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Cardiology 3 Flashcards

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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
Calcium Gluconate
Restores membrane potential Stabilized cardiac cell membrane decreases risk for lethal arrhythmias 1 gram as slow push Watch ECG
26
Salbutamol
Shifts potassium intracellularly, temporarily reducing serum K Double usual dose for bronchoconstriction Can give during arrest through ETT/King LT
27
Calcium Gluconate Side effects
Rapid: hypotension, bradycardia, syncope Chalky, N/V, dry mouth Local necrosis/abscess if extravasates
28
BER
Elevated J point with notching Global concave ST elevation Large symmetrical concordant T waves Absence of reciprocal changes or pathological Q
29
ST Segment/T wave ratio
Vertical height of ST elevation measured and compared to T wave amplitude in V6 Ratio >0.25 = pericarditis Ratio <0.25 = BER
30
Acute Pericarditis
Systemic effects of inflammation and pericardial damage Chest pain, fever, leukocytosis, malaise, tachycardia, friction rub
31
Chronic Pericarditis
Healed stage of acute form resulting from chronic pericardial dysfunction
32
Pericarditis treatment
ASA 650mg q 6 hours
33
Pericarditis Presentation
Retrosternal Chest pain worsening with position Dyspneic Tachycardic Possible fever Friction rub Evidence of pericardial effusion
34
Causes of Pericarditis
Infectious: viral Immunological: lupus, rheumatic fever Post-MI Uremia Trauma Following cardiac surgery Malignancy Post-radiotherapy Drug-induced
35
ECG Changes Pericarditis
Diffuse ST elevation No ST depression ST segment concave upwards PR segment depression PR segment elevation in aVR
36
Assessing STEMI vs Pericarditis
Reciprocal changes ST segment morphology convex or horizontal ST elevation lead 3 > lead 2 (STEMI if yes)
37
Beck's Triad
Hypotension JVD Muffled heart sounds
38
Amplitude and Pericardial Effusion
Large amounts of fluid lead to dampening effect
39
Characteristic of Pericardial Tamponade
Excess fluid accumulation in the pericardial space Build up impairs diastolic filling decreasing CO
40
Causes of pericardial tamponade
Pericardial effusion Trauma and hemorrhage
41
Pericardial Tamponade Manifestation
Reduced chamber filling during diastole Rising filling pressures in heart chambers Backup into SVC and IVC Reduced stroke volume Decreased CO
42
Other manifestations of pericardial tamponade
Tachycardia Pulmonary edema Pulsus paradoxus Dull chest pain Diminished ECG amplitude Compressed cardiac silhouette
43
Pericardial tamponade treatment
Pericardiocentesis Antibiotics Fluid, blood, inotropes as needed Surgery
44
Endocarditis
Inflammation of inner lining of the heart Caused by infection IV drug users at risk May include one or more heart valves
45
Infective Endocarditis
May cause mitral or tricuspid valve insufficiency and regurgitation
46
Presentation of Infective Endocarditis
Non-specific Symptoms 2 weeks from initiation of bacteremia Low grade fever Fatigue Weight loss Flu-like symptoms Heart murmur
47
Complication of Infective Endocarditis
Valvular insufficiency Myocardial abscess Embolization Renal disease
48
treatment Infective endocarditis
Antibiotics Anti-inflammatories Surgical valve replacement Hemodynamic support
49
Myocarditis
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
Symptoms Myocarditis
Fatigue Dyspnea on exertion Dysrhythmias
51
Cardiomyopathy
Dilated cardiomyopathy Restrictive cardiomyopathy Hypertrophic obstructive cardiomyopathy
52
Dilated Cardiomyopathy
Chambers of heart become hypertrophied and unable to pump out blood Dilated ventricular chambers Decreased ejection fraction Systolic failure
53
Restrictive cardiomyopathy
Muscles of heart chamber become thick with scar tissue, decreasing stretch Rarest form Particles in heart causing fibrosis Diastolic heart failure
54
Hypertrophic Cardiomyopathy
Enlarged walls of chambers Large septal wall impedes path for blood from LV to aorta
55
Causes of Dilated Cardiomyopathy
Unknown possible genetic component Myocarditis Ischemia Toxins Pregnancy
56
Path of Dilated Cardiomyopathy
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
Result of Dilated Cardiomyopathy
Dilation of ventricles Increased ventricular volume and reduced ejection fraction Decreased ejection of blood, atrial dilation, pulmonary and systemic venous congestion
58
Ejection Fraction
EDV-ESV / EDV x 100
