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Cardio1 PDF
Cardio1 PDF
1. Anatomy and physiology of the coronary arteries
Coronary artery :
- Left coronary artery
o Left anterior descending coronary artery
§ Septal branches
§ Diagonal branches
o Circumflex artery
- Right coronary artery
o Acute marginal branches
o AV nodal artery
o Posterior descending artery
2. Cardiac oxygen supply and demand
Myocardial oxygen supply.
Depends on oxygen content (hemoglobin and systemic oxygenation) and rate of coronary
blood flow.
Low aortic diastolic pressure -> low coronary artery perfusion pressure -> low myocardial
oxygen supply.
Coronary vascular resistance controlled by :
1) external compression
2) intrinsic control of coronary arterial tone
· Metabolic factor
Vasodilator - hypoxemia
· Endothelial factors
Vasodilator – prostacyclin & NO, EDHF
Vasoconstrictor – Endothelin 1, catecholamine
· Neural factors
Vasodilator - β2 adrenergic receptor
Vasoconstrictor – α adrenergic receptor
Myocardial oxygen demand
Depends on ventricular wall stress, heart rate, contractility.
High oxygen demand :
1) High ventricular pressure -> high wall stress
2) High LV filling and thinned wall heart -> high wall stress
3) High heart rate -> high ATP consumed
High oxygen consumption :
Positive inotropic drugs -> increase the level of contraction -> high oxygen consumption
3. Atherogenesis and pathophysiology of atherosclerosis and endothelial cells
1) Dysfunction endothelium
2) High LDL deposit in tunica intima
3) Oxidized
4) Activates endothelial cell
5) Release reactive oxygen species and metalloprotease
6) Adhesion of blood leukocytes into tunica intima
7) Monocytes move to tunica intima becomes macrophages
8) In macrophage surface, there is scavenger receptor that binds to ox-LDL
9) Become foam cell
10) Induce smooth muscle migration to tunica intima
11) Proliferate
12) Increase synthesis of collagen
13) Foam cell dies
14) Lipid amount release
15) Stop activation of collagen
16) Fibrous cap becomes thinner
17) Rupture
18) Thrombus formation
4. Biochemical changes affecting the heart and vessels (role & mechanism of cardiac enzymes)
- Cardiac specific troponin
TnC & TnI
Normal : absent in blood test
MI : rise in 3-4 hours after onset of chest discomfort
Peak level 18-36 hours
- Creatine kinase
Specific in heart CK-MB
MI : CK-MB : total CK > 2,5%
Rise 3 to 8 hours
Peak at 24 hours
Return to normal within 48-72 hours
- Myoglobin (rise in first hour, menurun dengan cepat)
- CPK (rise in 4-8 hours, ada di banyak tempat jadi tidak spesifik)
5. Pathophysiology of myocardial ischemia and myocardial infarction
Myocardial ischemia
1) Fixed vessel narrowing
o Fluid mechanism
o Anatomy
2) Endothelial cell dysfunction
o Inappropriate vasoconstriction (sympathetic nervous system)
o Loss of normal antithrombotic properties
3) Low perfusion pressure due to hypotension
4) Low oxygen content
Myocardial infarction
§ Transmural infarct : entire thickness of myocardial wall
§ Subendocardial infarct : innermost layer of myocardium
6. Management of myocardial ischemia and myocardial infarct
M – morphin
O – oxygen
N – nitrate
A – aspirin (slow agregat formation)
C – clopidogrel (antiplatelet & anticoagulant)
O – obat lain
7. Pharmacology treatment for atherosclerosis, myocardial ischemia, myocardial infarction
v Organic nitrates (first line)
Nitroglycerine, isosorbide dinitrate, isosorbide mononitrate
MOA : Lower oxygen demand
Increase oxygen supply
v β blocker
.....lol
MOA : Decrease myocardial oxygen demand
v CCB
Verapamil (non-dihydropyridine), diltiazem, .....dipin (dihydropyridin)
MOA : Lower myocardial oxygen demand
Increase oxygen demand
WEEK 5 - HEART FAILURE
Mitral Valve Disease
Mitral Stenosis
- Most common cause is rheumatic fever (complication of pharyngitis caused by A beta
hemolytic streptococci that mainly affect children and young adult) - treatment using
aspirin to reduce inflammation and penicillin to eliminate residual infection. Chronic
Rheumatic heart disease characterized by permanent deformity and impairment of one
or more cardiac valve. Manifest after 10 to 30 years after ARF.
- Caused by acute and recurrent inflammation due to ARF. These include fibrous
thickening and calcification of the valve leaflet, fusion of the commissures (border where
leaflet meet), and thickening and shortening of the chordae tendinae.
- Abnormal pressure gradient between LA and LV ( LA>LV). Cross-sectional area of the
valve normally 4 - 6 cm2 reduced to less than 2 cm2.
- High pressure in LA - Retrograde direction to pulmonal - High pressure in pulmonary
vein and capillary bed - transudation of plasma into lung interstitium and alveoli (causing
dyspnea). In severe case, significant elevation of pressure leads to the opening of
collateral channel between pulmonary and bronchial veins - leading to bronchial vein
rupture, resulting in hemoptysis *coughing in blood. (Passive hypertension)
- Reactive hypertension means medial hypertrophy and intimal fibrosis of the pulmonary
arterioles. This increase resistance of the arteriolar - reduce capillary hydrostatic
pressure - limited pressure in pulmo capillaries. This however cause decreased blood
flow through the pulmo and elevation of the right side heart pressure, as the right
ventricle pumps against the increased resistance - leads to hypertrophy and dilatation of
right chamber - right sided HF.
