Arterial blood volume is same as stroke volume and CO (cardiac output). When CO decreases, all physiologic processes occur to restore volume. With decrease CO (ie
hypovolemia), oxygenated blood will not get to tissues, and we can die. Therefore, volume is essential to our bodies.
We have baroreceptors (low and high pressure ones). The low pressure ones are on the venous side, while the high pressure ones are on the arterial side (ie the carotids and arch of aorta). They are usually innervated by CN 9 and 10 (the high pressure ones). When there is a decrease in arterial blood volume (decreased SV or CO), it will under fill the arch vessels and the carotid; instead of 9th or 10th nerve response, you have a sympathetic NS response, therefore catecholamines are released. This is good b/c they will constrict the venous system, which will increase blood returning to the right side of the heart (do not want venodilation b/c it will pool in your legs). Catecholamines will act on the beta adrenergic receptors on the heart, which will increase the force of contraction, there will be an increase in stroke volume (slight) and it will increase heart rate (“+” chronotropic effect on the heart, increase in systolic BP). Arterioles on the systemic side: stimulate beta receptors in smooth muscle. Diastolic pressure is really due to the amount of blood in the arterial system, while you heart is filling with blood. Who controls the amount of blood in arteriole system, while your heart is filling in diastole? Your peripheral resistance arterioles – that maintains your diastolic blood pressure. So, when they are constricted, very little blood is going to the tissues (bad news); good news: keep up diastolic pressure – this is important b/c the coronary arteries fill in diastoles. This is all done with catecholamines. Renin system is activated by catecholamines, too; angiotensin II can vasoconstrictor the peripheral arterioles (therefore it helps the catecholamines). AG II stimulates 18 hydroxylase, which converts corticosterone into aldosterone, and stimulates aldosterone release, which leads to reabsorption of salt and water to get cardiac output up.
With decreased SV, renal blood flow to the kidney is decreased, and the RAA can be stimulated by this mechanism, too. Where exactly are the receptors for the juxtaglomerlur apparatus? Afferent arteriole. There are sensors, which are modified smooth muscle cells that sense blood flow. ADH will be released from a nerve response, and pure water will increase but that does not help with increasing the cardiac output. Need salt to increase CO.
Example: bleeding to death and there is a loss of 3 L’s of fluid – how can you keep BP up?
Give normal saline is isotonic therefore the saline will stay in the ECF compartment. Normal saline is plasma without the protein. Any time you have hypovolemic shock, give normal saline to increase BP b/c it stays in the ECF compartment. Cannot raise BP with ½ normal saline or 5% dextrose; have to give something that resembles plasma and has the same tonicity of plasma. Normal saline is 0.9%.
Peritubular capillary pressures: you reabsorb most of the sodium in the proximal tubule (60-80%). Where is the rest absorbed?; in the distal and collecting tubule by aldosterone. The Na is reabsorbed into the peritubular capillaries. Starling forces in the capillaries must be amenable to it. Two starling forces: oncotic pressure (keeps fluids in the vessel) and hydrostatic (pushes fluids out of vessel).
Example: When renal blood flow is decreased (with a decreased SV and CO), what happens to the peritubular capillary hydrostatic pressure? It decreases. Therefore, the peritubular oncotic pressure is increasing (ie the force that keeps fluids in the vessel), and that is responsible for reabsorption of anything into the blood stream from the kidney. This is why PO (peritubular oncotic pressure) > PH (hydrostatic pressure of peritubular capillary), allows absorption of salt containing fluid back into blood stream into the kidney.
Tonicity of fluid reabsorbing out of proximal tubule is isotonic (like giving normal saline).
ADH is reabsorbing isotonic salt solution, but not as much as the proximal tubule. ADH contributes pure water, therefore, with all this reabsorption you have an isotonic sol’n add the ADH effect and the pt becomes slightly hyponatremic and hypotonic, therefore absorbs into the ECF compartment when there is a decreased CO.
Opposite Example: increased SV, and increase arterial volume, will lead to stretch of baroreceptors (innervated by 9th and 10th nerve), and a parasympathetic response will be elicited, instead of a sympathetic response. There will not be any venuloconstriction nor any increase in the force of contraction of the heart. This is fluid overload; therefore we need to get rid of all the volume. There is increased renal blood flow, so the RAA will not be
activated. Fluid overload does not ADH be released. The peritubular hydrostatic pressure is greater than the oncotic. Even of the pt absorbed salt, it wouldn’t go into the blood stream, and it would be pee’d out. Therefore pt is losing hypotonic salt solution with increased in arterial blood volume.
