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CCP S2 > CCP 216 - Cardiovascular Emergencies > Flashcards

CCP 216 - Cardiovascular Emergencies Flashcards

1
Q

Why is TNKase preferred over alteplase in the fibrinolysis of AMI?

A

It is associated with a lower rate of non-cerebral bleeding complications.

Described in the ASSENT-2 trial.

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2
Q

Summarize the eight benefits of beta blockers in AMI:

A

1) Decreased MVO2.
2) Decreased risk of VF.
3) Decreased automaticity.
4) Prolonged diastole & coronary perfusion.
5) Reduction in remodelling.
6) Slows progression of atherosclerosis.
7) Inhibits platelet aggregation and thromboxane synthesis.
8) Reduction in reperfusion injury.

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3
Q

When are beta blockers indicated in STEMI?

A

Certain benefit when no reperfusion strategy is used.

Probable benefit following PCI/fibrinolysis.

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4
Q

What are the five types of MI?

A

1) Occlusive
2) Demand
3) Sudden death
4) PCI-related
5) CABG-related

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5
Q

80% of VF/VT occurs within the ___ hours following AMI.

A

12 hours.

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6
Q

What receptors are responsible for acute modifications of HR and inotropy?

A

Baroreceptors.

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7
Q

When does the majority of ventricular filling occur?

A

EARLY diastole. This is because of the huge initial pressure gradient.

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8
Q

T or F:

Coronary plaque lesions are often < 50% following AMI.

A

True.

This indicates that the most important factors of AMI are plaque rupture, platelet aggregation, and thrombus formation.

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9
Q

How does mitral stenosis sound on auscultation?

A

MS is heard as an “opening snap” at the beginning of diastole, followed by a mid-diastolic rumble that tapers off in sound, and a final crescendo during atrial systole prior to ventricular contraction.

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10
Q

What is the S3 heart sound?

A

Ventricular gallop. Classically produced by VOLUME overload. Occurs during the rapid filling phase during early diastole. Occurs because of the tensing of the chordinae tendonae when fluid slams against the mitral valve.

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11
Q

What is the S4 heart sound?

A

Atrial gallop. Classically produced by PRESSURE overload. Occurs when the atria contract at the end of ventricular diastole. S4 is the sound of the atria contracting into a stiff ventricle.

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12
Q

What is the wall tension equation?

A

Wall tension = (P x Radius) / Wall thickness

P = Delta P (ie. P1-P2)

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13
Q

What is the oxygen delivery equation?

A

DO2 = (HR x [EDV x EF]) x ([SaO2 x 1.34 x Hgb] x [PaO2 x 0.0031])

Simplified:
DO2 = CO x CaO2

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14
Q

How many much ATP is produced in the Kreb cycle?

A

36 ATP.

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15
Q

What is the cardiac index?

A

CI = CO / TBSA

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16
Q

SVR is highest at the ____.

A

Distal capillaries.

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17
Q

How do right atrial pressure and CVP differ?

A

The RA is more compliant the SVC/IVC.

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18
Q

What is normal RAP?

A

< 5

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19
Q

What is normal RVP?

A

< 25 / < 5

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20
Q

What is normal LAP?

A

< 10

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21
Q

What is normal LVP?

A

< 130 / < 20

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22
Q

For CVP to be nearly identical to RVEDP, three factors need to be present:

A

I) Tricuspid needs to be functioning properly
II) Compliance of RA needs to be identical to vena cava.
III) An open column needs to be present between vena cava & RV.

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23
Q

Explain why CVP can’t be considered identical to RAP:

A

The RA is dynamic (ie. with respiration), and there is rarely a point in time where RAP is able to equalize with CVP.

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24
Q

Explain the importance of improving contractility prior to reducing afterload:

A

Sudden decreases in afterload prior to improvement of contractility may cause a rebound increase in HR.

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25
Q

What is tachyphylaxis?

A

Rapid decrease in response to a drug following administration.

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26
Q

Aortic regurgitant disease should be managed by:

A

Increasing HR.

This reduces diastolic regurgitation time into the LV.

