U5 Cardiac/Shock Flashcards Preview

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Flashcards in U5 Cardiac/Shock Deck (114):
1

Angina pectoris

Chest pain when ability to supply oxygen is not enough to meet cardiac muscle's demand

2

Ischemia with angina pectoris

Does not cause permanent damage to the heart

3

Chronic stable angina

Predictable following exercise
Relieved by nitroglycerine or rest

4

Unstable angina EKG changes

Depressed ST
Inverted T-wave
Changes resolve when pain resolves

5

Unstable angina

Occurs at rest or with exertion
May last >15 min
Not relieved with rest or nitros
NO changes in troponin or CK levels

6

Variant (Prinzmetal's) angina

Coronary spasm
Elevated ST; resolves when pain resolves
Usually responds to nitrates

7

New onset angina

1st angina symptoms felt during increased exertion

8

Pre-infarction angina

Occurs in days or weeks before an MI

9

Subendocardial

Not all the way through the muscle
Less effect on wall motion of the heart
More likely to extend later
Non-STEMI

10

Transmural

Affects all layers of the muscle
STEMI

11

STEMI EKG

ST elevation in 2 contiguous leads

12

Zone of necrosis

Area around the initial area of infarction
Abnormal Q
Too late to reverse

13

Zone of injury

Tissue that is injured, but not necrotic
ST elevation
Can be reverse, but requires immediate treatment

14

Zone of ischemia

Tissue that is oxygen deprived
T-wave inversion
Can be prevented with treatment

15

STEMI causes

Atherosclerosis
Plaque rupture
Coronary thrombi
Occlusion of coronary artery

16

Physical changes in MI

Obvious changes don't occur until 6 hrs after MI
Infarcted area is blue & swollen
After 48 hrs, gray with yellow streaks
8-10 days granulation tissue forms
2-3 months scar tissue

17

Ventricular remodeling

Scar tissue permanently change size & shape of the ventricle

18

Anterior (septal) MI

Caused by left anterior descending artery obstruction
ST elevation in V1-V4
Tachycardia
2nd & 3rd degree heart blocks

19

Posterior (lateral) MI

Caused by circumflex artery obstruction
ST elevation in V5 & V6
Sinus arrhythmias

20

Inferior MI

Obstruction of right coronary artery
1/2 of pts have obstruction of RCA that causes damage to R ventricle
ST elevation in 2, 3, & aVF
Sinus bradycardia
Heart blocks--usually temporary

21

MI in women

Post-menopause incidence is equal to men
Usually have NSTEMI

22

LDL level

<100mg/dL in pts with no known CAD risk factors

23

HDL level

>40mg/L

24

Triglycerides level

<150mg/dL in men

25

Alternative lipid-lowering therapy

Omega-3 fatty acids (fish oil)
Flaxseed
Canola oil
Lovaza (omega 3)

26

Metabolic syndrome risk factors

HTN
Decreased HDL
High LDL & triglycerides
Increased blood sugar
Large waist-->40 men; >35 women

27

Angina vs MI

Angina might be relieved with rest, nitros
MI does not go away with rest & nitro
MI has high troponin & CK

28

MI assessment

BP & pulse
EKGs
Distal pulses & skin temp
Heart sounds--S3
Resp rate & breath sounds
Increased temp

29

Creatinine kinase levels

Female--30-135 u/L
Male--55-170 u/L
Elevations--brain, myocardial, & skeletal muscle injury

30

Cardiac catheterization

Done to determine extent & exact location of coronary artery extremity
Dr decides if pt is candidate for PCTA or stent placement
Watch for cold extremities

31

Emergency care of pt with chest pain

ABCs
EKG within 10 min
Pt's description of pain
Vitals
02 therapy
Pain relief & aspirin

32

Code Heart

EKG within 10 min
Aspirin 324 mg
Troponin stat
Thrombolytic decision within 30 min
90 min to cath lab
Echo done before discharge (ejection fraction)
Beta blocker on discharge

33

Managing acute pain (MONA)

Morphine sulfate--small doses; watch for resp depression; can lower BP
O2--2-4L nasal cannula
Nitrates
Aspirin

34

Glycoprotein 2b/3a inhibitors

Unstable angina or NSTEMI
Given before & during PCTA to maintain patency of artery

35

Beta blockers

Decrease size of infarct
Slow heart rate & decrease force of contraction
Increase perfusion while reducing force of contraction

36

A/E beta blockers

Bradycardia
Hypotension
Decreased LOC
Chest discomfort
Crackles
Hypoglycemia

37

Angiotensin II Recptor Blockers (ARBs)

Prevent ventricular remodeling & heart failure post MI

38

ARBs assessment

Watch for decreased UO
Hypotension
Cough
Changes in K, BUN, & creatinine

39

Calcium channel blockers

Not used for post MI pts
Promotes vasodilation for pts with angina
HTN not controlled with beta blockers

40

Calcium channel blockers assessment

Hypotension
Peripheral edema

41

Reperfusion therapy

Thrombolytics
Used to reopen occluded coronary arteries
Given within 30 min in ER for STEMI