- Leads to LA enlargement - stretches the atrial conduction fibers - can cause atrial
fibrillation - reduce CO & stasis of blood flow - intra atrial thrombus formation -
thromboembolic - stroke
- Treatment using heart rate slowing agents (beta blocker, CCB, digoxin), anti coagulant.
Later use balloon
Mitral Regurgitation
- Primary cause because of structural defects, secondary cause because LV enlargement.
- Divided into acute and chronic. Acute resulted from sudden damage to components of
the valve apparatus. Chronic has multiple causes including myxomatous degeneration of
the valve in which floppy leaflets ( Mitral Prolapse)
- A portion of the left ventricular SV back to LA during systole. In result, CO is less than
LV total output.
- Direct consequences such as an elevation of left atrial volume and pressure, lower CO,
and increase volume-wall stress because the regurgitation volume returns + pulmo vein
- Frank-Starling mechanism
- Severity of MR and ratio of forward CO to backward flow are dictated by five factor
- Size mitral orifice during regurg., systolic pressure gradient between LA and LV,
Systemic vascular resistance oppose forward LV flow, LA compliance, and duration of
regurg with each systolic contraction.
- Prominent v wave
- Acute MR: Normal LA size and compliance → High LA pressure → High pulmonary
venous pressure → Pulmonary congestion and edema
- Chronic MR: Increased LA size and compliance → Relatively normal LA and pulmonary
venous pressures, but decreased forward cardiac output
- Surgical treatment needed, pharmacological is used only to stabilize patients.
Aortic Valve Disease
Aortic Stenosis
- Major causes including 1. Degenerative calcification, 2. Calcification of a congenitally
bicuspid aortic valve, 3. Rheumatic aortic valve disease.
- 1 and 2 results from a dynamic process of endothelial dysfunction, lipid accumulation,
inflammation, and alteration of signaling pathways. Over time, valvular myofibroblast
differentiate into osteoblast and deposit Calcium hydroxyapatite crystal, resulting in
stiffening and thickening of the valve.
- 3 causes inflammation of endocardial - fibrosis of the valve - fusion of the commissures
- Slow rate progression
- LV hypertrophy to overcome the impedance to flow to drive blood into the aorta.
(concentric hypertrophy)
- May cause syncope during exertion, angina, and heart failure (diastolic dysfunction)
- Treatment using AVR (Aortic Valve Replacement), Balloon is not good as it can
restenosis
Aortic Regurgitation
- Resulted either abnormal structure of leaflets or dilatation of the aortic root.
- 1. Bicuspid valve, 2. Infective endocarditis (perforation or erosion of a leaflet), 3.
Rheumatic (thickening and shortening)
- Acute AR - LV is normal size and relatively noncompliant
- LV high diastolic pressure - retrograde direction toward pulmo - pulmo edema
- Chronic AR - LV is adapted (eccentric hypertrophy), widened pulse pressure (high LV
Systolic pressure / reduced aortic diastolic pressure)
- Cause angina, and HF, DOE (dyspnea on exertion)
- Treatment for asymptomatic using vasodilator to reduce afterload
- Treatment for symptomatic patients using surgical correction
Tricuspid Valve Disease
Tricuspid stenosis - same like MS, but murmur is heard closer to the sternum.
Tricuspid Regurgitation - most commonly results from RV hypertrophy
Pulmonic Valve Disease
Pulmonic Stenosis - rare
Pulmonic Regurgitation - most commonly develops in the setting of severe pulmonary
hypertension
HEART FAILURE
1. Normal physiology
Frank-Starling relationship - the observation that ventricular output increases in relation to the
preload (the stretch on the myocardial fibers before contraction)
(The more a normal ventricle distended during diastole, the greater the volume that is ejected
during the next systole)
Three major determinants of SV:
- Preload - Ventricular wall tension at the end of diastole.
- Afterload - Ventricular wall tension during contraction.
- Contractility - Property of heart muscle that accounts for changes in the strength of
contraction resulted from chemical and hormonal influences.
Pressure-Volume loops
EDV = representation of preload
ESV = representation of afterload
a. HF with reduced EF
b. HF with preserved EF
Pathophysiology of Heart Failure
Etiologies can be grouped into:
SYSTOLIC DYSFUNCTION (HF with reduced EF)
1. Impaired contractility
A. Coronary Artery Disease
- Myocardial Infarct
- Transient myocardial ischemia
B. Chronic Volume overload (increases afterload)
- Mitral Regurgitation
- Aortic Regurgitation
C. Dilated Cardiomyopathies
2. High afterload (chronic pressure overload)
A. Advanced aortic stenosis
B. Uncontrolled severe hypertension
DIASTOLIC DYSFUNCTION (HF with preserved EF)
1. Impaired Diastolic Filling
A. LV hypertrophy
B. Restrictive cardiomyopathy
C. Myocardial fibrosis
D. Transient myocardial ischemia
E. Pericardial Tamponade - limits ventricular filling
Heart Failure with Reduced EF (Systolic Dysfunction)
Persistent elevated LV pressure is transmitted back to the pulmo (>20 mmHg) can cause
transudation of fluid into pulmo interstitium.
