Physiology Flashcards
intrinsic control of SV
changes brought about by changes in diastolic length/ diastolic stretch of myocardial fibres
EDV
volume of blood within each ventricle at the end of diastole
determines the cardiac preload
cardiac afterload
the resistance into which the heart is pumping
increase in afterload
at first: heart unable to eject full SV, so SV decreases > increase in EDV > force of contraction increase
eventually causing ventricular hypertrophy
hormones that regulate extracellular fluid volume
the renin-angiotensin aldosterone system
natriuetic peptides
antidiuretic hormones
rate liming step for RAAS
Renin secretion
RAAS regulated by mechanisms which stimulates renin release from juxtaglomerular apparatus in kidneys
Juxtaglomerular apparatus
region comprising of the macula densa, extraglomerylar mesangial cells and granular cells
Natriuretic peptides
peptide hormones synthesised by the heart and released in response to cardiac distension or stimuli
NPs function
Cause excretion of salt and water in kidneys > reducing blood volume and BP
decrease renin release =
decrease BP
two types of NPs released by the heart
atrial peptide
brain-type natriuretic peptide
shock
an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation
causes of shock
loss of blood
sudden severe impairment of heart function
physical obstruction to circulation
excessive vasodilation and abnormal distribution of blood flow
4 types of shock
hypovolaemic shock
cardiogenic shock
obstructive shock
distributive shock
hypovolaemic shock
caused by loss of blood volume
haemorrhagic or non-haemorrhagic
cardiogenic shock
caused by sudden severe impairment of cardiac function
obstructive shock
caused by physical obstruction to circulation either in or out the heart
- PE, pneumothorax
Distributive shock
caused by excessive vasodilation and abnormal distribution of blood flow
neurogenic or vasoactive
Systemic vascular resistance
sum of resistance of all vasculature in the systemic circulation
Resistance to blood flow
characteristics of blood, length of blood vessel, radius of blood vessel (inversely proportional to the power of 4)
nerve control of vascular smooth muscle
sympathetic nerves
noradrenaline acting on alpha receptors
- constrict
Vasomotor tone
means the vascular smooth muscle is partially constricted at rest
caused by tonic discharge of sympathetic nerves > continuous release of noradrenaline
Main hormone control of vascular smooth muscle
Adrenaline from the medulla
- acting on alpha (skin, gut, kidney arterioles) receptors causes vasoconstriction
- acting on beta2 (cardiac and skeletal) receptors causes vasodilatation
other hormones involved in control of vascular smooth muscle
angiotensin II- causes vasoconstriction
antidiuretic hormone- causes vasoconstriction
intrinsic control of vascular smooth muscles
match the blood flow of different tissues to their metabolic needs
can over-ride extrinsic controls
chemical and physical factors
chemical local metabolite factors causing relaxation of arteriolar smooth muscle
decreased PO2
increased PCO2
examples of chemical local humoral agents that cause vasodilation
histamine
bradykinin
NO
Nitric oxide
continuously produced by vascular endothelium from amino acid L-arginine through enzymatic action of nitric oxide synthase
potent vasodilator
examples of chemical local humoral agents that cause vasoconstriction
serotinin
thromboxane A2
leukotrienes
endothelin- potent vasoconstrictor, released from endothelial cells
factors influencing venous return
increased venomotor tone
increased blood volume
increased “skeletal muscle pump”
increased “respiratory pump”
Venomotor tone
increased venomotor tone increases venous return
what is an ECG
recording of potential changes, detected by electrodes that allow the electrical activity of the heart to be monitored
12 leads of the ECG
3 standard limb leadds
3 augmented voltage leads
6 chest leads- horizontal
Lead II
sees the heart from inferior view
PR interval
time for the SA node impulses to reach the ventricles
Leads I and aVL
lateral leads
views the heart from the left
Leads II, III, and aVF
inferior leads
V1 and V2
coming from right
look at interventricular septum
V3 and V4
lateral aspect
3 types of syncope
reflex syncope
orthostatic hypotension
cardiac syncope
physiological role of troponin I
binds to actin to hold the troponin-tropomyosin complex in place