42

C/I reperfusion therapy

Recent abdominal surgery
Previous intracranial hemorrhage
Vascular lesion
Malignant neoplasm
Stroke within 3 months
Significant head injury or facial trauma within 3 months

43

Indication a clot has been dissolved

Abrupt cessation of pain
Sudden onset of ventricular dysrhythmias
Resolution of ST changes & T wave inversion

44

Heart failure

Common post MI
Results from L or R ventricular dysfunction
Rupture of intraventricular septum
Papillary muscle rupture with valve dysfunction

45

Normal R atrial pressure

1-8 mmHg
Low indicates hypovolemia
High indicates R ventricular failure

46

Normal pulmonary artery pressure

15-26 mmHg systolic
5-15 mmHg diastolic

47

Normal pulmonary artery wedge pressure

4-12 mmHg
Elevated indicates L ventricular failure

48

Killip Class I heart failure

Absent crackles
S3
IV nitrates & diuretics

49

Killip Class II & III heart failure

Afterload reduction
Beta blocker once/day
ACE inhibitors & ARBs to prevent ventricular remodeling

50

Killip Class IV heart failure

Cardiogenic shock
40% L ventricle is necrosed
Stuttering chest pain

51

S/S cardiogenic shock

Tachycardia
Hypotension
BP <30/hr
Cold, clammy skin
Restlessness
Tachypnea

52

Cardiogenic shock drug therapy

Morphine--relieve pain
O2--decrease oxygen requirements
Hemodynamic monitoring--direct drug therapy
Vasopressors--increase cardiac output

53

Cardiogenic shock tx

Intra-aortic balloon pump--when pt not responding to drug therapy

54

Intra-aortic balloon pump

Invasive procedure
Balloon inflates during diastole
Increases blood flow to the arteries

55

Post-PTCA complications

Closure of vessel--chest pain
Bleeding from insertion site
Reaction to contrast media
Hypotension, hypokalemia, dysrhythmias

56

CABG

Occluded artery bypassed with pt's own venous or arterial blood vessel
For pts who don't respond to drug therapy

57

CABG candidates

Angina with >50% occlusion of left main that can't be stented
Acute MI with cardiogenic shock
Valvular disease

58

CABG complications
F/E imbalance

Edema is common
Monitor BP, wedge pressure, RA pressure, CO2, Cl, & UO
Watch Ca, Mg, & K

59

CABG complications
Hypotension

May result in collapse of graft
Vasopressors may be given

60

CABG complications
Hypothermia

Institute rewarming procedures if temp is t rewarm too quickly--increases O2 consumption
Stop rewarming when pt reaches 98.6

61

CABG complications
Hypertension

Systolic >140-150 mmHg
Give afterload reducers--nitroprusside--tubing must be covered in aluminum foil & protected from light

62

CABG postop

Monitor mediastinal drainage hourly
Report drainage >180ml/hr to dr

63

S/S cardiac tamponade

Sudden cessation of mediastinal drainage
JVD
Clear lung sounds
Pulsus paradoxus
Cardiovascular collapse

64

CABG postop assessment

Monitor neurological status q30 min until pt has awakened from anesthesia
Then check q2-4 hrs

65

Mediastinitis

Sternal wound infection--between 5 days to several wks postop
Fever beyond 4th day
Unstable sternum
Redness, swelling, or drainage from suture sites
Increased WBC

66

Minimally invasive direct coronary artery bypass

Indicated for pt with lesion of L anterior descending coronary artery
2 in incision made & 4th rib removed

67

Home care assessment

Recurrence of chest pain
Indications of heart failure--weight gain, crackles, cough
Dysrhythmias

68

Physical activity post-MI

1st wk--light housework
2nd wk--work part time
3rd wk--lift no more than 15 lbs for 6-8 wks
Monitor pulse before, halfway, & after exercise

69

Initial Stage of Shock

MAP decreased by <10
Lactic acid produced, but metabolism is still aerobic
Vascular constriction
Increased heart rate

70

Non-progressive Stage of Shock
Compensatory Shock

MAP decreased by 10-15
Acidosis & hyperkalemia--metabolism is anaerobic
Thirst
Anxiety/restlessness
Tachycardia/ increased respiratory rate
Decreased UO
Narrowing pulse pressure
Cool extremities

71

Progressive Stage of Shock
Intermediate Shock

Sustained decrease in MAP of >20
Compensatory mechanisms no longer deliver oxygen sufficiently
Feeling of impending doom
Confusion
Rapid, weak pulse
Hypotension
Anuria
Low blood pH

72

Intermediate Shock implications

Vital organs can only tolerate for short time before permanent damage
Must be corrected within 1 hr or less to save pt's life

73

Irreversible Stage of Shock
Refractory Stage

Too much cell damage has occurred
Therapy can't save pt's life even if cause of shock is corrected
Non-palpable pulse
Cold, dusky extremities
Unmeasureable O2 sats

