Cardiovascular

Present by :
Group XI

Chest pain
Medical Faculty of University Muhammadiyah Jakarta
 Member
Adhitya P.S
M. Derryatmiko
Agia Dwi N.
Nizlia Y.
Fauziah B.
Ridavianti
Fenny R.
Rijki R.S
H. Lutfi F.
Siti Heriah
Mia S.L

Facilitated by :
Dr. Yusnam S.
 Scenario
A bus driver 60 years old was carried to ICU with complaint hard painful
through chest wall and spread to hand. Before that, he felt healthy,
though he smoked 10 cigarrets/day. In examination he looked pale, with
cool skin and sweaty, weak artery pulse, with extrasistole sometimes
(ectopic ventricular beat). Artery blood pressure 90/75 mmHg. Heart
sound normal. In ECG was obtained big Q wave and elevation of ST
segment. He is entered to hospital with diagnose miocard infarc because
thrombosis of coronary artery. Analyse of plasma looked incresing of
heart enzyme (Lactat Dehidrogenase, Creatine phosphocinase, Aspartat
Aminotranferase). He had been given oxigene and morfine.
Streptocinase IV had been prepared to lysised coraonary thrombus and
he also had began aspirin reguler low dose.
Anatomy of HEART
Anatomy of HEART
Anatomy of HEART

Right Coronary Artery

Left Coronary Artery
Histology of Heart
 Tunica intima

Tunika media

Tunica adventitia

ARTERIOLE

VENULA
Tunica intima

Tunica media

Tunica adventitia
M
E M
D E
I D
U I
M U
M
A
R V
T E
E I
R N
Y
1. Tunica intima
2. Tunica media
3. Tunica adventitia
4. Internal elastic membrane
LARGE ARTERY

1. Tunica intima

2. Tunica media

3. Tunica adventitia
CAPILLARY OF LYMPH
Lumen kapiler limf

Lumen pembuluh
limf sedang
1. PURKINJE
FIBRE

2. ENDOCARDIUM

3. MYOCARDIUM
There has been a previous
extensive transmural myocardial
infarction involving the free wall of
the left ventricle. Note that the
thickness of the myocardial wall is
normal superiorly, but inferiorly is
only a thin fibrous wall. The
thinned area represents a
ventricular aneurysm that has
developed as a consequence of
the healed infarct. Such an
aneurysm represents non-
contractile tissue that reduces
stroke volume and strains the
remaining myocardium. The stasis
of blood in the aneurysm
predisposes to mural thrombosis.
This is mild coronary atherosclerosis. A few
scattered yellow lipid plaques are seen on
the intimal surface of the opened coronary
artery traversing the epicardial surface of a
heart. The degree of atherosclerosis here is
not significant enough to cause disease, but
could be the harbinger of worse
atherosclerosis to come.

The degree of atherosclerosis is

much greater in this coronary
artery, and the lumen is narrowed
by half. A small area of
calcification is seen in the plaque
at the right.
 Cardiac physiology
Cardiac circulation
 Conduction system

1.Sinoatrial Node
2.Atrioventricular Node
3.Bundle of His right and left
4.Purkinje fibers
Potential action
 Cardiac cycle
Stuffing phase
• Increased of atrium pressure
• Opening of tricuspid and mitral valvular
followed by closed of aorta and pulmonal
valvular
• Diasthasis
 Isovolumetric contraction
phase
• Ventricle pressure have already
increased
• Closed of tricuspid and mitral valvular
(S1)
• In this phase, ventricle need to adding
time to can push aorta and pulmonal
valvular
 Ejection phase
• Ventricle pressure get strong enough
to push the seminularis valvular
• Opening aorta and pulmonal valvular
• Including of two periods :
- Slow ejection period
- Rapid ejection period
 Isovolumetric relaxation
phase
• Closed of aorta and pulmonal
valvular (S2)
• Volume ventricle is not change
• Intraventricular pressure decrease
rapidly
• Phase over If atrium pressure higher
than ventricle
 Heart sounds
S1  is caused by the closure of the
atrioventricular valves mitral and tricuspid. at
the beginning of ventricular contraction, or
systole.
S2  caused by the closure of the aortic and pulmonic
valves at the end of ventricular systole
S3  entering the blood from atrium into ventricle
S4  atrium contraction
 Cardiac output
Amount of quit blood for a minutes

CO = SV x F

CO Influenced by :
• Contractility
• Frequency
• Freload
• Afterload
 Biochemistry of Heart

