Assessment & Management of Patients with Shock Flashcards
1
Q
Describe the hemodynamics involved in hypovolemic/cardiogenic/septic shock (Preload, PCWP, CI, SVR, Mixed O2 sat)
A
2
Q
In general, what is “shock”?
A
It is an acute, life-threatening acute syndrome of organ and systemic dysfunction; often times there is circulatory failure with hypotension often the original sign.
3
Q
In general, describe the pathophysiology of “shock”
A
The primary physiologic disturbance is the impaired cellular function that occurs when blood flow is disturbed.
- This leads to a disruption in the ability of the body to meet metabolic demands
- There is then a “Shock state” (Occurs when oxygen consumption is greater than oxygen delivered). And there is cellular hypoxia and resulting dysfunction
- Because of the reduced oxygen and nutrient supply from this shock state, this leads to anaerobic metabolism.
- This, in turn, causes the production of acids (lactic and pyruvic). Decreased adenosine triphosphate (ATP) then occurs causing reduced energy.
- Finally, activation of the inflammatory response occurs, releasing proinflammatory cytokines (tumor necrosis factor, interleukin-1), which cause systemic inflammation, and endothelial vasodilating oxygen free radicals
* Generally reversible if identified early but can quickly lead to an irreversible and fatal condition*
4
Q
What are the 4 main physiologic causes of shock?
A
- Decreased contractility. Seen in AMI, cardiomyopathy, CHF and valvular heart disease (stenosis, regurgitation)
- Decreased circulating volume. Hypovolemia, hemorrhage
- Obstruction of the central blood flow. Seen when there is a compression of the heart or great vessels
- Altered vascular resistance such as vasodilation and decreased peripheral vascular resistance. There is a pooling of venous blood with inadequate venous return. This results in relative hypovolemia. Examples are anaphylaxis, sepsis and neurological disorders
5
Q
What are the 3 compensatory mechanisms the body uses for shock?
A
1. Nervous system compensation:
- Baroreceptors sense a ↓ in CO and ↓BP.
- Signals go to the vasomotor center of the medulla stimulating the SNS → norepinephrine released
- ↑norepinephrine → ↑HR → ↑CO + ↑RR + constriction of vasculature in skin, GI tract and kidneys
2. Hormonal compensation:
- SNS actives the anterior pituitary → adrenocorticotropic hormone (ACTH) is released.
- ACTH → Adrenal Cortex → Aldosterone released → ↑Na reabsorption + ↑H20 absorption → ↓ Urine Output
- ↑preload to heart → ↑CO
3. Chemical compensation:
- Chemoreceptors in the aorta and carotid arteries sense an ↑ in pH
- Signals are sent to the Medulla → ↑RR & ↑Depth of respirations → ↓CO2
- Vasoconstriction of the cerebral vessels along with decreased O2 tension then leads to cerebral hypoxia and ischemia.
6
Q
What is and what causes hypovolemic shock?
A
Definition:
- Shock that occurs when circulating blood volume is inadequate to maintain circulation for tissue perfusion and nutritional requirements
- It is associated with a blood volume deficit of at least 15% - 25%.
Causes:
- Hemorrhage from trauma (Ex: long bone fractures, ruptured liver and/or spleen, and laceration of great vessels.
- Other blood lossess: GI bleed or hemorrhagic pancreatitis, ruptured abdominal aortic aneurysm.
- Non-hemorrhagic causes: vomiting, diarrhea, fistulas, large NG tube aspirate.
- Renal losses include excessive diuresis (think about diabetes insipidus, SIADH, Addison’s disease) or excessive diuresis from diuretics.
7
Q
What are the clinical manifestations of hypovolemic shock?
A
- tachycardia
- hypotension
- decreased CVP, CO, CI, pulmonary artery pressure
- The patient may be positive for postural hypotension: SBP decreases 20 mmHg or more OR the heart rate increases 20 bpm or more
- The more severe the hypovolemia, the more severe the symptoms
8
Q
Describe the symptoms seen in hypovolemic shock with progressive losses of blood
A
- Up to 10% blood volume lost – the patient may be asymptomatic or have slight tachycardia
- Up to 15% blood volume loss you will see slight hypotension and slight tachycardia in your exam. Capillary filling will be less than 3 seconds. The patient may feel anxious or slightly confused. They will be orthostatic; urine output will remain adequate at this point.
