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Patient Care > Cardiology 3 > Flashcards

Cardiology 3 Flashcards

1
Q

Prinzmetal’s Angina

A

Coronary artery spasm
Resolution of STE without revascularization
Occurs with baseline CAD

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2
Q

Prinzmetal’s Angina Treatment

A

ASA, Morphine, vasodilators

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3
Q

Causes of Prinzmetal’s angina

A

Recreational Substances
Catecholamine-like stimulants
Uterus-contracting drugs
Parasympathomimetic drugs
Anti-migraine drugs
Chemotherapeutic drugs
Stress causing increase in catecholamines
Uncontrolled release of thromboxane A2

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4
Q

HELP B

A

Hyperkalemia
Early Repolarization
Left ventricular hypertrophy; LBBB
Pericarditis
Brugada

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5
Q

Importance of K in the body

A

Regulate fluid + electrolyte balance
Maintain BP
Help transmit nerve impulses
Control muscle contraction in heart
Maintain healthy bones

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6
Q

Required Potassium intake

A

1mEq/kg/daily

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7
Q

Potassium Hemostasis

A

Primary intracellular cation
3.5-5mEq/L

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8
Q

Potassium Maintenance

A

Hormones
Cell membrane Transporters
Kidneys

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9
Q

Potassium Loss

A

Urine
Sweat
Stool

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10
Q

Causes of Hyperkalemia

A

Excessive Intake
Decreased excretion
Shift from intracellular to extracellular space

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11
Q

Medications causing hyperkalemia

A

ACE & ARB
Spironolactone
Digoxin
NSAID
Antifungals

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12
Q

Crush Injury

A

Compression of extremities or parts of body causing muscle swelling and neurological disturbances which affect areas of body

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13
Q

Crush Syndrome

A

Localized crush injury with systemic manifestations

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14
Q

Cellular Response to Crush Injury

A

Loss of membrane integrity: K leaking out, histamine release increasing vasodilation and capillary permeability
Continued pressure impairment causing local tissue hypoxia and build up of toxins

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15
Q

Insulin + Hyper K

A

Insulin treatment in hospital for hyperkalemia
Activates Na/K pump
Insulin deficiency deactivates pump, causing long repolarization
Decreases K in plasma
Stimulates K into cells by increasing Na efflux

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16
Q

S/Sx of Hyperkalemia Mild

A

General irritability
Rubber legs
Muscle twitching
Cramps
Nausea/diarrhea

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17
Q

Severe S/sx of Hyperkalemia

A

Hypotension
Decrease LOA
ECG changes

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18
Q

Hyper K and AP

A

Raises resting potential closer to threshold, causing AP to fire more easily
Effects slope of phase 0
Increased K inactivates sodium channels decreasing available during depolarization
Decreased Na slows depolarization, resulting in decreased upslope
Decreased conduction velocity

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19
Q

Prolong Hyper K and AP

A

K channels increase conductance
Increased slope of phase 2 and 3, shortening repolarization time
ST-T depression, peaked T waves, Q-T shortening

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20
Q

Mild Hyper K ECG

A

5.5-6.5mEq/L
Peaked T
Prolonged PR

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21
Q

Moderate Hyper K ECG

A

6.5-8 mEq/L
Loss of P wave
Prolonged QRS
ST elevation
Ectopic beats and escape rhythms

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22
Q

Severe Hyper K ECG

A

> 8.0mEq/L
Widening QRS
Sine wave
V fib
Asystole
Axis deviations
BBB
Fascicular blocks

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23
Q

Treatments of Sine Wave Hyper K

A

Fluid bolus
Symptomatic bradycardia directive
Calcium gluconate/salbutamol

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24
Q

Goal of HyperK Treatment

A

Stabilize the myocardial membrane
Drive extracellular potassium back into cells
Remove potassium from the body

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25
Q

Calcium Gluconate

A

Restores membrane potential
Stabilized cardiac cell membrane decreases risk for lethal arrhythmias
1 gram as slow push
Watch ECG