Need to know what happens if there is decreased CO, what happens when ANP is released from the atria, and give off diuretic effect; it wants to get rid salt. ANP is only released in volume overloaded states.
Example: pt given 3% hypertonic saline: what will happen to osmolality? Increase. What will that do to serum ADH? Increase – increase of osmolality causes a release of ADH.
Example: What happens in a pt with SIADH? decreased plasma osmolality, high ADH levels.
Example: What happens in a pt with DI? no ADH, therefore, serum Na increases, and ADH is low
How to tell total body Na in the pt: Two pics: – pt with dry tongue = there is a decrease in total body Na, and the pt with indentation of the skin, there is an increase in total body Na.
Dehydration: Skin turgur is preformed by pinching the skin, and when the skin goes down, this tells you that total body Na is normal in interstial space. Also look in mouth and at mucous membranes.
If you have dependent pitting edema that means that there is an increase in total body Na.
SIADH – gaining pure water, total body sodium is normal, but serum Na is low; have to restrict water.
Right HF and dependent pitting edema – fluid kidney reabsorbs is hypotonic salt solution with a decreased CO (little more water than salt), therefore serum Na will low. Numerator is increased for total body sodium, but denominator has larger increase with water.
What is nonpharmalogical Rx of any edema states? (ie RHF/liver dz) – restrict salt and water What is the Rx for SIADH = restrict H2O
What is the Rx for any pitting edema state? Restrict salt and water
Pharmacological Rx for pitting water – diuretics (also get rid of some salt).
III. Shock
A. Causes of hypovolemic shock – diarrhea, blood loss, cholera, sweating, not DI (b/c losing pure water, and not losing Na, total body Na is NORMAL! Losing water from ICF; no signs of dehydration; when you lose salt, show signs of dehydration).
Example: lady with hypovolemic shock – when she was lying down, her BP and pulse were normal; when they sat her up, the BP decreased and pulse went up. What does this
indicate? That she is volume depleted. This is called the TILT test. Normal BP when lying down b/c there is no effective gravity, therefore normal blood returning to the right side of the heart, and normal CO. However, when you sit the patient up, and impose gravity, you decrease the venous return to right heart. So, if you are hypovolemic, it will show up by a decrease in BP and an increase in pulse.
Cardiac output is decreased, and the catecholamine effect causes this scenario. How would you Rx? Normal saline.
Audio file 7: Fluid and hemodyn 3
Example: pt collapses, and you do a tilt test: 100/80 and pulse of 120 while lying down.
Sitting up, it was 70/60 and pulse of 150. The pt is severely hypovolemic, therefore Rx is normal saline. Treatment: One liter in, showed no signs, put another liter and the BP becomes normal, and is feeling better, but still signs of volume depletion (dry mouth). We have the BP stabilized, but the pt lost hypotonic salt solution, therefore we need to replace this. So on IV, give hypotonic salt sol’n (b/c was losing hypotonic salt solution). We do not give 5% dextrose and water b/c there’s not any salt in it. Therefore, we will give ½ normal saline. The treatment protocol is: when a pt loses something, you replace what they lost.
And when pt is hypovolemic, always give isotonic saline.
Example: DKA, have osmotic diuresis; tonicity of fluid in the urine that has excess glucose is hypotonic. Hypotonic fluid has a little more fluid than salt. So the pt is severely hypovolemic;
therefore the first step in management is correction of volume depletion. Some people are in hypovolemic shock from all that salt and water loss. Therefore need to correct
hypovolemia and then correct the blood sugar levels (DKA pts lose hypotonic solution).
Therefore, first step for DKA pt is to give normal saline b/c you want to make them normo-tensive. Do not put the pt on insulin b/c it’s worthless unless you correct the hypovolemia.
It can take 6-8 liters of isotonic saline before the blood pressure starts to stabilize. After pt is feeling better and the pt is fine volume wise. Now what are we going to do? The pt is still losing more water than salt in urine, therefore still losing a hypotonic salt solution, therefore need to hang up an IV with ½ normal saline (ie the ratio of solutes to water) and insulin (b/c the pt is loosing glucose).
So, first thing to do always in a pt with hypovolemic shock is normal saline, to get the BP normal. Then to correct the problem that caused the hypovolemia. It depends on what is
causing the hypovolemia (ie if pt is sweating, give hypotonic salt solution, if diarrhea in an adult give isotonic salt sol’n (ie normal saline), if pt with DI (ie stable BP, pt is lucid) give water (they are losing water, therefore give 5% dextrose (ie 50% glucose) and water).