* A = Systolic Dysfunction, B = Diastolic Dysfunction
Heart Failure with Preserved EF (Diastolic Dysfunction)
- Impaired early diastolic relaxation, increased stiffness of ventricular wall
- Elevated diastolic pressure is transmitted retrograde to pulmo
Right sided Heart failure is commonly caused by the presence of left sided heart failure.
This is because the left HF will cause high pressure in pulmonary vascular, that will affect the
right side of the heart to compensate. Right sided HF that results from a primary pulmonary
process is known as cor pulmonale.
Compensatory Mechanism
1. Frank - Starling Mechanism ( higher preload - increase stretch on the myofibers)
(limited)
2. Neurohormonal Alterations ( increasing venous return and stroke volume)
A. Adrenergic Nervous System
The fall in cardiac output sensed by baroreceptor - increasing sympathetic - causing
increase in HR, augmentation of ventricular contractility,and vasoconstriction
B. RAAS
Retain sodium, vasoconstriction, Increase in HR
C. Production of ADH
Increasing circulating volume
*These mechanism above can induce more peripheral edema and pulmonary congestion
D. Natriuretic Peptides
Have opposite reaction to those other hormone (excretion of sodium, vasodilation,
inhibition of renin secretion.
3. Development of ventricular hypertrophy and remodeling
Eccentric hypertrophy - increase in wall length (dilate)
Concentric hypertrophy - increase in wall thickness
Symptoms of Heart Failure
Class of NYHA
Class of AHA
Clinical Findings through X Ray
- Presence of Kerley B lines indicating pulmo edema
- Cardiomegaly
- Bat wing pulmonary opacities
Pulmonary Edema
- Rapid accumulation of fluid within the interstitium and alveolar space of lung due to LV
diastolic pressure >25 mmHg.
- Patient is tachycardic and may demonstrate cold, clammy skin owing to peripheral
vasoconstriction. Coughing of “frothy” sputum represents transudation of fluid into the
alveoli.
- Treatment using LMNOP (Lasix-furosemide, Morphine, Nitrates, Oxygen, Position-sit
upright)
Chapter 10 : Cardiomyopathies
3 main types
Dilated (impaired systolic contractile function) - concentric hypertrophy
- Caused by viral myocarditis, chronic excessive alcohol ingestion, peripartum state
specific gene mutation.
- Viral myocarditis mostly caused by coxsackievirus group B
- Chronic excessive alcohol ingestion is believed that ethanol can impair cellular function
by impacting mitochondrial oxidative function, myocyte apoptosis, cytosolic calcium
levels.
- Peripartum presents between the last month of pregnancy and up to 6 months
postpartum
*Lv dilatation can cause mitral regurgitation as the chamber dilates, the valve may fail to coapt properly in systole.
This can cause atrial enlargement that leads to atrial fibrillation, decreases forward stroke volume into the aorta.
Treatment using ACE inhibitor to reduce symptoms of HF, vasodilator, ARB, beta-blocker
Pacemaker for controlling electrical conduction (reducing atrial fibrillation)
Anticoagulant to prevent thromboembolic
Hypertrophic (abnormal diastolic relaxation)
- Mostly caused by an appearance of valvular stenosis
In Hypertrophic cardiomyopathy, there can be an outflow obstruction that caused by an
abnormal motion of the anterior mitral valve leaflet toward the LV outflow tract (Venturi forces)
S4 can be heard in HCM due to stiffening of the wall.
Treatment using beta blocker
Restrictive (stiffened myocardium because of fibrosis or an infiltrative process)
- Caused by fibrosis or scarring of the endocardium and infiltration of the myocardium by
an abnormal substance
- Most common cause is amyloidosis (amyloid deposition in heart) - deposition of
immunoglobulin light chain AL fragment secreted by a plasma cell tumor
- Resulted in an upward shift of the passive ventricular filling curve
- Most accurate diagnostic tools is biopsy to find the presence of amyloid deposition
- Treatment using salt restriction, chemotherapy
4) The physiologic basis of the management of HF
a) Clinical Manifestations of HF
Mainly caused by:
· Impaired forward cardiac output.
· Elevated Venous Presure
Left- Ventricular Heart Failure
1) Dyspnea (Shortness of Breath):
- Caused by Pulmonary congestion / Reduced cardiac output.
- Transudation of fluid from pulmonary vein to interstitial space and lung parenchyma.
- Decreased pulmonary compliance and increases work of breathing.
- Excess fluid in the wall increases resistance to airflow and increases respiration
effort.
- Juxtacapillary receptors stimulated which results in rapid, shallow breathing.
- HF with dyspnea (without pulmonary congestion) is a result of impeded blood flow to
respirating muscles and accumulation of lactic acid due to anaerobic respiration.
- Initial Stage;; Dyspnea on Exertion, Severe stage;; Dyspnea at rest.
2) Dulled mental state:
- Reduced cerebral perfusion.
3) Decreased urine output
- Decreased renal perfusion
- Increased frequency at night (nocturia);; usually when supine because blood flow
redistributed to kidney promoting renal perfusion and diuresis.