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26
Q

Salbutamol

A

Shifts potassium intracellularly, temporarily reducing serum K
Double usual dose for bronchoconstriction
Can give during arrest through ETT/King LT

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27
Q

Calcium Gluconate Side effects

A

Rapid: hypotension, bradycardia, syncope
Chalky, N/V, dry mouth
Local necrosis/abscess if extravasates

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28
Q

BER

A

Elevated J point with notching
Global concave ST elevation
Large symmetrical concordant T waves
Absence of reciprocal changes or pathological Q

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29
Q

ST Segment/T wave ratio

A

Vertical height of ST elevation measured and compared to T wave amplitude in V6
Ratio >0.25 = pericarditis
Ratio <0.25 = BER

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30
Q

Acute Pericarditis

A

Systemic effects of inflammation and pericardial damage
Chest pain, fever, leukocytosis, malaise, tachycardia, friction rub

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31
Q

Chronic Pericarditis

A

Healed stage of acute form resulting from chronic pericardial dysfunction

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32
Q

Pericarditis treatment

A

ASA 650mg q 6 hours

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33
Q

Pericarditis Presentation

A

Retrosternal Chest pain worsening with position
Dyspneic
Tachycardic
Possible fever
Friction rub
Evidence of pericardial effusion

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34
Q

Causes of Pericarditis

A

Infectious: viral
Immunological: lupus, rheumatic fever
Post-MI
Uremia
Trauma
Following cardiac surgery
Malignancy
Post-radiotherapy
Drug-induced

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35
Q

ECG Changes Pericarditis

A

Diffuse ST elevation
No ST depression
ST segment concave upwards
PR segment depression
PR segment elevation in aVR

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36
Q

Assessing STEMI vs Pericarditis

A

Reciprocal changes
ST segment morphology convex or horizontal
ST elevation lead 3 > lead 2 (STEMI if yes)

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37
Q

Beck’s Triad

A

Hypotension
JVD
Muffled heart sounds

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38
Q

Amplitude and Pericardial Effusion

A

Large amounts of fluid lead to dampening effect

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39
Q

Characteristic of Pericardial Tamponade

A

Excess fluid accumulation in the pericardial space
Build up impairs diastolic filling decreasing CO

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40
Q

Causes of pericardial tamponade

A

Pericardial effusion
Trauma and hemorrhage

41
Q

Pericardial Tamponade Manifestation

A

Reduced chamber filling during diastole
Rising filling pressures in heart chambers
Backup into SVC and IVC
Reduced stroke volume
Decreased CO

42
Q

Other manifestations of pericardial tamponade

A

Tachycardia
Pulmonary edema
Pulsus paradoxus
Dull chest pain
Diminished ECG amplitude
Compressed cardiac silhouette

43
Q

Pericardial tamponade treatment

A

Pericardiocentesis
Antibiotics
Fluid, blood, inotropes as needed
Surgery

44
Q

Endocarditis

A

Inflammation of inner lining of the heart
Caused by infection
IV drug users at risk
May include one or more heart valves

45
Q

Infective Endocarditis

A

May cause mitral or tricuspid valve insufficiency and regurgitation

46
Q

Presentation of Infective Endocarditis

A

Non-specific
Symptoms 2 weeks from initiation of bacteremia
Low grade fever
Fatigue
Weight loss
Flu-like symptoms
Heart murmur

47
Q

Complication of Infective Endocarditis

A

Valvular insufficiency
Myocardial abscess
Embolization
Renal disease

48
Q

treatment Infective endocarditis

A

Antibiotics
Anti-inflammatories
Surgical valve replacement
Hemodynamic support

49
Q

Myocarditis

A

Inflammation of heart muscle
Caused by recent viral infection, could also be bacteria or cardio toxins
Left ventricular dysfunction or general dilation of all heart chambers

50
Q

Symptoms Myocarditis

A

Fatigue
Dyspnea on exertion
Dysrhythmias

51
Q

Cardiomyopathy

A

Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic obstructive cardiomyopathy