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27
Q

Aortic stenotic disease should be managed by:

A

Increasing EDV and slowing HR.

This facilitates a high LV pressure to promote LV outflow.

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28
Q

What are the four causes of hypoxia?

A

1) Hypoxic
2) Histotoxic
3) Hypemic
4) Stagnant

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29
Q

What are the five causes of hypoxemia?

A

1) Low FiO2
2) VQ mismatch
3) Diffusion impairment
4) Hypoventilation
5) Shunt (venous admixture)

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30
Q

What is cardiac steal?

A

Coronary perfusion following the path of least resistance.

For example: Nitrate vasodilation of the LAD during occlusion of the LCX may shunt blood to the LAD, further reducing perfusion of the LCX.

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31
Q

What components of the DO2 equation are modifiable?

A

1) Cardiac output
2) Hgb
3) SaO2
4) PaO2 (environmental PO2)

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32
Q

Why is unstable angina disappearing as a diagnosis?

A

UA is essentially early NSTEMI that has not yet produced detectable troponin.

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33
Q

What are the contraindications of nitrates in the realm of critical care?

A

1) Cardiogenic shock
2) Fixed occlusive lesion (cardiac steal)
3) Preload dependent AMI (ie. RV MI)

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34
Q

Who needs rescue PCI?

A

1) Persistent STE that hasn’t decreased by at least 50%.

2) Persistent C/P.

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35
Q

What is the time-frame for rescue PCI?

A

Preferably within 2 hours. Necessary within 24 hours.

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36
Q

STEMI management includes:

A

1) DAPT
2) Anticoagulation
3) Reperfusion

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37
Q

What is the preferred P2Y12 inhibitor for primary PCI?

A

Ticagrelor (180mg) or prasugrel.

If clopidogrel, double the usual dose.

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38
Q

What is the preferred anticoagulant in primary PCI?

A

UFH (5000U + infusion).

UFH can be reversed and controlled better than GP IIb/IIIa inhibitors.

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39
Q

What is the preferred P2Y12 inhibitor for primary fibrinolysis?

A

Clopidogrel (Age ≤ 75 300mg; Age > 75 75mg).

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40
Q

What is the preferred anticoagulant in primary fibrinolysis?

A

UFH (4000U + infusion), because it can be reversed with protamine sulphate.

Enoxaparin is acceptable, but enoxaparin eliminates the opportunity for rescue PCI is required.

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41
Q

What is the MOA of P2Y12 inhibitors?

A

Irreversible blockade of the P2Y12 component of the ADP receptor on platelet surface.

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42
Q

What is the MOA of ASA?

A

Irreversibly inhibits COX 1 and COX 2 enzymes, ultimately irreversibly inhibiting formation of thromboxane A2, inhibiting platelet aggregation.

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43
Q

What is the MOA of UFH?

A

Inactivates thrombin and prevents the conversion of fibrinogen to fibrin.

44
Q

What is the best measurement of heparin levels?

A

Anti-Xa levels, which directly measure the amount of heparin in the blood.

INR indirectly measures heparin levels.

45
Q

What is the timeline cutoff for reperfusion?

A

Fibrinolysis max is 24 hours following onset, but no benefit after 12 hours.

PCI can be considered over any timeline.

46
Q

The preferred timeline of PCI is within ___ minutes from first medical contact.

A

90 minutes.

47
Q

Transfer to PCI-capable centre is preferable compared to fibrinolysis if PCI can be achieved within ___ minutes of first medical contact.

A

120 minutes.

48
Q

An NSTEMI patient who is being catheterized within 24 hours should receive which anticoagulant?

A

UFH.

49
Q

An NSTEMI patient who is being catheterized in > 24 hours should receive which anticoagulant?

A

Fondaparinux.

Single dose fondaparinux provides 24 hours of coverage, has a lower risk of re-thrombosis than UFH, and also anticoagulants DVT.

50
Q

The indications for PCI in NSTEMI are:

A

I) Hemodynamic instability.
II) Electrical instability.
III) Persistent C/P.

