C A R D IO V A S C U LA R

EM ER G EN C IES

dr VENICE CHAIRIADI, SpJP

FIHA

 Cardiovascular emergencies are

life-threatening disorders that

must be diagnosed quickly to
avoid delay in treatment and to
minimize morbidity and mortality
Patients may present with severe
hypertension,
chest
pain,
dysrhythmia, or cardiopulmonary
arrest

CARDIAC
ARREST ???

 Cardiopulmonary arrest occurs

as a result of a multitude of
cardiovascular,
metabolic,
infectious,
neurologic,
inflammatory, and traumatic
diseases

SALAH SATU PEN YEBAB

CARD IAC ARREST
ACUTE CORONARY
SYNDROME

SINDROM KORONER AKUT

Merujuk pd sekumpulan keluhan dan tanda klinis yang sesuai
dengan iskemia miokard akut
Mencakup Infark miokard akut ( dgn elevasi /depresi segmen
ST , gelombang-Q dan non gel Q) dan angina tidak stabil
( UAP)

Sindrom Koroner Akut

Tanpa elevasi ST

Elevasi ST

NSTEMI

Infark Miokard
Akut
Angina Tdk Stabil

NQMI
Kursus SKA

Qw MI

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS
Diagnosis
Kerja
ECG
Biochemistry
Stratifikasi
risiko

SAKIT DADA
Curiga Sindrom Koroner Akut
Elevasi ST
menetap
Troponin
(CKMB)

Tanpa Elevasi Normal atau

ST menetap Tdk dpt ditentukan
ECG
Troponin
2 X negative

Troponin

Risiko tinggi Risiko rendah

Mungkin bukan SKA

Pengobatan
Pencegahan
sekunder
Esc/EHJ 2002

Acute InferiorW allM I

http://homepages.enterprise.net/djenkins/ecghome.html

SALAH SATU PENCETUS VT/VF

Acute extensive anteriorM CI

BEBERAPA G AM BARAN
ARITM IA LAIN

TakikardiVentrikel

11

Takikardia ventrikuler torsade de pointes

m enyusulfenom ena R diatas T karena
intervalQ T yang m em anjang
12

Torsade de pointes

13

FibrilasiVentrikel

14

Fibrilasiventrikuler
Undulasi-undulasiyang tidak teratur dan cepat,
diikutioleh hentiventrikelatau asistol
ventrikuler :tak ada kom pleks Q RS
15

PEA

Identifying Asystole

D IAG N O SIS AN D TH ERAPY

The American Heart Association, in

collaboration with the International Liaison
Committee on Resuscitation, has established
guidelines for resuscitation of cardiac arrest
patients :
Activate EMS or the designated code team.
Perform basic life support (CPR).
Evaluate heart rhythm and perform early
defibrillation as indicated.
Deliver advanced life support (e.g., intubation,
intravenous [IV] access, transfer to a medical
center or intensive care unit).

CPR
NO TRAINING : HANDS ONLY CPR
TRAINED : 30:2 CPR
HIGHLY TRAINED : MULTIRESCUER

COORDINATED CPR

BAN TU AN H ID U P D ASAR

H EN TIN APAS D AN H EN TI
JAN TU N G
Penyebab henti napas

- sumbatan : benda asing, muntahan, edema

laring atau bronkus, tumor
- gangguan paru : infeksi, aspirasi, edema
paru, kontusio paru
- gangguan neuromuskular yg menyebabkan
penurunan kemampuan otot dada
Penyebab henti jantung : gagal jantung,
tamponade jantung, miokarditis,
kardiomiopati hipertropi, fibrilasi veentrikel

PRO TO KO L BCLS

PELAKSAN AAN TIN D AKAN RJP

D APAT TID AK D ILAKU KAN PAD A
Henti
: jantung pada sarana kesehatan

- permintaan keluarga yg berhak secara sah

- henti jantung pada stadium akhir
- neonatus atau bayi dgn angka mortalitas
tinggi
Henti jantung diluar fasilitas kesehatan
- tanda kematian klinis yg ireversibel
- upaya RJP dgn resiko membahayakan penolong
- penderita dgn trauma yg tdk bisa diselamatkan

PEN G H EN TIAN RJP

- tindakan bhd sudah optimal tanpa
respon
- penderita terpapar bahan beracun
yg menghambat ssp
- kejadian henti jantung yg tdk
disaksikan penolong dlm jangka
waktu tertentu
- asistol menetap selama 10 menit
atau lebih

