CCRN PRACTICE TEST
1. How does Nifedipine (Procardia) work?: Nifedipine decreases myocardial oxygen
consumption by dilating veins and arteries, thereby decreasing preload andafterload. Nifedipine
also decreases vasospasm and potential for vasospasm. Unlikediltiazem and verapamil,
nifedipine does not significantly decrease contractility
2. What are the components of the pulmonary artery waveform?: In a pulmonary artery
waveform the three components of the waveform are systole, dicroticnotch, and diastole.
Systole is the pressure generated by the right ventricle so thatthe pulmonic valve will be
pushed open, the dicrotic notch is caused by the closureof the pulmonic valve, and diastole is
the pressure in the pulmonary artery during ventricular diastole. The diastolic pressure is a
reflection of the vascular tone in thepulmonary vascular bed. If the vessels are constricted or
if there is back pressure from the left side of the heart, the diastolic pressure will be high
3. What is ankle-brachial index?: ABI is ankle-brachial index, or ankle artery pressure
divided by brachial artery pressure. The pressure at the ankle normallyis higher than the
pressure at the brachial artery, and the normal ABI is 1 or greater. This measurement is more
quantitative than the presence or absence ofaudible Doppler pulses. If an occlusion is
developing, the ankle artery pressure
(measured with a blood pressure cuff and a Doppler stethoscope) will decrease andthe
calculated ABI will decrease long before the pulses are no longer audible
4. How does hypoxemia affect pulmonary vascular pressures?: It causes the vasculature to
constrict, which can lead to pulmonary hypertension
5. If you notice a sudden change in diastolic pulmonary artery pressures you should suspect
what?: Proximal movement of the catheter. Recall that the systolic pressure of the pulmonary
artery and the right ventricle are approximately the same. The diastolic pressure in the
pulmonary artery is normally approximately 10 mm
Hg, whereas the diastolic pressure of the right ventricle is normally close to 0. Anysudden
decrease in the PA diastolic pressure should lead you to suspect that the catheter has flipped
back into the right ventricle
6. What is DIC?: DIC is a consumptive coagulopathy. The clotting cascade is stimulated,
causing clotting in the microcirculation. Platelet and clotting factors (including fibrinogen) are
consumed and become depleted. Clotting studies areprolonged. The massive clotting
stimulates the fibrinolytic system. FDPs are theresult of this fibrinolysis, and they trigger
more bleeding
7. Management of care for pt with DIC includes...: Avoidance of injections, replacement of
fluids/blood/clotting factors, turning frequently and gently, and notusing automated BP cuffs
(risk of injury/trauma)
8. Drugs that may cause torsades de pointes: Amitriptyline (Elavil) causes QTinterval
prolongation and may cause torsades . Other drugs- Class IA antidysrhyth-mics (e.g.,
procainamide, quinidine, and disopyramide), Class III antidysrhythmics (e.g., sotalol and
amiodarone), tricyclic antidepressants (e.g., imipramine [Tofranil]),and phenothiazines (e.g.,
, chlorpromazine [Thorazine])
9. Advantages of an IABP vs pressors?: If you have a hypotensive patient withhigh afterload
giving them pressors will increase SVR, work on the heart, and myocardial oxygen
consumption. IABP increases coronary artery perfusion and myocardial oxygen without
increasing afterload or decreasing BP
10. What are the determinants of oxygen diffusion: Surface area available forgas transfer
Thickness of the alveolar-capillary membraneDiffusion coefficient of gas
Driving pressure
11. What affects the driving pressure of oxygen?: Oxygen concentration (FiO2) and
barometric pressure- so to increase SaO2 you either have to increase FiO2 or increase pressure
(either by hyperbarics or PEEP/CPAP)
12. How do you manage fluid status in a patient with a subarachnoid hemor-rhage?: You
keep the patient hypervolemic with a PAOP (LV preload) greater than12mmHg (normal is 8-
12). Keeping them hypervolemic aids in the prevention andtreatment of vasospam, which
increases the morbidity
13. What is the goal of medical management of stable angina and how is thatachieved?: The
goal of medical management in angina is to decrease myocardialoxygen consumption and to
prevent progression of the disease. Beta-blockers decrease myocardial oxygen consumption by
decreasing heart rate and contractility.Nitrates decrease myocardial oxygen consumption by
decreasing preload primarilyand may decrease afterload also, depending on the dosage. Calcium
channel block-ers decrease myocardial oxygen consumption by decreasing preload and
afterload.
Aspirin is used for primary and secondary prevention of a myocardial infarction byinhibiting
platelet aggregation
14. What do these hemodynamic parameters indicate and how to tx?
HR-112 BP-90/46 (60) RAP-16 PAP 26/10 PAOP- 5 CI-2: Right ventricular dysfunc-tion- High
RAP, normal PAP, PAOP low= decreased blood return to the left side of heart
Goal to improve LV filling to enhance CO. Achieve this by increasing RV filling pressure
(RAP) to higher than normal to increase the passive flow of blood into LV. Discontinue
venous vasodilators (nitroglycerin) and given fluid boluses. Don't
give diuretics because they would decrease RAP and CO. Dobutamine is needed toimprove RV
contractility
15. How does Milrinone work?: Inotropic agent, has arterial and venous vasodi- lating
qualities- decreases preload and lessens the filling of the left side of the heart.Is indicated for
chronic LV failure.
