Lets do this: Care Of Patients In Shock!

Shock is defined as: impaired delivery of oxygen to the tissues. Oxygen delivered to the tissues is imperative for function of tissues.

From a metabolic standpoint, the largest problem we will encounter in a patient suffering from shock is Lactic Acidosis. 

What causes lactic acidosis? When there is impaired oxygen deliver to the tissues, they are forced to switch from aerobic to anaerobic respiration. The byproduct of anaerboic respiration is lactic acid which will lower the patients pH. 

Septic Shock (which i will discuss later) generates the most lactic acid due to cellular hypoxia. To treat the lactic acidosis in septic shock we would have to treat the infection! Some other causes of lactic acidosis include; Hypovolemic + Cardiogenic + Distributive shock

Other causes NON-related to shock that cause Lactic acidosis are:

1. Cardiac Arrest because there is not alot of breathing or perfusion going on during a cardiac arrest, because of the amount of time from last heart beat until we can gain a return of spontaneous circulation (downtime). To treat the lactic acidosis in this case we would try to return spontaneous circulation. 
2. Seizures because you are not breathing during a tonic clonic seizure for example, and there is lactic acid build up during these periods of apnea. Severity of course depends on how long the patient had apnea. To treat the lactic acidosis in this case we would try to stop the seizure and get the patient to start breathing.

Lets talk about Oxygenation and Tissue Perfusion. Oxygen reaching the tissues depends on the amount of arterial blood that is reaching the tissues.  We are directly focusing on arterial blood when we are talking about perfusion.

Three Factors Affecting Perfusion & r/t MAP

• Total Blood Flow 
• Cardiac Output (ml/min)
• Size of the vascular bed.

MAP is the Mean Arterial Pressure it is the average of your systolic and diastolic blood pressure (so add your systolic + diastolic and divide by 2) this measures the mean pressure, which is the average pressure during an entire cardiac cycle.  We need the tissues to be perfused during systole as well as diastole which is why we focus on this mean pressure. 

If the total blood flow increases, then the MAP increases (and vice versa)

If the cardiac output increases then the MAP increases (and vice versa)

The Size of the Vascular bed on the other had has an inverse relationship with MAP.

As the vascular beds dilate (or enlarge) the MAP decreases, likewise as the vascular beds constrict the MAP increases.

✔A Normal MAP is 80 - 100 mm Hg, in the clinical setting, a MAP of 60 is the minium required to perfuse the brain, so if the MAP drops below 60, your patients cerebral perfusion will be impaired.

OKAY… Still with me? Lets move on to the SPECIFIC STAGES OF SHOCK. Remember: the stages are determined by the volume of loss (blood or plasma). Other factors that influence the severity of shock would be: etiology of loss, rate of loss, and patients comorbities.

Before we being I’d like to tell you about Pulse Pressure. This is the difference between systolic and diastolic blood pressure. (For example 120/80) the Pulse pressure will be 40. (120 minus 80) ✔ normal pulse pressure is 30-40 mmHg.  The reason we look at a patients pulse pressure, is to see if their body is able to maintain a pressure between systole and diastole.  If the pulse pressure is high, (like if a patient has a bp of 100/20 their pulse pressure will be 80 mm Hg) So 80 mm Hg is considered wide  which means that during diastole the patients body is not able to maintain enough pressure to perfuse the tissues! If the pulse pressure is narrow (say the patient has a bp of 200/180, making the pulse pressure 20) this means that the heart and the patients cardiovascular system is not able to fully relax so the patient will have decreased filling.

OKAY! Now lets get to the stages already!

SPECIFIC STAGES OF SHOCK

INITIAL STAGE OF SHOCK

• 750 mL of blood lost (15% of total blood volume)
• Baseline MAP decreases about 10 mm Hg.
• Heart rate and respiratory rate increase due to compensatory mechanisms.
• Sympathetic nervous system kicks in to keep your MAP at an acceptable rate, This is the key component of the initial stage of shock, the patients MAP is typically normal, just slightly lowered.
• Patients pulse pressure will increase. (wide)

2nd NON-PROGRESSIVE / COMPENSATORY STAGE OF SHOCK

• 750-1500 mL of blood loss (15-30% of total blood volume)
• Baseline MAP decreases about 10-25 mm Hg. 
• At this point your bodies compensatory mechanisms are all maxed out. This is your bodies last all forward effort to combat this so in addition to the sympathetic nervous activation the RAAS system will also be activated

QUICK REFRESHER: RAAS = Renin-Angiotensin-Aldosterone System is stimulated when there is decreased perfusion to the kidneys. The kidneys will then stimulate the RAAS system to reabsorb sodium and water, so the patient will most likely have a decrease in urine output.

