CARDIAC SHOCK

CARDIOGENIC SHOCK

H. Sukma Wicaturatmashudi, S.Kp.M.Kep.Sp.KMB

 DEFINITION OF SHOCK
 Clinical condition resulting from acute generalised
state of inadequate tissue perfusion causing tissue
hypoxia
 Insufficient blood (oxygen+nutrients) reaching tissues
and insufficient removal of waste from tissues
 Not to be confused with cardiac arrest which is the
acute cessation of the cardiac pump.
 Shock can lead to a cardiac arrest.
Shock: The state in which profound and
widespread reduction of effectivetissue
perfusionleads first to reversible, and then if
prolonged, to irreversible cellular injury (Kumar
and Parillo, 1995).

Shockis defined as a clinical syndrome due to

inadequate tissue perfusion that results in end-
organ dysfunction.
 DIFFERENT TYPES OF SHOCK

 Hypovolaemic Shock- Fluid loss

 Cardiogenic Shock- Failure of heart to pump

effectively

 Distributive Shock- (septic shock, anaphylactic

shock, neurogenic shock)-Peripheral
vasodilatation causing a fall in the volume of
blood returning to the heart
 CARDIOGENIC SHOCK

Failure of the heart to pump

effectively resulting in inadequate
circulation of blood
HEMODYNAMIC PARAMETERS

 Systemic Vascular Resistance (SVR)

 Cardiac Output (CO)
 Mixed Venous Oxygen Saturation (SvO2)
 Pulmonary Capillary Wedge Pressure
(PCWP)
 Central Venous Pressure (CVP)
 Cardiac Output (CO) = HR x SV (L/min)
Normal CO = 4 to 8 L/min

 Cardiac Index (CI) = CO/BSA (L/min/m2)

Normal CI = 2.5-4.2 L/min/m2
 Stroke Volume Index (SVI): CI/HR (ml/beat/m2)
Normal SVI = 40-85 ml/beat/m2
 Systemic Vascular Resistance = MAP – CVP / CO x 80
Normal SVR = 900-1600 dynes/sec/cm-5
 Systemic Vascular Resistance Index = MAP – CVP / CI x 80
Normal SVRI = 1970-2390 dynes/sec/cm-5
Oxygen Delivery (DO2) [520-570 mL/min x m2]: rate of
oxygen transport in arterial blood
DO2= CI x 13.4 x Hb x SaO2

Oxygen Uptake (VO2) [110-160 ml/min x m2]: rate of

oxygen taken up from the systemic microcirculation
VO2 = CI x 13.4 x Hb x (SaO2 – SvO2)
 NORMAL VALUES
Right Atrial Pressure, CVP Mean 0-6mmHg

Pulmonary Artery Systolic 15-30mmHg

Pressure End-diastolic 4-12mmHg
mean 9-19mmHg

PCWP Mean 4-12mmHg

Cardiac Output 4-8 L/min
Mixed Venous O2 Sat >70%

SVR 800-1200
Harus disingkirkan penyebab
hipotensi lain :

Hipovolemia, perdarahan, sepsis,

emboli paru, tamponade, diseksi
aorta, kelainan katup
 CAUSES

 Myocardial Infarct
 Cardiomyopathy ( Heart muscle disease)
 Cardiac valve disorders
 Congenital defects (ventralseptal defect)
 Prolonged cardiopulmonary bypass
Etiology
PATHOPHYSIOLOGY
 Decrease in Cardiac Output
– Fall in blood pressure
– High Left Ventricular Filling Pressures

 Compensatory response
– Increase systemic vascular resistance (increase blood flow to the
heart)
– Increase heart rate (increase blood to the tissues)

 Resulting physical manifestations

– Cool peripheries
– Weak thready pulse
– Decreased urine output
 SIGNS OF DECREASED TISSUE
PERFUSION

 Restlessness or decreased conscious level

 Hypotension
 Increased respiratory rate
 Poor urine output
 A weak thready pulse or absent pulse
 Cool, clammy, and mottled skin
 Poor signal on pulse oximeter
 Distended jugular vein
 Fatigue due to hyperventilation
CLINICAL MANIFESTATIONS

RADIOGRAPHIC FINDINGS
Enlarged Heart
Pulmonary Congestion

PULMONARY FINDINGS
Dyspnoea
Increased respiratory rate
Inspiratory crackles, possible wheeze
Arterial blood gases show a low O2
Respiratory Alkalosis
 NON INVASIVE FINDINGS

Thready, rapid pulse

Narrow pulse pressure
Distended neck veins
Arrythmias
Chest pain
Cool, pale, moist skin
Oliguria
Decreased mentation
 HAEMODYNAMIC FINDINGS

 Systolic Blood Pressure < 90 mmHg

(sustained > 30min.)
 Mean Arterial Pressure <70 mmHg
 Cardiac Indexes< 2.2 L/min/m2
 Pulmonary Artery Wedge Pressure > 18
mmHg
Echocardiogram image from a patient with cardiogenic
shock shows enlarged cardiac chambers;
PULMONARY ARTERY WEDGE PRESSURE

Measured by a Swan-Ganz catheter, is the

pressure measured in a pulmonary artery after
occlusion of that artery.