4) Fatigue and Weakness
- Decreased skeletal muscle perfusion.
- Nocturnal cough- Hemoptysis (coughing up blood)
5) PND (Paroxysmal Nocturnal Dyspnea)
- Breathlessness that often awakens the patient due to lower extremity interstitial
edema.
6) Orthopnea
- Temporary relief in symptoms when seated upright.
- Expansion of intravascular volume which increases venous return to the heart.
Right-Ventricular Heart Failure
1) Abdominal discomfort (Ascites)
- Systemic Venous Pressure increases, liver engorged and capsule stretched.
2) Anorexia and Nausea
- Edema in GI tract
3) Peripheral Edema
- Increase in venous hydrostatic pressure.
- Worsens during the day due to gravity and improved when supine at night.
4) Unexpected weight gain
- Increase in interstitial fluid.
b) Components of Treatment of HF
Treatment of HF with Reduced EF
1) Diuretics (eg: Furosemide (Lasix) , Thiazide diuretics)
- Should only be used if there is evidence of pulmonary congestion (rales)/ edema.
- Elimination of Na and Water through kidney reduces intravascular volume and
venous return to the heart.
- Decreases preload to the left ventricle and decreases diastolic pressure which
decreases hydrostatic pressure without a fall in stroke volume.
- Acts in renal loop of Henle and is less effective if there is a decrease in renal
perfusion.
- Overuse causes diuresis that may decrease cardiac output / lead to other conditions
such as;; hypokalemia, hypomagnesmia which causes arrhythmia.
2) Vasodilators
· ACE Inhibitors (-pril)
- Reverse neurohormonal compensatory mechanism by inhibiting RAAS.
- Causes sodium elimination and increases the level of bradykinin (Vasodilator)
- Decreases heart workload.
· Venous vasodilators (eg;; nitrates)
- Increases venous capacitance and decreases venous return to the heart to decrease
pressure in LV and decreases hydrostatic pressure so pulmonary congestion
improves.
· Arterial Vasodilators (eg: hydrasalazine)
- Decreases systemic vascular resistance and afterload decreased.
- Induces Ventricular muscle fiber shortening during systole that increases stroke
volume.
· Nesitiride
- IV vasodilator for decompensated HF
- Rapid and potent vasodilatation and lowers intracardiac pressure and increases
cardiac output.
3) Inotropic drugs;;
- To increase contractility where strove volume and cardiac output increased
- Usually to treat HF with systolic dysfunction.
· ß- Adrenergic agonists (eg: dobutamine, dopamine)
- Temporary hemodynamic support
· Phosphodiesterase Inhibitors
- IV treatment for CHF.
· Digitalis
- Increases contractility and decreases cardiac enlargement
- Increases cardiac output with systolic HF and increases sensitivity of baroreceptors
to fire sympathethic drive in the heart
- Reduces LV afterload by slowing AV conduction.
· ß- blockers
- Increases cardiac output and decreases hemodynamic deterioration.
- Negative Inotropic effect.
- Carvedilol- non selective ß1, ß2 receptor blocker with weak alpha blocking
properties.
- Metoprolol- ß1 selective properties.
· Aldosterone Antagonist Therapy (eg: Spironolactone, Eplenerone)
- Prevents excess aldosterone in HF causing cardiac fibrosis and adverse ventricular
filling.
- Usually given after MI
Additional Therapy
1) Anticoagulation with warfarin – prevents intracardiac thrombus formation if LV systolic
function is severely impaired.
2) Treatment of AF/ Ventricular Arrythmias- Improves Cardiac ouput when in sinus rhythm.
3) Implantable CD (Cardioverter Deffibrilator)
4) Cardiac Replacement Therapy- Cardiac Transplant.
Treatment of HF with preserved EF
1) Relief pulmonary congestion and peripheral edema with diuretics.
2) Inotropics have no role because contractility unchanged.
5) Infections of the heart
a) Infective and non-Infective endocarditis.
Acute Bacterial Endocarditis
Clinical
Sub-Acute
Infective Endocarditis Host-Substrate native valve
Prosthethic valve
IV drug abuse
Specific infecting organism
Pathogenesis:
· Endocardial Surface Injury
- Endothelial Injury- turbulent blood flow and foreign material.
- Platelets adhere to exposed subendocardial connective tissue and initiate formation
of sterile thrombus (vegetation) through fibrin deposition
· Thrombus formation
· Bacterial entry to circulation.
· Bacterial adherence to injured endocardial surface.
Non Bacterial thrombotic endocarditis
· Usually caused by trauma hospitable to microbes and spresds to bloodstream
causing Infective endocarditis
· Fibrin-platelets deposit adherence to bacteria.
· Fibrin covers adherent organisms and protects from host defenses by inhibiting
chemotaxis and migration of phagocytes.
· Causative agents are usually S. Aureus, Enterococci spp, Pneumococci (gram
positive bacteria)
· Gram + bacteria dextran are resistant to destruction in circulation by complement
and adhere to endothelial and platelet surface proteins.
· Cell wall binds to thrombus causing endocarditis which causes mechanical
cardiac injury, thrombotic/ septic emboli/ Immune injury which may cause;;
valvular damage, abcess and erosion to cardiac conducting system.
