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Critical Care > Cardiac > Flashcards

Cardiac Flashcards

1
Q

what is directly related to blood flow?

A

tissue perfusion

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2
Q

what is directly related to cardiac output?

A

blood flow

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3
Q

what influences blood flow & are components of SV?

A

“pump, pool & pipes”
pump (contractility)
pool (blood & fluid)
pipes (blood vessels)

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4
Q

what does unstable angina, NSTEMIs & STEMIs all result from?

A

coronary artery disease

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5
Q

describe the difference between unstable angina, NSTEMIs & STEMIs

A

unstable angina: has the most blood flow through a coronary artery but slightly blocked still
NSTEMI: heart attack; more blood flow blocked compared to unstable angina
STEMI: most severe form of a heart attack of MI; NO blood flow through a coronary artery

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6
Q

when do the coronary arteries fill?

A

during diastole

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7
Q

how do you determine a bundle branch block when looking at an EKG?

A

QRS is prolonged

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8
Q

what specific part of the heart could cause bradycardia if it is not receiving enough O2 & blood?

A

SA node (primary pacemaker of the heart)

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9
Q

what specific part of the heart could cause various heart blocks if not receiving enough O2 & blood?

A

AV node

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10
Q

what is angina pectoris?

A

chest pain or discomfort caused by decreased blood flow to the heart

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11
Q

describe the difference between stable & unstable chest pain

A

stable: chest pain usually w activity, gets better w rest, O2 demand is increased & supply is inadequate
unstable: chest pain that does not stop w rest

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12
Q

describe the difference between myocardial O2 supply & demand

A

supply: when the heart does not have adequate O2 supply
demand: when the heart is demanding too much O2

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13
Q

name 3 ways angina could present itself

A
  1. epigastric (heart burn)
  2. radiating down the arm, neck, etc. (not always in the chest)
  3. fatigue
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14
Q

which types of patients have atypical angina?

A

women, > age 65 & diabetic patients

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15
Q

what is a patient at risk for when they have a new onset of unstable angina?

A

MI, dysrhythmias or SCD (sudden cardiac death)

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16
Q

describe the difference in waves on an EKG w an NSTEMI & STEMI

A

NSTEMI: ST depression
STEMI: ST elevation

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17
Q

what is a common cardiac biomarker used to show the heart is releasing its injured proteins?

A

troponin

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18
Q

do we want to see troponin elevated or decreased?

A

decreased! we want to see peaks go down & continue to draw until we have the first peak & then first down trend

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19
Q

describe the difference between a positive cardiac biomarker & negative cardiac biomarker

A

+ = means troponins are high & pt has an NSTEMI
- = pt has unstable angina

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20
Q

what are the #1 complications with acute MIs?

A

dysrhymias

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21
Q

when should a pt be given oxygen?

A

when they are hypoxemic (O2 <90% or in resp distress)

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22
Q

how does aspirin help w an MI?

A

decreases mortality rate (diminishes platelet aggregation & prevents thrombus plaque from getting bigger)

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23
Q

why is nitroglycerin often administered in MI situations?

A

helps w chest pain (CP for a pt must be at 0!)

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24
Q

which med is administered for chest pain if pain is not relieved by nitroglycerin?

A

Morphine IV

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25
Q

describe preload

A

PULL
volume status (what is coming back to the heart)

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26
Q

describe afterload

A

PIPES
tells how vasoconstricted or vasodilated the patient is or the resistance the heart has to overcome
deals w ARTERIES!

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27
Q

describe contractility

A

the PUMP

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28
Q

how should a patient w HF be positioned & why? what should they avoid?

A

semir or high fowlers to decrease preload
they should avoid the valsalva manuever (bearing down to have a BM) because it stimulates the vagus nerve & can cause a decrease in HR & BP & puts them at risk for developing dysthymias

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29
Q

how does nitroglycerin affect the CVP, wedge pressure, PA pressures, SVR & BP?

A

decreases all of them! major vasodilator

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30
Q

when should you hold nitro?

A

if systolic BP is less than 90!

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31
Q

which meds should NOT be given w nitro & why?

A

Viagra or Sidenafil, will cause pt to be fatal!

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32
Q

how does morphine sulfate affect preload & afterload?

A

decreases them both (dilates both veins & arteries) decreasing O2 demand & myocardial workload

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33
Q

how do ACE inhibitors & ARBs effect preload & afterload?

A

decreases both but more affect on afterload (decreasing SVR & BP)

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34
Q

which two types of meds must be given within 24 hours of admission for a pt with an acute MI unless contraindicated?