- 15% - 30% blood volume loss you will see a MAP greater than 65 mmHg, tachycardia, decreased pulse pressure, cool extremities with pallor and capillary filling greater than 3 seconds. The patient will be lethargic and weak. Urine output will begin to decrease to less than the normal of 0.5 ml/kg/hr.
- >40% blood volume loss, you will see moderate to severe hypotension (MAP less than 65 mmHg) with tachycardia. The patient’s LOC will be severely compromised; they will have cold clammy skin.
9
Q
How do you manage a patient in hypovolemic shock?
A
- Give a fluid challenge of 250mL-500mL NS or LR
- If the CVP or BP remains low, continue to bolus
- Give appropriate products for type of fluid loss:
- Blood/blood products – transfuse PRN depending on the severity of shock. One unit of PRBCs should increase the hematocrit by approximately 3 ml/dl and hemoglobin by 1 gram/dl.
- Consider coagulation factors when you are not transfusing with whole blood. Fresh frozen plasma (FFP) may be needed to correct clotting factors (except platelets). If the patient is receiving massive transfusions then FFP will be required. The patient may need a platelet transfusion to control bleeding if the count is low of if there is platelet dysfunction
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Crystalloids – this is the initial fluid to be used in resuscitation of severe sepsis and septic shock. Points to remember about them include: They are inexpensive, convenient and relatively free of adverse effects. They are rapidly distributed across intravascular and interstitial cell spaces. The two most common are Ringer’s Lactate and Normal Saline.
- Ringer’s contains physiologic concentrations of sodium, chloride, calcium, potassium and lactate in water. It is a very effective volume expander and buffer in the patient with acidosis.
- Normal saline increases plasma volume. You will see it used most often when the hypovolemic state is NOT due to blood loss. The expansion in volume is transient as the fluid will eventually accumulate in the interstitial spaces (pulmonary edema). If you compare it to a colloid, it usually requires 2-4 times more of NS than a colloid to achieve hemodynamic stability.
- Colloids – Albumin. Recommended when patients with severe sepsis and septic shock are requiring large amounts of crystalloids as they produce a greater and more sustained increase in plasma volume. This then improves cardiac function and transport of oxygen. When there is hypovolemia that occurs more from plasma loss rather than blood (burns, third degree spacing, peritonitis, bowel obstruction) plasma protein fractions like albumin and Plasmanate are the treatment of choice. Monitoring should include observation of the patient for pulmonary edema, coagulopathies and anaphylaxis.
- Military antishock trousers – an external counterpressure device that may be applied to trauma patients by first responders (especially with fractures of pelvis and long bones) to splint, increase venous return and hopefully improve vital organ perfusion. Its use is controversial.
Vasopressors are contraindicated until the circulating volume has been restored with fluid replacement!
10
Q
What is and what causes cardiogenic shock?
A
Definition:
- Occurs when there is an impaired ability of the heart to pump effectively. There will be a decrease in stroke volume (SV) and cardiac output (CO). This results in poor tissue perfusion and tissue hypoxia.
Causes:
- Acute myocardial infarction (AMI)
- Arrhythmias
- CHF
- Myocardial trauma with contusions
- dissecting aortic aneurysm
- myocarditis
- end-stage cardiomyopathy and septic shock with severe myocardial depression
11
Q
What are the clinical manifestations associated with cardiogenic shock?
A
- Patients with crushing chest pain and EKG changes consistent with AMI will benefit from early intervention to reverse the cardiogenic shock
- You will see ↓ SV, ↓ CO & ↓ CI
- A CI less than 1.8 L/min/m2 suggests cardiogenic shock
- LVEF of less than 30%, if left heart failure is the cause, will be seen, on echocardiogram. If the cause is right heart failure this will be seen on echo also.