Myocarditis
Inflammation of myocardium causing myocyte damage and Inflammatory cardiomyopathy.
1) Dilated- Chamber enlargement due to heavy preload volume
2) Hypertrophic- Thickened ventricular wall
3) Restrictive- Stiffened by myocardium
Pericarditis
Inflammation in the pericardium. Usually acute and occurs post MI due to arrhythmia or viruses
such as HSV, HIV, CMV. May also be caused by respiratory tract infection.
6) Cardiac Rehabilitation
Effect of exercise on a healthy heart:
50 min/ week has positive impact on heart as it regulates tissue perfusion, increases contractility
and stimulates HR and lowers BP. It also lowers the chances of high LDL cholesterol which
prevents risk for atherosclerosis leading to MI.
Effect of exercise on abnormal heart:
Only light exercises should be conducted on an abnormal heart because the higher workload on
an abnormal heart may cause further dyspnea.
Stress tests are conducted to see STEMI on ECG. If patient feels discomfort, immediately stop
because of exercise intolerance in HF. Light exercises may improve exercise tolerance.
7) RHD
- Inflammatory condition that involves the heart, skin and connective tissues.
- Complication of upper respiratory tract infections caused by a group of streptococci
- Tachycardy, decreased ventricular contractility, pericardial friction rub, transient
murmur of mitral or aortic regurgitation or a mid diastolic murmur (inflamed valve
leaflets) at cardiac apex.
WEEK 3 - CARDIO
1. Describe nodal, purkinje fibers and ventricular/atrial action potentials with particular
reference to:
a. Phases and ion movement
b. Relative and Absolute Refractory Periods
c. Conduction Velocity
2. Decribe the anatomy of the cardiac electrical system with particular reference to SA
node, atria,AV node, bundle of His, LBB, RBB Purkinje fibers
3. Einthoven’s triangle, Action Potencial gives rise to the ECG? Normal EKG, Rhytm EKG
(Normal sinus rhytm, Sinus bradycardia, Sinus tachycardia, AV block, Atrial flutter and
fibrillation, SVT,VT, V-fib, Asystole, dan segala arrythmia
4. Mechanism of arrythimas;;
a. Tachycardiac Arrythimas
i. Physiologic
ii. Re-entry (large circuit and ectopic pacemaker)
iii. After-depolarization
b. Bradycardiac Arrythmias
i. Sinus
ii. Block
5. Treatment of tachycardia dan bradycardia (conservative, pharmacologic, dan invasive)
6. Hemodynamic consequences of tachycardia, including preload, CO, BP, and coronary
flow.
7. Pharmacologic of :
a. Class 1, 2,3,4, anti arrythmia
b. Adenosine
1.
a. Phases and ion movement:
Fase 4 : Resting State. Dimana sodium dan
kalsium channel ketutup.
Fase 0 : Sodium channel kebuka,
depolarisasi, hingga mencapai treshold
potential.
Fase 1 : Aktivasi K+ channel , K+ keluar
Fase 2 : Plato Channel - karena K+ keluar
dan Ca++ masuk jadi seimbang.
Fase 3 : Repolarisasi- Keluarnya K+ sampai
ke resting potential lagi.
b. Relative and Absolute Refractory Periods
Refractory Period : Ketidakmampuan sel untuk merespon berbagai stimulus dalam beberapa
periode waktu.
Absolute Refractory Period : Dimana cel tidak akan bisa diberi
stimulus baru. Terjadi ari awal depolarisasi hingga fase
plateau.
Relative Refractory Period: is a period that follows the
absolute period, and the excitability begins to recover
gradually until it reaches its normal value. RRP coincides with
the period od rapid polarization following the plateau.
c. Conduction Velocity
5.
Treatment of Bradycardia
- Pharmacologic:
- Anticholinergic (atropine): - IV
Obat ini berikatan dengan reseptor muscarinic
yang akan menurunkan vagal stimulation
dengan menurunkan depol sinus node dan
menurunkan konduksi melalui AV node, yang
ditandai dengan lepasnya ACh ke reseptor
muscarinic. maka heart rate akan naik.
- Beta-1- Receptor Agonist (Isoproterenol) IV-
Mengurangi efek endogenous cathecolamines
dengan meningkatkan HR dan kecepatan
konduksi AV node
- Electronic Pacemarker
- Temporary
- Permanent
Treatment of Tachyarythmias
- Pharmacologic (no 7)
- Non Pharmaco:
- Vagal Maneuvers- carotid sinus massage
- Electric Cardioversion and Defibbrilation
- Implantable Cardioverter- Defibrillators
- Catheter Ablation
6. Tachycardia of atrial or ventricular origin reduces stroke volume and cardiac output
particulary when the ventricular rate is greaeter than 160 beats/min. The stroke volume
becomes reduced because of decreased ventricular filling (preload) at high rates of contraction.
Furthermore, if the tachyarrythmia is associated with abnormal ventricular conduction, the
synchrony and therefore effectiveness of ventricular contraction will be impaired leading to
reduced ejection. Another consequence of tachycardia is increase myocardia oxygen demand.
This can cause angina, particularly in patients having underlying coronary artery disease.
Finally, chronic states of tachycardia can lead to systolic heart failure.
