L8 - Cardiovascular Physiology II Flashcards
describe the autonomic nervous system control over heart rate
- parasympathetic NZ (acetylcholine, ACh) activated muscarinic receptors in the heart
- a) Sympathetic NS (norepinephrine, NE) activates adrenergic receptors in the heart. b) Adrenal medulla -> epinephrine (Eli, hormone) activates adrenergic receptors in the heart
- sympathetic uses both neurotransmitter and hormone
describe how the heart rate is controlled by the PSNS and the SNS
Chronotopic event -> effect on heart rate
Dromotopic event -> effect on conduction velocity
Increase HR:
- increased plasma epinephrine
- increased activity of sympathetic nerves of heart
- decreased activity of parasympathetic nerves to heart
- SA node: increase HR
Decrease HR:
- PSNS (ACh release)
- lowers membrane potential (K+ channel activity increases - which causes hyper polarisation)
- reduces slope of pre potential (funny Na+ channel decrease)
- delays reach of the threshold potential (takes longer to overcome the change)
- reduces heart rate
describe the preload (Frank-Starling) mechanism and contractility of the heart
Increase in venous return, preload or end diastolic volume (EDV)
-> frank-starling mechanism
Stretch of cardiomyocytes causes more optimal actin myosin overlap
Cardiac muscle do not stretch beyond optimal length (Lo) in contrast to skeletal muscle
- so increase filling = more contracting since more length to contract with
Increase in sympathetic activation causes increase in contractility (at any given EDV)
Effects on strength of contraction -> inotropic -> increase in intracellular Ca2+
- and filling is the same but more sympathetic activation results in heart contracting more strongly
describe after load - resistance to output
- aortic valves are closed, isovolumetric contraction (11)
- when LV pressure reached aortic pressure (14) valves open, blood is ejected into the aorta - SV (stroke volume)
- however, if aortic pressure is higher (green line), then LV will have to generate more contraction to open the valves, which also will take longer, so less blood will be ejected - lower SV
Afterload = aortic pressure (-> resistance to the LV output)
More afterload, more resistance, less SV -> reduced cardiac function
describe how control of the heart is integrated (could draw diagram)
- all discussed processes (sympathetic/parasympathetic control, preload, contractility, after loaf) can occur at the same time influencing cardiac output (HR x SV)
describe the vessels - structure and function
structure determines function (anatomy determines physiology)
function defines structure (physiology defines anatomy)
Large vein:
- few layers of smooth muscle and connective tissue
- few elastic layers
- endothelium
- wide lumen
Large artery:
- many layer of smooth muscle and connective tissue
- several elastic layers
- endothelium
- lumen
Venule:
- connective tissue, endothelium, lumen
Arteriole:
- smooth muscle cells, endothelium, lumen
Capillary:
- endothelial cells, lumen
describe vessel physiology
- blood flow distribution fo specific organ
- all vessels together (mostly arterioles) - provide the total peripheral resistance
Regulation of blood flow:
- Vasodilation: smooth muscle cells relax, vessel radius increases, resistance drops
- Vasoconstriction: smooth muscle cells contracts, vessel radius decreases, resistance rises
Heart -> arteries -> arterioles -> capillaries -> venues -> venes -> heart
- get oscillation of bp due to the contracting and relaxing of the heart, effect decreases the further from the heart you get
describe the control of the arterioles
- local control - intrinsic tone - autocrine
- vasoconstrictors: internal BP (myogenic response)
- vasodilators: decreased oxygen, K+, CO2, H+, osmolarity
a) active hyperemia (regulation of resistance to local metabolic demand - well developed in skeletal muscle, heart, glands)
b) flow auto regulation (regulation of resistance to maintain constant local flow, myogenic responses) - extrinsic control - reflex, nerves, hormones
Neural controls:
- vasoconstrictors: sympathetic nerves that release NE
- vasodilators: neurons that release nitric oxide (NO)
Hormonal controls:
- vasoconstrictors: epinephrine, angiotensin II, vasopressin
- vasodilators: epinephrine, atrial natriuretic, peptide
a) control for whole-body needs (not control for local metabolic demand)
how do capillaries facilitate exchange?
