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CEN > 19 CEN: cardiac > Flashcards

19 CEN: cardiac Flashcards

19 items on exam

1
Q

What is cardiac output?

A

Cardiac output (L/min) = heart rate (HR) X stroke volume (SV)
HR is bpm. SV is the volume w/ each beat

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2
Q

What is the primary compensatory mechanism for low CO in pediatric patients?

A

tachycardia
-because they cannot increase SV
NOTE: hypotension is a late sign, bradycardia is an ominous sign in pediatrics

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3
Q

How is SV influenced?

A

preload, afterload, and contractility

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4
Q

How is preload evaluated?

A

CVP

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5
Q

What decreases preload and how is it increased?

A

hypovolemia (fluid loss, diuretics, or vasodilators)
-increased with volume (fluids, blood) and vasoconstictors:
alpha-adrenoceptor agonists.
vasopressin
epinephrine.
norepinephrine.
phenylephrine
dopamine.
dobutamine

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6
Q

How is afterload evaluated?

A

SVR.
-It is the resistance to ventricular emptying

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7
Q

How is afterload decreased and how it is treated?

A

↓ in distributive shock (neurogenic, septic, anaphylactic) and with vasodilation
-tx: vasopressors like Norepi

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8
Q

In a state of shock, how does the body respond?

A

-SNS stimulation causes catecholamines epi and Norepi to release which ↑HR
-adrenal glands release catecholamines as well which ↑BG through glycogenolysis
*Glycogenolysis occurs primarily in the liver and is stimulated by the hormones glucagon and epinephrine (adrenaline)

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9
Q

What increases afterload and how is it treated?

A

↑ by HTN, Aortic stenosis, and through other shock compenstation
-tx: vasodilators like NTG

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10
Q

What happens to HR in neurogenic shock and why?

A

the PSNS ↓HR because the SNS response is blocked

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11
Q

What does a narrowed pulse pressure indicate?

A

Early shock

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12
Q

What does a widened pulse pressure indicate?

A

↑ICP

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13
Q

What is cushing’s triad?

A

The 3 signs of ↑ICP
-widened PP or ↑SBP
-bradycardia
-irregular breathing pattern

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14
Q

How do chronotropes affect the heart? Examples.

A

HR at the SA node
Diltiazem or Cardizem (negative) reduces HR and BP.

Diltiazem is a calcium channel blocker. It works by affecting the movement of calcium into the cells of the heart and blood vessels. This relaxes the blood vessels, lowers blood pressure, and increases the supply of blood and oxygen to the heart while reducing its workload.

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15
Q

How do inotropes affect the heart? Examples.

A

Contractility
Dopamine (positive)
Dobutamine (positive)

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16
Q

How do dromotropes affect the heart? Examples.

A

Automaticity (electrical impulse) at the AV node
-Epinephrine (positive)
-Beta blocker (negative)

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17
Q

What does Beta Blockers mask signs of?

A

Shock and hypoglycemia

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18
Q

What organs do Beta-1 medications affect? Examples.

A

Heart only
The cardio-selective beta-1-blockers include atenolol, betaxolol, bisoprolol, esmolol, acebutolol, metoprolol, and nebivolol.
**nonselective carvedilol affects the lungs and not given to asthma and COPD patients

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19
Q

Angiotensin Converting Enzymes Inhibitors:
What are ACE-I given for? Examples.

A

↓BP by blocking converstion of angiotensin 1 to 2
Lisinopril, Benazepril (Lotensin), Enalapril (Vasotec)

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20
Q

What are adverse effects of ACE-I medications?

A

-dry non-productive cough (leads to noncompliance), ARB prescribed instead
-angioedema

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21
Q

Angiotensin Receptor Blockers:
What are ARBs given for? Examples.

A

↓BP by inhibiting angiotensin 2 receptors
Irbesartan (Avapro).
Losartan (Cozaar).
Telmisartan (Micardis).
Valsartan (Diovan).

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22
Q

What are indications for CCBs (calcium channel blockers)? Examples.

A

Diltiazem (Cardizem) controls ventricular rate in A-fib and HTN
Amlodapine (Norvasc) for HTN and chest pain
Nifedipine (Adalat CC) for HTN and prophylaxis angina

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23
Q

What effects does NTG have on the body?