51
Q

Contraindications of PCI include:

A

1) Risk of bleeding during procedure.
2) Inability to take DAPT for 1yr.
3) Severe renal failure.
4) Triple vessel disease (ie. needs CABG).
5) Palliative status.

52
Q

The goal of TNK is ___ minutes.

A

30 minutes.

53
Q

Enoxaparin is contraindicated in patients with:

A

CKD/AKI.

54
Q

What AMI patients receive BB?

A

Everyone. Unless there is an outstanding contraindication.

55
Q

Which AMI patients receive statins?

A

Everyone.

56
Q

ACE-Is are given to which AMI patients?

A

Hypertensive patients who DO NOT have AKI.

57
Q

Differentiation of Type I versus Type II AMI can be performed by:

A

1) Assessing wall motion abnormality. Typically Type II AMI will not have wall motion abnormality.
2) Type II AMI is classically in the presence of another insult.
3) Type II AMI has fairly stable troponin.

58
Q

What are the three types of fluid that may be present in the pericardium?

A

1) Arterial blood
2) Venous blood
3) Lymph

59
Q

What is the first ventricle to collapse from pericardial tamponade?

A

The RA. Followed by the RV.

60
Q

Tamponade affects the heart most at what phase of filling?

A

End diastole. Essentially all filling occurs at the beginning of diastole when tamponade is present.

61
Q

Pulsus paradoxus is defined by ___% variation in pulse pressure.

A

10%.

62
Q

What are the causes of cardiac tamponade?

A

1) Trauma.
2) Free wall or lateral wall rupture of ventricle.
3) Renal failure.
4) Autoimmune disease (ie. SLE)

63
Q

What two treatments need to be avoided in LVOT obstruction, that are frequently used in the management of HF?

A

Inotropes and vasodilators.

64
Q

How should LVOT obstruction from SAM be managed?

A

With fluid and high afterload. Dilation of the ventricle will stretch the mitral valve leaflet away from the LVOT.

65
Q

Which patients are at risk of SAM?

A

Patients with subvalvular HCM (hypertrophy of the upper septum).

66
Q

What is the cause of HCM?

A

Derangement of sarcomeres in the myocardium.

67
Q

How is systolic anterior motion of the mitral valve into the LVOT produced?

A

Caused by a venturi effect, which pulls the leaflet into the LVOT.

68
Q

Dagger Q waves on ECG may indicate:

A

HCM.

69
Q

Young healthy adults who have LVH on ECG may have what underlying disease?

A

HCM.

70
Q

Explain the controversy of beta blocker use in patients with HCM:

A

PRO: BB will allow higher preload and subsequent dilation of the ventricle to separate the anterior leaflet from the LVOT.

CON: BBs may reduce afterload, which may allow for faster outflow, producing a venturi effect in the LVOT.

71
Q

What lesion can produce a relative LVOT obstruction from akinesia of the lower LV septum, and hyperkinetic movement of the basal septum?

A

LAD lesion.

72
Q

What are “kissing ventricles”?

A

Complete closure of the ventricles during systole, indicating hypovolemia.

73
Q

Why is PEEP generally capped at approximately 25mmHg?

A

25mmHg is when the esophageal sphincters are typically opened.

74
Q

Outline the approach to SCAPE:

A

1) Nitrates (hydralazine is also an option, but it is less titratable and less predictable).
2) PEEP
3) Diuretics
4) Beta blocker (if HR > 150)
5) Transition to long-term antihypertensive (ie. labetalol and hydralazine).

75
Q

The majority of organs auto regulate blood pressure between which range?

A

50 to 150 mmHg.

76
Q

MAP is the BP seen at the ____, whereas SBP reflects BP at the _____.

A

MAP = Arterioles.

SBP = Proximal aorta.

77
Q

What is the dosing regimen of labetalol for hypertensive emergencies?

A

10, 20, 40, 80.
Deliver at 10 minute intervals, doubling dose PRN.

MAX single-dose:
80mg
MAX total dose:
300mg

78
Q

Aortic dissection involving the ascending aorta is ‘x’ Stanford classification.

A

Stanford Type A.

Surgical emergency.