- high CSA, low constant flow
- fast delivery through larger arteries, with slow exchange in capillaries
Modes of exchange: (of O2, CO2 and glucose)
- diffusion (majority, gradient driven)
- vesicle transport (end-/exocytosis)
- bulk flow (pressure gradients)
describe angiogenesis in dental practice
Angiogenesis: formation of new blood vessel from pre-existing capillaries - oxygen and nutrient dependent
- growth factors (VEGF), cytosines, transcription factors, adhesion molecules, matrix metalloproteinases
Angiogenic therapies:
- antiangiogenic angainst malignancies (cancer)
Wound healing:
- proangiogenic to repair cardiovascular diseases (stroke, infarct)
Human dental pulp is highly vascularised with high regenerative capacity
The regenerative endodontic concept:
- use stem cells, biochemical factors, and engineering materials to replace lost or impaired biological tissues for dental pulp regeneration
describe the veins and venules (CO improving techniques, veins in general, path of how SV can be increased)
Cardiac output improves via:
1. systemic venous constriction
2. skeletal muscle pump
3. respiratory pump
4. increase in blood volume
High blood store capacitance
Low pressure differences but enough to maintain blood flow
Very low venous resistance
to increase SV:
- those for CO improvement mechanism
- increase venous pressure
- increase venous return
- increase atrial pressure
- increase end-diastolic ventricular volume
- increase stroke volume
how is blood pressure regulated short term (two ways)
- baro-reflex
- increased arterial pressure
- arterial baroreceptors (aortic arch and carotid sinus) increase firing
reflex via medullary cardiovascular centre
- decrease sympathetic outflow to heart, arterioles, veins
- increase parasympathetic outflow to heart - Blood loss - haemorrhage (draw out diagram)
- hypotension
main goal -> maintain circulation
concerted action targeting the heart, arteries and veins
describe postural hypotension and vasovagal syncope
- postural hypotension: sudden drop in blood pressure when standing up, due to venous pooling, less venous return, should be quickly restored by baroreflex via autonomic system
- vasovagal syncope: sudden drop in blood pressure due to anxiety (emotions), drops sympathetic and ups parasympathetic system
More common in people with autonomic dysfunctions (diabetes, medications, beta blockers)
What to do?
increase preload by increasing venous return
contract (leg) muscles (muscle pump) and take a good deep breath (respiratory pump) before standing up
describe the control of blood pressure long term
Blood volume important determinant of blood pressure
Important role of the kidneys in regulating blood volume
Increase in arterial pressure:
- Kidneys increase urinary loss of sodium and water
- causing a decrease in plasma volume
- which decreases blood volume
Increased arterial pressure:
- increased urinary loss of sodium and water
- decreased plasma volume - negative feedback
- increase blood volume
describe systemic hypertension and its vascular cause
- high blood pressure at rest
Psystolic >130mmHg or Pdiastolic >80 mmHg - however, guidelines are diff in diff countries so need to stay up to date with latest research
Vascular cause:
Elevated pressure ->damage arteries, impairs organ function in affected areas (eg. decreased oxygen supply)
1. Increased preiphreal resistance - decreased arterial radius
a) arteriosclerosis - stiffer arteries (remodelling) - aging, genetic
b) atherosclerosis - blockage of arteries (deposition of material) - lifestyle, genetic
- atherosclerosis is a major risk factor for infarction/stroke
2. increased blood volume (kidneys)
what are the considerations for dental practice?
- hypertension need to be well controlled to prevent excessive bleeding
- chest pain might occur if cardiac stress suddenly increases - the coronary supply is outweighed by oxygen demand. episodes of chest pain - stable angina - can be precipitated by the stress of dental treatment
- in general, bleeding can be minimised by local vasoconstriction (epinephrine, via alpha adrenergic receptors), which is given after local anaesthetic will also localise drug and the anaesthetic
