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CVS Flashcards

1
Q

How do the LV and RV contract differently?

A

The LV contracts concentrically while the RV twists and contracts.

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2
Q

Afterload is also known as….

A

Wall tension across the ventricles at the end of systole.

P1: SVR (120)
P2: Pleural pressure (0-5)
T = [(P1-P2) x radius] divided by wall thickness. The smaller the delta P, the less the afterload. Lessen afterload by decreasing P1 (vasodilation) or increasing P2 (PEEP).

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3
Q

Preload is also known as…

A

Wall tension across the ventricle at the end of diastole. It generally represents the volume that stretches the ventricles before contraction.

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4
Q

What is a normal ejection fraction and what is a normal stroke volume?

A 
EF = ESV/EDV
(EF = 75/120, EF = 63%), normal EF = >60%

SV = EDV - ESV
Usually about 70mL in a 70kg male.

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5
Q

How does PPV affect the two ventricles?

A

To an extent, PPV props the LV up and decreases the pressure difference between the LV and intrathoracic space. This helps more than the detriment it causes to aortic compression so net benefit for the LV.

However, it also compresses the pulmonary vasculature and forces the RV to work harder, possibly decreasing LV preload. RV preload is already reduced due to great vessel compression.

*Generally speaking, PPV reduces CO, except in the case of high SVR.

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6
Q

Delta down must have a _____% change in order for a patient to be considered fluid responsive. They must be in sinus rhythm, paralyzed and be on a controlled tidal volume @10ml/kg for it to be considered accurate.

A

10

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7
Q

Murmur intensity is graded on a scale from 1-6. What grade is associated with a corresponding thrill?

A

4

1: only a cardiologist can hear
(6: you can hear that thing without a stethoscope!)

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8
Q

When describing a heart murmur, what characteristics are worth mentioning?

A 
Shape (crescendo)
Timing
Location (A, P, T, M)
Radiation (carotids, subclavians)
Intensity (1-6)
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9
Q

Useful labs when assessing a CVS patient:

A 
Troponins (HS, I, T)
BNP
Lactate
SvO2
Extended lytes
BUN:Cr
CBC
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10
Q

There are five types of MI. What are they?

A
  1. Atherosclerosis
  2. Oxygen imbalance
  3. Sudden death
  4. PCI mediated
  5. CABG mediated
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11
Q

Standard therapy for NSTEMI pathway:

A

+ASA (162-325)
+P2Y12 inhibitors (Plavix 300/150, Ticagralor 180/90)
+Statins (Atorvastatin 80mg)
-Beta blockers (Metoprolol 5/25), or ACE-I if BP/HR high
-Nitrates (10mcg/min TNG infusion, TNG patch, TNG spray)
-Anticoagulation (Enoxaparin, heparin)
-O2/MSO4
-Optimize Mg++, K+
-Integrillin if there is a high clot burden
-Pantaloc 80mg bolus, then 8mg/hr infusion

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12
Q

Killip Score (assesses HF in setting of MI)

A

I - No HF
II - Pulmonary edema <50%, S3, SBP > 90
III - Pulmonary edema >50%, S3, SBP > 90
IV - Cardiogenic shock, SBP < 90

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13
Q

Target electrolyte levels for MI:

A

Ca++ > 1.0
K+ 4.0-5.0
Mg++ >0.8

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14
Q

When converting AFib, which PO cardioverting agent tends to lower BP less? Beta blockers or CCBs?

A

Beta Blockers.

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15
Q

STEMI Imposters

A 
BER
Pericarditis
LBBB
LVH
Paced
Increased ICP
Aortic dissection (more likely affects RCA)
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16
Q

Timelines for PCI vs TNK and what study is it based on?

A

For PCI, door to balloon must occur < 90 minutes, or consider it if access to TNK is delayed > 2 hours.

PRAGUE/DANAMI-2

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17
Q

Absolute contraindications for TNK/tPA:

A
  • Hx of ICH
  • Hx of ischemic CVA < 3mo
  • Known cerebral vascular lesion
  • Metastatic intracranial malignancy
  • Possible aortic dissection
  • Active bleeding or bleeding diathesis
  • Significant head/face trauma < 3mo
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18
Q

When is thrombolysis considered effective?

A

When ST segments decrease by at least 50% and ischemic symptoms are completely resolved within 90 min.