A

Vasodilation
-↓ preload and afterload
-↓ BP
-↓ O2 consumption

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24
Q

With what drugs is NTG contraindicated? Examples.

A

Do not give if Phosphodiesterase inhibitors taken within the past 24Hrs.
-Viagra (Sildenafil), Cialis (tadalafil), Levitra (vardenafil)

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25
Q

What effects does Nitroprusside have on the body?

A

This is a potent preload and afterload reducer
-often used in HTN crisis** [180/120 millimeters of mercury (mm Hg) or greater => MEDICAL EMERGENCY. It can lead to a heart attack, stroke or other life-threatening health problems.]

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26
Q

3 primary Vasopressors and 1 that augments?

A

Primary: Epi, Norepinephrine (Levophed) and Phenylephrine
Secondary: Vasopressin

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27
Q

Stable vs Unstable Angina?

A

BOTH have negative troponin
Stable: CP with exertion, short duration, relieved with rest or NTG
Unstable: CP with little exertion, longer duration, unrelieved

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28
Q

What is NSTEMI and how is it dx?

A

(+) troponin with no STE

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29
Q

What does a STEMI indicate?

A

(+) troponin with STE (meaning there is arterial obstruction w/ thrombosis

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30
Q

What is variant angina (Prinzmetal’s)? What are the causes?

A

Coronary vasospasms that cause cyclical pain at rest d/t ischemia
-causes: stress, Raynaud’s, and migraines.
STE resolves and pain relieved when vasospasm resolves
**BB may exacerbate vasospasm due to unopposed alpha stimulation

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31
Q

S/S of Acute coronary syndrome? How might women and diabetics present differently?

A

chest tightness, jaw pain, neck pain, left arm pain, epigastric (indigestion-like) pain, scapular discomfort; N/V; signs of shock; dysrhythmias; diaphoresis; dizziness
-women c/o ↑ fatigue, scapular and RUQ pain
-diabetics more likely to have silent MI

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32
Q

When does troponin elevate and peak?

A

Elevation in 3-12hrs, peaks at 10-24hrs.

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33
Q

When should you get posterior V7-V9 ECG?

A

When there is ST depression in V1 & V2, ECG may show STE in V7-V9 for Posterior infarct

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34
Q

Which leads indicate an inferior infarct?

A

II, III, aVF; Inferior is RCA
-you want to get a R-sided ECG to look at V4R

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35
Q

Which leads indicate an anterior infarct?

A

V1-V4 Anterior = LAD
It is anterior septal if V1-V2

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36
Q

Which leads indicate lateral infarct?

A

If I, aVL, V5-V6; LAD/circumflex
High lateral STEMI: High lateral STEMI can present as ST-elevation involving lead I and aVL. Subtle ST elevation in V5, V6 and reciprocal changes in lead III and avF may be present. This is usually caused by occlusion of the first diagonal branch of LAD

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37
Q

Ischemia vs Injury vs Infarction

A

-A zone of ischemia typically produces ST segment depression and/or inverted or tall T waves.
-A zone of injury produces ST segment elevation (STEMI) , T wave may invert
-A zone of infarction produces a large Q wave in the QRS complex. If old, Q is deep and wide.

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38
Q

What vessel is occluded and what type of infarct is the “widow maker”? S/S?

A

LAD- left anterior descending

S/S: CRUSHING CHEST PAIN, ventricular dysrhythmias, tachycardia, FEELING OF IMPENDING DOOM, BBB, SOB, crackles in lungs and S3 from LV failure (cardiogenic shock),

**second degree type 2 (Mobitz 2) is an OMINOUS SIGN.
*a new onset heart murmur = VSD –> EMERGENCY

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39
Q

What vessel is occluded with INFERIOR infarct? S/S?

A

most commonly RIGHT CORONARY ARTERY– supplies SA and AV nodes

S/S: Epigastric pain, bradycardias resulting in hypotension, second degree heart block type 1, N/V, risk of mitral regurg and papillary muscle rupture (new onset heart murmur)

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40
Q

If an inferior infarct is suspected, what other diagnostic test should be done?

A

a RIGHT-SIDED ECG to look at V4R
-30 to 50% of inferior MIs are RIGHT VENTRICLE

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41
Q

What S/S are associated with a RV infarction? Treatment?