A

ACE inhibitors & Beta blockers (reduces incident of sudden cardiac cath post MI)

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35
Q

how do beta blockers work on the heart?

A

they have - inotropic action & reduce myocardial O2 demand & contractility

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36
Q

when are Ca channel blockers used?

A

only used if pt cannot tolerate nitrates or beta blockers

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37
Q

what are examples of Ca channel blockers?

A

Diltiazem & Verapamil

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38
Q

how do Ca channel blockers affect afterload & work on the heart?

A

decrease afterload; decrease dromotropic, chronotropic & inotropic action of the heart

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39
Q

name the 1st line treatment drug for preload reduction

A

Nitroglycerin

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40
Q

name the 1st line tx drug for afterload reduction

A

ACE inhibitors / ARBs

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41
Q

name the 1st line tx drug that is considered a - inotrope

A

Beta-blockers

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42
Q

name the 1st line tx drug that is considered a - chronotrope

A

Beta-blockers

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43
Q

name an anti-platelet agent & how does it work?

A

aspirin - prevents stickiness of platelets so they don’t form clots

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44
Q

name an anticoagulant agent

A

heparin

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45
Q

what is the purpose of anti-thrombotic therapy?

A

to prevent further thrombus / clot formation

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46
Q

what is the purpose of fibrinolytic therapy & when are they used?

A

it destroys clots

47
Q

fibrinolytic therapy is only used w which type of patients?

A

STEMIs!

48
Q

which drugs are often combined w aspirin for a dual anti-platelet therapy?

A

P2Y12 receptor inhibitors (Clopidogrel & Ticagrelor) & llb / lla inhibitors (Eptifibatide & Tirofiban)

49
Q

what is a risk factor of all anti platelet agents?

A

bleeding!!

50
Q

which drugs are often started in cath lab & sometimes continued after an intervention?

A

llb / lla inhibitors (Eptifibatide & Tirofiban)

51
Q

which med dose is often adjusted based on monitoring of PTT or APTT?

A

Heparin Sodium

52
Q

how is Enoxaparin (Lovenox) different from heparin sodium?

A

more effective & expensive, less bleeding risk but w less control
do not have to monitor PTT & APTT because the half life is longer

53
Q

what type of Heparin route is necessary to monitor the APTT every 6 hours?

A

only continuous infusion of heparin due to the half life

54
Q

how does heparin affect PTT when it is therapeutic?

A

Increases PTT (takes more time to clot)

55
Q

which drug is used to antagonize the effects of Heparin?

A

Protamine sulfate

56
Q

other than bleeding what is another complication associated w heparin therapy? what drugs are used for this complication?

A

Heparin induced thromobocytopenia
stop all heparin completely & administer Bivarudin (Angiomax) or Argatroban (Acova)

57
Q

name 2 interventional therapies for acute coronary syndromes

A
  1. PCI (percutaneous coronary intervention)
  2. CABG (coronary artery bypass graft)
58
Q

what are some signs of reperfusion? name 4

A
  1. cessation of CP
  2. elevated ST segments return to baseline
  3. reperfusion dysrhythmias
  4. early & marked peaking of troponin
59
Q

when are fibrinolytic therapy agents typically given for STEMIs? give some examples

A

given within 30 min of arrival to ED; Alteplase, Tenecteplase, Reteplase & Streptokinase

60
Q

when is PCI used for STEMIs?

A

will only be used if a pt cannot be performed on within 90 minutes in a cath lab

61
Q

what is also a big risk with fibrinolytics in addition to bleeding being a big risk?

A

stroke

62
Q

describe a percutaneous coronary intervention (PCI)

A

coronary stents are placed

63
Q

in general, what can cardiac catheterization do?

A

diagnose & provide interventions

64
Q

name some complications post PCI

A
  1. coronary spasm (angina, CP)
  2. coronary artery dissection (tearing of the coronary artery)
  3. coronary thrombosis (cath can dislodge a clot)
  4. bleeding & hematoma formation at the insertion sites
  5. compromised blood flow to exremity
  6. retroperitoneal bleeding (abdominal / back pain)
  7. contrast induced renal failure
  8. ventricular dysthymias (reprofusion dysthymias)
  9. vasovagal response (bradycardia, hypotension, loss of consciousness)
65
Q

what is mandatory in a post PCI assessment?

A

pulse & hematoma checks!

66
Q

how do you handle a vasovagal response after a cath is removed from the groin area?

A

hold pressure from 20-30 min straight!