79
Q

Aortic dissection involving only the descending aorta is ‘x’ Stanford classification.

A

Stanford Type B.

Medically managed.

80
Q

Aortic dissection involving both the ascending and descending aorta is ‘x’ Stanford classification.

A

Stanford Type A.

Surgical emergency.

81
Q

What does PRES stand for?

A

Posterior reversible encephalopathy syndrome.

82
Q

How is PRES managed?

A

PRES is a hypertensive encephalopathy. It is managed by reduction of SBP by ~25%, guided by LOC improvement.

83
Q

What is often the cause of death in bradycardia?

A

Polymorphic VT related to prolonged QTc.

84
Q

Stimulation of the alpha-2 results in:

A

CNS depression and decrease in HR.

85
Q

What are two common alpha 2 agonists used in critical care?

A

Clonidine and dexmedetomidine.

86
Q

What is the trade name of dexmedetomidine?

A

Precedex.

87
Q

List some common causes of bradycardia:

A

1) Hypothermia
2) Hyperkalemia
3) Hypothyroidism.
4) Hypoglycemia.
5) End-stage hypoxia, hypercapnia, and acidosis.
6) Neurogenic shock (from reduced sympathetic outflow).
7) Pacemaker failure
8) Drugs (ie. digoxin, BB, alpha 1 antagonists, alpha 2 agonists)

88
Q

Outline the approach to bradycardia management:

A

1) Atropine.
2) Pacing.
3) Chronotrope (ie. epi).
4) Calcium (to manage hyperK)
5) Insulin for beta blockade.

89
Q

What ECG changes may be present from ICH?

A

T wave changes.

90
Q

How does alcoholism associated with hypokalemia?

A

It impairs uptake of K in the gut.

91
Q

Narrow QRS PEA is generally considered a ____ problem, and is associated with what disease states?

A

Mechanical RV problem.

Tamponade, tension, PTX, mechanical hyperinflation, PE.

92
Q

Wide QRS PEA is generally considered a ___ problem, and is associated with what disease states?

A

Metabolic LV problem.

Hyperkalemia, sodium-channel blocker toxicity.

93
Q

What is the indication for CT scan in all-cause cardiac arrest?

A

Investigation for bleeding.

94
Q

What does TTM stand for, and what is the current recommendation for TTM?

A

Targeted temperature management.

Prevent hyperthermia, by targeting a temperature of 36C.

95
Q

“Pocket change” is useful for remembering:

A

Pressure within the cardiac chambers.

5, 10, 25, 100 (RA, RV, LA, LV).

96
Q

List the scoring systems for HF:

A

1) Killip
2) NYHA
3) Forrester

97
Q

List the scoring systems for AMI-associated mortality:

A

1) TIMI

2) GRACE

98
Q

List the scoring systems for CAD:

A

1) Framingham

99
Q

What is daltaparin typically used for?

A

Anticoagulation in PE and DVT.

100
Q

What is the utility of methylene blue in cardiogenic shock?

A

Functions by scavenges excess cGMP to reduce the vasodilatory effect of cGMP. Ultimately results in vasoconstriction

101
Q

Outline the approach to the management of aortic dissection:

A

1) Reduce HR (goal of 60
2) Reduce SBP (goal of 100)

Avoid hydralazine, as it may increase wall shear stress.

102
Q

How does hypocalcemia appear on an ECG?

A

QTc prolongation.

103
Q

How does hypercalcemia appear on ECG?

A

QTc shortening.

104
Q

How does hypomagnesemia appear on ECG?

A

QTc prolongation.

Changes contiguous with hypokalemia.

105
Q

How does hypermagesemia appear on ECG?

A

Changes contiguous with hyperkalemia.

106
Q

How does hyperkalemia appear on ECG?

A

1) Peaked T waves (>5.5).
2) P wave flattening and PR prolongation (>6.5).
3) QRS prolongation, sine wave appearance, bradycardia, and AV block (>7.0).
4) Asystole, VF, or wide PEA (>9.0).

107
Q

How does hypokalemia appear on ECG?

A

1) PR prolongation, T wave inversion, and prominent U wave.

2) SVTs.

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