zachow Flashcards
describe epinephrine and norepinephrine receptor affinity
Epinephrine: at low concentrations it binds beta1 and beta2 and at higher concentrations it only binds alpha1 and beta1.
Norepinephrine: at low concentrations it binds alpha1 > beta1> beta2. At high concentrations only alpha1 and beta1. It has highest affinity for alpha1.
Describe the pathway for turning on SNS activity?
It starts with the high pressure baroceptor in the carotid sinus/ aortic arch and the low pressure baroceptor in the right atrium.
The sensation is passed via sensory vagal and glossopharyngeal pathways to the brain (parasympathetic sensory). The sensory cell body is in the inferior vagus ganglion just under the jugular foramen.
Then the vasomotor center of the medulla is like okay ramp up inotropy, chronotropy and cause vasoconstriction.
Preganglionic sympathetics come from the lateral horn, synapse at postganglionics which always carry cholinergic nicotonic receptors and respond to acetylcholine.
The depolarizations get brought through the postganglionic sympathetics and synapse on the effector tissue, releasing norepinephrine.
Parasympathetic (would come from the brain stem in the vagus nerve and their postganglionics will be in the cardiac plexus. They use acetylcholine in both synapses (cholinergic muscarinic)
So why does blood pressure and heart rate go up when you go from laying down to standing?
What would happen if you had autonomic failure
The gravity causes a momentary decrease in venous return, leading to a drop in right atrial pressure and a decrease in cardiac output. Your low pressure barroreceptors in the right atrium pick up on this and quickly turn on sympathetics. Your heart rate goes up, cardiac output goes up, blood pressure goes up.
If you had autonomic failure as in your barroreceptors aren’t working, you couldn’t restore MAP and as you a result you would feel orthostatic hypotension.
What makes orthostatic hypotension worse in people with hypertension.
For people with hypertension, the RAAS system is secreting more volume than the normal person. So when someone has orthostatic hypotension when standing up, they have even less blood volume to make up for the loss of MAP>
Describe the clinical presentation of pheochromocytoma.
They would have huge levels of epi and norepi. This would result in drugs not being effective (diuretics and calcium channel blockers)
So she would have chronic hypertension but because of this chronic hypertension, her barroreceptor range got elevated.
So that when she went from supine to upright, her body couldn’t sense the drop in MAP/venous return and couldn’t compensate leading to orthostatic hypertension.
Where is there a splitting of S2 on inspiration?
Upon inspiration there is a decrease in thoracic pressure. This leads to increased venous return to the right side of the heart and when that increased volume is ejected, it takes longer due to the increased volume and the pulmonic valve closes later.
On the other hand, there is less blood in the pulmonary venous side and with less blood, the aorta closes earlier.
Why does exertion during aortic stenosis lead to syncope.
Upon exertion, there should be increased CO but CO can not accommodate due to the stenosis. Vasodilators are increased and this decreases TPR, leading to decreased perfussion pressure and as a result, you get syncope.
