Episode 86: Four categories of shock intuitively with respiratory and metabolic acidoses.
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).
Cross-Synaptic Learning Principle = Epidemiology. Other examples include most common causes of death by age group (MC genetic cause of MR = Down Syndrome, MCC of MR = Fetal Alcohol Syndrome, MCC death in youth = accidents).
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.
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 normotensive. 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).
B. Four kinds of shock:
1. Hypovolemic shock:
Blood loss, diarrhea (adult or child), basically whenever you are lose salt, you could end up with hypovolemic shock. Give volume.
2. Cardiogenic shock:
MC due to MI. Right Ventricular Assist Device and await transplant.
3. Neurogenic shock:
Assoc. with spinal cord injuries. Example: diver in a shallow pool; may see priapism.
4. Septic shock:
MC due to E. coli; also MCC sepsis in hospital and is due to an indwelling of the urinary catheter. Staph aureus is not the MC cause of IV related septicemia in the hospital, E.Coli wins hands down because of sterile technique. Endotoxin in cell wall is a lipopolysacharide, which are seen in gram negative bacteria. The lipids are endotoxins. Therefore, gram negatives have lipids (endotoxins) in their cell wall, gram positive do not. So if you have E.Coli sepsis, you will have big time problems, and it’s called septic shock.
5. Classical clinical presentations:
a) Hypovolemic and cardiogenic shock: you would see cold and clammy skin, b/c of vasoconstriction of the peripheral vessels by catecholamines (release is due to the decrease in SV and CO) and AG II after decreased volume sensed in the aortic arch and carotid bodies. These will vasoconstrict the skin and redirect the blood flow to other important organs in the body like brain and kidneys, leading to a cold clammy skin. BP is decreased, pulse is increased.
b) Pouseau’s laws: is a concept that teaches you about peripheral resistance of arterioles which control the diastolic blood pressure.
TPR = V/r^4
TPR = Total peripheral resistance of the arterioles
V = Viscosity
r = radius of the vessel to the 4th power
Cross-Synaptic Learning Principle = PreMed throw-backs. Other examples include Force = Mass x Area; The physics of how drum brakes work in cars, multiplying for force based in increased area.
The main factor controlling TPR is radius to the 4th power. What controls the viscosity in the blood? Hb. So if you are anemic, viscosity of blood is decreased (ie low hemoglobin), and if you have polycythemia (high hemoglobin), viscosity will be increased. Therefore, TPR in anemia will decrease, and in polycythemia will increase.
c) Septic shock – There is a release of endotoxins which activates the alternative complement system. The complement will eventually release C3a and C5a which are anaphylatoxins, which will stimulate the mast cells to release histamine. The histamine causes vasodilation of arterioles (the same ones of the peripheral resistance arterioles). Therefore blood flow is increased throughout the peripheral resistance arterioles and the skin feels warm. The endotoxins also damage the endothelial cells; as a result, two potent vasodilators (NO and PGI2) are released. Therefore, 2 or 3 vasodilators are released, and affect the TPR to the fourth power. Therefore, the TPR will decrease (due to vasodilation).
TPR arterioles control your diastolic BP b/c when they are constricted; they control the amount of blood that remains in the arterial system while your heart is filling up in diastole. Therefore, when the TPR arterioles are dilated, the diastolic BP will pan out. Think of a dam (with gates): if all the gates are wide open all that water will come gushing through. This is what happens to the arterioles when they are dilated. The blood gushes out and goes to the capillary tissues, supposedly feeding all the tissues with O2. Think in the context of fishing: when the dam wall opens, all the water rushes thru causing turbulent waters, therefore this would be a bad time to go fishing. The fishes would be trying to save themselves. That is what the O2 is doing. Therefore, with all this blood going by, the tissues cannot extract O2 b/c it is going too fast and b/c it isn’t a controlled release of blood. Therefore, the blood is coming back to the right side of the heart faster than usual, b/c all the arterioles are widely dilated. Due to the blood going back to the heart faster, the cardiac output is increased. This is seen in septic shock and the skin feels warm b/c the vessels are dilated. Therefore, with septic shock, there is a HIGH output failure, with warm skin.