*Runs of idioventricular rhythm are highly indicative of reperfusion and successful thrombolysis. Do not treat them. They are usually self limiting.

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19
Q

Why do successful TNK patients still need to go for angio?

A

If there was 90% occluded vessel that received the thrombus, the 90% occlusion is still there after the TNK dissolves the thrombus.

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20
Q

Complications of untreated STEMI…

A 
Q waves (necrosed tissue)
LV wall rupture
LVA
Papillary muscle rupture
Dysrhythmias
Cardiogenic shock
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21
Q

Front line vasoactive therapies for cardiogenic shock:

A

Always start them on levophed first, then start the dobutamine. Consider milrinone only in tachycardia and extreme cases since it stays in the system for so long and is hard to correct.

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22
Q

There are two types of HF. Diastolic (preserved EF) and systolic (reduced EF). What must your EF be less than to be considered as systolic failure?

A

<40%

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23
Q

What does the NYHA score measure? What study suggests that an NYHA score of 4 should get ACE-Is?

A

Heart failure
Class 1: No symptoms
Class 2: Slight SOB/angina on physical activity
Class 3: Marked limitation on walking 20-100m. Comfortable at rest.
Class 4: Severe limitations. Symptomatic even at rest.

CONSENSUS-1

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24
Q

Chronic Tx for HF:

A

*ACE-I/ARB
*Beta blockers
*Spironolactone
TNG patch
Diuretics
CRT/ICD

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25
Q

Acute Tx for HF:

A 
Lasix (IV dose should = home PO dose)
Nitro (start at 10mcg/min and move up quickly)
Oxygen
Position
BIPAP/CPAP
Dobutamine
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26
Q

Cardinal signs of a right sided MI:

A
  • Hypotension
  • Clear lungs (except with posterior-medial papillary muscle rupture)
  • JVD
  • Increased CVP
  • Bradycardia
  • V4R findings, or STE III > II
  • *Avoid TNG, MSO4
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27
Q

What does the TIMI score measure?

A

Ha! It actually measures two things!

1 - Risk score for STEMI (0 to 14). A score of 8 or higher comes with a 8.8% chance of death.

2 - Flow during percutaneous coronary angioplasty (0 to 3). 3 is normal perfusion/flow.

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28
Q

What are the goals of therapy when starting a nitroglycerin infusion for ACS?

A

Target total pain relief, but limit yourself using the patient’s blood pressure.

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29
Q

What does the Forrester score assess?

A 
Cardiogenic shock. A true Forrester needs a PAC.
I. Warm and dry
II. Warm and wet
III. Cold and dry
IV. Cold and wet
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30
Q

Causes of right sided heart failure:

A

RVMI
Pulmonary HTN
PE

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31
Q

What wall of the RV is affected in RCA occlusion?

A

The lateral wall. The septum is supplied by the LAD and remains functioning normally. A fluid bolus for RVMI can help improve CO since the septum becomes a more effective pumping mechanism when distended.

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32
Q

Well, shiiiiiiit. How you going tell the difference between a PE and an RVMI?
(Both will likely have hypotension, JVD, clear lungs/SOB, high CVP)

A
  • 15-lead (ITWs/S1Q3T3 vs STE)
  • Hx (Virchow’s vs Frammingham’s).
  • Perform an echocardiogram (subxiphoid view)
  • Tachycardia (PE) vs bradycardia (RVMI)
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33
Q

What is Virchow’s triangle?

A

Stasis: Bed rest, long flight, varicose veins, F# limb
Hypercoaguability: CA, pregnancy, smoking
Endothelial Injury

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34
Q

Describe an alternate mechanism of hypoxemia in PE:

A

It’s not dead space ventilation. Vessels surrounding PE release cytokines that cause inflammation, increased A-C thickness and, therefore, shunt.

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35
Q

Right heart strain pattern on ECG and labs

A

Sinus tachycardia with right axis deviation
ITWs in septal leads
Elevated BNP and troponins
CT and echo
D-dimer (a negative result can rule out a PE)

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36
Q

Main difference when treating PE vs RVMI:

A

Provide fluid bolus in RVMI will improve preload. It assists with septal pumping. Do not bolus if RV failure present. Assess CVP.

A fluid bolus will decrease coronary perfusion pressures (Ohm’s Law) in PE and decrease DO2.

PEs will get heparin and possibly tPA. RVMIs will get TNK/PCI and ACS pathway.