52
Q

Dilated Cardiomyopathy

A

Chambers of heart become hypertrophied and unable to pump out blood
Dilated ventricular chambers
Decreased ejection fraction
Systolic failure

53
Q

Restrictive cardiomyopathy

A

Muscles of heart chamber become thick with scar tissue, decreasing stretch
Rarest form
Particles in heart causing fibrosis
Diastolic heart failure

54
Q

Hypertrophic Cardiomyopathy

A

Enlarged walls of chambers
Large septal wall impedes path for blood from LV to aorta

55
Q

Causes of Dilated Cardiomyopathy

A

Unknown possible genetic component
Myocarditis
Ischemia
Toxins
Pregnancy

56
Q

Path of Dilated Cardiomyopathy

A

Systolic failure
Ventricles unable to eject all blood in the chambers
Ventricles dilate to compensate for decreased ejection fraction
Ventricle walls thin
Eventually ventricles cannot dilate to compensate

57
Q

Result of Dilated Cardiomyopathy

A

Dilation of ventricles
Increased ventricular volume and reduced ejection fraction
Decreased ejection of blood, atrial dilation, pulmonary and systemic venous congestion

58
Q

Ejection Fraction

A

EDV-ESV / EDV x 100

59
Q

Ejection fraction NOrmal

A

55-70

60
Q

Ejection fraction below normal

A

40-55%

61
Q

Ejection fraction suggesting heart failure

A

<40%

62
Q

Life threatening ejection fraction

A

<35%

63
Q

Prognosis of dilated cardiomyopathy

A

High mortality from progressive cardiogenic shock and ventricular dysrhythmias

64
Q

Right Ventricular Failure S/Sx

A

Pulmonary HT
JVD
Peripheral edema
RVH
Right atrial enlargement
Ascites
Hepatomegally

65
Q

Left Ventricular Failure S/Sx

A

Pulmonary edema
Hypoxia
Acidosis
Increased WOB
Renal failure
Arrhythmias
A fib
LVH
Hemoptysis
Increased MVO2 demand
Persistant cough

66
Q

Causes of Restrictive Cardiomyopathy

A

Amyloidosis
Sarcoidosis
Genetic inheritance
Scleroderma
Radiation
Exposure to agents promoting fibrosis
Iron overload
Idiopathic

67
Q

Clinical Presentation of Restrictive Cardiomyopathy

A

RVF and LVF symptoms
JVD
Dependent edema
Hepatomegaly
Ascites
Dyspnea, pulmonary edema
Exercise intolerance
Fatigue

68
Q

Treatment of Restrictive Cardiomyopathy

A

Treat underlying problem
Diuretics
Vasodilators
Monitor

69
Q

Mitral Valve Stenosis

A

A fib common
Atrial enlargement and fibrillation increase risk for thrombus
Pulmonary congestion
Orthopnea
Cough
Exertional dyspnea
Paroxysmal nocturnal dyspnea
Abnormal breath sounds
Decreased SpO2

70
Q

Atrial Hypertrophy

A

Left atrial enlargement caused by mitral valve disease
Biphasic P wave with wide terminal component

71
Q

Causes of Hypertrophic Cardiomyopathy

A

Genetic disorder
Abnormal SNS responsiveness of heart
Abnormal catecholamine levels
Systemic hypertension

72
Q

Mitral Valve Regurgitaiton

A

Backflow of blood from LV to left atrium during systole
Increased outflow resistance
LV compensates
Left atrium and LV dilate and hypertrophy

73
Q

Pathogenesis of Hypertrophic Cardiomyopathy

A

LVH occurring in absence of stimuli such as HTN or aortic stenosis
Restrict ventricles from filling properly
Cells become larger to compensate
Septum extremely hypertrophied

74
Q

Diastolic Dysfunction Hypertrophic Cardiomyopathy

A

Decreased chamber size
Decrease filling of heart, decreased output
Diastolic heart failure