59
Ejection fraction NOrmal
55-70
60
Ejection fraction below normal
40-55%
61
Ejection fraction suggesting heart failure
<40%
62
Life threatening ejection fraction
<35%
63
Prognosis of dilated cardiomyopathy
High mortality from progressive cardiogenic shock and ventricular dysrhythmias
64
Right Ventricular Failure S/Sx
Pulmonary HT JVD Peripheral edema RVH Right atrial enlargement Ascites Hepatomegally
65
Left Ventricular Failure S/Sx
Pulmonary edema Hypoxia Acidosis Increased WOB Renal failure Arrhythmias A fib LVH Hemoptysis Increased MVO2 demand Persistant cough
66
Causes of Restrictive Cardiomyopathy
Amyloidosis Sarcoidosis Genetic inheritance Scleroderma Radiation Exposure to agents promoting fibrosis Iron overload Idiopathic
67
Clinical Presentation of Restrictive Cardiomyopathy
RVF and LVF symptoms JVD Dependent edema Hepatomegaly Ascites Dyspnea, pulmonary edema Exercise intolerance Fatigue
68
Treatment of Restrictive Cardiomyopathy
Treat underlying problem Diuretics Vasodilators Monitor
69
Mitral Valve Stenosis
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
Atrial Hypertrophy
Left atrial enlargement caused by mitral valve disease Biphasic P wave with wide terminal component
71
Causes of Hypertrophic Cardiomyopathy
Genetic disorder Abnormal SNS responsiveness of heart Abnormal catecholamine levels Systemic hypertension
72
Mitral Valve Regurgitaiton
Backflow of blood from LV to left atrium during systole Increased outflow resistance LV compensates Left atrium and LV dilate and hypertrophy
73
Pathogenesis of Hypertrophic Cardiomyopathy
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
Diastolic Dysfunction Hypertrophic Cardiomyopathy
Decreased chamber size Decrease filling of heart, decreased output Diastolic heart failure
75
Aortic Outflow Obstruction
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
Clinical Manifestations of Hypertrophic Cardiomyopathy
Exertional syncope or presyncope Symptoms of pulmonary congestion chest pain Palpitaitons
77
ECG Changes of Hypertrophic Cardiomyopathy
LVH Deep narrow Q waves in lateral and inferior leads from septal hypertrophy P mitre from left ventricular diastolic dysfunction Dysrhyhtmias
78
Dysryhthmias + hypertrophic cardiomyopathy
WPW Atrial fibrillation SVT
79
Arrhythmogenic Right Ventricular Cardiomyopathy
Inerited disease with paroxysmal ventricular arrhythmias and sudden cardiac death Fatty tissue replaces heart tissue Surviving pts develop features of RVF
80
Etiology ARVC
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
Clinical Features of ARVC
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
ECG Features ARVC
Epsilon Wave T wave inversion V1-3 Prolonged S wave upstroke Localized QRS widening in V1-3 Paroxysmal episodes of VT with LBBB
83
Epsilon wave
Small positive deflection buried in end of qrs
84
Treatment of ARVC
Anti-arrhythmic drugs if no high risk features Defibrillator if high risk Ablation Heart failure treatment
85
Brugada Syndrome
Faulty sodium ion channel inhibiting conduction of AP causing abnormal repolarization Leading cause of death among young men in east/southeast asia
86
Brugada Considerations
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
When Brugada may appear
Fever, Ischemia, Drug use, hypokalemia, hypothermia, post cardioversion
88
Brugada ECG
Coved ST elevation >2mm in >1 of V1-V3, negative T wave
89
Brugada Type 2
Saddle-like appearance >2mm in V1-V3
90
Brugada Treament
ICD
91
Characteristics of Brugada
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
Left Ventricular Hypertrophy
Abnormally large left ventricle
93
Causes of LVH
Outflow problem, pressure overload Volume overload Heart attempting to overcome pressure or volume
94
Components affecting height of QRS
Size and direction of vectors Direct opposition of various vectors Effusion Body fat Amyloid deposits
95
Tall QRS Complexes
Increased hypertrophy of one or both ventricles Increased abnormal pacer Increased aberrantly conducted beat
96
Abnormally Small QRS
Decrease voltage in all limb leads <5 Decreas waves <10mm high in precordial
97
LVH ECG changes
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
Effect of hypertrophy on cardiac axis
Greater muscle mass equals excess generation of electrical potential on affected side Greater time required for movement of depolarization wave through large muscle

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