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37
Q

PE treatment:

A
  • tPA
  • Anticoagulation
  • Oxygenation
  • Permissive hypotension
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38
Q

Normal mean pressure for each chamber:

A 
RA: 5
LA: 10
RV: 25
LV: 100
In RV strain, pressures are increased and coronary perfusion gradient is decreased.
39
Q

The LV is perfused during diastole only. What about the other chambers?

A

They are low pressure chambers (except in RV strain). They are normally perfused during systole and diastole.

40
Q

How much cardiac output does diaphragmatic breathing use up during passive breathing? Active breathing?

A

At rest: 3%

Active: 30%

41
Q

Why is areflexia so damn lethal in right ventricular failure?

A

Hypoxia/hypercapnia causes pulmonary vasoconstriction, which causes increased right sided afterload. BMV will also kill these patients since it compresses pulmonary vasculature and also increases RV afterload. Just try not to intubate or BMV these patients.

42
Q

Mech vent strategy for RV failure:

A

Low pressure/volumes. High rates. Minimize PEEP. High FiO2.

43
Q

Dose of Amiodarone (bolus and infusion):

A

Initial bolus: 150mg
First 6 hours: 1mg/min
Next 18 hours: 0.5mg/min

44
Q

DDx for sinus bradycardia

A 
HyperK+
Increased ICP
RCA Ischemia
Hypothermia
Drugs
Carotid artery trauma
45
Q

Causes of pericardial effusion:

A 
Inflammation (post MI)
Uraemia
Trauma
CA
Autoimmune disorder
46
Q

Concerns when managing an LAD MI:

A
  • Ventricular dysrhythmias
  • LVA
  • Apical rupture
  • Purkinje/Bundle of His dysfunction (AV blocks)
  • LV failure
  • Papillary muscle rupture
47
Q

Treatment for cardiac tamponade:

A

Full: Fluid bolus
Fast: Allow tachycardia
Forward: Levophed

48
Q

Patient has a surgical drain in for their tamponade. All of a sudden they become SOB and hypotensive. Thoughts?

A

Probably not infection this early in the game. Check for an iatrogenic pneumothorax.

49
Q

Cardinal signs of pericarditis:

A

Positional pain
Friction rub
Diffuse concave STE with PR depression

50
Q

Of pericarditis, myocarditis, endocarditis, which one will be associated with elevated troponins?

A

Myocarditis

*Myocarditis means sick heart muscle. It can deteriorate into cardiogenic shock.

51
Q

Risk factors for aortic dissection:

A

HTN, age, Marfan’s, smoking, Caucasian

52
Q

Differentiate type A from type B aortic dissection:

A

Type A is proximal to the LSCA while type B is distal to it.

Type A requires surgical intervention.

53
Q

What is the main concept behind treating aortic dissection?

A

Lower Delta P/Delta T
Delta P: pulse pressure
Delta T: chronotropy

54
Q

What is the actual treatment for aortic dissection?

A
  • Labetalol to target BP < 120 but keep HR > 60.
  • If HR < 60, use nitroprusside to continue to lower BP.
  • Don’t overlook analgesia or anxiolysis in lowering HR.

*Nitroprusside must be taken from the sending hospital

55
Q

Define HTN crisis:

A

SBP > 180 or DBP > 120 with signs of end organ damage (vision loss, decreased UO, chest pain, CVA)

56
Q

Conditions where you would use heparin, instead of Enoxaparin in the setting of ACS:

A

Poor renal function
Patient is going for CABG
Heparin is already running

Heparin is good if pt has renal failure. Enoxaprin is good if pt has liver failure.

57
Q

Nitroprusside vs Nitroglycerin infusion:

A

Nitroprusside: Start at 40mcg/kg/min. Used for lowering BP since it is both an arterial and venous dilator.

Nitroglycerin: Start at 10mcg/min. Used for ACS and CHF. Mostly, a venodilator.

58
Q

Dosing regimen for labetalol:

A

5mg -> 10mg -> 20mg -> 40mg -> 80mg. Stop at total of 300mg and consider another vasodilator like hydralazine, phentalomine, nitroprusside or nifedipine.

59
Q

Approximate infusion equivalent of 0.6mcg patch of TNG:

A

10mcg/min

60
Q

Standard infusion rate for 40mEq KCl-.

A

100mL/hr = 4mEq/hr through a central line only.

