Dr. Walton presents the case of an elderly gentleman in severe cardiogenic shock in the setting of monomorphic VT and prior history of MI and VT arrest.
This patient was admitted and started on amiodarone for monomorphic VT (ultimately converted to NSR), milrinone drip for inotropic therapy, and hydralazine for afterload reduction.
Shock is a state of hypoperfusion resulting in end organ damage (demand is higher than delivery)
Shock can be compensated, decompensated, or lead to irreversible multiorgan failure
Shock is classified in four ways:
Hypovolemic: decreased intravascular volume --> decreased preload and stroke volume --> compensatory vasoconstriction (hemorrhagic, GI losses, skin losses, renal loses, third spacing); treat with fluid/product administration and pressor support
Distributive: relative hypovolemia due to excess vasodilation (septic, anaphylactic, neurogenic, adrenal insufficiency); treat with fluids and pressor support
Obstructive: extra-cardiac causes of pump failure (PE, pneumothorax, severe PH, tamponade, constrictive pericarditis, restrictive cardiomyopathy); treat the underlying process
Cardiogenic: pump failure (cardiomyopathy, ACS, arrhythmia, mechanical issue); treat underlying process and use supportive therapies and inotropes
What is a "mixed venous"??
A mixed venous blood content (SvO2) measures the amount of oxygen in venous blood returning to the R side of the heart. This represents the amount of oxygen "left over" after the tissues remove what they need. This can help to assess tissue oxygen delivery.
A true "mixed venous" comes from a PA catheter (including blood from the coronary sinus). For our purposes, we are typically getting these measurements from the SVC (Scv02), which is technically a "central venous".
Oxygen delivery is dependent on cardiac output (Q) and arterial oxygenation (CaO2 - which is also dependent on hemoglobin):
Oxygen consumption is the rate at which oxygen is removed from the blood for use by the tissues. This can be directly measured by respirometry or calculated by the Fick equation.
The normal SvO2 is 65-75%, which denotes a normal oxygen extraction of 25-35%. Under normal circumstances, oxygen consumption (VO2) is proportional to delivery and extraction. If metabolic demand increases (think, exercise), consumption also increases by increasing delivery and oxygen extraction.
This can help serve as a surrogate for tissue perfusion and can help to differentiate between the types of shock.
Decreased oxygen delivery and increased metabolic demand frequently happen during shock. In the setting of diminished delivery, maintenance of normal oxygen consumption occurs by an increase in oxygen extraction. A low SvO2 indicates that cardiac output is not high enough to meet tissue oxygen needs.
A rise in SvO2 may either indicate that the cardiac output is meeting the metabolic needs of the tissue, OR it may indicate that the patient has resorted to anaerobic metabolism.
Low mixed venous (<65%) is seen in pump failure - cardiogenic shock, or pericardial tamponade. It can also be seen in very late hypovolemic shock.
Elevated mixed venous (>65%) is seen in high circulatory states - distributive shock, early hypovolemic shock, and PE, severe PH or tension pneumothorax.
What is the management approach to monomorphic VT?
1. Is the patient hemodynamically stable? If NO, patient needs urgent electrical cardioversion (initially should be a sychronized shock at maximal energy)
2. If they are hemodynamically stable --> initiate antiarrythmic drug therapy (amiodarone, lidocaine or procanaimide). If this doesn't result in pharmacologic cardioversion, may need to proceed to electrical cardioversion.
3. If at any point the patient becomes pulseless--> transition to standard ACLS algorithms and CPR
Why were this patient's liver enzymes so elevated?
Just like above, hepatic ischemia develops when there is an imbalance between hepatic oxygen supply and demand.
The liver is particularly susceptible to circulatory disturbances, and can both suffer from ischemic hepatitis as well as congestion due to heart failure. Passive congestion is often intertwined and co-exists with reduced cardiac output.
Congestive hepatopathy often occurs in patients with right sided heart failure. Elevated central venous pressure is transmitted to the hepatic veins and venules, leading to atrophy of hepatocytes and development of fibrosis (over time)
-The most common lab finding is elevation in serum bilirubin
-Other liver biochemical tests are mildly increased - alk phos is usually normal or minimally elevated, aminotransferase levels are elevated in 1/3rd of patients (but no more than 2-3x upper limit of normal). Striking transaminitis typically indicates hypotension contributing as well.
-Patients who have preexisting passive congestion of the liver are at increased risk for ischemic injury.
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