Because of the large compliance of the pulmonary

circulation, it provides an indirect measure of
the left atrial pressure.
 CARDIAC INDEX
Cardiac index (CI) is a parameter that relates the
cardiac output to body surface area, thus relating
heart performance to the size of the individual.

Cardiac output is the volume of blood being

pumped by the heart, in particular by a ventricle
in a minute.

The normal range of cardiac index is 2.6 - 4.2 L/min

per square meter.
 DIAGNOSIS KEPERAWATAN

 Penurunan curah jantung b.d. gangguan

kontraktilitas otot jantung.
 Nyeri dada b.d. iskemi otot jantung.
 Gangguan pertukaran gas b.d. gangguan ventilasi-
perfusi.
 Intoleransi aktivitas b.d. Ketidakseimbangan antara
suplai oksigen dengan kebutuhan miokard jantung.
 Cemas b.d. proses penyakit.
MANAGEMENT OF CARDIAC SHOCK
AIM
Increasing Myocardial Oxygen Delivery
Maximising Cardiac Output
Decreasing Left Ventricular Workload
 MEDICATION

 Fluid Resuscitation if required

 Oxygenation and Airway Protection
 Correct electrolyte imbalance
 Analgesia if required
 Discontinue - Nitrates, beta-blocker and ace
inhibitors as they reduce blood pressure
 INTERVENSI
 Observasi tanda-tanda vital, parameter hemodinamik setiap 15 menit
atau sesuai dengan kondisi pasien.

 Kaji semua aspek tentang nyeri dada ( dengan menggunakan skala nyeri
1 – 10 ).
 Observasi pola, suara nafas serta analisa gas darah.
 Beri oksigen 100 % melalui non rebreathing mask untuk
mempertahankan saturasi oksigen lebih dari 90 %.
 Monitor irama jantung secara terus menerus, kaji irama dan
dokumentasikan adanya perubahan.
 Berikan titrasi Obat-obat inotropik untuk mempertahankan perfusi sesuai
dengan program pengobatan.
 Monitor status cairan masuk dan keluar.
 Ciptakan suasana yang tenang, jelaskan kondisi pasien dan tindakan
yang akan dilakukan , tingkatkan support system.
 Inotropic Agents, increase the force of muscle
contraction

 Diuretics, increase the excretion of water and

therefore reduce the workload of the heart
 Nitrates once B.P. has stabilised
 Thrombolytic s??? too late
 Dopamine
 <2 renal vascular dilation
 <2-10 +chronotropic/inotropic (beta effects)
 >10 vasoconstriction (alpha effects)

 Dobutamine – positive inotrope, vasodilates,

arrhythmogenic at higher doses

 Norepinephrine (Levophed): vasoconstriction, inotropic

stimulant. Should only be used for refractory
hypotension with dec SVR.

 Vasopression – vasoconstriction
IABP MAXIMISE CARDIAC OUTPUT
REVASCULARISATION

Percutaneous Transluminal Coronary Angioplasty

(PTCA)

OR

Coronary Artery Bypass Grafting

(CABG)
 ANGIOGRAPHY/ANGIOPLASTY

A patient with cardiogenic shock demonstrates severe stenosis of the left

anterior descending coronary artery.
 Following angioplasty of the critical stenosis, coronary flow is
reestablished. The patient recovered from cardiogenic shock.
COMPLICATIONS OF CARDIOGENIC SHOCK

 Cardiopulmonary arrest
 Dysrythmias
 Renal failure
 Multisystem Organ Failure
 Ventricular Aneurysm
 Stroke
 Death
 MORTALITY

> 55% inpatients treated medically

die from cardiogenic shock
 CONCLUSION

 Cardiac shock is life-threatening

 The key to successful management is early
diagnosis and prompt medical management
 Be aware of the signs of decreased tissue
perfusion
 Assess total perfusion (peripheries, urine
output) and not simply blood pressure
ANY QUESTIONS?