CVS

Question 1

Why is CV research important

Answer 1

The ageing population:
Baby boomers make up a large proportion of the population and are heading into the age where CVD mortality risk increases

Question 2

What are some recent trends in CVD

Answer 2

Acute coronary events have been declining due to treating risk factors. However, there has been an increase in heart failure (preventative measures?)

Question 3

What are the 2 main functions of the CVS

Answer 3

Function as a distribution system (nutrients/water/gases, hormones, immune, waste, heat)
Maintain homeostasis

Question 4

Name all the heart valves and where they are located

Answer 4

Tricuspid valve - right AV
Bicuspid valve - left AV
Aortic semilunar - left V to Aorta
Pulmonary semilunar - right V to Pulmonary arteries

Question 5

What are the functions of the AV and semilunar valves

Answer 5

AV - Prevent back flow into the atria during ventricular contraction
Semilunar - Prevent back flow into the ventricle during ventricular relaxation

Question 6

Features of myocardial muscle cells

Answer 6

Branched, single nuclei, connected by specialised junctions called intercalated disks

Question 7

Features of intercalated disks

Answer 7

Contain desmosomes which transfer force from cell to cell. Contain gap junctions which allow electrical signals to pass rapidly from cell to cell

Question 8

2 types of cardiac cells and their differences

Answer 8

Contractile cells - striated fibres organised into sarcomeres
Auto-rhythmic (pacemaker) cells - Signal for contraction, smaller and fewer contraction fibres, not organised into sarcomeres

Question 9

Discuss the major events in the cardiac contractile cycle as it relates to left ventricular and aortic pressures, and valve sounds

Answer 9

1 - Ventricular diastole (fast and slow filling) causes pressure to drop close to 0mmHg
2 - AV valves close (HS 1) when ventricular pressure exceeds atrial pressure, and a ventricular isometric contraction causes ventricular pressure to rapidly rise
3a - Aortic semilunar valve opens when ventricular pressure exceeds aortic blood pressure. This causes rapid ejection of blood into the aorta, increasing pressure.
3b - Ejection of blood slows as ventricular capacity is depleted, causing pressure to flatten.
4 - Isometric relaxation of the left ventricle causes pressure to drop rapidly. When ventricular pressure falls below aortic pressure, the aortic semilunar valves close (HS 2), preventing a drop in aortic blood pressure.
5 - As left ventricular pressure falls below left aortic pressure, AV valves open and the ventricle begins filling with blood again.

Question 10

Discuss blood volume and pressure changes throughout the CVS

Answer 10

Blood flows down a pressure gradient. Pressure is greatest in the aorta and drops in an S-shaped manner until it is lowest in the vena cava. Distribution of blood volume is inversely proportional to this - least blood volume in the systemic arteries while most blood volume in the systemic veins.

Question 11

What is flow rate?

Answer 11

The volume of blood that passes a given point per unit of time (mL/min)

Question 12

Vasoconstriction vs vasodilation?

Answer 12

Vasoconstriction is a decrease in blood vessel diameter which decreases blood flow.
Vasodilation is an increase in blood vessel diameter which increases blood flow.
Flow though a tube is inversely proportional to resistance

Question 13

Flow =

Answer 13

change in pressure/resistance (R)

Question 14

Total blood volume

Answer 14

~5L

Question 15

What is diastole and systole?

Answer 15

Diastole is cardiac muscle relaxation

Systole is cardiac muscle contraction

Question 16

What is auscultation?

Answer 16

Listening to the heart through the chest wall using a stethoscope

Question 17

What is the major parameter controlled by the CVS?

Answer 17

Systemic mean arterial pressure

Question 18

What happens when BP is too high or low?

Answer 18

Too high = hypertension (can lead to organ damage)

Too low = shock

Question 19

What feedback loops act to regulate MAP?

Answer 19

Short term via neural pathways

Long term via the vasculature and kidneys

Question 20

Formula for MAP?

Answer 20

MAP = CO (SV x HR) x TPR

Question 21

Formula for SV?

Answer 21

SV = EDV - ESV

Question 22

Average SV and CO

Answer 22

CO = 5L/min
SV = 70mL

Question 23

What are some challenges to BP regulation?

Answer 23

Posture (lying to standing)
Dehydration
Haemorrhage
Surgery, wounds, burns
Exercise
Abnormal hormonal regulation

Question 24

What are baroreceptors and how do they work?