10mEq will increase serum K+ by approximately 0.1 mmol so 40mEq should bump K+ up by 0.4mmol. Shifts in pH will also alter serum K+ levels.

Consider oral K+ if patient is conscious. It’s safer, more effective and faster.

61
Q

Major caveat before administering Mg++ to correct hypomagnesia:

A

The patient must be making urine.

62
Q

Initial dose of hydralazine:

A

5-20mg (will cause reflex tachycardia)

63
Q

Standard dose of Lasix and its effects on decreasing preload:

A

20-80mg (Or match their home PO dose with an IV dose)

Increases venous capictance and decreases venous volume.

64
Q

Steps to take when you lose capture on a TVP:

A

Roll the patient on their side
Increase TVP output
Switch to transcutaneous pacing

65
Q

When assessing an aortic dissection, what two systems other than CVS must you assess?

A

Neuro and renal

And GI (celiac, mesenteric arteries)

66
Q

How does an intra-aortic balloon pump (IABP) work?

A

Used to treat cardiogenic shock. It inflates during diastole, thus providing counterpulsations and increasing pressure pushed back onto the coronary ostia. This helps with coronary perfusion.
Also decreases LV P1 pressure (and thus afterload), by the negative pressure “pulled” on the LV when the balloon deflates. The decrease in wall tension decreases MVO2.
It inflates to 80-90% diameter of aorta immediately after the aortic valve closes and deflates just before aortic valve opening.

67
Q

Tx for pulmonary hypertension:

A
  • Optimize pH, improve PaO2 (but keep PEEP low)
  • Nitric oxide or flolan
  • Milrinone, then dobutamine with levophed
  • Maybe a fluid bolus, unless the patient worsens. Then give diuretics.
68
Q

Treatment for RVMI:

A 
Fluid bolus
ACS/STEMI pathway
Permissive hypotension
Dobutamine +/- levophed only if you have to.
No morphine or nitro!
69
Q

What was the DANAMI-2/PRAGUE-2 trial about?

A

The benefit of PCI within 120 min vs TNK.

70
Q

Why is tachycardia in ACS a bad thing?

A
  • Increases MVO2
  • Decreases coronary perfusion since diastole is less and coronary arteries fill during diastole.

-Before treating with beta blockers, though, make sure there are no signs of heart failure and the patient isn’t relying on tachycardia for CO.

71
Q

What is Beck’s triad?

A

Assesses for cardiac tamponade:

  • Hypotension
  • JVD
  • Muffled heart sounds
  • Also look for electrical alternans and ultra sound
72
Q

Other body systems affected my endocarditis:

A

Valvular vegetations can dislodge and travel to cause emboli in renal or neurological systems.

73
Q

Predictors of failed NIPPV in ACPE at baseline (1) and after one hour of therapy (2):

A
  1. RR > 39, SBP < 102, SpO < 85%, lactate > 2.4

2. RR > 33, SPB < 90%, pH < 7.37, PF < 147, lactate > 2.6

74
Q

Independent risk factors for failing NIPPV in the setting of ACPE:

A
  • Killip IV score
  • LVEF < 30%
  • BNP > 3350
  • Fluid balance > 400mL since onset of ACPE
75
Q

How does a paralytic effect blood pressure?

A

Loss of skeletal muscle tone reduces venous return to RA.

76
Q

Describe a cardiac appropriate RSI strategy:

A

-Heavy on fentanyl, light on sedatives and paralytics. Use ketamine, unless super arrhythmogenic or hypertensive.

77
Q

BNP can be used as a marker for severity of ADHF, but it must be taken with two grains of salt (figuratively, not literally of course… That would be bad)

A
  • BNP can be chronically elevated in HF patients
  • It’s dynamic and will change. BNP will likely decrease in the face of insensible losses from increased respiratory rate and losses from diuretic therapy.
78
Q

DDx for STE in cardiogenic shock

A
  • MI
  • Dissection
  • LVA
  • Hyperkalemia
  • LVH strain
  • SAH
  • Myopericarditis
  • Do an ultrasound, check CXR, bilateral BPs, labs
  • Consider Levophed for increased diastole (better coronary perfusion and increased preload/contractility)
79
Q

5 most immediate concerns with CP. Better rule these out!

A
  • MI/ACS
  • PE
  • Tension PTX
  • Aortic dissection
  • Boerhaave
80
Q

How much pericardial fluid can cause tamponade physiology?

