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78 Cards in this Set
- Front
- Back
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What is the formula for constriction of blood vessels?
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Pressure = Flow x resistance (MAP) = Cardiac Output (flow) x Peripheral resistance (systemic)
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How much cardiac output is the atrial kick responsible for?
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20-30%
Without atrial kick, you only passive motion of blood to veins |
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How much of the cardiac cycle is systole vs diastole?
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systole = 1/3
diastole = 2/3 |
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What are the three phases of ventricular systole?
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1. Isometric contraction (isovolumetric contraction)
2. Rapid ventricular ejection 3. Reduced ventricular ejection |
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What are the four parts of ventricular diastole?
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1. Isovolumetric relaxation
2. Period of rapid filling 3. Period of slow filling 4. Atrial systole, which provides the atrial kick |
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What is cardiac output?
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The volume of blood in liters pumped by the heart in 1 minute.
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What is the cardiac index?
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Measurement of the Cardiac Ouput (CO) adjusted for Body Surface Area (BSA). It is a more precise measurement of the efficiency of the pumping action of the heart.
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What is the stroke volume? Stroke volume index?
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Stroke volume is the volume ejected with each heartbeat. Stroke volume index is adjusted for BSA.
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What determines BP?
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Cardiac output and the Systemic Vascular Resistance (SVR), which is the opposition encountered by the Left Ventricle.
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What is Pulmonary Vascular Resistance (PVR)?
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The resistance to blood flow encountered by the Right Ventricle.
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What is Left Ventricular End-Diastolic Pressure a measure of? What is the measure tool?
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Left ventricular Pre-load (amt of L Ventricle stretch)
PAWP measures pulmonary capillary pressure and, under normal conditions, measures Left Ventricular Pre-load Mitral Valve dysfunction, Intracardiac defect or dysrhythmia interferes with this measure |
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What is CVP?
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Central Venous Pressure
Measured in the Right Atrium or the Vena Cava close to the heart Equates to the Right Ventricular Pre-load or Right Ventricular End-Diastolic Pressure Tricuspid Valve dysfunction, Intracardiac defect or dysrhythmia interferes with this measure |
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What is Frank-Starling's law?
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Explains the effects of preload and states that the more a myocardial fiber is stretched during filling, the more it shortens during systole and the greater the force of the contraction. As preload increases force generated in the subsequent contraction increases, thus SV and CO increase. The increased myocardial stretch causes greater O2 need of the myocardium. Stretched out sweat pants analogy.
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What is after load?
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Refers to the forces opposing ventricular ejection, including systemic arterial pressure, the resistance offered by the aortic valve, and the mass/density of the blood being moved.
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What is preload?
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The volume within the ventricle at the end of diastole.
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What are the measures of after load?
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SVR and arterial pressure = left ventricular after load.
PVR and pulmonary arterial pressure = right ventricular after load. Increased after load often results in decreased CO. Vasodilators will reduce after load |
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What is contractility? How do you measure it?
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The strength of the contraction of the heart. Said to increase when the preload is unchanged but the heart contracts more forcefully. Positive Inotropes increase contractility. Negative inotropes decrease it, i.e., beta blockers, Ca++ channel blockers, alcohol, acidosis.
No direct measures of contractility; measuring CO and PAWP indirectly measures. If preload, HR, and after load remain constant then contractility is changed. |
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What is the phlebostatic axis?
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The point at which the transducer is placed (4th intercostal space and mid-chest).
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What are you measuring with an arterial line?
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systolic, diastolic and mean BPs
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What does a Pulmonary Artery Flow-Directed Catheter measure, i.e. Swan-Ganz?
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PA pressure -- PA diastolic pressure and PAWP with balloon inflation (Left Ventricular preload); SvO2; CVP at the right atrium
These measures increase with heart failure and fluid volume overload; decreases with volume depletion The distal lumen sits in the PA |
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What is the normal range for SvO2 in the L ventricle? Right atrium?
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Left ventricle = 95-99%
Right atrium = 60-75% |
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What do you test to measure fluid status?
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CVP and Wedge pressure
(and lung sounds) |
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What is normal cardiac output? Cardiac index?
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4 - 8 L/min (rough depending on size of patient)
2.5 - 5.0 L/min/m2 |
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What is a normal wedge pressure (PAWP/PCWP)?
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8-12 or 10-12
Low PCWP = dehydration High PCWP = Fluid overload 18-20 = onset of pulmonary congestion 20-25 = moderate 25-30 = severe congestion >30 pulmonary edema |
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What is a normal CVP (Right Ventricular preload)
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2-6 mmHg
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What conditions increase preload? Basic treatments?
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Conditions:
-Congestive heart failure -Hypercoloid (elevated proteins) -Bradydysrhythmias Treatments: -Diuretics -Volume displacement -ACE inhibitors |
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Afterload = BP. True?
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False. It is a component of BP. SVR is after load
left Ventricular after load = SVR Right Ventricular after load = PVR (not common in adults) |
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What is a normal SVR? PVR?