74

Vasoconstrictors

Improve blood flow by increasing peripheral resistance
Increases venous return to the heart & improves heart contractility

75

Dopamine infusion
Nursing interventions

Assess for chest pain
Monitor UO hourly

76

Norepinephrine (Levophed)
Nursing interventions

Assess BP q15min
Assess for headache

77

Phenylephrine HCL
Nursing interventions

Assess q30min for extravasation
Check extremities for color & perfusion
Assess for chest pain

78

Inotropic agents

Improve heart muscle cell contraction

79

Dobutamine
Nursing interventions

Assess for chest pain

80

Milrinone
Nursing interventions

Assess BP q15min

81

Agents enhancing myocardial perfusion

Improves blood flow to the heart by dilating coronary arteries

82

Sodium nitroprusside
Nursing interventions

Protect drug from light
Assess BP q15min

83

Hypovolemic shock

Loss of blood volume from vascular space
Loss of circulating RBCs--low oxygen
Reduced MAP

84

Causes of hypovolemic shock

Hemorrhage
Dehydration

85

Hypovolemic shock lab assessment

Decreased PaO2
Increased PaCO2
Increased lactic acid
Decreased H&H
Increased potassium

86

Hypovolemic shock
Nursing interventions

ABCs
Elevate pt's ft & keep HOB no greater than 30*
Restore fluid with colloids
Blood & blood products

87

Hypovolemic shock
Drug therapy--dopamine, levophed

Cause vasoconstriction of blood vessels, decrease venous pooling, increase MAP & O2

88

Hypovolemic shock
Drug therapy--dobutamine, milrinone

Improve heart muscle cell contraction

89

Hypovolemic shock
Drug therapy--nipride, nitroglycerine

Dilate coronary blood vessels to improve cardiac contraction & aerobic metabolism in the heart

90

Drug therapy parameters

Assess q15min
Pulse
BP
RR
Skin color
O2 sat
Mental status
UO

91

Distributive shock

No loss of blood volume, but is not effectively circulated

92

Causes of distributive shock

Loss of sympathetic tone
Blood vessel dilation
Pooling of blood in venous & capillary beds
Increased capillary leak

93

Neurogenic shock

Loss of MAP
Decreased sympathetic nerve impulses
Smooth muscles relax causing vasodilation

94

Causes of neurogenic shock

Pain
Anesthesia
Stress
Spinal cord injury
Head trauma

95

S/S neurogenic shock

Flushed skin
Diaphoresis
Can persist 1-6 wks

96

Chemical induced distributive shock
Anaphylaxis

Seconds to minutes after exposure to antigen
Causes widespread loss of blood vessel tone & decreased cardiac output

97

Capillary leak syndrome

Fluid shifts from blood vessels into interstitial tissues

98

Causes of capillary leak syndrome

Severe burns/wounds
Liver disorders
Ascites
Paralytic ileus
Malnutrition
Hyperglycemia

99

Obstructive shock

Heart remains normal but factors outside the heart prevent adequate filling & adequate contraction of the heart

100

Sepsis

Infectious organisms have entered the blood stream
Begins with bacterial or fungal infection & progresses to a dangerous condition over a period of days

101

Septic Inflammatory Response Syndrome (SIRS)

Increase in organisms that escape local control & trigger inflammatory response

102

SIRS criteria

Temp >100.4 or 20 or PaCO2 12,000 or <4,000

103

Sepsis criteria

2 or more present
Hypotension
UO less than intake
Positive fluid balance
Decreased cap refill
Hyperglycemia >120
Change in LOC
Increased creatinine

104

Severe sepsis

All tissues involved & hypoxic to some extent
Widespread microthrombi formation
Anaerobic metabolism
Hyperglycemia
Increased HR

105

S/S severe sepsis

Low O2 sat
Rapid resp rate
Decreased to absent UO
Change in mental status

106

Common organisms leading to sepsis

E-coli
Klebsiella
Pseudomonas
Staph
Strep

107

Sepsis interventions

O2 therapy
IV antibiotics
Low dose cortisone for adrenal insufficiency
Insulin to manage blood sugar
Heparin therapy for microthrombi

108

Adult Respiratory Distress Syndrome (ARDs)

Common in sepsis
Makes air exchange difficult

109

S/S that suggest ARDs cause is sepsis

Productive cough
Fever >100.9
Pleuritic pain
Pulse >90
Tachypnea
Altered LOC
Elevated or low WBCs
Hypotension
High lactate

110

Disseminated Intravascular Coagulopathy (DIC)

Widespread intravascular activation of coagulation system caused by disruption in homeostasis
Can occur with septic shock

111

DIC lab tests

D-dime--indicates formation & breakdown of fibrin clots
PT
PTT
Fibrinogen level

112

DIC presentation

Oozing from bodily orifices
Hemorrhaging
Bruising, petechiae
Oozing from IV sites, puncture sites,wounds

113

DIC tx

Replacement of platelets & clotting factors
Control of initiating disease process

114

Troponin levels

Rises first & quickly
Troponin T--<0.03 ng/ml
Elevation--myocardial damage