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NSCC 7320 > Hemodynamic Instability > Flashcards

Hemodynamic Instability Flashcards

1
Q

What causes AAA?

A

Degeneration of collagen fibres and elastin, loss of smooth muscle fibres which results in thinning of medial layer and dilation of affected area

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2
Q

What is AAA?

A

Full thickness dilation of a BV that is greater that 50% the normal aortic diameter

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3
Q

What is the normal diameter of the aorta? If the aorta is considered aneurysmal, what does the diameter have to be?

A

2 cm. >3cm.

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4
Q

What are other locations for aortic aneurysms? What is the most common?

A

Ascending thoracic aorta, descending thoracic aorta, and abdominal aorta (most common).

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5
Q

What are the manifestations of a symptomatic AAA?

A

Abdominal, back, flank pain. N/V if pressing on adjacent bowel, back pain from pressure on spinal nerves or ischemia from embolization to distal circulation (lower limbs, gut, kidneys)

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6
Q

What is the triad of symptoms for AAA rupture?

A

Severe acute abdominal/back pain, profound decreased BP, pulsatile abdominal mass.

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7
Q

What is the most useful predictor of repairs for AAA?

A

AAA greater than or equal to 5.5 cm

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8
Q

When would someone get an open repair versus an EVAR?

A

Open repair if ruptured, EVAR for high risk patients

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9
Q

What are some common post-op complications from open repair of AAA?

A

Spinal ischemia and neuro deficits (from prolonged cross-clamp time), Fluid imbalances, embolization of thrombus or debris from inside of aneurysm to distal sites including circulation to lower limbs, gut, kidneys. Most common are bowel ischemia and AKI (prolonged cross clamp time).

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10
Q

What are nursing priorities caring for someone post AAA repair?

A

Control BP, close hemodynamic monitoring, assess distal circulation, check incision site, may have difficulty ventilating patient due to distended abdomen/pain

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11
Q

What is the definition of shock?

A

Hemodynamic instability and impaired widespread EOP that goes untreated

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12
Q

What is the predominant issue in hypovolemic shock? How are other determinants of CO affected?

A

Decreased preload. Increased after load (SNS comp mech), decreased contractility (decreased preload), increased HR (SNS comp mech), decreased CO overall.

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13
Q

What is the main treatment for hypovolemic shock? How will it help?

A

Fluid resuscitation (will help preload). Afterload, contractility and HR should all improve once CO is restored.

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14
Q

What is the main issue in cardiogenic shock? How are other determinants of CO affected?

A

Contractility is poor. Preload is increased (blood backing up as it isn’t pumping forward), after load is increased (comp mech from decreased CO and poor perfusion, SNS and RAAS), increased HR (SNS), decreased CO overall.

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15
Q

What is the main treatment for cardiogenic shock? How will it help?

A

Nitro or diuretic to decrease preload, + inotrope to support contractility, and nitro or vasodilator to support after load.

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16
Q

What is the main issue in distributive shock? How are other determinants of CO affected?

A

Reduced afterload is the primary problem (PNS>SNS, sepsis), preload is decreased (due to decreased venous return), contractility is decreased (due to decreased preload), HR is increased (due to SNS). Initially CO may be increased or normal due to decreased after load (less force to pump against) but will eventually decrease.

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17
Q

How would we want to treat distributive shock?

A

Fluid resus (help preload), vasopressors (afterload). Fluid rests should improve contractility and support increased CO.

18
Q

Once we start to adequately oxygenate tissues, how long does it usually take for lactate levels to go down? What might happen to these levels during the ‘washout’?

A

12-24 hours. Might initially go up.

19
Q

Based on the SAFE study, what fluid is recommended for fluid resuscitation?

A

NS (albumin just as effective but it is more expensive and not as readily available)

20
Q

Based on TRICC trails, what are the transfusion requirements with ACS and non-cardiac pt?

A

Non-Cardiac: Hgb <70

Cardiac: Hgb <80

21
Q

How does Levophed (norepi) work? Potential SE?

