BUNYI JANTUNG

Dr. Suhaemi, SpPD, Fiansim

Heart sounds

2nd sound and opening snap of MS are best heard

on the base.
LSB: TR, AR, VSD, HCM
Apex: MR, MS, AS.
Below L clavicle: PS, PDA as continuous.
Radiation to L axila: MR.
Radiation to RSB and carotids: AS
Radiation all over the precordium: VSD
MS: Loud S1, Split S2, opening snap, rumbling
diastolic murmur in apex. Area <2.5 cm,
symptoms correlate.
PR: Diastolic, decrescendo at LSB (Graham Steel)

Splitting of S2
INSPIRATION

EXPIRATION

Normal
splitting

s1

A2
P2

s1

A2

P2

Wide splitting
(PS,MR,RBB
B, VSD,PDA

s1

A2
P2

s1

A2

P2

Paradoxical
splitting (AS,
LBBB, HCM,
LVH)

s1

P2

A2 s1

P2

A2

Fixed splitting
(ASD)

s1

A2
P2

s1

A2

P2

Mitral Valve Regurgitation

Etiology:

Myxomatous degeneration
Rheumatic disease
Endocarditis

Grades 1 to 4
Surgical indications

If symptomatic
EF<60%
LVES diameter >4.5cm
Pulmonary pressure >55mmg Hg

Aortic Stenosis
Aortic Stenosis
Location of
murmur

Second
sound
Carotid
Pulse

HCM

Apex and R 2nd

intercostal space
radiating to
carotids.
No component A2

LSB,
With thrill
Not radiating

Slowly rising

Brisk or bifid

Present A2

Life Threatening Causes of Chest

Pain

Acute Coronary Syndromes

Pulmonary Embolus
Tension Pneumothorax
Aortic Dissection
Esophageal Rupture
Pericarditis with Tamponade

Acute Coronary Syndromes EKG Findings

STEMI - ST segment elevation (>1 mm) in

contiguous leads; new LBBB
T wave inversion or ST segment depression
in contiguous leads suggests
subendocardial ischemia
5% of patients with AMI have completely
normal EKGs

Acute Coronary Syndromes Cardiac Markers

Marker

Initial
Rise

Peak

Return to
normal

Benefits

Troponin

2-4 hr

10 -24 hr

5 -10 days

Sensitive and specific

CK-MB

3-4 hr

10-24 hr

2 4 days

Unaffected by renal failure

LDH

10 hr

24 -72 hr

14 days

Myoglobin

1-2 hr

4 -8 hr

24 hours

Very sensitive, powerful

negative predictive value

Acute Coronary Syndromes Cardiac

Markers

Acute Coronary Syndromes Treatment

Aspirin
Nitroglycerin
Oxygen
Analgesia

Treatment
Beta-Blockers
Anticoagulation
Anti-Platelet Agents
Thrombolysis
Percutaneous Coronary
Interventions (PCI)

Acute Coronary Syndromes - Treatment

STEMI (ASA, B-blocker, NTG, anti-platelet,

anticoagulation, thrombolysis, PCI)

NSTEMI (ASA, B-blocker, NTG, anti-platelet,

anticoagulation, PCI)

Unstable Angina (ASA, B-blocker, NTG,

anticoagulation, risk stratification)

Causes of Syncope

Syncope: Pathophysiology

Decreased cerebral
perfusion is common to all
causes of syncope
Cessation of cerebral
perfusion for as little as 35 seconds can result in
syncope
Decreased cerebral
perfusion may occur as a
result of decreased cardiac
output or decreased
systemic vascular
resistance.

More Pathophysiology

Bilateral hemisphere
dysfunction or
reticular activating
system (RAS)
midbrain knockout.
Generally acute
hypoperfusion is
responsible.

Regional
(vasoconstriction)
Systemic (global
hypotension)

Loss of consciousness
causes loss of postural
tone leading to collapse
35% reduction in
cerebral blood flow will
cause syncope.
Modifying factors

Cardiac output
Systemic and local vascular
resistance/occlusion
Blood volume
Ability to compensate

Syncope: Etiology

Mnemonic: PASSOUT
P-ressue (hypotensive causes)
A-rrthymias
S-eizures
S-ugar (hypo/hyper glycemia)
O-utput (cardiac)/ O2 (hypoxia)
U-nusual causes
T-ransient (TIAs, strokes, CNS diseases)

Syncope

CAUSES (Head---Heart---Vessels)

Reflex mediated

Cardiac

Mechanical , arrhythmias

Orthostatic

Vasovagal, carotid sinus, situational

Drugs, autonomic failure

Cerebrovascular
Unknown
Nonsyncopal causes

sinus bradycardia

ventricular tachycardia
3 or more beats

WPW

Prolonged QT interval

Other: sinus pause> 2 sec, SVT, afib, 2nd or 3rd AV block, PM malfunction

Syncope Evaluation Flow

Chart