However, in hypovolemic and cardiogenic shock, the cardiac output is decreased (b/c the vessels are constricted by catecholamines and angiotensin II), and the skin feels cold and clammy.
C. Swan Ganz Catheter
The Catheter is inserted in the right side of the heart and it measures all parameter that is taught in physiology. All of these things are measured in a swan ganz catheter.
1. Cardiac Output: measured by swan gang or “right heart cath”
2. Systemic vascular resistance: this is a calculation. The basically measures the TPR, ie measures what arterioles are doing
3. Mixed venous O2 content. You know normally that the O2 content is equal to = 1.34 x Hb x O2 sat’n + pO2. Measured in RA with swan ganz catheter; this is the BEST TEST for evaluating tissue hypoxia. Cardiac output in cardiogenic and hypovolemic shock is low, therefore, blood not being pushed ahead with a great deal of force. So, tissue will have a lot of time to extract O2 from what little blood that is being delivered. As a result, mixed venous O2 content in hypovolemic and cardiogenic shock will be decreased ie very low b/c the blood going through the vessels is very slow (no force is helping to push it through). Therefore, it extracts more O2 than normal. Mixed venous O2 content in septic shock (when blood is passing through vessels at a very fast rate) will lead to a HIGH mixed venous content (b/c tissues unable to extract O2). Example is in in high output cardiac failure as a result of phospholipid A release from bacterial cell walls in sepsis.
4. Pulmonary capillary wedge pressure – measures Left ventricular end diastolic volume and pressure (EDV and EDP). Catheter in right heart will tell you what the pressure is in the left ventricle.
5. Differences between Hypovolemic, Cardiogenic, and Septic Shock using Swan Ganz catheter:
- CO in hypovolemic and cardiogenic? both decreased
- CO in septic shock? Increased
Systemic vasc resistance (TPR) is a measure of what the ARTERIOLES are doing.
- What is TPR in hypovolemic and cardiogenic shock? Increased due to vasoconstriction
- TPR in septic shock? Decreased due to vasodilation.
- Mixed venous in hypovolemic and cardiogenic? Low.
- Mixed venous in septic shock? High.
How do we separate hypovolemic and cardiogenic?
Pulmonary capillary wedge pressure (measures left ventricular EDV)
- In Hypovolemic, what is LVEDV? Low.
- In Cardiogenic, what is LVEDV? High.
- In Endotoxin shock? it’s decreased.
1. Example: Of all organs in the body, which suffers the greatest due to decreased BP? Kidneys. What part? Medulla, which makes sense because the cortex can rob all the oxygen and the medulla is more sensitive in this way. The kidneys normally receive 1/4 of all cardiac output so even 1-2 liters less of total blood volume is noticed. Not the brain b/c with decreased CO, the circle of willis will distribute blood flow to certain areas in the brain, especially the areas where there are neurons. Someone with hypovolemic, or cardiogenic, or septic shock: oliguria, result in an increased in BUN/Creatinine. Recall that both are byproducts of protein and amino acid catabolism and that creatinine is the closest in vivo model to inulin for measuring the glomerular filtration rate. This occurs b/c the patient is going into acute tubular necrosis. Nephrologists want to correct the renal blood flow, so that you can prevent ATN b/c a pt can die. What type of necrosis? Coagulation necrosis. The dead renal tubules will slough off and produce renal tubular casts in the urine which will block urine flow, thereby producing oliguria. There is also a decrease in GFR, leading to ATN (chances of survival are NOT zero). So it is the kidneys that are the most affected when the cardiac output is decreased, ie decreased blood flow. Brain would be a close second to necrosis (no direct marker; EEG shows diffuse slowing, non-paroxysmal pattern consistent with encephalopathy). The heart has a bit of a collateral circulation as well, releasing cardiac enzymes such as troponins and CK-MB. The liver takes a hit as well and releases transaminases (and all its other contents of dead and dying cells). Remember that laboratory testing CONFIRMS the diagnosis that you’ve already made. You should always consider WHY you need a test.