Answer 24

Mechanical receptors in the carotid sinus and aortic arch which detect changes in BP

Increased firing triggers efferent pathways to decrease SNS and increase PSNS activity (decreases HR and hence BP). Few blood vessels innervated

Decreased firing triggers efferent pathways to increase SNS and decrease PSNS activity. Increases HR, contractile strength and hence BP. Also has impact on arterioles (vasoconstriction increases TPR) and veins (vasoconstriction increases venous return and hence SV, CO and BP)

Question 25

Describe the effects of long-term regulation on the CVS

Answer 25

Regulation of ECF volume major pathway for long term regulation of MAP. ECF volume impacted by changes in input and output. Kidneys predominant organ

Question 26

Describe the response to decreased MAP in order of increasing severity

Answer 26

``` Arterial baroreceptor reflex Autonomic response Renin-angiotensin system Aldosterone release Vasopressin release Increased erythropoietin release ```

Question 27

What is the Frank-Starling law?

Answer 27

Increased venous return stretches the ventricle and makes the next contraction stronger (i.e. the more blood that comes back to the heart [increasing EDV] the more blood the heart will eject)

Question 28

What impacts venous return?

Answer 28

Skeletal muscle pump Respiratory pump - inhalation increases blood flow into thoracic veins; exhalation increases blood flow into the heart and abdominal veins Sympathetic innervation of veins (vasoconstriction)

Question 29

What is inotropy?

Answer 29

Inotropes are chemicals which increase contractility and hence increase SV (e.g. epinepherine, norepinepherine, digitalis)

Question 30

What is lusitropy?

Answer 30

Lusitropes are chemicals which decrease contractility and hence decrease SV

Question 31

Describe the factors which integrate to control CO

Answer 31

CO is a function of HR and SV HR determined by depolarisation in auto-rhythmic cells. Decreases due to parasympathetic innervation. Increases die to sympathetic innervation and epinephrine SV is determined by force of contraction in ventricular myocardium. This force is influenced by contractility (sympathetic innervation and epinephrine increases this) and end-diastolic volume. EDV varies with venous return influences by the skeletal muscle pump, respiratory pump and venous constriction.

Question 32

How does the action potential of the auto-rhythmic cells differ to that in normal contractile cells?

Answer 32

In auto-rhythmic cells slow inward depolarising Na+ currents ("funny" currents) lead to spontaneous depolarisation (no stimulus required) Provides stimulus for contractile cells to depolarise

Question 33

How does the action potential spread throughout the conduction system? Why is this important for optimal filling/ejection from the heart?

Answer 33

1. Action potential originates at SA node in auto-rhythmic cells 2. AP spreads throughout right and left atria 3. AP can only pass from atria into ventricles via AV node, after a brief delay (due to slower conduction signals through node) a. Allows atrial contraction to complete ventricular filling before ventricular contraction begins 4. AP travels rapidly down interventricular septum via Bundle of His (AV bundle), left and right bundle branches, then rapidly throughout the myocardium through Purkinje fibres a. Ventricle begins contracting from base upward 5. Remainder of ventricular cells activated by APs moving through gap junctions Important for optimal filling so the heart contracts from the base upwards, allowing all blood to be ejected from the ventricles during systole

Question 34

If the SA node is not functioning normally, how does the heart respond?

Answer 34

Atrioventricular (AV) node (50bpm) and Purkinje fibres (25-45bpm) can act as pacemakers under some conditions SA node = 70bpm

Question 35

Sympathetic and parasympathetic effect on auto-rhythmic depolarisation?

Answer 35

Parasympathetic = hyperpolarizes the membrane potential and slows depolarisation, slowing HR Sympathetic & epinephrine = depolarises the membrane potential & speeds up pacemaker potential (funny current), increasing HR

Question 36

Steps in cardiac contractile cell action potential

Answer 36

0. Na+ channels open 1. Na+ channels close 2. Ca2+ channels open; fadt 3. K+ channels close Ca2+ channels close; slow K+ channels open 4. Resting potential Plateau results from decreased K+ and increased Ca2+ (required for contraction). Plateau ends when flux is reversed

Question 37

What is the difference between an action potential and an ECG?

Answer 37

Action potential = change in membrane potential ECG = average electrical changes across two electrodes. PQRST waves allow us to monitor rate rhythm, intervals, pathology

Question 38

Events caused by P wave, QRS complex and T wave

Answer 38

P = depolarisation of the atria P-R segment = conduction through AV node and AV bundle (pause that occurs which allows AV node to block conduction, allowing atria to empty into ventricle) QRS complex = wave of ventricular depolarisation T = repolarisation of the ventricle Atrial repolarisation part of the QRS (lost in larger wave)

Question 39

Conclusions from EMG?

Answer 39

HR = time between 2 P waves or 2 Q waves Rhythm = regular pattern Wave analysis = presence and shape Segment length constant

Question 40

Describe the excitation-contraction coupling process

Answer 40

1. Action potential starts with the heart pacemaker cells 2. Voltage-gated L-type Ca2+ channels in the cell membrane open and Ca2+ enters the cell 3. Ca2+ induces Ca2+ release through ryanodine receptors which open in the sarcoplasmic reticulum (SR) 4. Calcium binds to troponin to initiate contraction via crossbridge cycle (as in skeletal muscle) 5. Relaxation occurs when Ca2+ unbinds from troponin 6. Calcium is removed from cytoplasm back into the SR for storage with Ca2+ ATPase, or out of the cell through the Na+-Ca2+ exchanger (NC) 7. Na+ gradient is maintained by the Na-K-ATPase

Question 41

What factors impact force of contraction

Answer 41

Force generated is proportional to number of active cross-bridges. This is determined by how much calcium is bound to troponin Sarcomere length impacts force of contraction (filling the heart more increases force - Frank Starling Law)