7. Klasifikasi obat arrythmia
- Kelas 1 - Na channel blockade
- Tipe a : Moderate Block (depress phase 0, prolonging repolarization)
- Quinidine, Procainadmide, Disopyramide
- Untuk: A-fib dan flutter, PSVT, VT
- Tipe b : Mild block (depress phase 0 selectively in abnormal/ischemic tissue,
shorten repolarization)
- Lidocaine, Phenytoin, Mexiletine
- VT, Digitalis-induced arrythmias
- Tipe c : Marked block (markedly depress phase 0, minimal effect on
repolarization)
- Flecainide, Propafenone, Moricizine
- A-fib dan PSVT
- Kelas 2 - Beta-adrenegic receptor bloackade (decrease slope of phase 4)
- Propranolol, Esmolol, Metaprolol, Timolol, Atenolol
- Atrial or Ventricular Premature Beats, PSVT, A-fib dan flutter, VT
- Kelas 3 - K+ channel blockade
- Amiodarone (prolongs phase 3, also acts on phase 1,2,4), Sotalol (Prolongs
phase 3, decrease slope of phase 4), Ibutilide (prolongs phase 3), Dofetilide
(prolongs phase 3)
- VT(amiodarone dan sotalol), Afib, Aflutter, Bypass tract- mediated PSVT
- Kelas 4 - Ca++ channel blockade
- Verapamil (prolongs phase 2), Diltiazem (prolongs phase 2)
- PSVT, Afib dan flutter, Multifocal atrial tachycardia
Sequence of ECG interpretation
1) Patient
Identity
a. Name
b. Date
and
Time
2) Calibration
a. Check
1.0
mV
vertical
box
inscription
(normal
standard
=
10
mm)
3) Rhythm
a. Sinus
Rhythm
is
present
if
i. Each
P
wave
is
followed
by
a
QRS
complex
ii. Each
QRS
is
preceded
by
a
P
wave
iii. P
wave
is
upright
in
leads
I,
II,
and
III
iv. PR
interval
is
>0,12
sec
(3
small
boxes)
b. If
these
criteria
are
not
met,
determine
type
of
arrhythmia
4) Heart
Rate
a. Use
one
of
these
methods:
i. 1500
/
(number
of
mm
between
beats
=
small
boxes)
ii. Count
off
method:
300
–
150
–
75
–
60
–
50
iii. Number
of
beat
in
6
sec
x
10
b. Normal
rate
=
60-‐100
bpm
(bradycardia
<60,
tachycardia
>100)
5) Intervals
a. Normal
PR
=
0,12-‐0,20
sec
(3-‐5
small
boxes)
b. Normal
QRS
≤
0,10
sec
(≤2,5
small
boxes)
c. Normal
QT
≤
half
the
R-‐R
interval,
if
heart
rate
normal
d. Normal
QTc
Interval
≤
0,44
sec
(QT/ 𝑹𝑹)
<orang
aritmia
punya
QT
bisa
beda2
jadi
di
corrected
dulu
itungannya
jadi
pake
ini
bukan
≤
half
RR
e. Normal
RR
0,6
–
1,0
sec
6) Mean
QRS
axis
a. Normal
if
QRS
is
primarily
upright
in
leads
I
and
II
(+90º
to
-‐30º)
b. Otherwise,
determine
axis
by
isoelectric
/
perpendicular
method
7) P
wave
abnormalities
a. Normal
P
wave:
≤2,5
mm
tall
and
<0,11sec
b. Inspect
P
in
leads
II
and
V1
for
left
and
right
atrial
enlargement
i. RaH
=
Tall
P
wave
and
sharp
(P
pulmonal)
in
I,
II,
III,
and
aVF
ii. LaH
=
Broad
P
wave
and
P
wave
notched
(P
mitral)
in
I
and
II
8) QRS
wave
abnormalities
a. Normal
QRS
duration:
0,08
–
0,10
sec
b. Inspect
for
left
and
right
ventricular
hypertrophy
i. RvH
=
V1
R>S
and
Right
Axis
deviation
ii. LvH
=
S
in
V1
+
R
V5
or
R
V6
≥
35mm;
and
R
in
aVL
>
11mm;
and
R
in
lead
I
>
15mm
c. Inspect
for
bundle
branch
blocks
i. RBBB
=
RSR
in
V1
and
Prominent
S
in
V6
ii. LBBB
=
RSR
in
V6
and
absent
R
+
prominent
S
in
V1
d. Inspect
for
pathologic
Q
waves
(Q
pathologic
≥
1/3