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SVR = 800-1200 dynes/sec/cm5
PVR = 200 dynes/sec/cm5 |
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Can you have low BP and have high after load?
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Yes due to low cardiac output (Low BP) and vasoconstriction (high SVR); can also have high SVR and be in a hypertensive crisis
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What conditions decrease preload? Basic treatments?
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Conditions:
- Hypovolemia - increased intrathoracic pressure - Cardiac tamponade - Tachydysrhythmias - Loss of atrial kick (a-fib) Treatments: - Crystalloid solutions (LR, NS) - Colloid solutions (albumin, plasmanate) - Blood or blood products -Adjust vasodilators (decrease nitrates) |
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What conditions increase afterload? Basic treatments?
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Conditions:
- Vasoconstriction - HTN - Aortic Valve Disease - Hypercoaguability Treatments: - Arterial vasodilators - ACE inhibitors - Phosphodiesterase inhibitors - Intraaortic balloon pump - Pulmonary vasodilators - O2 to reduce Right ventricular after load (reducing work of lungs) |
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What conditions decrease afterload? Basic treatments?
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- Vasodilation
Treatment: vasopressors to increase afterload |
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What conditions increase contractility? Basic treatments?
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Conditions:
- sympathetic nervous system stimulation Treatment: - Beta blockers - Ca++ channel blockers |
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What conditions decrease contractility? Basic treatments?
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Conditions:
- Myocardial ischemia or infarction - Cardiomyopathy - Hypoxemia & acidosis - Negative inotropes Treatment: - Cardiac glycosides (digoxin) - Sympathomimetics - Phosphodiesterase inhibitors (milrinone) - Calcium - Glucagon |
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What conditions increase heart rate?
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Conditions:
- sympathetic stimulation Treatment: - Cardiac glycosides (digoxin) - beta blockers - CCBs - Overdrive pacing - Vagal maneuvers |
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What conditions decrease heart rate?
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Conditions:
- parasympathetic stim - Conduction abnormalities Treatment: - Sympathomimetics - Parasympatholytics, ie, atropine - Pacemaker |
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What are complications of PA catheters?
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- During insertion (tickling SA node, can temp or perm stop working; v-tach from right ventricle; infection)
- During monitoring (movement) - During removal (make sure not embedded in PA; could result in PE or air embolism |
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What are the impacts of inotropic medications?
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Positive:
Increase myocardial contractility, primarily As that happens, following also occurs: - Ventricular emptying increases - Filling pressure of the heart decreases - Stroke volume increases - Cardiac output increases - Increases BP - Improves tissue perfusion Negative, Increases: - myocardial O2 demand - workload of the heart - vascular resistance **used for shock and low cardiac output syndromes |
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What are the classes of inotropic medications?
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Cardiac glycosides = digoxin
Sympathomimetics = stimulate adrenergic receptors - natural catecholamines (epinephrine, dopamine, norepinephrine) - Synthetic: (dobutamine, neosynephrine, phosphodiesterase inhibitors = milrinone) |
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What are the drugs most commonly used for cardiogenic shock with hypotension?
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Dopamine (moderate dose)
Levophed Epinephrine Neosynephrine |
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What are the drugs most commonly used for cardiogenic shock, caused by cardiac failure, with normotension?
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Dobutamine
Dopamine (low dose) Milrinone Epinephrine (low dose) |
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What are the drugs most commonly used for septic shock with hypotension?
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Levophed
Dopamine (low-mod) Dobutamine Milrinone |
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What are the most commonly used drugs for hypovolemic shock?
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Fluids
Blood Blood products |
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What are the most commonly used drugs for shock related to bradycardia?
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Epinephrine
Isuprel |
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What is the most commonly used drug for anaphylactic shock?
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Epinephrine
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What is dopamine used for?
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Hypotensive arrest
NOT for septic shock Heart failure (use with caution) Increase renal perfusion Correct hemodynamic imbalance in shock syndrome |
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What receptors are activated by Dopamine?
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Alpha (increases with dose)
Beta 1 (peaks and then effect declines high dose) Beta 2 (low-moderate, not dose-dependent) |
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What are the cardiovascular effects of dopamine?
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- Increases cardiac output (most with low dose, diminishing response with high dose)
- Increases heart rate (most with moderate dose) - increases SVR (most with high dose) |
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What receptors are activated by Dobutamine?
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- Alpha (NO effect)
- Beta 1 (high activation with all doses) - Beta 2 (Moderate activation) |
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What are the cardiovascular effects of Dobutamine?
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- Increases Cardiac Output
- Increases heart rate (effect increases with dose) - DECREASES SVR (reason it is good for pump failure) |
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Where are alpha receptors located and what is the response to stimulation?
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Located on vessels of skin and kidneys
vasoconstriction of peripheral arterioles to shunt blood |
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Where are beta1 receptors located and what is the response to stimulation?
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Located in cardiac tissue
Increase HR, conduction, and contractility |
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Where are beta2 receptors located and what is the response to stimulation?
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Located in vascular and bronchial smooth muscle
Vasodilation of peripheral arterioles Bronchodilation |
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What receptors are activated by epinephrine?
