Download Sheet #3 / Rawan Al-Majali

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Coronary artery disease wikipedia , lookup

Heart failure wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Jatene procedure wikipedia , lookup

Myocardial infarction wikipedia , lookup

Cardiac surgery wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Transcript
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
(Part 2/ Management of shock) Dr. Firas Obeidat
In normal conditions, the heart generates power, and any physically fit patient can do this
efficiently. This power generated by the heart will deliver nutrients and remove the waste products
from the peripheral tissues. Once the heart fails to induce this power, we will have a state of shock.
So what is shock?
It is a state of inadequate tissue perfusion. This will lead to anaerobic condition or metabolism
because there is no sufficient oxygen.
Usually healthy people will try to compensate for this insufficieny by different mechanisms to
reproduce this power or oxygen generated by the heart at least for the vital organs, but up to a
limit, beyond which the body can’t compensate for anything, and we will have a state of shock. If
left untreated, will end up with multi organ failure.
We’re concerned here with two definitions:
Preload: blood coming back to the heart. So it’s the blood in the venous system (Inferior vena cava
IVC, and superior vena cava SVC). This preload or blood in the venous system will induce ventricular
end diastolic pressure.
Afterload: peripheral vascular resistance, this will resist the mayocardial function.
Peripheral vascular system will try to collapse or to spasm to try to minimize the expenditure of
oxygen or nutrients.
Stages of shock:
Before entering the frank stage of shock, we have a pre-shock state or compensated state (a
compensatory mechanism due to stress).
Normal body will compensate for around 10% loss of intravascular volume, this is usually
compensated either by increasing the heart rate, or by spasm of the peripheral vascular system or
redistribution of blood to vital organs.
If this state of preshock continues, we will reach a frank shock state.
If the blood loss is more than 20-25%, you will have signs of organ dysfunction, and the
compensatory mechanism will be overwhelmed.
If the state of shock continues without resuscitation or any intervention, we will go into MOF (multi
organ failure) and as more organs fail to function, the mortality rate becomes more than 90%.
Page 1 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
The mortality rate associated with Renal/respiratory failure is more than 60-70%.
Tissue perfusion is determined by: cardiac output and peripheral or systemic vascular resistance.
Types of shock:
The major elements of the circulatory system are: Preload, pump (heart), and the peripheral
vascular system. Any abnormality in these three, will induce a type of shock.
Hypovolemic shock:
The most common one in surgical patients. There is a decrease in intravascular volume. So the
preload is decreased. the problem is in the preload.
Causes: hemorrhage, dehydration, burns, sepsis (patients with sepsis will either have septic shock or
hypovolumic shock).
Cardiogenic shock:
The underlying cause is pathology in the heart, occurs in medical patient not in surgical patients.
Cardiogenic: the problem is inherent in the heart itself, which may be any one of these: myocardial
infarction (one of the most common causes), valvular disease, arrhythmias, heart failure. Cardiac
problem will manifest itself as a decreased output, and decreased volume. Both are consistent with
shock.
Mechanical shock: (Or obstructive type of shock)
The problem is in blood entry and exit.
Veins have a very thin and collapsible walls. Which makes it easy to retard the blood flow in veins.
So any external compression decreases the preload.
Pneumothorax (presence of gas) or hemothorax (presence of blood in the pleural cavity) can
compress on inferior vena cava or SVC, and decrease preload volume,
infusion in the pericardium, can also cause compressive shock.
These conditions, cause inflow obstruction.
While in outflow obstruction, blood flow is impeded as it leaves the heart, for example Pulmonary
embolism, may delay blood flow from cardiac right ventricle to the lung.
Page 2 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
Distributive or vasodilatory shock:
This is the general name, other names: neurogenic shock, septic shock, anaphylaxis, and
addinisonian crisis.
Regional anaesthesia if improperly given can lead to neurogenic shock. The affected part here is the
autonomic innervation of the vessels. This results in paralysis, dilatation, relaxation and pooling of
blood in these vessels, thus decreased preload.
In septic shock, production of inflammatory mediators causes peripheral vascular relaxation, Here
the cause is not in preload, but it is the afterload.
General features of shock:
-Cool skin: due to blood redistribution, skin supply becomes compromised as the body tries to
spare whatever left in the circulation for the vital organs, so spasms in peripheral vascular system
supplying the skin happen. But this doesn’t hold true for septic shock. On the contrary, the patient
experiences hotness and warm skin in early stages (dilatations rather than spasms).
-The kidneys will be affected because the body will try to decrease the output or the excretions of
fluids from the body, so patients will have oligurea.
- Mental status is also affected, you will notice confusion and dizziness.
-Metabolic acidosis due to anaerobic metabolism.
In general, how do we approach patients with shock?
- I have to have an IV access, preferably peripheral lines not central lines, they are easier. Don’t look
for a central access when your patient is hypotensive, this will waste your time and induce more
trauma.
- Oxygenation: apply the oxygen mask to the patient, to provide a consistent concentration of
oxygen and compensate for tissue hypoxia.
So in general we aim for optimizing the intravascular volume, and at the same time, looking for the
underlying cause. If the problem was in fluids, the routine administrative tools are IV access, and
oxygen mask. but you have to know the underlying cause. For example, in case of a cardiogenic
shock, due to MI or heart failure, it’s not appropriate to administer IV fluids 1 or 2 liters, because he
will die!
Page 3 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