R)
9) ST
segment
or
T
wave
abnormalities
a. Inspect
for
ST
elevations:
i. ST
segment
elevation
MI
• Precordial
lead
elevation
≥
2mm
• Limb
lead
elevation
≥
1mm
ii. Pericarditis
• Diffuse
ST
segment
elevation
• PR
segment
depression
b. Inspect
for
ST
depressions
or
T
wave
inversions
i. Myocardial
ischemia
or
non-‐ST
elevation
MI
• ST
depression
≥
0,5mm
precordial
/
limb
ii. Usually
accompany
ventricular
hypertrophy
or
bundle
branch
blocks
iii. Metabolic
or
chemical
abnormalities
10) Compare
with
patient’s
previous
ECG
Normal Sinus Rhythm
• Irama
:
Teratur
• HR
:
60
–
100
bpm
• P
wave
:
Normal,
setiap
P
selalu
diikuti
QRS,
T
• PR
interval
:
Normal
(0,12
–
0,2
sec)
• QRS
complex
:
Normal
(0,06
-‐0,12
sec)
Bradyarrhythmia
1. SinoAtrial
Node
a. Sinus
Bradycardia
•
Smua
normal
hanya
HR
<
60
bpm
•
Tanda2
Sinus
Rhythm
Normal
b. Sinus
Arrest
(SA
Block)
• Terdapat
episode
hilangnya
satu
atau
lebih
gelombang
P,
QRS
dan
T
• Irama
:
Teratur,
kecuali
pada
yang
hilang
• HR
:
biasanya
<60
bpm
• P
wave
:
Normal
• PR
interval
:
Normal
• QRS
Complex
:
Normal
c. Sick
Sinus
Syndrome
• Inappropriate
bradycardia
• Irama
:
Ada
yang
tachycardia
ada
yang
bradycardia
2. Escape
Rhythm
a. Junctional
Escape
Rhythm
• Impuls
dari
AV
/
proximal
bundle
of
His
• HR
:
40
–
60
bpm
• P
wave
:
Tidak
sebelum
QRS
karna
awal
mulainya
bukan
dari
SA
atau
retrograde
/
inverted
P
wave
sebelum
QRS
di
lead
II,
III,
aVF
b. Ventricular
Escape
Rhythm
• Impuls
dari
Ventricular
ectopic
pacemaker
(RBB
/
LBB)
• HR
:
30
–
40
bpm
• QRS
wave
:
Widened
• P
wave
:
Tidak
sebelum
QRS
/
tidak
terlihat
3. Atrioventricular
Conduction
System
a. First
Degree
AV
Block
• Irama
:
Teratur
• HR
:
60-‐100
bpm
• PR
Interval
:
>
0,20
sec
b. Second
Degree
AV
Block
i. Mobitz
1
/
Wenckebach
• Irama
:
Tidak
teratur
• HR
:
<60
bpm
• P
wave
:
Normal,
ada
satu
gelombang
P
yang
tidak
diikuti
QRS
• PR
interval
:
Makin
lama
makin
panjang,
kemudian
terjadi
block,
selanjutnya
siklus
berulang
ii. Mobitz
2
• Irama
:
Tidak
teratur
• HR
:
<60
bpm
• P
wave
:
Normal,
ada
satu
atau
lebih
gelombang
P
yang
tidak
diikuti
QRS
• PR
interval
:
Normal
/
Memanjang
secara
konstan,
kemudian
ada
block
c. Third
Degree
AV
Block
• Irama
:
Teratur
• HR
:
<60
bpm
• P
wave
:
Normal,
akan
tetapi
gel
P
dan
gel
QRS
berdiri
sendiri2,
P
wave
lebih
cepat
dari
pada
QRS
dan
gel
P
kadang
diikuti
QRS
kadang
tidak
• PR
interval
:
Berubah-‐ubah/tidak
ada
• QRS
Complex
:
Normal
/
>0,12
sec
Tachyarrhythmia
1. Supraventricular
Arrhythmias
a. Sinus
Tachycardia
• Smua
normal
hanya
HR
>
100
bpm
• Tanda2
Sinus
Rhythm
normal
b. Atrial
Premature
Beats
• Re-‐entry
dari
focus
atrial
selain
SA
Node
• Irama
:
Teratur
kecuali
saat
penambahan
• P
wave
:
Abnormal
• QRS
complex
:
Kalau
APB
(p
wave)
muncul
saat
refractory
period,
QRS
tidak
muncul…
Kalau
APB
muncul
saat
fase
akhir
diastolic,
QRS
wide.
c. Atrial
Flutter
• Re-‐entry
of
large
anatomical
fixed
structure
atrial
tissue
along
with
Tricuspid
valve
annulus
• Depolarization
wave
circulate
up
interatrial
septum
>
Roof
>
down
the
face
wall
>
floor
of
R.