AIRW AY
HEAD TILT
CHIN LIFT
JAW THRUST

BREATH IN G
Berikan napas bantuan dalam 1 detik
Volume tidal yg cukup untuk mengangkat dinding

dada
2 kali napas bantuan setelah 30 x kompressi dada
Kondisi 2 atau lbh penolong dgn terpasang alat
bantu napas, bantuan diberikan setiap 6-8 detik
(8-10x per menit)
Penderita dgn masalah hambatan jalan napas
memerlukan tekanan tinggi
Pemberian bantuan napas berlebih tidak
diperlukan

 Bagaimana menilai korban tidak

sadar.
Cara melakukan kompresi dada
dan bantuan pernapasan.
Bagaimana mengoperasikan
defibrillator eksternal secara aman.
Bagaimana menempatkan korban

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

A PPR O A CH SA FELY!

Scene
Rescuer
Victim
Bystanders

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

CH ECK R ESPO N SE
Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

CH ECK R ESPO N SE

Shake shoulders
gently
Ask Are you all
right?
If he responds
Leave as you find him.
Find out what is
wrong.
Reassess regularly.

SH O U T FO R H ELP

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

O PEN A IR W AY
Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

CH ECK B R EATH IN G

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

CH ECK B R EATH IN G

Look, listen and

feel for NORMAL

breathing
Do not confuse

agonal breathing
with NORMAL
breathing

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

30 CH EST CO M PR ESSIO N S

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

CH EST CO M PR ESSIO N S
Place the heel of one
hand in the centre of the
chest
Place other hand on top
Interlock fingers
Compress the chest
Rate 100 min-1
Depth 5 cm
Equal compression :
relaxation

When possible change

CPR operator every 2 min

R ESCU E B R EATH S

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

R ESCU E B R EATH S

Pinch the nose

Take a normal

breath
Place lips over
mouth
Blow until the
chest rises
Take about 1
second
Allow chest to fall

CO N TIN U E CPR

30

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest
compressions
2 rescue breaths

D EFIB R ILLATIO N

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
Attach AED
Follow voice
prompts

SW ITCH O N A ED

Some AEDs will

automatically
switch themselves
on when the lid is
opened

ATTA CH PA D S TO
CA SU A LTYS B A R E CH EST

A N A LYSIN G R H YTH M
D O N O T TO U CH V ICTIM

SH O CK IN D ICATED

Stand clear
Deliver shock

SH O CK D ELIV ER ED
FO LLO W A ED IN STR U CTIO N S

30

N O SH O CK A D V ISED
FO LLO W A ED IN STR U CTIO N S

30

IF V ICTIM STA RTS TO

B R EATH E N O R M A LLY PLA CE
IN R ECO V ERY PO SITIO N

CPR IN CH ILD R EN

Adult CPR

techniques can be
used on children
Compressions 1/3

of the depth of the

chest

AED IN
CHILDREN
Age > 8 years
use adult AED
Age 1-8 years
use paediatric
pads / settings if
available (otherwise
use adult mode)
Age < 1 year
use only if
manufacturer
instructions indicate
it is safe

Approach safely

Approach safely

Check response

Check response

Shout for help

Shout for help

Open airway

Open airway

Check breathing

Check breathing

Call 118

Call 118

30 chest
compressions
2 rescue breaths

Attach AED
Follow voice

AcuteHeart
Failure
Globaltimebomb?

HEART FAILURE

Clinical syndrome that can result

from any structural or functional
cardiac disorder that impairs the
ability of the ventricle to fill with
or eject blood

Acute Heart Failure ESC Guideline, Eur Heart J 2005

ClinicalSyndrom es ofAcute H eart

Failure

Acute Heart Failure ESC Guideline, Eur Heart J 2005

Acute Heart Failure ESC Guideline, Eur Heart J 2005

Acute Heart Failure ESC Guideline, Eur Heart J 2005

Causes of acute heart failure

Main causes

Ischemic heart disease, Cardiomyopathy,

Hypertension
Other causes: Valvular heart disease, Congenital
heart
disease, Alcohol and drugs, Hyperdynamic circulation
(anaemia, thyrotoxicosis, haemochromatosis, Paget's
disease), Right heart failure (RV infarct, pulmonary
hypertension, pulmonary embolism, cor pulmonale
(COPD)), Arrhythmia and Pericardial disease.

Mechanisms leading to heart failure

Impaired cardiac contractility as in

myocardial infarction and

cardiomyopathy
Ventricular outflow obstruction
(pressure overload) as in
hypertension and aortic stenosis
Impaired ventricular fillings as in
mitral stenosis and constrictive
pericarditis
Volume overload as in mitral

H em odynam ic Profi
le ?

