Cardiovascular system Flashcards
Explain the path of blood flow through the heart - the cardiac cycle
- Superior and inferior vena cava
- Right Atrium
- Tricuspid Valve
- Right Ventricle
- Pulmonary semilunar valve
- Pulmonary arteries
- Lungs
- Pulmonary veins (L+R)
- Left atrium
- Bicuspid valve
- Left ventricle
- Aortic semilunar valve
- Aorta
- Body: arteries -> capillaries -> veins
Electrical conduction pathway of the heart (6)
- Sinoatrial node
- internodal pathways
- AV node
- AV bundle of His
- bundle branches (R+L)
- perkinje fibres (R+L)
P-wave
atrial depolarisation (atrial repolarisation obscured by QRS complex)
PR interval (PQ)
time delay between atrial depolarisation and conduction through AV node for ventricular activation (0.12-0.2s)
QRS complex
ventricular depolarisation (0.06-0.1 sec)
ST segment
electrical plateau of ventricular activation
T Wave
ventricular repolarisation
Normal HR - how to find HR on ECG
60-100bpm
- number of QRS complexes in a 6 second strip x 10
Stroke Volume (SV) - definition and normal values, formula
amount of blood pumped out of each ventricle during a single beat
○ ~ 70-80ml @ rest
○ EDV - ESV = SV
Heart rate (HR) - definition and normal values, bradycardia, tachycardia
number of times the heart beats (per minute)
○ 60-100 bpm
○ Bradycardia = <60 bpm
○ Tachycardia = >100 bpm
Cardiac Output (CO) - definition and formula
the amount of blood pumped by each ventricle in 1 minute
○ CO (ml/min) = SV (ml/beat) x HR (beat/min)
The difference between resting and maximal CO is cardiac reserve
End Diastolic volume (EDV) - definition and normal value
amount of blood in each ventricle at the end of ventricular diastole (the beginning of ventricular systole)
~ 120ml @ rest
End Systolic Volume (ESV) - definition and normal value
amount of blood remaining in each ventricle at the end of ventricular systole (start of ventricular diastole)
○ ~ 50 ml @ rest
Ejection Fraction (EF) - definition and normal value
percentage of EDV ejected represented by SV i.e. SV/EDV (x100 to get %)
○ ~ 55-70%
○ Varies with changing demand
○ Represents the efficiency of the heart. A diseased heart will have a reduced EF
Preload - definition, how it affects CO
end-diastolic volume/pressure = stretch placed on myocardial fibres just before contraction
○ Greater the end-diastolic volume, the more ventricular muscle fibres are stretched (Frank Starling mechanism)
Affects CO:
- Preload too low => amount of blood available to pump out is decreased => SV decreased -> CO decreased
- Preload too high and ventricles stretched out => reduced SV -> reduced CO
Afterload - definition, how it affects CO
resistance to ventricular contraction
Affects CO:
- Increased Afterload => increased demands of the heart
Blood Pressure (BP) - definition, SBP, DBP definition, normal BP, hypertension, folrmula
Pressure the blood exerts against the inner wall of the blood vessels
○ Systolic BP (SBP) - ‘high’ pressure in arterial system
○ Diastolic BP (DBP) - ‘low’ pressure in arterial system
○ Normal arterial BP = 120/80
○ Hypertension = >140/90
○ BP = CO x TPR
Pulse pressure
Pulse Pressure = SBP - DBP
Mean arterial pressure (MAP)
- DBP +1/3 pulse pressure
- Average driving pressure propelling blood from LV to RA
What are the (2) determinants of blood flow rate? How do they affect blood flow?
- Driving pressure - Flow is directly proportional to gradient pressure; blood flow increases when pressure increases and vice versa
- Vascular resistance - Flow is inversely proportional to resistance; as resistance increases, blood flow decreases
What are the determinants of vascular resistance? How do they affect resistance?
- Length of blood vessels - longer blood vessel = more resistance
- Radius/diameter of the blood vessels (physiological) - smaller radius/diameter = more resistance
- viscosity of blood - thicker blood = harder to pump -> increases vascular resistance
What causes BP changes (3)?