Atrium
(could
alse
be
left)
• Irama
:
Biasanya
teratur
,
bisa
juga
tidak
• HR
:
180
–
350
bpm
• Gelompang
:
Bentungnya
seperti
gigi
gergaji
(saw
tooth),
dimana
gelombang
P
timbulnya
teratur
dan
dapat
dihitung,
P
:
QRS
=
2:1,
3:1
atau
4:1
• PR
interval
:
Tidak
dapat
dihitung
• QRS
complex
:
Normal
d. Atrial
Fibrillation
• Multifocal
Firing
from
R
&/
L
atrium
• Irama
:
Tidak
teratur
• HR
:
Bervariasi
• P
wave
:
Banyak
tapi
tidak
dapat
diidentifikasi
• PR
interval
:
Berubah-‐ubah
• QRS
complex
:
Normal
e. Paroxysmal
Supraventricular
Tachycardias
(PSVT)
• Re-‐entry
involve
AV
node,
Atrium,
or
Accessory
pathway
• Irama
:
Teratur
• HR
:
150-‐250
bpm
• P
wave
:
sulit
dilihat
/
retrograde,
kadang
terlihat
kecil
• PR
interval
:
tidak
dapat
di
hitung
/
sangat
sedikit
ii. Atrioventricular
Reentrant
Tachycardias
(AVRT)
• Due
to
bypass
tract
of
AV
node
allowing
retrograde
(from
ventricle
able
to
go
back
to
atrial),
anterograde
(from
atrium
to
ventricle),
or
both
ü Ventricular
Pre-‐Excitation
Syndrome
o A.K.A
Wolff
Parkinson
White
Syndrome
(WPWS)
o Orthodromic
AVRT,
Antidromic
AVRT,
Sinus
Rhythm
o Orthodromic
:
electrical
impulse
goes
down
from
SA
to
the
AV
Node
to
ventricle,
however
the
impulse
doesn’t
stop
and
goes
up
from
the
ventricle
to
the
SA
node
through
Bundle
of
Kent
(Retrograde
P
waves)
o Antidromic
:
electrical
impulse
goes
down
from
SA
node
to
the
Bundle
of
kent
>
ventricle
>
septum
(bundle
of
his)
>
AV
node
>
SA
node
(Retrograde
P
waves
with
wide
QRS)
ü Concealed
Accessory
Pathway
o Retrograde,
during
sinus
Rhythm
ventricles
depolarize
through
AV
alone
and
ECG
normal
iii. AV
Nodal
Re-‐entrant
tachycardia
(AVNRT)
• Most
common
form
of
PSVT
• Due
to
branch
AV
connection
to
bundle
of
His
(with
fast
and
slow
branch)
iv. AVRT
v.
AVNRT
• AVRT
ada
delta
wave,
P
wave
masih
terlihat
(PR
interval
>0,7sec)
• AVNRT
P
wave
tidak
terlihat
/
retrograde
f. Focal
Atrial
Tachycardia
(AT)
• Impuls
atrial
dari
yang
bukan
SA
node
(hanya
1)
• P
wave
:
Terdapat
premature
p
wave
dengan
bentuk
yang
berbeda
g. Multifocal
Atrial
Tachycardia
(MAT)
• Impuls
atrial
dari
yang
bukan
SA
node
(≥3)
• P
wave
:
Terdapat
premature
P
wave
dengan
≥3
bentuk
yang
berbeda
2. Ventricular
Arrhythmia
a. Ventricular
Premature
Beats
(VPB)
• Irama
:
Tidak
teratur
karna
ada
gelombang
yang
timbul
dini
• HR
:
Bergantung
pada
irama
dasarnya
• P
wave
:
Tidak
ada
• PR
interval
:
Tidak
ada
• QRS
complex
:
>0,12
sec
• Nomenclature
a. Ventricular
Bigeminy
–
Satu
normal,
satu
VPB
b. Ventricular
Trigeminy
–
Dua
Normal,
satu
VPB
c. V.
Quadrigeminy
–
Tiga
Normal,
satu
VPB
d. Couplet
–
1
Normal,
2
VPB
(gandeng)
– 1 Normal, 3 VPB (gandeng)
e. Run
of
6
–
1
Normal,
6
VPB
(gandeng)
f. VPB
continuous
–
Ventricular
Tachycardia
(VT)
b. Ventricular
Tachycardia
(VT)
i. Monomorphic
VT
• Irama
:
Teratur
• P
wave
:
Tidak
ada
• QRS
Complex
:
>0,12
sec
ii. Polymorphic
VT
–
Torsades
de
Pointes
• Electrical
impuls
dari
beberapa
source
ectopic
pacemaker
di
ventrikel
• Irama
:
Tidak
teratur
• P
wave
:
Tidak
ada
• QRS
complex
:
Tidak
teratur,
beberapa
bentuk
QRS
(QRS
naik
turun)
c. Ventricular
Fibrillation
(VF)
• SMUANYA
BRANTAKAN
dan
ga
jelas
Asystole
Pulseless Electrical Activity
• Terdapat
electrical
impulse
tapi
tidak
ada
nadi
Other ECG abnormalities (dr. Antonia)
1. Chronic
Obstructive
Pulmonary
Distress
(COPD)
–
CorPulmonale
i. QRS
morphology
limb
leads
• Right
axis
deviation
• S>R
in
lead
I
Precordial
Leads
• S>R
in
V5-‐V6
• Lead
V1
rs,
RS,
or
rS
Orthogonal
Lead
• S>R
in
Lead
I
• Tall
R
wave
in
Lead
II
ii. P
wave
Limb
Leads
• P>3mm
in
lead
II
or
III
Precordial
Leads
• Negative
P
in
Lead
V1
2. Pulmonary
Embolism
a. S1
Q3
T3
<
wajib
inget
• Prominent
S
wave
in
lead
I
• Pathologic
Q
waves
in
lead
III
• Inverted
T
waves
in
lead
III
3. Electrolyte
Imbalance
a. Kalium
(N
3,7-‐5
mEq/L)
4. Cardiac
Tamponade
5. Sudden
Death
• Kematian
karna
penyakit
CardioVascular
≤1
hour
6. Cardiac
Arrest
a. Pre-‐Arrest
b. Arrest
Induction
c. Arrest,
Post
Arrest
d. Post
Return
of
Spontaneous
Circulation
(ROSC)
*catetan gw, abaikan2… fibrinolytic therapy (alteplase, tPA), reteplase (rPA), and
tenecteplase (TNK-tPA )