Cardiology Flashcards
Name local, endothelial, neurohormonal and neural factors that cause VASOCONSTRICTION
LOCAL
- decreased local temperature
- autoregulation
ENDOTHELIAL
- endothelin 1
- serotonin (from platelets)
- thromboxane A2
NEUROHORMONAL - Adrenaline (except in skeletal muscle and liver) - Noradrenaline - Vasopressin - Angiotensin II **** Digitalis-like substance - neuropeptide Y
NEURAL
- sympathetic discharge
Name local, endothelial, neurohormonal and neural factors that cause VASODILATION
LOCAL
- increase CO2, decreased O2
- increased K, adenosine, lactate
- decreased pH
- increased temp
ENDOTHELIAL
- NO
- kinins
- prostacyclin (PGE1)
NEUROHORMONAL
- Adrenaline (skeletal muscle and liver)
- calcitonin G protein
- substance p
- histamine
- ANP
- VIP
NEURAL
- decreased sympathetic tone
- cholinergic vasodilator nerves to vasculature of limb skeletal muscles
Where are our baroreceptors?
- Carotid sinus: innervated by carotid sinus nerve (branch from glossopharyngeal)
- Aortic arch: innervated by aortic depressor nerve (branch from vagus)
- Right atrium at entrance of IVC and SVC
- Left atrium at entrance of pulmonary vein
- In pulmonary circulation
What is the pathway for enacting hypotension with increasing cerebral pressures?
- Increase firing when pressure rises , stimulating NTS in medulla with glutamate (excitatory).
- NTS excitatory input to CVLM, which depresses RVLM and depresses sympathetic output.
- Excitatory projections from NTS to vagal motor neurons in nucleus ambiguus and dorsal motor nucleus result in increased vagal stimulation.
Outline the processes in eliciting bradycardia with the Valsalva Manouevre
- Initial hypertension due to increase of intrathoracic pressure leading to increased aortic blood pressure
- Fall in BP due to venous compression, decrease in venous return and cardiac output
- Decreased arterial pressure inhibits baroreceptors, causing tachycardia and rise in TPR
- When glottis reopened, intrathoracic pressure returns to normal, output restored
- BP peripherally high due to TPR high, stimulating baroreceptors, causing bradycardia and drop to normal levels
Where are our peripheral chemoreceptors, what activates them and what is their effect?
Present in carotid and aortic bodies.
Activated by reduction in PaO2, and increase in PaCO2 and pH.
Activation leads to vasoconstriction and increased vagal nerve activity
Where are our central chemoreceptors, what is their mechanism of action?
Receptors on or within medulla
Increased ICP –> decreased blood supply to RVLM –> hypoxia and hypercapnoea increase discharge –> rise in systemic arterial pressure to restore blood flow
What are some of the factors that inhibit and activate endothelin II?
Stimulated by AT II, catecholamines, hypoxia, insulin, HDL, shear stress, thrombin
Inhibited by NO, ANP, prostacyclin, PGE2
What are some of the effects of dopamine?
- renal vasodilatation via specific dopaminergic receptors
- (+) vasodilatation in the mesentery
- (+) heart via B1 receptors therefore inotropic effect
- (+) general vasoconstriction therefore increasing SBP a net increase in peripheral vascular resistance
- decrease appetite via specific dopaminergic receptors
What are the key actions of prostacyclin on the circulation?
Where is it released from?
Inhibits platelet aggregation, promotes vasodilation
released from endothelium and vascular smooth muscle
What are 5 actions of ANP?
- Inhibits release of ADH (vasopressin) water diuresis
- Increases GFR increase Na loss
- Inhibit release of renin reduce Na retention
- Lowers BP by inhibiting actions of several vasoactive substances
- May have a role in the brain in the central control of BP (ANP & CNP)
What is the vasomotor region of the brain?
- actions
- stimulators
- inhibitors
- when activated, uses glutamate to signal increased sympathetic discharge (HTN/TACHY)
- Direct stimulation = CO2, hypoxia
- Excitatory inputs = cortex, PAG, reticular formation, pain pathways, carotid/aortic chemoreceptors
- Inhibitory inputs = cortex, caudal ventrolateral medulla, carotid/aortic/cardiopulmonary baroreceptors
In pacemaker cells of the heart, what are the key channels that open in close in
- phase 4
- phase 0
- phase 3
Do these result in depolarisation or hyperpolarisation?
phase 4 - Ih channels open that allow slow depolarisation with Na coming INTO cell until action potential reached
phase 0 - voltage gated Ca2+ influx with swift depolarisation, turn off once peak
phase 3 - K+ channels that result in efflux and hyperpolarisation (repolarisation) allowing ifunny channels to be activated again
How does the parasympathetic nervous system act on pacemaker cells?
acetylcholine acting on M2 muscarinic receptors at the SA node to
- open a special set of K+ channels. The resulting IKAch slows the depolarizing effect of Ih
- activate of the M2 receptors and cAMP in the cells, and this slows the opening of Ca2+ channels
How does the sympathetic nervous system act on pacemaker cells?
Noradrenaline β1 receptors
Increase in intracellular cAMP facilitates the opening of L-type calcium channels channels, increasing rapidity of the depolarization phase of the impulse