A

S/S: JVD, hypotension, shock, STE at V4R

Tx: infuse NS bolus and dobutamine for contractility
-caution with preload-reducing agents like NTG and morphine

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42
Q

What is the PCI goal for STEMI tx?

A

<90min door to balloon

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43
Q

When is fibrinolytic therapy given instead of PCI?

A

If PCI unavailable in 90-120 min
**expect reperfusion dysrhythmias like accelerationed IVR or VT (good sign of reperfusion!)

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44
Q

What are other interventions for STEMI tx?

A

-O2 at 4L NC if SpO2 <94% or respiratory distress
-NTG SL (q5 x3 tab max)
-ASA 162-325 chewable to prevent platelet aggregation
-BB for HTN STEMI
-ACE-I or ARB to reduce infarct size and improve venticular remodeling
-Antiplatelets: aspirin, plavix, effient, brilinta
-Anticoagulants: heparin, lovenox, coumadin, eliquis, xarelto, pradaxa

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45
Q

What is aortic dissection and what are the causes?

A

This is a tear in the intimal layer d/t:
HTN,
age >60,
cocaine use,
trauma (1st & 2nd rib fractures),
heart disease,
connective tissue dz like Marfan’s and Ehlers Danlos.

46
Q

What are the S/S of aortic dissection?

A

S/S: sudden onset of tearing, ripping pain to chest, shoulders, flank or back not relieved by analgesics, **difference of 20 mmHg SBP b/w arms, pulsatile mass
a) Ascending: stroke-like symptoms, Horner’s Syndrome (Ptosis, Anhidrosis, Miosis- a drooping eyelid, ↓ sweating on the affected side of the face, ↓ pupil size, .)
b) Descending: loss of distal pulses, lower extremity weakness, ↓UO

47
Q

How is an aortic dissection diagnosed and treated?

A

Dx: TTE or TEE, chest CT or MRI
-will see widened mediastinum and obscured aortic knob on films

Tx: support ABCs and anticipate rapid deterioration so start 2-18g IVs;
-maintain HR 60-80
-SBP 100-120 mmHg with BB (to avoid reflex tachycardia), nitroprusside, or NTG; analgesia; prepare for surgical repair

48
Q

What are the BLS CPR expectations?

A

100-120 compressions per minute at 30:2
-do not delay BLS and defibrillation for an advanced airway
-if adv airway present, then continuous compressions with 1 breath q6sec
-keep ETCO2 >10. If less then switch compressors.

49
Q

Defibrillation. What are shockable rhythms?

A

V-fib and pulseless V-tach
*have defib charging before pulse check to ↑ compression time

50
Q

How many joules are used in adult shockable cardiac arrest?

A

Biphasic 120-200 joules
Monophasic 200-360 joules

51
Q

How many joules are used in PEDIATRIC shockable cardiac arrest?

A

Initially 2-4 joules/kg;
then 4 joules/kg;
then 4-10 joules/kg

52
Q

5H’s & 5T’s causes for cardiac arrest?

A

Especially in asystole and PEA

H: hypovolemia, hypoxemia, hydrogen ion, Hyper or hypokalemia, hypothermia
T: Toxins, Trauma, Tension Pneumothorax, Tamponade, Thrombosis

53
Q

What are the medications for cardiac arrest?

A

-epinephrine (1mg/10ml)
-antiarrhythmic: amiodarone 300mg IV/IO or Lidocaine 1-1.5mg/kg for refractory VF
-Sodium bicarb 1mEq/kg for metabolic acidosis-induced cardiac arrest, hyperkalemia, and TCA overdose

54
Q

What are causes of maternal cardiac arrest? How should CPR be performed?

A

Causes: DIC, embolism, eclampsia, abruption
CPR: higher compressions and manually displace the uterus to the left to prevent vena cava syndrome –> prepare for C-section

55
Q

What are interventions for post arrest resuscitation? ROSC

A
  1. secure airway and optimize ventilation/oxygenation (ETCO2 35-45 and O2 90%)
  2. ↑ circulation with 1-2L of NS and vasopressor by weight to get SBP >90 mmgHg
  3. Targeted temperature management (TTM) at 32-36 degrees for 24hrs. Control shivering, provide sedation, analgesia, and neuromuscular blockade.
56
Q

What is considered stable tachycardia? How can it be treated without meds?

