstem.
(ii) Medullary Cardiovascular Control Center
Located in medulla oblongata
Collects information from arterial baroreceptors
Determines appropriate response
Alters sympathetic and parasympathetic tone:
Heart Arterioles
Veins
Be able to describe what capillary exchange is and the mechanisms that enable it.
Movement of materials between blood and tissues
Capillaries well adapted for function:
Endothelium
Small diameter
Slow blood flow
High density:
50,000 miles of capillaries
Most cells with 0.1 mm of capillary
Massive surface area 6300 m2
Intercellular spaces
Three mechanisms:
(i) Diffusion
Movement down concentration gradient
Across plasma membrane
Lipid‐soluble materials by simple diffusion
Others by facilitated diffusion
Gases, nutrients & metabolic end products
(ii) Transcytosis
Endocytosis into cell
Exocytosis out of cell
Non‐lipid soluble macromolecules
(iii) Bulk Flow
Mass movement of water and small solutes through intercellular spaces
Driven by hydrostatic pressure (pushing fluid out of capillary)
Opposed by osmotic (oncotic) pressure (sucking fluid back into capillary)
Referred to as Starling’s Forces:
Know what net filtration pressure is and how to calculate it.
NFP = difference between the hydrostatic and the oncotic pressure gradients:
NFP = (HPc -HPi) - (OPc -OPi)
Understand the mechanisms responsible for the development of oedema following a soft tissue injury.
soft tissue injury -> plasma proteins in interstitial space -> increase interstitial fluid oncotic pressure -> increase filtratin & decrease reabsorption -> oedema
If cardiac output is 18 L/min, and heart rate is 150 beats per minute, what will the stroke volume be?
120mL
18000mL/150
Frank-Starling’s law states which of the following?
stroke volume is proportional to end-diastolic volume
stroke volume is inversely proportional to resistance
blood flow is proportional to pressure differences
stroke volume is proportional to cross-sectional area
stroke volume is inversely proportional to pressure
stroke volume is proportional to end-diastolic volume
Venous return to the heart is assisted by which of the following?
low resistance of veins
low pressure in the right atrium
valves in veins
the skeletal muscle pump
all
The T wave of an electrocardiogram is associated with which of the following electrical events?
ventricular repolarisation
During the early phase of systole, which of the following events occur?
Ventricular pressure rises.
Ventricular volume decreases.
The ventricles contract.
Ventricular pressure rises.
The ventricles contract.