2. Example: Pt with the sickle cell trait can get kidney dz; b/c the renal medulla’s O2 tension is low enough to induce sickling. Therefore if you have a young black woman with microscopic hematuria coming to the office, what is first test you should do? Sickle cell screen, b/c she probably has the sickle cell trait. Therefore, sickle cell trait has problems, b/c O2 tension in renal medulla is low enough to induce sickling in peritubular capillaries, which produces microinfarctions in the kidneys. Therefore, don’t want to produce Coagulation necrosis (aka ATN).
IV. Acid-base and Blood Gas
Acidosis – increase in H+ ions, therefore decrease in pH
Alkalosis – decrease in H+ ions, therefore increase in pH
A. Equation for acid/base physiology:
pH = [HCO3 -] / pCO2
- Increase in bicarb = increase pH = metabolic alkalosis
- Decrease in bicarb = decrease pH = metabolic acidosis
- Increase pCO2 = decrease pH = respiratory acidosis
- Decrease pCO2 = increase pH = respiratory alkalosis
B. Compensation = bodies attempt to try to maintain a normal pH (which it never does).
1. Example: if you have metabolic alkalosis (increase in bicarb: which is in the numerator), then have to increase denominator (pCO2) to keep it normal, therefore, compensation is due to respiratory (pCO2) acidosis. A nice way of memorizing it is what is the opposite of metabolic? Respiratory and what is the opposite of acidosis? Alkalosis, and vice versa.
2. Example: if you have metabolic acidosis (decrease bicarb) what do we have to do with the pCO2? We have to get rid of it. If we decrease the nominator, we have to decrease the dominator in order for the equation to stay the same. Therefore, we have to blow off the CO2 (hyperventilation).
3. Ventilation is a CO2 term!
- Hyperventilation = Increase in respiratory rate allows for the blowing off of CO2, therefore results in respiratory alkalosis. For the treatment of respiratory alkalosis is to give the pt a paper bag and ask to breath in it, b/c then they are re-breathing their own CO2.
- Hypoventilation = Decrease in respiratory rate allows for the retention of CO2, therefore results in respiratory acidosis. Example, can appear to be acutely delirious and combative.
Full compensation does not exist; you never bring back the pH to the normal range. There is one exception: chronic respiratory alkalosis in high altitude; ie mountain sickness (ie Peru).
C. Respiratory conditions: acidosis and alkalosis
1. Things that deal with CO2:
a) Respiratory center is in medulla oblongata, which controls the breathing rate
b) Upper airways – if obstructed, there will be a problem getting rid of CO2.
c) Chest bellows – most imp muscle of respiration is diaphragm. On inspiration: the diaphragm goes down, the negative intrathroacic pressure increases, and air follows the negative pressure into the lungs and blood is sucked into the right side of the heart (this is why neck veins collapse on inspiration). Negative vacuum sucks blood and air into your chest. On expiration, there is a “+” intrathrocic pressure, pushing things out. It helps the left heart to push blood out and it also helps the lungs by pushing out air.
(a) Barbiturates or any drug that depresses the respiratory center will leads to respiratory acidosis
(b) CNS injury to medulla oblongata – resp acidosis
(c) Anxiety = MCC resp alkalosis. When you take a test, sometimes you feel strange, and get numb and tingly, especially around mouth and on the tips of fingers, and become twitchy (b/c you are in tetany) its all caused by being alkalotic and ionizing calcium level gets lower and you really are getting tetany. Therefore you become twitchy and paresthesias (ie carpal pedal sign or trousseau’s sign are both signs of tetany). All due to tetany b/c of breathing too fast from anxiety.