67
Q

what is the point of a compression device? (TR band)

A

air is pushed into device to compress the artery & prevent bleeding (a few hours after the procedure, nurses will start to deflate air very slowly) always look for bleeding!!

68
Q

which position should a patient be kept in post femoral PCI?

A

HOB no higher than 30 degrees; keep extremity straight

69
Q

describe a coronary artery bypass graft (CABG)

A

rerouting piping & taking grafts to function as new coronary arteries
blood is bypassed & rerouted by suturing!

70
Q

name 4 complications associated w acute MIs

A
  1. life threatening ventricular dysrhymias
  2. HF
  3. pulmonary edema
  4. cardiogenic shock
71
Q

what do statins do to the heart?

A

decrease plaque formation

72
Q

if a pt is unable to have a PCI within 90 minutes, which drugs must be given?

A

fibrinolytics

73
Q

what does MONA BASH stand for & what are they used to treat?

A

M - morphine
O - oxygen
N - nitrates
A - aspirin
B - beta-blockers
A - ACE-inhibitors
S - statins
H - Heparin

used to treat the 3 types of ACS!

74
Q

explain how to treat unstable anginas

A

MONA BASH & possible interventional treatment depending on how the pt presents

75
Q

explain how to treat NSTEMIs

A

MONA BASH until pt is able to get into PCI

76
Q

explain how to treat STEMIs

A

requires emergent treatment! pt must have PCI within 90 minutes & if unable adminiter fibrinolytics & MONA BASH until PCI

77
Q

How do you treat a thrombus?

A

Fibrinolytics (only for STEMIs) because of bleeding risk OR with PCIs or CABG if PCI can’t work

78
Q

what type of med removes a clot that is causing ischemia / infarction?

A

Fibrinolytic agent

79
Q

which med reduces preload and afterload, dilates coronary arteries, increases myocardial O2 supply & reduces myocardial O2 demand?

A

Nitroglycerin

80
Q

which med reduces preload & afterload by venous & arterial vasodilation decreasing myocardial O2 demand & relives pain?

A

Morphine

81
Q

which med reduces heart rate to decrease myocardial O2 demand, infarct size & improve survival rate?

A

Beta-blocker

82
Q

which med decreases afterload & myocardial O2 demand?

A

ACE inhibitor

83
Q

describe heart failure

A

impairment in the ability of the ventricle to fill or eject blood effectively

84
Q

what does ventricular remodeling cause the heart to do?

A

stiffen up & enlarge

85
Q

name some clinical manifestations of left sided HF

A
  1. SOB
  2. orthopnea
  3. crackles
  4. elevated PAP (pulmonary artery pressures)
  5. post nocturnal dyspnea, S3, tacypnea, cough & hypothysis
86
Q

name some clinical manifestations of right sided HF

A
  1. lower extremity edema
  2. jugular vein distention
  3. Hepatojugular reflex (when liver is pushed on, there is an increase in JVD)
  4. elevated CVP
  5. hepatomegaly, cytomegaly, ascites, pulmonary hypertension & weight gain
87
Q

what does the BNP determine?

A

determines the severity of disease & prognosis (the higher it is, the worst off) it is well correlated w LV preload

88
Q

describe the BNP

A

secreted by the ventricles in response to excessive stretching of the heart muscle cells

89
Q

name some medications that manage chronic HF

A

ACEIs or ARBs, nitrates, Hydralazine, Beta-blockers, diuretics, digoxin, spironolactone & statins

90
Q

name two nursing interventions for management of chronic HF

A
  1. cardiac resynchronization therapy (bioventricular pacing therapy)
  2. ICD (implantable cardioverter defibrillator) (senses when a pt is in a lethal rhythm & shocks them)
91
Q

list 5 ways a patient could self manage chronic HF?

A
  1. adherence to drug regimen
  2. daily weights ( gaining of 3 lb. in a day or 5lb. in a week, notify MD)
  3. low Na diet
  4. exercise
  5. smoking & alcohol cessation
92
Q

which three classes of meds are often given to patients experiencing acute HF?

A
  1. preload reduction meds
  2. afterload reduction meds
  3. inotropic support meds
93
Q

which two devices can be used for patients experiencing acute HF?

A
  1. intraaortic balloon pump (inserted during emergencies; decreases afterload & enhances coronary artery blood flow)
  2. left ventricular assist device (continuously takes blood from the left ventricle into the aorta to help out the left ventricle; pt could have this long term & it could be a bridge to transplantation)
94
Q

which two types of meds are used to reduce preload in acute HF?