But if the patient was subjected to severe bleeding and fluid loss, try to compress the area of
bleeding and provide fluids.
So it depends on the primary survey done in the emergency unit.
So hypovolemic shock requires IV administration, and usually we use primary types of fluids like
crystalloids, they are available and cheap.
Colloids: volume by volume, like albumin, blood, fresh frozen plasma, but these are not available on
spot, they’re expensive, and may induce allergic reactions.
So the primary fluids for hypovolemia are crystalloids, like normal saline and ringer lactate.
Septic shock: treated as in hypovolemia, because there is pooling of blood. So I give fluids, because
there is dehydration. So the primary treatment is hydration. Same in acute pancreatitis and third
space loss.
At the same time, I look for the sepsis, determine the most likely bacteria causing this sepsis, and
search for the underlying cause, UTI or pyelonephritis.
And I give empirical antibiotic treatment.
Neurogenic shock: the problem here is not in the intravascular volume, but the innervation of blood
vessels “flaccid or infection of the autonomic nervous innervations” which causes them to relax and
dilate. So we try to restore the contractility of the peripheral vascular system.
How to deal with neurogenic shock?
These patients have pooling of blood, so lifting their legs would help to increase the preload. At the
same time, vascoconstrive agents here have a role, in contrast to hypovolemia, we don’t go first for
adrenaline to increase the pressure, the problem is in fluids, whereas here the problem is in
contractility. In addition, you give fluids but not in that aggressive way as in hypovolemia.
Cardiogenic shock:
The problem is in the pump, you have to be careful with fluids, if you gave too much fluid, you will
end up with pulmonary edema and death. We want to decrease the load on the heart, so we
basically give diuretics in addition to beta blockers and other drugs that enhance the contractility
and the effectiveness of the heart.
Page 4 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
most common causes of Hypovolemic shock in surgical patients:
-Blood loss or bleeding.
-Plasma loss as seen in burns or sepsis.
-Extracellular fluid loss. As seen in third space loss, gastroenteritis, and severe pancreatitis.
Vascular access is the most important. Try to give 20 cc/kg, or one liter push, then take two reading
values, see if the patient is improving or not. Usually they improve. If they didn’t, you have to look
for a major cause, bleeding or another underlying cause.
Usually we give two liters; give the first liter and we assess. How to reassess? By central venous
pressure. After the administration of fluids, veins are full with blood and easy to access so I can
measure the preload which reflects the intravascular volume and the effectiveness of the heart.
Compressive shock:
Compression either on blood inflow or outflow (Mostly on inflow).
Veins are collapsible and easy to compress compared with arteries, unless they contain thrombus.
pulmonary artery may cause massive pulmonary embolism and induce blockage to the arteries.
What are the causes of compressive shock?
Pericardial tamponade, pneumothorax, obesity, hepatomegaly, or sepsis in the abdomen, it will
push the diaphragm and limits the cardial function.
Cardiogenic shock other causes: electrolytes imbalances, arrhythmias, atrial fibrillations, and
decreased contractility and cardiac output.
Our aim in patients with pump failure is to reach an acceptable left ventricular end systolic pressure,
and to give a sufficient peripheral oxygenation with acceptable heart rate, so you have to be careful
in prescribing the right drug, it doesn’t have to increase or exaggerate the ischemic condition of the
patient’s heart by inducing tachycardia or other risky side effects. But at the same time you need to
have an efficient cardiac output.
Diuretics are very important to decrease the preload, also we usually use adrenaline as the first
choice because it will increase the cardiac output and at the same time will give an alpha effect on
the vasoconstriction of the peripheral vascular system.
Neurogenic shock:
Happens in patients with spinal injury, quadriplegia, general and regional anesthesia patients. The
cause as we said is the affection of the autonomic innervation.
Page 5 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
Sometimes administration of drugs affecting the adrenergic nervous system, may induce aunotomic
affection and neurogenic shock .
These patients we bring them to Trendelenburg position, with the use of vasoconstrictors.
Regarding the septic shock, before reaching the frank stage of shock, the patient first goes through
these stages: bacteremia, sepsis, severe sepsis, and finally shock.
Systemic inflammatory response syndrome SIRS:
Criteria for diagnosis:
-Temperature more than 38 or less than 37.
-Heart rate more than 90.
-Respiratory rate more than 20.
-WBC’s more than 12,000 or less than 4,000
What is sepsis? Sepsis is the presence of at least two of the previously mentioned abnormalities plus
documentation of Infection.
For example a patient with a WBC count of 15,000 + heart rate 120 + positive blood culture, we call
this sepsis.
Severe sepsis: when signs of organ dysfunction start to develop, such as oliguria and mental
changes.
Septic shock: mostly due to gram negative bacteria.. The patient reaches decompensation, and
some of the patients will not respond to the resuscitative measures.
It is the only type of shock peripherally warm compared with others, but if it persists, you will see
cold peripheries, more hypotension and decrease in the cardiac output. Because septic shock
patients usually to compensate for this, they have tachycardia, and flaccid peripheries due to the
release of inflammatory mediators induced by sepsis (while it’s because of autonomic innervation
affection, in regional anesthesia patients).
Management:
-IV fluids are important.
-Culture of the expected focus of infection.
-Administration of antibiotics.
Page 6 of 7
17/2/2015
General Surgery/Lec 2+3
Rawan Al-Majali
In general, you have to know the definition of shock and its different types. General and specific
signs of shock.
Usually we use aggressive resuscitation, by iv fluid, except in cardiogenic shock.
Vasopressor is one of the first line management in patients with neurogenic shock.
Page 7 of 7