Occur in response to:
- baroreceptors and chemoreceptors in the arteries (short term regulation )
- renin-angiotensin system (long term regulation)
- the kidneys (long term regulation)
What are the short term regulators of BP?
define short term and list methods (sensor, control, effectors)
short term = regulation of minute to minute changes in arterial pressure due to e.g. postural changes or manoeuvres
methods:
- sensors: aortic and carotid baroreceptors via vagus and GP nerves. Sense change -> alert cardiac control centre
- control: cardiovascular control centre in the medulla oblongata regulates CV activity through nervous and endocrine systems
- vasomotor centre = changes arterial diameter of;
- skeletal muscle arterioles -> vasodilation
- visceral arterioles -> vasoconstriction
- cardio-accelerator centre = increased HR and contractility
- cardio-inhibitor centre = decreased HR and contractility - effectors: sympathetic nerves to heart and blood vessels, vagus nerve, vasomotor nerves
- endocrine influence: threat/stress -> sympathetic NS stimulation -> adrenaline & noradrenaline -> increased BP and HR
What are the long term regulators of BP?
define long term and list methods
Long term = regulating overall arterial bp over time, involving endocrine and renal systems
Controls: (low bp) -> Renin-angiotensin-aldosterone system -> increased total circulating blood volume -> increased BP
Controls of CO
- heart rate
- stroke volume
How does HR affect CO
- sympathetic activity: increases HR, conduction velocity and ventricular contractility -> increase CO
- parasympathetic activity: depresses the SA node -> decreases HR and impedes conduction velocity -> decreased CO
- reflexes: acute changes in BP sensed by stretch receptors in carotid and aortic arch result in an inverse change in HR i.e. increased BP = decrease in HR
What determines Stroke Volume?
- preload 2. afterload 3. contractility
EDV reduced -> SV reduced -> CO reduced
How does SV affect CO?
increased SV = increased CO
decreased SV = decreased CO
How does increased myocardial contractility affect CO? What causes contractility to increase?
increased contractility -> increased EF -> increased SV -> increased CO
Increased contractility caused by:
- circulating adrenaline
- sympathetic stimulation
(3) transport methods of substances into and out of the capillaries
- diffusion
- transcytosis (transport from one side of a cell to the other within a membrane-bounded carrier)
- bulk flow (passive movement from high to low pressure)
What is filtration? what pressures promote it?
Pressure-driven movement of fluid and solutes from blood capillaries
promoted by:
- blood hydrostatic pressure
- interstitial fluid osmotic pressure
What is reabsorption? what pressures promote it?
pressure-driven movement of fluid from interstitial fluid into blood capillaries
promoted by:
- interstitial fluid hydrostatic pressure
- blood colloid osmotic pressure
What is the net result of capillary exchange?
filtration > reabsorption
What is net filtration?
the balance between the fluid pressure. It determines whether blood volume and interstitial fluid remain steady or change
What is oedema? why does it occur?
oedema = abnormal increase in interstitial fluid volume
occurs when filtration greatly exceeds reabsorption
excess filtration:
- increased capillary BP
- increased permeability of capillaries
inadequate reabsorption:
- decreased concentration of plasma protein
When do the AV valves open? phase, cause, function, how
In diastole (relaxation)
- open when ventral pressure is lower than atrial pressure
- allows blood flow from atria into ventricles
- occurs when ventricles are relaxed, chordae tendinae are slack and papillary muscles are relaxed
When do the AV valves close? phase, cause, function, how
in systole (contraction)
- close when ventricles contract (‘Lub’)
- prevents backflow of blood into atria
- ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taught and papillary muscles contract to pull cords and prevent cusps from everting
When do the semilunar valves open? phase, cause, function
open with ventricular contraction
in systole
allow blood flow into pulmonary trunk and aorta
When do the semilunar valves close? phase, cause, function
close with ventricular relaxation (‘Dub’)
in diastole
prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the valves
