Cardiology 3 Flashcards
Prinzmetal’s Angina
Coronary artery spasm
Resolution of STE without revascularization
Occurs with baseline CAD
Prinzmetal’s Angina Treatment
ASA, Morphine, vasodilators
Causes of Prinzmetal’s angina
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
HELP B
Hyperkalemia
Early Repolarization
Left ventricular hypertrophy; LBBB
Pericarditis
Brugada
Importance of K in the body
Regulate fluid + electrolyte balance
Maintain BP
Help transmit nerve impulses
Control muscle contraction in heart
Maintain healthy bones
Required Potassium intake
1mEq/kg/daily
Potassium Hemostasis
Primary intracellular cation
3.5-5mEq/L
Potassium Maintenance
Hormones
Cell membrane Transporters
Kidneys
Potassium Loss
Urine
Sweat
Stool
Causes of Hyperkalemia
Excessive Intake
Decreased excretion
Shift from intracellular to extracellular space
Medications causing hyperkalemia
ACE & ARB
Spironolactone
Digoxin
NSAID
Antifungals
Crush Injury
Compression of extremities or parts of body causing muscle swelling and neurological disturbances which affect areas of body
Crush Syndrome
Localized crush injury with systemic manifestations
Cellular Response to Crush Injury
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
Insulin + Hyper K
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
S/Sx of Hyperkalemia Mild
General irritability
Rubber legs
Muscle twitching
Cramps
Nausea/diarrhea
Severe S/sx of Hyperkalemia
Hypotension
Decrease LOA
ECG changes
Hyper K and AP
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
Prolong Hyper K and AP
K channels increase conductance
Increased slope of phase 2 and 3, shortening repolarization time
ST-T depression, peaked T waves, Q-T shortening
Mild Hyper K ECG
5.5-6.5mEq/L
Peaked T
Prolonged PR
Moderate Hyper K ECG
6.5-8 mEq/L
Loss of P wave
Prolonged QRS
ST elevation
Ectopic beats and escape rhythms
Severe Hyper K ECG
> 8.0mEq/L
Widening QRS
Sine wave
V fib
Asystole
Axis deviations
BBB
Fascicular blocks
Treatments of Sine Wave Hyper K
Fluid bolus
Symptomatic bradycardia directive
Calcium gluconate/salbutamol
Goal of HyperK Treatment
Stabilize the myocardial membrane
Drive extracellular potassium back into cells
Remove potassium from the body
Calcium Gluconate
Restores membrane potential
Stabilized cardiac cell membrane decreases risk for lethal arrhythmias
1 gram as slow push
Watch ECG
Salbutamol
Shifts potassium intracellularly, temporarily reducing serum K
Double usual dose for bronchoconstriction
Can give during arrest through ETT/King LT
Calcium Gluconate Side effects
Rapid: hypotension, bradycardia, syncope
Chalky, N/V, dry mouth
Local necrosis/abscess if extravasates
BER
Elevated J point with notching
Global concave ST elevation
Large symmetrical concordant T waves
Absence of reciprocal changes or pathological Q
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
Acute Pericarditis
Systemic effects of inflammation and pericardial damage
Chest pain, fever, leukocytosis, malaise, tachycardia, friction rub
Chronic Pericarditis
Healed stage of acute form resulting from chronic pericardial dysfunction
Pericarditis treatment
ASA 650mg q 6 hours
Pericarditis Presentation
Retrosternal Chest pain worsening with position
Dyspneic
Tachycardic
Possible fever
Friction rub
Evidence of pericardial effusion
Causes of Pericarditis
Infectious: viral
Immunological: lupus, rheumatic fever
Post-MI
Uremia
Trauma
Following cardiac surgery
Malignancy
Post-radiotherapy
Drug-induced
ECG Changes Pericarditis
Diffuse ST elevation
No ST depression
ST segment concave upwards
PR segment depression
PR segment elevation in aVR
Assessing STEMI vs Pericarditis
Reciprocal changes
ST segment morphology convex or horizontal
ST elevation lead 3 > lead 2 (STEMI if yes)
Beck’s Triad
Hypotension
JVD
Muffled heart sounds
Amplitude and Pericardial Effusion
Large amounts of fluid lead to dampening effect
Characteristic of Pericardial Tamponade
Excess fluid accumulation in the pericardial space
Build up impairs diastolic filling decreasing CO
Causes of pericardial tamponade
Pericardial effusion
Trauma and hemorrhage
Pericardial Tamponade Manifestation
Reduced chamber filling during diastole
Rising filling pressures in heart chambers
Backup into SVC and IVC
Reduced stroke volume
Decreased CO
Other manifestations of pericardial tamponade
Tachycardia
Pulmonary edema
Pulsus paradoxus
Dull chest pain
Diminished ECG amplitude
Compressed cardiac silhouette
Pericardial tamponade treatment
Pericardiocentesis
Antibiotics
Fluid, blood, inotropes as needed
Surgery
Endocarditis
Inflammation of inner lining of the heart
Caused by infection
IV drug users at risk
May include one or more heart valves
Infective Endocarditis
May cause mitral or tricuspid valve insufficiency and regurgitation
