Circulation Flashcards
Major categories of shock
- Hypovolemia
- Cardiogenic
- Obstructive
- Distributive
Bedside assessment of shock? How is BP determined
BP = SVR x (HR x SV)
(CO = SV x HR)
Feel patient’s extremities - if warm, vasodilated SVR is low. If cool, mottled SVR is high
If BP low, SVR high then CO must be low - need to determine HR/SV
Look at HR - too fast or slow
SV - check JVP
Rule out obstructive causes of low SV (tamponade, tension pneumo, massive PE)
If low JVP and low SV need volume first (fluid vs. blood)
If volume and obstruction are not the issue -think contractility
What is the mechanism and dosing of dobuatmine?
Mechanism: inotrope, works on B1 cardiac receptors
Dosing: 2-20 mcg/kg/min
Caution: may cause tachydysrhythmias, cardiac ischemia from increased demand
Mechanism of norepinephrine? Dosing?
Mostly alpha agonist, some B1 activity.
Useful as a vasopressor in wide variety of situations
Less reflexive bradycardia compared to phenylephrine due to beta activity
0.01-0.5 mcg/kg/min, once you hit >0.3-0.4 with no improvement always think about other causes of shock
Mechanism of phenylephrine? Dosing?
Alpha 1 agonist
Vasopressor only, no inotropy
Short acting, easy pocket pressor
50-200 mcg IV q5 min as needed
Mechanism of dobutamine?
B1 agonist
Inotrope
Also induces some vasodilation with B2 activity
Risk of tachydysrhythmias
Mechanism of milrinone?
Phosphodiesterase (PDE3) inhibitor, inodilator
acts on increasing cAMP to increase intracellular calcium levels
In cardiac cells - leads to increase inotropy and contractility
In peripheral vasoactive cells - leads to vasodilation
Watch for hypotension
Long acting, increased in renal failure - difficult to “take back” once started
Differentiate between systolic and diastolic dysfunction
Systolic dysfunction: poor contractility of myocardium, decreased stroke volume
Diastolic dysfunction: Preserved systolic function, but decreased ventricular compliance and relaxation
End diastolic pressure increases with little improvement in end diastolic volumes (SV). Reduces pressure gradient for flow into the ventricles, leads to decreased cardiac output
10 major causes of AV block
- Ischemia
- Fibrosis/sclerosis of conduction system
- Medications - amiodarone, adenosine, beta-blockers, calcium channel blockers, clonidine, digoxin
- Hyperkalemia
- cardiomyopathy
- myopericarditis
- Hyper/hypothyroidism
- . Infiltrative diseases (rheum, amyloid, malignancy)
- Trauma
- Cardiac surgery
What forces contribute to ventricular afterload?
End diastolic volume (chamber radius)
Vascular resistance
Vascular compliance
Pleural pressure
What are 5 indications for plasma transfusion
- Clinically significant bleeding in patients with severe liver disease and increased INR/PTT
- Massive transfusion
- DIC with active bleeding
- TTP
- Patients with coagulation factor deficiencies when factor concentrates are ineffective/unavailable
What is the INR of FFP?
1.4-1.5
What are 3 indications for cryoprecipitate?
- Hypofibrinogenemia (s disease
What 3 components are involved in hemostasis?
- Vessels
- Platelets
- Coagulation factors