A

150mL

81
Q

Definition of cardiogenic shock:

A

Persistent hypotension (SBP < 80-90) with CI < 1.8 (unsupported) or < 2.2 (supported)

82
Q

What are the 5 categories of pulmonary artery hypertension?

A 
I - Idiopathic, meth
II - Left heart failure
III - Lung disease, chronic hypoxia
IV - Chronic pulmonary artery obstructions
V - Chronic hemolytic disease
83
Q

What is the single best test to determine a patient’s fluid responsiveness?

A

Passive leg raise
-Lift a supine patient’s legs up to 45 degrees for 45-60 seconds. If MAP increases by 10mmHg, then give fluid. Not to be used on trauma patients.

84
Q

Three cardinal signs of an aortic dissection:

A
  • Knife-like, stabbing shoulder/back pain
  • Widened mediastinum on CXR
  • Unequal bilateral BPs

*If one of these signs is present, a CT angiogram is required to rule it out.

85
Q

What is CRT

A

Cardiac Resynchronization Therapy

-Used with CHF patients with intraventricular conduction delays, to improve LV systolic dysfunction.

86
Q

Diagnosing a tamponade… Go!

A
  • Beck’s (JVD, muffled HS, low BP)
  • Compressed RA
  • Non-collapsible IVC
  • By the time the LV is involved, pulsus paradoxus will also likely exist and the patient will be using accessory breathing muscles to create negative pressure in pulmonary vasculature to ‘pull’ blood in.
  • Pulusus paradoxus can be confirmed with placement of an A-line.
  • Pts with pulusus paradoxus will die during intubation. Use an awake approach.
  • Locate descending aorta on long axis view to differentiate tamponade from pleural effusion. Also look at the lungs.
  • Really, only an anterior pericardial effusion can be safely drained.
87
Q

What is the equation to determine DO2

A

DO2 = CO x CaCO2

CO: (SV x HR)
CaO2: [(1.34 x Hgb x SaO2) + (0.003 x PaO2)]

88
Q

Your patient is in cardiogenic shock and after starting them on levophed, they still require some inotropic support. What will guide your decision making?

A

Okay, you’ve looked at things such as peripheral perfusion and ScVO2 and the suck. Levophed is helping coronary perfusion and improving myocardial function but it ain’t enough. Start them on some low dose dobutamine to get some better contractility and maybe even a bit of vasodilation to improve peripheral perfusion. Once the patient’s kidneys are working again, you can think about switching to milrinone in order to bring heart rate down and reduce the risk of dysrhythmias. Remember, milrinone is renally cleared and very slow to metabolize so don’t start it unless the patient is making urine.
P.S. Fuck dopamine

89
Q

What’s more concerning? Second degree heart block in the setting of inferior or anterior MI?

A

Inferior MI may cause isolated ischemia to the AV nodal artery whereas if it’s an anterior MI, large swathes of conduction pathways need to be taken out for the patient to go into a second degree block. Definitely, be more concerned about the anterior 2AVB.

90
Q

What could pericardial free fluid mean in the setting of post MI?

A
  • Pericarditis
  • Aortic dissection
  • Ventricular free wall rupture
91
Q

You’re transporting a post-STEMI patient and they suddenly crash. What could be going on? List your DDx.

A
  • Ventricle Wall rupture
  • Chordae tendinae rupture
  • Septal wall defect
  • Reinfarct
  • Inflammatory pericarditis now a tamponade
  • Dissection
  • Cardiogenic shock
92
Q

Your post STEMI patient has abruptly crashed and you suspect a chordae tendinae rupture. How do you treat it?

A

-High dose NTG infusion to reduce the regurgitation gradient and possibly some inotropic support.

93
Q

What should pucker your butthole more? A second degree AV block from an inferior or an LAD STEMI?

A

LAD is worse. Instead of just the AV nodal artery being bad, an LAD 2AVB means enough myocardium has been wiped out to fry a lot of electrical pathways.

94
Q

Signs of HOCM

A
  • LVH on 12-lead when there is no reason for LVH such as HTN or AS
  • Dagger Q waves in inferior leads
  • Exertional syncope or presyncope
  • AS like systolic murmur
  • Respiratory such as dyspnea, orthopnea, fatigue
  • Palpitations
  • Chest pain

CCP (18 decks)

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