Presentation of Infective Endocarditis
Non-specific
Symptoms 2 weeks from initiation of bacteremia
Low grade fever
Fatigue
Weight loss
Flu-like symptoms
Heart murmur
Complication of Infective Endocarditis
Valvular insufficiency
Myocardial abscess
Embolization
Renal disease
treatment Infective endocarditis
Antibiotics
Anti-inflammatories
Surgical valve replacement
Hemodynamic support
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
Symptoms Myocarditis
Fatigue
Dyspnea on exertion
Dysrhythmias
Cardiomyopathy
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic obstructive cardiomyopathy
Dilated Cardiomyopathy
Chambers of heart become hypertrophied and unable to pump out blood
Dilated ventricular chambers
Decreased ejection fraction
Systolic failure
Restrictive cardiomyopathy
Muscles of heart chamber become thick with scar tissue, decreasing stretch
Rarest form
Particles in heart causing fibrosis
Diastolic heart failure
Hypertrophic Cardiomyopathy
Enlarged walls of chambers
Large septal wall impedes path for blood from LV to aorta
Causes of Dilated Cardiomyopathy
Unknown possible genetic component
Myocarditis
Ischemia
Toxins
Pregnancy
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
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
Ejection Fraction
EDV-ESV / EDV x 100
Ejection fraction NOrmal
55-70
Ejection fraction below normal
40-55%
Ejection fraction suggesting heart failure
<40%
Life threatening ejection fraction
<35%
Prognosis of dilated cardiomyopathy
High mortality from progressive cardiogenic shock and ventricular dysrhythmias
Right Ventricular Failure S/Sx
Pulmonary HT
JVD
Peripheral edema
RVH
Right atrial enlargement
Ascites
Hepatomegally
Left Ventricular Failure S/Sx
Pulmonary edema
Hypoxia
Acidosis
Increased WOB
Renal failure
Arrhythmias
A fib
LVH
Hemoptysis
Increased MVO2 demand
Persistant cough
Causes of Restrictive Cardiomyopathy
Amyloidosis
Sarcoidosis
Genetic inheritance
Scleroderma
Radiation
Exposure to agents promoting fibrosis
Iron overload
Idiopathic
Clinical Presentation of Restrictive Cardiomyopathy
RVF and LVF symptoms
JVD
Dependent edema
Hepatomegaly
Ascites
Dyspnea, pulmonary edema
Exercise intolerance
Fatigue
Treatment of Restrictive Cardiomyopathy
Treat underlying problem
Diuretics
Vasodilators
Monitor
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
Atrial Hypertrophy
Left atrial enlargement caused by mitral valve disease
Biphasic P wave with wide terminal component
Causes of Hypertrophic Cardiomyopathy
Genetic disorder
Abnormal SNS responsiveness of heart
Abnormal catecholamine levels
Systemic hypertension
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
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
Diastolic Dysfunction Hypertrophic Cardiomyopathy
Decreased chamber size
Decrease filling of heart, decreased output
Diastolic heart failure
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
Clinical Manifestations of Hypertrophic Cardiomyopathy
Exertional syncope or presyncope
Symptoms of pulmonary congestion
chest pain
Palpitaitons
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
Dysryhthmias + hypertrophic cardiomyopathy
WPW
Atrial fibrillation
SVT
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
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
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
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
Epsilon wave
Small positive deflection buried in end of qrs
Treatment of ARVC
Anti-arrhythmic drugs if no high risk features
Defibrillator if high risk
Ablation
Heart failure treatment
Brugada Syndrome
Faulty sodium ion channel inhibiting conduction of AP causing abnormal repolarization
Leading cause of death among young men in east/southeast asia
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
When Brugada may appear
Fever, Ischemia, Drug use, hypokalemia, hypothermia, post cardioversion
Brugada ECG
Coved ST elevation >2mm in >1 of V1-V3, negative T wave
Brugada Type 2
Saddle-like appearance >2mm in V1-V3
Brugada Treament
ICD
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
Left Ventricular Hypertrophy
Abnormally large left ventricle
Causes of LVH
Outflow problem, pressure overload
Volume overload
Heart attempting to overcome pressure or volume
Components affecting height of QRS
Size and direction of vectors
Direct opposition of various vectors
Effusion
Body fat
Amyloid deposits
Tall QRS Complexes
Increased hypertrophy of one or both ventricles
Increased abnormal pacer
Increased aberrantly conducted beat
Abnormally Small QRS
Decrease voltage in all limb leads <5
Decreas waves <10mm high in precordial
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
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