A

Pt is alert with a normal BP.
If narrow complex tachycardia, vagal maneuvers.

57
Q

When is Adenosine indicated for dysrhythmias?

A

For narrow SVT or wide monomorphic VT, Adenosine 6mg rapid IV push with NS flush to slow SA and AV node conduction. If effective in ↓ HR, but not at desired base then a 12mg dose of adenosine can be given.

58
Q

What 3 drugs can be given for stable SVT?

A

Adenosine (1st line tx)
Cardizem (CCB) or Labetalol (BB)

59
Q

What is HR for SVT?

A

140-180 but up to 250

60
Q

What medications can be given for stable V-tach?

A
  1. Amiodarone 150mg slow
  2. Lidocaine (esp. if d/t prolonged QTi) [also given for PVCs]
  3. Procainamide 20-50mg/min up to 17mg/kg
  4. Sotalol (monitor for hypotension or prolonged QT)
61
Q

What is the intervention for unstable SVT or VT?

A

Sync cardioversion, on the R wave (ventricular contraction)
Biphasic 50-200 joules.
Pediatric 0.5-1.0j/kg but up to 2 joules/kg

62
Q

How far must defib pads be kept from generator of ICD?

A

10cm or 4in

63
Q

What is A-fib with RVR rate?

A

> 100 quivering atria with rapid ventricular rate

64
Q

What is the concern or risk with A-fib?

A

Emboli or stroke

65
Q

How does WPW present on ECG?

A

delta wave on upstroke of QRS and short PR interval
risk of tachycardia

66
Q

What is considered prolong QT interval? Risk?

A

QTi > half the total R-R length;
the risk is R on T phenomenon, leading to polymorphic Vt (Torsades de pointes)

67
Q

What are th ABCDE causes of prolonged QTi?

A

AntiArrythmics: sotolol, amiodarone, procainamide
AntiBiotics: flouroquinolones (-floxacin, Levo & Cipro), macrolides (-mycins), aminoglycosides
AntiCychotics: haloperidol, risperidone, thorazine, geodon
AntiDepressants: SSRIs, TCAs- Elavil, Tofranil
AntiEmetics: Ondansetron, Droperidol, Compazine

68
Q

How do you treat Torsades? (w/ pulse and pulseless)

A

Palpable pulse: cardioversion and Mg sulfate slow infusion
Pulseless: BLS, defib, Epi, and Mg 2g IV push

69
Q

What is 1° block?

A

prolonged PR interval (>0.20)

70
Q

What is 2° block, type 1?

A

progressively longer PR interval, R-R consistent

71
Q

What is 2° block, type 2?

A

PR wave consistent, R-R inconsistent because there are P waves without a QRS

72
Q

What is 3° block?

A

R-R interval consistent, with hidden P waves. The atria and ventricles are not communicating.

Without appropriate conduction through the AV node, the SA node cannot act to control the heart rate, and cardiac output can diminish secondary to loss of coordination of the atria and the ventricles.

73
Q

How do treat bradycardia and heart blocks?

A

BVM assisted breathing
Atropine 1mg IVP q3-5min up to 3mg
Consider transcutaneous pacing
Epi infusion 2-10 mcg/min
Dopamine infusion 5-20 mcq/kg/min
Pacemakers for refractory bradycardia and heartblocks

74
Q

How is transcutaneous pacing initiated?

A

Anterior-posterior pad placement preferred. (anterior-lateral ok)
Rate 60-80at 60 mA and increase until capture obtained

Electrical capture is confirmed by an ECG reading – widened QRS following every pacer spike. Mechanical capture is determined by a palpable pulse (NOT CAROTID) and other signs of increased circulation (increased blood pressure, improvements in skin color and warmth, and improved level of consciousness).

75
Q

What are S/S of Pericarditis?

A

S/S: sudden onset of retrosternal CP exacerbated by inspiration, activity, and supine position; pain relieved by leaning forward or sitting up; pericardial friction rub heard best while leaning forward; tachycardia and tachypnea; low-grade fever

76
Q

How is Pericarditis Dx and Tx?

A

Dx: CXR, echo, 12-lead ECG: global STE without reciprocal changes; tall, peaked T waves in all leads except aVR

Tx: NSAIDs, allow pt to lean forward. (**Do not give NTG)

77
Q

How is Endocarditis Dx and Tx?