16. Hyperthermia cause what change on the oxyhemoglobin dissociation curve?: It causes it
to shift to the right, which decreases hemoglobin's affinity foroxygen (doesn't like it so it
doesn't hold on to it). So your O2 sats would be lowerthan normal
1. How does Nifedipine (Procardia) work?: Nifedipine decreases myocardial oxygen
consumption by dilating veins and arteries, thereby decreasing preload andafterload. Nifedipine
also decreases vasospasm and potential for vasospasm. Unlikediltiazem and verapamil,
nifedipine does not significantly decrease contractility
2. What are the components of the pulmonary artery waveform?: In a pulmonary artery
waveform the three components of the waveform are systole, dicroticnotch, and diastole.
Systole is the pressure generated by the right ventricle so thatthe pulmonic valve will be
pushed open, the dicrotic notch is caused by the closureof the pulmonic valve, and diastole is
the pressure in the pulmonary artery during ventricular diastole. The diastolic pressure is a
reflection of the vascular tone in thepulmonary vascular bed. If the vessels are constricted or
if there is back pressure from the left side of the heart, the diastolic pressure will be high
3. What is ankle-brachial index?: ABI is ankle-brachial index, or ankle artery pressure
divided by brachial artery pressure. The pressure at the ankle normallyis higher than the
pressure at the brachial artery, and the normal ABI is 1 or greater. This measurement is more
quantitative than the presence or absence ofaudible Doppler pulses. If an occlusion is
developing, the ankle artery pressure
(measured with a blood pressure cuff and a Doppler stethoscope) will decrease andthe
calculated ABI will decrease long before the pulses are no longer audible
4. How does hypoxemia affect pulmonary vascular pressures?: It causes the vasculature to
constrict, which can lead to pulmonary hypertension
5. If you notice a sudden change in diastolic pulmonary artery pressures you should suspect
what?: Proximal movement of the catheter. Recall that the systolic pressure of the pulmonary
artery and the right ventricle are approximately the same. The diastolic pressure in the
pulmonary artery is normally approximately 10 mm
Hg, whereas the diastolic pressure of the right ventricle is normally close to 0. Anysudden
decrease in the PA diastolic pressure should lead you to suspect that the catheter has flipped
back into the right ventricle
6. What is DIC?: DIC is a consumptive coagulopathy. The clotting cascade is stimulated,
causing clotting in the microcirculation. Platelet and clotting factors (including fibrinogen) are
consumed and become depleted. Clotting studies areprolonged. The massive clotting
stimulates the fibrinolytic system. FDPs are theresult of this fibrinolysis, and they trigger
more bleeding
7. Management of care for pt with DIC includes...: Avoidance of injections, replacement of
fluids/blood/clotting factors, turning frequently and gently, and notusing automated BP cuffs
(risk of injury/trauma)
8. Drugs that may cause torsades de pointes: Amitriptyline (Elavil) causes QTinterval
prolongation and may cause torsades . Other drugs- Class IA antidysrhyth-mics (e.g.,
procainamide, quinidine, and disopyramide), Class III antidysrhythmics (e.g., sotalol and
amiodarone), tricyclic antidepressants (e.g., imipramine [Tofranil]),and phenothiazines (e.g.,
, chlorpromazine [Thorazine])
9. Advantages of an IABP vs pressors?: If you have a hypotensive patient withhigh afterload
giving them pressors will increase SVR, work on the heart, and myocardial oxygen
consumption. IABP increases coronary artery perfusion and myocardial oxygen without
increasing afterload or decreasing BP
10. What are the determinants of oxygen diffusion: Surface area available forgas transfer
Thickness of the alveolar-capillary membraneDiffusion coefficient of gas
Driving pressure
11. What affects the driving pressure of oxygen?: Oxygen concentration (FiO2) and
barometric pressure- so to increase SaO2 you either have to increase FiO2 or increase pressure
(either by hyperbarics or PEEP/CPAP)
12. How do you manage fluid status in a patient with a subarachnoid hemor-rhage?: You
keep the patient hypervolemic with a PAOP (LV preload) greater than12mmHg (normal is 8-
12). Keeping them hypervolemic aids in the prevention andtreatment of vasospam, which
increases the morbidity
13. What is the goal of medical management of stable angina and how is thatachieved?: The
goal of medical management in angina is to decrease myocardialoxygen consumption and to
prevent progression of the disease. Beta-blockers decrease myocardial oxygen consumption by
decreasing heart rate and contractility.Nitrates decrease myocardial oxygen consumption by
decreasing preload primarilyand may decrease afterload also, depending on the dosage. Calcium
channel block-ers decrease myocardial oxygen consumption by decreasing preload and
afterload.
Aspirin is used for primary and secondary prevention of a myocardial infarction byinhibiting
platelet aggregation
14. What do these hemodynamic parameters indicate and how to tx?
HR-112 BP-90/46 (60) RAP-16 PAP 26/10 PAOP- 5 CI-2: Right ventricular dysfunc-tion- High
RAP, normal PAP, PAOP low= decreased blood return to the left side of heart
Goal to improve LV filling to enhance CO. Achieve this by increasing RV filling pressure
(RAP) to higher than normal to increase the passive flow of blood into LV. Discontinue
venous vasodilators (nitroglycerin) and given fluid boluses. Don't
give diuretics because they would decrease RAP and CO. Dobutamine is needed toimprove RV
contractility
15. How does Milrinone work?: Inotropic agent, has arterial and venous vasodi- lating
qualities- decreases preload and lessens the filling of the left side of the heart.Is indicated for
chronic LV failure.
16. Hyperthermia cause what change on the oxyhemoglobin dissociation curve?: It causes it
to shift to the right, which decreases hemoglobin's affinity foroxygen (doesn't like it so it
doesn't hold on to it). So your O2 sats would be lowerthan normal