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Alpha (response is higher with higher dose)
Beta 1 (response peaks with moderate dose) Beta 2 (response is moderate with any dose) |
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What are the cardiovascular effects of epinephrine?
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- Increases CO (highest response with moderate dose)
- Increases HR (moderate response with high dose) - Increases SVR (moderate response with high dose) |
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What receptors are activated by Norepinephrine?
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Alpha (response is higher with higher dose; higher than epinephrine)
Beta 1 (moderate response with any dose) Beta 2 (No response) |
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What are the cardiovascular effects of Norepinephrine?
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- Increases CO (low response)
- Increases HR (low response) - Increases SVR (very high response) good for septic shock to reduce vasodilation |
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What receptors are activated by Phenylephrine?
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Alpha (high response)
Beta 1 (No response) Beta 2 (No response) |
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What are the cardiovascular effects of Phenylephrine?
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- DECREASES CO (low response)
- DECREASES HR (low response) - Increases SVR (very high response) |
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Why is dobutamine the best choice for pump failure or with dopamine for MI/shock?
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- Primarily beta1 effects
- mild beta2 effects with mild vasodilation - increases contractility without increasing HR, B/P or SVR |
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Why is Norepinephrine (levophed) used for septic shock? What are primary adverse effects?
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- Increases CO
- Increases SVR Adverse effects: - arrhythymias, HTN, chest pain - anxiety - respiratory distress (even tho no Beta 2 effect) - EXTRAVASATION! |
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What are epinephrine and phenylephrine typically used for?
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- Code situation/shock
- Very potent alpha stimulator - Increases BP without stimulating myocardium - Increases SVR ** watch peripheral circulation; use heat packs if color/pulses/cap refill are diminshed |
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What is milrinone typically used for?
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- Strictly for pump failure; usually acute exacerbations
- Positive inotrope and vasodilator - Increases CO (contractility and decreased after load) ** Incompatible with Lasix |
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How do vasodilators work on after load and preload?
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Afterload reduction:
- arterial dilation, results decreased resistance to ventricular ejection; may improve CO without increasing myocardial O2 demand Preload reduction: - venous dilation to increase capacitance; results in decreased filling pressure for the failing ventricle |
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What are the effects of nitroglycerin?
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Arterial and venous dilation; at low doses, mainly VENOUS; at high doses, mainly ARTERIAL
Adverse effects: postural hypotension, headache, reflex tachy ***Antagonist to Heparin!!! (if both given together, PTT appears elevated until nitro stopped and then dangerous high PTT) |
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What are the effects of niprusside (nitride)?
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Very potent venous and arterial vasodilator
Used for hypertensive crisis; decrease after load in pulmonary edema and heart failure Avoid in renal failure - breaks down to thiocyanate (psychosis, tinnitus, coma) Avoid in liver failure - breaks down to cyanide (almond smell on breath) ** MIX only with D5W, not NS; protect from light |
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What is Phentolamine (regitine) used for?
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alpha adrenergic antagonist used in treatment of dermal necrosis after extravasation
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What drugs should ideally be given through a central line?
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- dopamine
- epinephrine - levphed - neosynephrine |
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What is shock?
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Failure of the circulatory system to maintain adequate perfusion of vital organs
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What are the three stages of shock?
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1. Compensatory (non-progressive)
- maintain CO, vasoconstriction, decreased urine, tachycardia 2. Reversible (progressive) 3. Irreversible - Multiple organ damage - Endotoxin release |
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What is cardiogenic shock?
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shock caused by pump failure, i.e., MI, PE, valve dysfunction, dysrhythmias (filling/emptying defects); occurs when >40% of myocardium is involved
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What are the phases of septic shock?
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Early or Warm phase: total vasodilation, Low BP, resistant to fluid resuscitation, low urine, tachypnic; expect PA cath to be low <800, CO will be high 8-10 bc so much fluid floating around but too vasodilated to move.
Late or Cold phase: vasoconstriction, hypotension, altered mental status, poor outcomes |
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What is the defining feature of neurogenic shock?
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Bradycardia
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What are the hemodynamic changes for cardiogenic shock?
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HR: Increased
Stroke volume: Decreased CO: Decreased SVR: Increased PAWP: Increased CVP: Increased |
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What are the hemodynamic changes for hypovolemic shock?
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HR: Increased
Stroke volume: no change or decreased CO: decreased SVR: increased PAWP: decreased CVP: decreased |
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What are the hemodynamic changes for septic shock (warm or hyperdynamic)?
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HR: Increased
Stroke volume: Increased CO: Increased SVR: Decreased PAWP: decreased CVP: decreased |
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What are the hemodynamic changes for septic shock (cold or hypodynamic)?
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HR: Increased
Stroke volume: decreased CO: decreased SVR: increased PAWP: increased CVP: increased |
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What are the hemodynamic changes for neurogenic shock?
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HR: decreased or normal
Stroke volume: no change CO: decreased SVR: decreased PAWP: decreased CVP: decreased |