75
Q

Aortic Outflow Obstruction

A

Strenuous activity precipitates profound outflow obstruction
Decreased diameter to aorta from enlarged septum
Stretching LV causes opening of aortic valve to increase
Diastolic phase decreased due to increase in HR

76
Q

Clinical Manifestations of Hypertrophic Cardiomyopathy

A

Exertional syncope or presyncope
Symptoms of pulmonary congestion
chest pain
Palpitaitons

77
Q

ECG Changes of Hypertrophic Cardiomyopathy

A

LVH
Deep narrow Q waves in lateral and inferior leads from septal hypertrophy
P mitre from left ventricular diastolic dysfunction
Dysrhyhtmias

78
Q

Dysryhthmias + hypertrophic cardiomyopathy

A

WPW
Atrial fibrillation
SVT

79
Q

Arrhythmogenic Right Ventricular Cardiomyopathy

A

Inerited disease with paroxysmal ventricular arrhythmias and sudden cardiac death
Fatty tissue replaces heart tissue
Surviving pts develop features of RVF

80
Q

Etiology ARVC

A

2nd cause of sudden death in young people
20% sudden death in pts <35
More common in men than women and italian or greek
1/5000

81
Q

Clinical Features of ARVC

A

Symptoms due to ventricular ectopic beats or sustained VT, palpitations syncope, cardiac arrest
First symptom may be death
Usually family history of sudden death

82
Q

ECG Features ARVC

A

Epsilon Wave
T wave inversion V1-3
Prolonged S wave upstroke
Localized QRS widening in V1-3
Paroxysmal episodes of VT with LBBB

83
Q

Epsilon wave

A

Small positive deflection buried in end of qrs

84
Q

Treatment of ARVC

A

Anti-arrhythmic drugs if no high risk features
Defibrillator if high risk
Ablation
Heart failure treatment

85
Q

Brugada Syndrome

A

Faulty sodium ion channel inhibiting conduction of AP causing abnormal repolarization
Leading cause of death among young men in east/southeast asia

86
Q

Brugada Considerations

A

Documented v fib or polymorphic VT
Family history of SCD <45
Coved type ECGs
Inducibility of VT with electrical stimulation
Syncope
Nocturnal atonal respiration

87
Q

When Brugada may appear

A

Fever, Ischemia, Drug use, hypokalemia, hypothermia, post cardioversion

88
Q

Brugada ECG

A

Coved ST elevation >2mm in >1 of V1-V3, negative T wave

89
Q

Brugada Type 2

A

Saddle-like appearance >2mm in V1-V3

90
Q

Brugada Treament

A

ICD

91
Q

Characteristics of Brugada

A

Abnormalities localized to V1-V3
Sudden cardiac death
Structurally normal heart
Familial occurrence
Partial RBBB with ST elevation and biphasic T waves
May come and go
Sodium channelopathy

92
Q

Left Ventricular Hypertrophy

A

Abnormally large left ventricle

93
Q

Causes of LVH

A

Outflow problem, pressure overload
Volume overload
Heart attempting to overcome pressure or volume

94
Q

Components affecting height of QRS

A

Size and direction of vectors
Direct opposition of various vectors
Effusion
Body fat
Amyloid deposits

95
Q

Tall QRS Complexes

A

Increased hypertrophy of one or both ventricles
Increased abnormal pacer
Increased aberrantly conducted beat

96
Q

Abnormally Small QRS

A

Decrease voltage in all limb leads <5
Decreas waves <10mm high in precordial

97
Q

LVH ECG changes

A

Deepest S wave in V1 or 2 + tallest R wave in V5 or V6 >35 mm or

R in aVL >12
S in V1 or V2 > 20-25
R in V5 >20 or V6 >25
Left ventricular strain pattern of ST segment and T wave

98
Q

Effect of hypertrophy on cardiac axis

A

Greater muscle mass equals excess generation of electrical potential on affected side
Greater time required for movement of depolarization wave through large muscle

Patient Care (11 decks)

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