EROBIC
GLYCOLISIS

OXIDATION- VATTY
ACID

CREB CYCLE
Biochemistry of Heart
 Cytosol
Glucose 2 Piruvat 8 ATP

2 Ko ASH
2 CO2

2 Acetyl co. A 6 ATP

2 Piruvat

SAS 24 ATP
2 NAD
2 NADH + H+

6 ATP
Fosfolirasi
Oksidatif
 Anoxia of heart muscle

Rare of O2 NADH 6 ATP

Glucose Piruvat

NADH + H+
Lactate Dehydrogenase
Acetyl co. A

NAD

Lactate 2 ATP
SAS

LDH (Lactate Dehydrogenase) in blood increase

 For overcoming rare of ATP

Anoxia of heart muscle

Kreatin Fosfokinase

Kreatin-Fosfat + ADP creatin

+

Brittle heart muscle membrane ATP

Heart muscle damage

Anoxia of heart muscle Enzyme out SGOT

SGPT
 Myocard ischemic

Muscle release some

substances

If high concentration of
the substances

Stimulated nerves of pain

Afferen nerve will Send it

to CNS

CNS  efferen nerve

Efferen nerve  C-3 , T-5

Mechanism of reffered pain Reffered pain

 Myocardial Infarction
Acute myocardial infarction (MI) is the rapid development of
myocardial necrosis resulting from a sustained and complete
absense of blood flow to a portion of the myocardium, produced
by a superimposed thrombosis, and generated by a ruptured
atherosclerotic plaque

patophysiology
• Myocardial necrosis
• Atherosclerosis, if etiologic
• Thrombosis; not usually seen because spontaneous
thrombolysis occurs within 24 hours
 causes
• Most frequent cause is rupture of an atherosclerotic lesion
within coronary wall with subsequent spasm and thrombus
formation
• Coronary artery vasospasm
• Ventricular hypertrophy
• Hypoxia
• Coronary artery emboli

EPIDEMIOLOGY • Predominant age: >40 years

• Predominant sex:
- Age 40-70: Male > Female
- Age >70: Male = Female
 Risk factors for
atherosclerosis

• Age
• Male gender
• Smoking
• Hypercholesterolemia and triglyceridemia
• Diabetes Mellitus
• Poorly controlled hypertension
• Type A personality
• Family History
• Sedentary lifestyle
SIGNS AND SYMPTOMS
• Pain¾arm, back, jaw, epigastrium, neck, chest
Anxiety
• Lightheadedness, pallor, weakness, syncope
• Nausea, vomiting, diaphoresis
• Chest heaviness, tightness
• Cough, diaphoresis, dyspnea, rales, wheezing
• S4 heart sound
• Arrhythmias
• Hypertension, hypotension
• Jugular venous distention
• Cannon jugular venous A waves (in presence of heart block
or right ventricular failure)
 Electrocardiography (ECG)
- ST segment elevation in a regional pattern:
Typical of acute transmural ischemia
- ST segment depression with T wave inversions:
Typical of subendocardial ischemia
- New or presumably new bundle branch block
- ST segment changes are findings of ischemia;
transmural infarction may show normal ECG.
- Q waves representing transmural myocardial
necrosis appear within 24-48 hours.

Acute anteriolateral MI
 Lab.
• Troponin I is a specific indicator of MI; appears 3-6 hours after
MI, peaks at 16 hours, and decreases in 9-10 days.
• Creatine kinase (CK): Rises following infarction within 4-8
hours; peaks 18-24 hours; and subsides over 3-4 days. Specific
indicator for myocardial necrosis; has 15% false-positive rate
• CK isoenzymes: BB in brain and kidney, and MB in cardiac
muscle
• Lactate dehydrogenase: Rises within 24 hours, peaks within 3-6
days, and returns to baseline within 8-12 days
• ESR: Rises within 3 days and may remain elevated for several
weeks
• Leukocytes: Rise within several hours after MI, peak in 2-4 days,
and normal within 1 week
 Farmacology
Aspirin : 325 mg PO acutely

(Alteplase); tissue plasminogen activator: 15 mg IV bolus, 50 mg over 30

minutes, then 35 mg over 60 minutes

Heparin by protocol or low-molecular-weight heparin; enoxaparin (Lovenox) 1

mg/kg q12h SC (preferred)

- Nitrates: 5 ug/min IV, increase slowly. Do not lower arterial blood pressure beyond
90 mm Hg. Change to oral or topical when stable.
- Oxygen: 2-4 L/min
Acute MI - Morphine: 2-6 mg IV q2-4h as needed for pain relief/sedation
- Metoprolol (Lopressor): 5 mg IV ´ 3, 5 minutes apart, followed by 50 mg PO q6h
starting 15 minutes after last IV dose
- Stool softeners: Docusate sodium (dioctyl sodium sulfosuccinate) 100 mg 2 b.i.d.
- Lidocaine: 1-2 mg/kg IV once, then 1-4 mg/min IV drip. Use for ventricular
arrhythmias only, not for prophylaxis
 Post MI
• b-Blockers reduce mortality.
• Nitrates may be needed for angina.
• ACE inhibitors may assist with remodeling.
Contraindications
- b-Blockers contraindicated in acute heart failure and bronchospasm
(may use IV esmolol (short-acting) safely)

- IV thrombolysis is contraindicated  active internal hemorrhage

recent head trauma
intracranial neoplasm
hemorrhagic cerebrovascular accident
pregnancy
persistent hypertension (>200/120 mm Hg)
traumatic CPR
hemorrhagic retinopathy
trauma or major surgery within 2 weeks
peptic ulcer or heme-positive stools
 SURGERY
- Coronary reperfusion
- Emergency stenting is a mechanical form of coronary
reperfusion. It is considered superior to IV thrombolysis
if within 1st 12 hours.
- Can be accomplished with low mortality.
- Pump failure: Intra-aortic balloon pump