A
  1. diuretics
  2. nitrates
95
Q

which three types of meds are used to reduce afterload in acute HF?

A
  1. ACE’s & ARBs
  2. nitro (monitor BP every 5-15 min; cannot be used long term or will cause cyanide toxicity)
  3. hydralazine
96
Q

which three types of meds are used for inotropic support in acute HF patients?

A
  1. Dobutamine
  2. Dopamine (low to mid dose)
  3. Milirinone (long half life)
97
Q

The nurse is caring for a patient in an acute exacerbation of HF. Which of the following meds should the nurse anticipate?
A. Metoprolol
B. 0.9% normal saline bolus
C. Morphine
D. Dobutamine

A

D. Dobutamine (acute exacerbation of HF warrants meds that decrease preload, decrease afterload & improve inotropy. Dobutamine is a positive inotrope

98
Q

describe an abdominal aortic aneurysm. name 6 risk factors

A

Localized dilatation of a portion of the aorta, >1.5 times its normal diameter; Usually at a weakened area of the aortic wall
risk factors:
1. age
2. HTN
3. Lipid disorders
4. Atherosclerosis
5. genetic predisposition (Marfan symdrome; tall w long limbs)

99
Q

name 3 symptoms / assessment findings of a patient w a stable abdominal aortic aneurysm

A
  1. palpable, pulsatile mass in the umbilical area of the abdomen
  2. abdominal pain
  3. lower back pain
100
Q

name 2 assessment findings of a patient w an acute rupture of an abdominal aortic aneurysm

A
  1. sudden onset of severe abdominal pain
  2. hypotension w abrupt loss of consciousness because of the severe loss of blood
101
Q

how do you treat a stable abdominal aortic aneurysm?

A

risk factor modification & elimination
EX: if they smoke, have them stop & control their HPN

102
Q

how do you treat an acute rupture of an abdominal aortic aneurysm?

A

surgical repair but this is less preferred because of the invasive risks

103
Q

what are 7 S/Sx of an acute aortic dissection?

A
  1. sever & sudden HPN (around 200 systolic)
  2. sudden onset of intense & excruciating pain present in the back between the shoulder blades, chest & arms*
  3. ripping or tearing sensation within the chest
  4. radiation of pain down into the abdomen & lower back
  5. worse pain in the patient’s life
  6. syncope or LOC w onset of pain
  7. development of a murmur from aortic insufficiency; unequal pulses
104
Q

describe an aortic dissection. which type is more serious?

A

weakened aortic medial layers, a false channel or lumen is created as blood is pumped through the tear, classified according to location; type A is more serious

105
Q

how do you treat an aortic dissection? name 3 things

A
  1. BP reduction w IV beta blockers
  2. further systolic BP reduction w vasodilators like Nitro
  3. pain relief & sedation
106
Q

how do we manage an aortic dissection post operatively?

A

IV nitro to prevent HPN & to keep sysstolic BP below 120!

107
Q

what is PAD?

A

peripheral arterial disease (processes that obstruct the blood supply of the lower or upper extremities)

108
Q

name some risk factors for PAD (9)

A
  1. atherosclerosis
  2. smoking
  3. diabetes
  4. age > 70
  5. male gender
  6. HPN
  7. hyperlipidemia
  8. family history
  9. history of MI, HF, TIA or stroke
109
Q

what are the clinical manifestations of PAD?

A

classic 5 P’s:
1. pain! intermittent claudication (cramping, burning, aching in legs that is relieved w rest)
2. pulselessness
3. pallor
4. paresthesia
5. paralysis

110
Q

what is the difference between early & late intermittent claudication?

A

early: cramping, burning, or aching pain in the legs or buttocks w activity that is relieved by rest
late: pain at rest is a warning sign of an anoxic limb & loss of blood supply

111
Q

how can PAD be diagnosed at the bedside?

A

ankle brachial index: blood pressure cuff applied to one upper arm & above the ankle to obtain blood pressure readings

112
Q

what is chronic venous insufficiency? name some s/sx

A

“pulling effect” blood cannot get back to the heart
S/SX:
1. brown pigmentation of the skin
2. edema
3. thick, flaky skin
4. ulcerations

113
Q

which of the following medications is indicated for a patient w PAD?
A. Clopidogrel
B. Tenectecplase
C. Norepi
D. Nipride

A

A. Clopidogrel; patients should be on an anti-platelet med to prevent further thrombus formation in PAD

Critical Care (5 decks)

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