• In addition to the RAAS system, you will also see the activation of baro-receptors (specifically due to the decreased MAP and BP) these receptors are located in the carotid sinuses, aortic arch, and left atrium). They are very sensitive to pressure changes, and when they sense a decrease they will stimulate the adrenal medulla in the brain to release catecholamines; epinephrine and norepinephrine. 
• These two catecholamines increase vasoconstriction, increase heart rate and contractility
• During this stage, the body will start shunting blood away from non-vital organs such as the kidneys, the G.I. tract and the skin. 
• The patient will also start to become acidotic due to decreased perfusion and anaerobic respiration that produces the lactic acid.
• This stage is the last stage where the effects of the shock are reversible so at this point, even though the blood is shunted from the kidneys, G.I. and skin, there is no permanent harm… YET. because as we know the body can’t sustain this for very long, and without proper and rapid intervention the patient will progress into the next stage.

3rd PROGRESSIVE STAGE OF SHOCK

• 1500-2000 mL of blood (30-40% of total blood volume)
• This is when the patient will experience full activation of the sympathetic nervous system.
• Heart rate will be >120 (due to the epinephrine and norepinephrine)
• Respiratory rate will be very high usually 30-40 breaths per minute.
• Oliguria (urine production will fall to zero)
• HYPOTENSION and a very Narrow  pulse pressure.
• The organs will now start developing hypoxia, and permanent damage occurs which deems this a life threatening emergency
• Because the MAP often falls below 60, patients will be confused (due to the lack of cerebral perfusion) and agitated (due to the hypoxia).

4th REFRACTORY STAGE OF SHOCK

• >2000 mL of blood lost (>40% of total blood volume)
• At this point the patient is probably unconscious, and if they are conscious they they are profoundly lethargic (which is a patient who can’t open their eyes, DOES have spontaneous respiratory drive but will do nothing more than moan or groan to painful stimuli)
• Severe Hypotension in this stage and very narrow pulse pressure.
• Sometimes the blood pressure is SO LOW that we can’t really auscultate it so what we do is use a doppler or palpate for the systolic pulse only.
• Chart as follows: “75/doppler or 75/palpate” this way the other nurses know that you couldn’t get the diastolic and you used a doppler or you palpated.
• At this 4th stage there is significant cell death and tissue damage related to hypoxia. The body can’t respond effectively to intervention and shock continues
• If the body loses the ability to respond to our medical interventions then 100% death will occur in a short period of time. 
• The reason that our body lacks the ability to respond at this stage, is due to the profound anaerobic respiration, because we are not able to perfuse the tissues enough to meet up to the current oxygen demands as well as making up for the deficit that the first 3 stages created!
• Heart rate will be > 140
• If not on a ventilator respiratory rate >40
• Oliguria
• Skin will feel cool and clammy and look mottled; splotchy. not perfused at all
• Capillary refill will be >5 seconds

PHEWF! So now that we got through the stages, LETS TALK ABOUT WHAT ACTUALLY KILLS THE PATIENT FROM SHOCK… (sorry that sounds a bit insensitive).

⚡MULTIPLE ORGAN DYSFUNCTION SYNDROME - or “MODS” or just Multiple organ failure.

• This is when the organs have lost their ability to function because of the metabolites produced by cell death. As we know from going through the 4 stages of shock, cells are slowly starting to die off, the metabolites or cellular contents from these dead cells enter into the circulation. These are toxic to other organs.
• To add insult to injury, we also start to have a dysfunction of our clotting cascades so the patient will now start to form microthrombi. This is related to the fact that the contents of the dead cells are seen as foreign in the circulatory system and they get attacked by platelets and clotting factors and from little micro-emboli that travel through our circulatory system and lodge in small capillary beds. 
• These micro-emboli greatly effect the tips of the fingers, the tip of the nose, the penis, the toes and the lungs. As these micro-clots lodge in these areas it causes a further decrease in perfusion, further limits oxygenation and speeds up the decline of the patient!
• the Liver, Heart, Brain and Kidneys are especially susceptible to MODS, because these organs depend upon constant profusion and oxygenation in order to maintain their function.
• Also, as the pancreas loses perfusion and becomes ischemic, it releases a peptide chain, which has been named  the myocardial depressant factor. 
• This myocardial depressant factor reduces contractility to the myocardium, causes arterial constriction & prevents phagocytosis.
• Because we have decreased perfusion naturally we are going to need maximum cardiac output, but of course this myocardial depressant factor reduces contractility, and makes the problems of shock a million times worse!
• HOW AWFUL IS THAT!!  In Summary: You’ve got cell death due to hypoxia releasing toxic metabolites into the circulatory and now this myocardial depressant factor prevents phagocytosis from ingesting and destroying this waste, so now the patient has uncontrolled toxins and metabolites in the bloodstream causing tons and tons of micro-clots, which are able to lodge anywhere, and not only that, but because the myocardial depressant factor causes arterial constriction, it increases the chances that micro-clots will actually get lodged there!!

You may be wondering, well.. what can we as nurses do for a patient experiencing MODS?

»>Honestly, there is not a whole lot we can do because their body will start fighting against any of our interventions as we are trying to fix the various problems they are having. This is the point in time where you continue the interventions you have in place already but don’t start new ones. You halt everything, let it be, let the family in and focus on comfort care. Some families may even ask that you stop some of the interventions that you have already started.

Okay i’m going to go take a little break from type and eat dinner. My next post will be on the TYPES OF SHOCK; Hypovolemic, Cardiogenic, Distributive, Obstructive including, pathogenesis and management.