Low perfusion at rest

Congestion at rest?

No

No

Yes

Warm & dry

Warm & wet

Cold & dry

Cold & Wet

Yes

Sign of congestion:
Orthopnea, elevated JVP,
edema,pulsatile hepatomegaly,
asites, rales,louder S3,
P2 radiation left ward,
abdomino-jugular reflex,
valsava square wave

Sign of low perfusion:

Narrow pulse pressure,cool
extremities,sleepy, suspect from
ACEI hypotension, low Na, renal
worsening

European Heart Journal of Heart Failure,2005;

March. Vol 7:323-331

M AN AG EM EN T ACU TE H EART
FAILU RE?

M anagem ent ofAcute H eart Failure

ConventionalTreatm ents of
AD H F
Diuretics

Vasodilators

Reduce
fluid
volume

Decrease
preload
and/or
afterload

Inotropes

Augment
contractility

Fonarow GC. Rev Cardiovasc Med 2001;2(suppl 2):S7S12

79

AD H F treatm ent Algorithm

Diagnosis of ADHF, Initiate therapy based on presenting signs and symp

A) Signs and Symptoms of Volume Overload

Orthopnea/PND
Increased JVD
DOE/SOB
S3 or S4
Pitting Edema
Rales
Chest Xray; pulmonary congestian HJR
Recent Weight Gain
BNP

(C) Mild
Volume Overload

(B) Signs and Symptoms of Low Cardiac

Output
Narrow pulse pressuure
Decreased urine output
Altered Mental status inadequate response
Prerenal Azotemia
IV diuretic
Cool extremities

(E) Mod-Severe
Volume Overload

(G) MildModerate
SBP > 90 mmHg

(J) Very Low

Cardiac Output
No

On a -Blocker
Yes Chronically

Pulmonary artery cathether Placed

High SVR
High PCWP
Low CI
SBP > 90 mmHg
consider vasodilators after initiation
of inotropic support

No
(H) Milrinone
(I) Dobutamine
Inadequate Response
Very Low Cardiac Output (J)

(D) IV Diuretics

(F) IV Diuretics + IV Vasodilators

D iuretics and H eart Failure

There have been no long-term studies of diuretic
therapy for the treatment of heart failure and, thus,
its effects on morbidity and mortality are not known.1
Patients may become unresponsive to high doses of
diuretic drugs if they:
Consume large amounts of dietary sodium2
Are taking agents that can block the effects of
diuretics
(eg, NSAIDs, COX-2 inhibitors)1
Have significant impairment of renal function or
perfusion1

Diuretic resistance can generally be overcome:

By the IV administration of diuretics2
The use of two or more diuretics in combination2
1.Ravnan SL et al. Congest Heart Fail 2002;8:8085
2.Brater DC. N Engl J Med 1998;339(6):387-95 81

Role of Inotropic Therapy in Patients

With Heart Failure
The routine use of inotropes as heart failure
therapy is not indicated in either the short- or
long-term setting
The use of inotropes as a treatment of
cardiogenic shock, diuretic/ACE inhibitor
refractory heart failure decompensations, or as a
short-term bridge to definitive treatment, such
as revascularization or cardiac transplantation,
is potentially appropriate
Inotropes may be appropriate as a palliative
measure in patients with true end-stage heart
failure as part of hospice care
Felker GM. Am Heart J 2001;142:393401

82

Lim itations ofCurrent Therapies

for Acute CH F:Positive Inotropes
Increased mortality with oral inotropes
Aggravation and induction of arrhythmias -need telemetry (milrinone, dobutamine,
dopamine)
Tachycardia
Tachyphylaxis (dobutamine)
Neurohormonal activation and/or lack of
suppression
Physiologic effects antagonized
by -blockade (dobutamine, dopamine)
83

G uidelines ofuse ofIV

vasodilators for AD H F

IV vasodilators (nitroglycerin or nitroprusside) and

diuretics are recommended for rapid symptom

relief in patients with acute pulmonary edema or
severe hypertension

Strength of evidence = C, HFSA 2006 Practice Guideline, Recommendation 12.16

IV vasodilators (nitroprusside, nitroglycerin or

nesirite) may be considered in patients with ADHF

and advanced HF who have: Persistent severe HF
despite aggressive treatment with diuretics and
standard oral therapies
Strength of evidence = C, HFSA 2006 Practice Guideline, Recommendation 12.17