- Patients will have signs of congestion with rales/rhonchi, a decreased PaO2, an increase in the PaCO2 initially followed by a decrease in the PaCO2 as shock progresses
- You will hear S3 and S4 heart sounds; the presence of a precordial thrill may occur as well as a systolic murmur of mitral regurgitation. Acute MR may warrant immediate surgical intervention
- Peripheral edema, distended neck veins
- Oliguria, altered mental status and cool skin may occur as tissue perfusion decreased
- Cardiogenic shock is diagnosed after documentation of myocardial dysfunction and exclusion/correction of hypovolemia, hypoxia and acidosis
12
Q
What diagnostic tests are done to diagnose cardiogenic shock?
A
- EKG to evaluate for ischemia or arrhythmia
- Echocardiogram should be done immediately at bedside
- CXR – look for cardiomyopathy, aortic abnormalities
- Lab – ABG, electrolytes (abnormalities can cause arrhythmias), CBC (severe anemia can result in ischemia), BNP (elevated in CHF), cardiac enzymes
- Left and right heart catheterization – right to assess hemodynamics, left to assess coronary arteries
- Continuous hemodynamic monitoring – may be useful to exclude volume depletion, cardiac output and index
13
Q
How do you manage a patient with cardiogenic shock?
A
- Goal = improve cardiac output
- Initially fluid resuscitation may be indicated unless pulmonary edema is present. Electrolyte imbalances and acidosis should be corrected
- Inotropic agents to improve cardiac contractility may be needed: Dopamine, Dobutamine, Milrinone, Vasodilating agents
- Afterload reduction: Nitroprusside, Vasopressor agents
- Preload reduction: May be necessary for BP support. Vasopressin, Norepinephrine, Dopamine, epinephrine, Phenylephrine, Nitroglycerine, Diuretics
- Counter-pulsation (intra -aortic balloon pump) may be needed to increase pump efficiency, increase end organ perfusion and reduce myocardial oxygen demand. Other devices include Impella and LVAD (discussed in next module)
- Revascularization for patients with AMI with resultant cardiogenic shock
14
Q
What is and what causes obstructive shock?
A
Definition:
- Due to obstruction of flow in the cardiovascular system. You may see an impairment of diastolic filling or excessive afterload. Patients with obstructive shock usually have hypotension associated with distended neck veins but usually without other evidence of volume overload
Cause:
- Etiologies include a direct venous obstruction by an intrathoracic tumor, an increased intrathoracic pressure caused by a tension pneumothorax or high ventilator positive end expiratory pressure (PEEP), decreased cardiac compliance due to constrictive pericarditis or cardiac tamponade and an increase in ventricular afterload caused by an aortic dissection, pulmonary embolus or acute pulmonary hypertension
15
Q
What is and what causes Distributive shock?
A
Definition:
- There is vasodilation and loss of vasomotor tone resulting in venous pooling of blood with decreased venous return, decreased CO and inadequate tissue perfusion
Cause:
- Occurs in septic, neurogenic and anaphylactic shock
16
Q
What is and what causes Septic Shock?
A
Definition:
- It is a systemic inflammatory response (SIRS) PLUS infection. It is a systemic inflammatory response to infective organisms in the blood stream that alter vascular tone resulting in relative hypovolemia. This systemic infection then begins the vicious cycle of coagulation and inflammation
Cause:
- Nosocomial infections in the critically ill
- Genitourinary (GU) tract (this is the most common cause of sepsis in the older adult)
- Respiratory tract
- Wounds, surgical or trauma
- Catheter sites (peripheral or central)
- Meninges
- GI tract – overuse of broad-spectrum antibiotics has led to resistant strains of bacteria
- Some causative organisms include these gram-negative bacilli:
- E Coli
- Klebsiella pneumonia
- Enterobacter
- Proteus
- Pseudomonas
- Serratia
- Meningococci
- And gram positive organisms including:
- Staphylococci including staph aureus, staph epidermidis and staph saprophyticus
- Streptococci – strep pyogenes, strep viridins and strep pneumonia (there are others)
- Clostridia – clostriium perfringens, clostridium difficile and clostridium botulinum
- Bacteriodes.
- Viruses and fungi may also be causative agents