A

Dx: ↑ WBC, ↑ ESR, blood cultures, ECHO to assess valves

Tx: IV abx, prepare for admit and possible valve repair

78
Q

What are S/S of Endocarditis?

A

S/S: FEVER, chills, night sweats, myalgia’s, NEW ONSET MURMUR (d/t vegetation on valves); pleuritic CP; splinter hemorrhages in nail beds; conjunctival petechiae (eyes); Osler’s nodes on digits (tender nodules); Janeway lesions (macules on palms/soles); Roth spots (retinal hemorrhages)

79
Q

What is a main cause of endocarditis if the patient has not had recent cardiac surgery?

A

IV drug use

80
Q

What are S/S of Left sided HF?

A

S/S: SOB, S3 heart sound, paroxysmal nocturnal dyspnea (PND), dyspnea, crackles, Kerly B lines on XR, pulmonary edema

-most from anterior MI

81
Q

What are S/S of Right sided HF?

A

S/S: JVD, peripheral edema, ascites, hepatomegaly, ↑ CVP from Cor pulmonale from COPD for pulmonary HTN, or RV MI

82
Q

Whare are supportive measures for HF?

A

support ABCs, cardiac monitoring, titrate O2 to >90%
**caution w/ IVFs,
**caution w/ loop diuretics (vasodilation) to ↓preload; monitor K+
**caution w/ vasodilators (NTG)
**caution w/ ACEI/ARB to interrupt RAAS

83
Q

What defines Hypertensive Emergency/Crisis?
How quickly is it reduced?

A

SBP >180 or DBP >120 + PLUS evidence of impending end-organ damage
i.e. AMI, aortic dissection, HF, pulmonary edema, intracranial hemorrhage;
HTN encephalopathy; and eclampsia.

↓MAP by 20-25% over 1-2hrs with Nipride (pre and afterload reducer)

84
Q

What defines Hypertensive urgency?

A

SBP >180 or DBP >120 + WITHOUT evidence of new end-organ damage or dysfxn
i.e. pulmonary edema, cardiac ischemia, neurologic deficits, or acute renal failure

85
Q

What are S/S of HTN urgency?

A

headache, dizziness, shortness of breath, chest pain, vomiting, or vision changes.

86
Q

What are S/S of HTN emergency?

A

altered LOC, chest pain, dizziness, epistaxis, headache, seizures, visual disturbances

87
Q

What diagnostics are performed for hypertensive urgency and emergency? Immediate interventions and medications?

A

Dx: ECG, CXR, UA, BUN, Creat

Tx: O2, IV, consider ART line (allen’s test first)

Meds:
-NTG or nitroprusside (Nipride)- slow infusion to ↓ MAP by a max of 25% in the first 2hrs of tx. → SBP goal 140-160 mmHg
- Labetalol has slower onset; safe and effective during pregnancy

88
Q

What are S/S of pericardial (Cardiac) tamponade?

A

S/S:
Beck’s triad (JVD, hypotension, muffled (distant) heart sounds;
kussmaul sign (↑ in JVD on inspiration);
pulus paradoxus (↓ in BP upon inspiration);
small ECG amplitude;
electrical alternans (alternating amplitude of QRS);
tachycardia, anxiousness, restlessness;
risk of PEA

89
Q

What kind of shock can cardiac tamponade cause and how to tx?

A

OBSTRUCTIVE SHOCK
-needle pericardiocentesis subxiphoid if emergent OR
resuscitative thoracotomy (pericardial window)
-support BP with vasopressors

90
Q

What is Virchow’s triad and what is it a risk for?

A

Virchow’s triad: venous stasis (immobility, air travel), vein damage (fracture), hypercoagulability (estrogen therapy, pregnancy)

Risk for DVT

91
Q

What causes PVD? S/S of peripheral vascular dz? Risk?

A

damaged venous valves.
S/S: aching, throbbing pain more common with walking (dorsiflexion)
Risk: PE

92
Q

S/S of PAD? How is PAD dx and tx?

A

S/S: shiny skin, hair loss, constant excruciating burning pain, cold extremity, ↓ pulses or pulseless

Dx: ankle brachial index (ABI; normal 0.9-1.3)
Tx: DO NOT ELEVATE. If critical ischemia present, prepare for embolectomy

93
Q

Which part of the heart is typically affected by blunt injury?