(d) Pregnant woman have resp alkalosis b/c estrogen and progesterone over stimulate the respiratory center. Located in the lungs are spider angiomas due to AV fistulas related to high estrogen, therefore clear more CO2 per breath than a normal woman. A lot of shunting occurring within lungs. These spider angiomas go away after delivery of the baby.
(e) Endotoxins over stimulate the system. All pts in endotoxic shock have resp alkalosis. They are also in anaerobic metabolism, producing lactic acid, therefore are also in metabolic acidosis. Therefore, endotoxic resp alkalosis due to overstimulation, and metabolic acidosis due with normal pH.
(f) Salicylate overdose – overstimulate resp center, leading to resp alkalosis. Salicylic acid is an acid, hence metabolic acidosis, and pH will be normal b/c they balance e/o out. (Tinnitus in salicylate OD – also a MIXED disorder!)
(g) 6 y/o child with inspiratory strider – do a lateral x-ray, and see thumbprint sign, with a swollen epiglottis. The diagnosis is acute epiglottitis, due to H. influenza; vaccination has decreased incidence, hence you don’t see any kids with H. meningitis b/c of the vaccination. The MC of meningitis in 1 month – 18 yrs = N. meningitis.
(h) 3 month old – croup, a larygiotracheobronchitis dz due to parainfluenza virus. Want to do a lateral x-ray and see a steeple sign. Where is the obstruction in croup? Trachea
(i) Pt shoving food in their mouth (café coronary) – Heimlich maneuver; if they can talk, leave alone and let them cough it out.
(j) Diaphragm innervated by the phrenic nerve – ie erb Duchene palsy, with brachial plexus injury, and child has resp difficulty, and diaphragm on right side is elevated. Paralysis of the diaphragm will lead to increased CO2.
(k)Lou Gehrig’s dz – amyotrophic lateral sclerosis dz, a LMN’s and UMN’s gone therefore cannot breath b/c no innervation to the diaphragm (ie diaphragm and intercostals are paralyzed)
(l)Guillain-Barre – ascending paralysis in a patient who a week ago had a respiratory infection. The spinal fluid shows increased protein, slight increase in lymphocytes, and a gram stain negative. Dz: Guillain-Barre, demyelinating dz
(o) Polio – destroys LMN’s and eventually UMN’s. Therefore, anything that paralyzes muscle of resp will lead to resp acidosis.
(p) LUNGS: obstructive and restrictive lung dz’s:
- Obstructive lung dz – problem getting air out, compliance increased and elasticity is decreased, therefore, have a resp acidosis.
- Restrictive lung dz – ie Sarcoidosis and pneumonocionioses, there is a problem in getting air in therefore has a resp alkalosis (?)
Caisson’s Disease –Underwater: for every 30 ft, increase 1 atm, (ie 760 at level, but 30 ft lower it will be 2 atm); the reverse is true when you go to high altitudes – ie at top of mt everst, the atmospheric pressure is 200 atm; still breathing 21% O2; breathing the same, but atmospheric pressure is different, depending on where you are.
Formula for calculating: alveolar O2 = (0.21 x atmospheric pressure) – PCO2 / .8
High Altitude: (.21 x 200) – 40mmHb/.8 = 2mmHg of air in alveoli, therefore will have to hyperventilate at high altitudes, b/c lower pCO2= increased PO2 (you HAVE to hypverventilate otherwise you die).
However, when you go under, the atm pressure increases, and the nitrogen gases are dissolved in your tissues, leading to an increase in pressure. Ie 60 ft below, want to get up fast; like shaking a soda bottle; as you ascend, the gas comes out of fat in bubbles; the bubbles get into tissues and BV’s; this is called the bends; leads to pain, and quadriplegia, loss of bladder control. Rx = hyperbaric O2 chamber.