84

TraditionalVasodilators:
Lim itations

Nitroglycerin

? Efficacy in CHF
Tachycardia
Tachyphylaxis
Neurohormonal

activation due to
reflexive sympathetic
activity

Nitroprusside
Difficult titration
ICU/arterial line monitoring due

to excessive hypotension risk

Tachycardia
Coronary steal
Pulmonary shunting
Toxic metabolites
Neurohormonal activation due
to reflexive sympathetic
activity
85

Treatm ent Algorithm for AD H F

86

ESC guideline 2005

IdealAgent for AD H F

Vasodilation (venous and arterial)

Rapidly decreases ventricular filling pressures
Rapidly decreases symptoms of congestion
Does not increase heart rate or directly increase
contractility (decreases myocardial oxygen demand)
Is not proarrhythmic
Has no tachyphylaxis
Provides neurohormonal suppression
Promotes diuresis / natriuresis
Is conveniently dosed (can be used with or without
pulmonary artery catheterization)
Minimal titration needed

Fonarow GC. Rev Cardiovasc Med 2001;2(suppl 2):S7S12

87

InitialTreatm ent Algorithm

for AD H F

Acutely Decompensated Heart Failure

(Volume overloaded, dyspneic, with SBP > 90 mm Hg)
IV
Diuretics

Oxygen

Compensation
Optimize oral drug regimen
Optimize patient education
Discharge home

Initial Therapy

Nesiritide
2 mcg/kg bolus followed
by
0.01 mcg/kg/min infusion

Inadequate
Response
Increase
Nesiritide
MonitoringDose

Refractory Therapy
Hemodynamic

V Inotropic
Agent(s)

Mechanical
Assist

88
Abraham WT et al. Prev Cardiovasc
Med 2001;2:235236

G oalofTreatm ent
for AD
HF
Hemodynamic
:
Clinical :

symptoms
clinical signs
body weight
diuresis
oxygenation

Laboratory:
serum electrolyte

normalization
BUN and/or creatinine
plasma BNP
blood glucose
normalization

PCWP to < 18 mmHg;

cardiac output and/or

stroke volume
Outcome:
length of stay in the ICU
duration of

hospitalization
time to hospital readmission
mortality
Tolerability:
low rate of withdrawal from

therapeutic measures
low incidence of adverse
effects
89

Pulm onary O edem a

PULMONARY OEDEMA
This is a very frightening, life threatening emergency
characterized by
Extreme breathlessness.
Clinical features
Patients with alveolar oedema are acutely breathless,
wheezing, anxious and perspiring profusely.
Cough productive of frothy, blood-tinged (pink) sputum,
which can be copious with tachypnea and peripheral
circulatory shutdown.
Tachycardia, a raised venous pressure and a gallop
rhythm.
Crackles and wheezes are heard throughout the chest.
The arterial Po2 falls and initially the Paco2 also falls,
owing to overbreathing. Later, the Paco2 increases
because of impaired gas exchange.
The chest X-ray shows diffuse haziness, owing to alveolar
fluid, and the Kerley B lines of interstitial oedema.

Pulm onary O edem a

TREATMENT
- The patient must be placed in a sitting position.
High-concentration oxygen is given. In severe cases,
ventilation is
necessary.
Intravenous diuretic treatment with furosemide or
bumetanide is
given. These diuretics induce an acute venodilatory response
with a reduction in preload that helps to relieve pulmonary
congestion in addition to the more delayed diuretic response.
- Morphine (10-20 mg i.v.) together with an antiemetic such as
metoclopramide (10 mg i.v.) is given.
- Venous vasodilators, such as glyceryl trinitrate, may produce
prompt relief by reducing the preload.
- Aminophylline (250-500mg or 5mg/kg IV) is infused over 10
minutes

Cardiogenic Shock

SHOCK is a severe failure of tissue perfusion, characterized

by hypotension, a low cardiac output and signs of poor tissue
perfusion such as oliguria, cold extremities and poor cerebral
function. Cardiogenic shock is commonly due to myocardial
infarction, acute massive pulmonary embolus, pericardial
tamponade & sudden-onset valvular regurgitation.

TREATMENT: Patients require intensive care

General measures such as complete rest, continuous 60%
oxygen administration and pain and anxiety relief are
essential.
The infusion of fluid is necessary if the pulmonary capillary
wedge pressure is below 18 mmHg.
Short-acting venous dilators such as glyceryl trinitrate or
sodium nitroprusside should be administered intravenously if
the wedge pressure is 25 mmHg or more.
Cardiac inotropes to increase aortic diastolic pressure.
Emergency revascularization of occluded arteries

TERIMA KASIH