A

RV d/t positioning

94
Q

What are S/S of cardiac contusion (blunt cardiac injury)? Tx?

A

chest pain unrelieved by NTG,
dysrhythmias (ST and PVC’s most common, VT, blocks), STE,
hypotension, cardiac failure

Tx: OXYGEN!, con’t cardiac monitoring; possible vasopressors and positive inotropes TO INCREASE BP

95
Q

What kind of shock to LV heart failure? S/S?

A

Cardiogenic shock

S/S: Tachypnea, crackles, pulmonary edema, S3 heart sound, Kerly B lines on CXR, cool clammy skin, hypotension

96
Q

What is tx for cardiogenic shock?

A

oxygenation;
↓ preload with NTG and diuretics;
↓ afterload with NTG or nitroprusside
↑ contractility with positive inotropes (dobutamine) and IABP;
treat dysrhythmias

97
Q

What are causes of obtructive shock and their interventions?

A

Pericardial tamponade - pericardiocentesis
Tension pneumo- needle decompression
Thrombolytics- PE
Supine vena cava syndrome (adv pregnancy)- turn left side 15-30­°
Abdominal compartment syndrome- surgery

98
Q

What is the Diamond of death?

A

hypothermia (prevent in all SHOCK)- (impairs thrombin production and platelet fxn)
acidosis (impairs thrombin production and other coag factors, ↑ lactate)
coagulopathy (CAN’T CLOT, whole-blood loss depletes clotting factors)
+hypocalcemia added (b/c must Ca must be replaced with massive blood transfusions)

99
Q

For hypovolemic shock, what is the isotonic crystalloid dosing?

A

Adults 30ml/kg
Peds 20ml/kg

100
Q

For hemorrhagic shock, what are the interventions in order?

A

1 DIRECT PRESSURE

#2 Tourniquets tightened until bleeding stops, pelvic binder over greater trochanter for pelvic fracture
#3 Transfuse blood 1:1:1 (plasma, platelets, pRBC’s)

101
Q

What does hypocalcemia occur with massive blood transfusions?

A

b/c the citrate in the blood binds with calcium and removes from system

102
Q

Why is permissive hypotension allowed in blunt abdominal trauma and pelvic fractures?

A

to reduce bleeding and NOT POP A CLOT
a SBP <100

103
Q

Fluid resus for hemorrhagic shock?

A

500ml WARMED boluses can be given until blood products available, with MAX OF 1 LITER
OR SBP 90 achieved

104
Q

What is shock?

A

insufficient O2 to meet the metabolic demands of cells and organs, INADEQUATE TISSUE PERFUSION

105
Q

How are the 4 types of shock differentiatived with 1 word each?

A

Hypovolemic- volume problem
Obstructive- mechanical problem
Cardiogenic- pump issue
Distributive- pipe problem

106
Q

What are the 3 types of distributive shock?

A

anaphylactic- bronchospasm and vasodilation
septic
neurogenic- bradycardia and hypotension

107
Q

What is given instead of atropine for transplanted hearts?

A

Isoproterenol (Isuprel)

108
Q

Examples of primary blast injuries?

A

Primary injuries are those that result from the over-pressurization or under- force impacting the body.

-blast lung
-tympanic membrane rupture
-ABD hemorrhage & perforation
-Globe (eye) rupture
-Mild TBI

109
Q

Examples of secondary blast injuries?

A

Secondary injuries result from projectiles propelled by explosion

-primary fragmemts rom expoding weapon
-eye penetration (can be occult)
-closed and open brain injury
-secondary fragments: projectiles from the environment (debris, vehicular metal)

110
Q

Examples of tertiary blast injuries?

A

tertiary injuries result from displacement of the victim by the blast wind and stutural collapse

Quaternary injuries are all other injuries resulting from the blast.

111
Q

Examples of Quaternary blast injuries?

A

Quaternary injuries are all other injuries resulting from the blast. Heat or combustion fumes)

-external or internal burns
-crush injuries
-asthma, COPD, breathing issues from dust, smoke, toxic fumes
-angina
-hyperglycemia, HTN

112
Q
A

CEN (10 decks)

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