A

Peripheral vasoconstrictor, primarily acts on alpha receptors. Increases after load. Ischemic limbs, inc cardiac O2 demand from inc after load and could dec CO.

22
Q

How does Phenylephrine work? Potential SE?

A

Arterial vasoconstrictor, increases after load. Works on alpha receptors. May cause bradycardia related to vagal stimulations from rapid rise in BP, dec SV due to increased after load.

23
Q

How does Nitro work? Why is this effective?

A

Causes venodilation which results in decreased preload. Dilates coronary arteries.

24
Q

What are four examples of vasoconstrictors? What is the primary treatment in vasodilatory shock? Second line?

A

Epi, norepi, phenylephrine, vasopressin.

Levophed, epi (2nd).

25
Q

What are three examples of inotropes?

A

Dobutamine, dopamine, milrinone.

26
Q

What are three examples of vasodilators?

A

Nitro, hydralazine, sodium nitroprusside

27
Q

How does Epi work? Potential SE?

A

Binds at alpha, beta 1 and 2, increases after load and CO. Dysrhythmias, inc HR, inc myocardial demand.

28
Q

How does vasopressin work? Potential SE?

A

Stimulates V1 receptors (vasoconstrictor in smooth muscles) and V2 receptors (increase reabsorption of h20 in nephron collecting ducts). Increases after load. Potential gut ischemia (smooth muscle contraction in gut), distal limb ischemia.

29
Q

How does dobutamine work? Potential SE?

A

Mainly beta 1, some beta 2, some alpha stimulation. Increases contractility, decreases after load, may cause inc HR. BP may inc/dec, inc HR or dysrhythmias could occur.

30
Q

How does dopamine work? Potential SE?

A

Some alpha and beta 1. Hemodynamic effects are dose-dependent. Increases contractility (mid dose), increases afterload (high dose), inc renal perf (low dose). Inc HR common. Possible HTN, inc HR, palpitations, dysrhythmias.

31
Q

How does milrinone work? Potential SE?

A

Phosphodiesterase 3 inhibitor. Increases calcium. Increases contractility, causes vasodilation (including in pulmonary arteries). Ventricular dysrhythmias, dec BP, headache.

32
Q

How does hydralazine work? Potential SE?

A

Arterial vasodilator. Decreases after load. Reflexive tacky.

33
Q

How does sodium nitroprusside work? Potential SE?

A

Venous and arterial smooth muscle dilation, combines with hub to produce cyanide. Decreases after load from peripheral vasodilation/decreased peripheral resistance. Dec BP, myocardial ischemia, N/V, abdo pain, cyanide poisoning.

34
Q

What are symptoms of cyanide poisoning from sodium nitroprusside?

A

Confusion, decreased LOC, decreased O2sat.

35
Q

What are the recommendations for dose adjustments of vasoactive drugs? How are the drugs normally ordered?

A

Adjust dose in small increments. With a MAP goal and/or SBP goal (more often MAP goal).

36
Q

Can levophed be administered via PIV?

A

Yes, but only for a short period of time at a low concentration until central access can be obtained.

37
Q

Under what SBP do we often try to keep patients? In what types of patients is it most important to keep BP controlled?

A

<160-180. Head injury, AAA, post-op

38
Q

What medications might be used to treat HTN?

A

Labetalol/beta blocker, hydralazine

39
Q

How does hydralazine work? Potential SE?

A

Direct arterial vasodilator. Decreases after load. Decreases HTN. May cause reflexive tacky.

40
Q

How does labetalol work? Potential SE?

A

Beta 1, 2, alpha antagonist. Dec HR, dec afterload. Bronchospasm, heart block, Brady, postural hypotension.

41
Q

How does metoprolol work? Potential SE?

A

Beta antagonist (beta 1 specificity). dec HR, dec contractility, may decrease BP as a result of dec HR (unless given IV then has large effect on BP). Bradycardia, heart block.

42
Q

Why are dec preload and dec after load commonly seen post intubation?

A

Dec preload due to increased intrathoracic pressure and decreased venous return. Decease after load related to sedation and analgesia medications.

NSCC 7320 (7 decks)

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