Left and Right Heart Failure: What Is

the Differences and How to Diagnose

Anna Fuji Rahimah, MD, FIHA
 What is Heart Failure?

A chronic, progressive condition in which

the heart muscle is unable to pump
enough blood through the heart to meet
the body's needs for blood and oxygen

HF usually results in an enlarged heart

 HEART FAILURE ̴ can’t meet demands

SYSTOLIC HF DIASTOLIC HF
can’t PUMP can’t FILL
hard enough enough
BLOOD
in
LUNGS

CONGESTION
Fluid buildup
 CONGESTIVE HEART FAILURE (CHF)

SYSTOLIC HF DIASTOLIC HF
can’t PUMP can’t FILL
hard enough enough
BLOOD
in
LUNGS

CONGESTION
Fluid buildup
CONGESTIVE HEART FAILURE (CHF)
MILLIONS of people

DEATH
ISCHEMIA VALVULAR
DISEASE

CONGESTIVE HEART FAILURE (CHF)

MILLIONS of people

DEATH
RIGHT-SIDED LEFT-SIDED
HEART FAILURE HEART FAILURE
RIGHT-SIDED LEFT-SIDED
HEART FAILURE HEART FAILURE

BIVENTRICULAR
HEART FAILURE
they work in series

RIGHT-SIDED LEFT-SIDED
HEART FAILURE HEART FAILURE

BIVENTRICULAR
HEART FAILURE
LV Failure
ISCHEMIC HEART LEFT-SIDED
DISEASE HEART FAILURE

coronary atherosclerosis * usually SYSTOLIC

(pumping)

DAMAGE to
MYOCARDIUM

plaque
buildup
ISCHEMIC HEART LEFT-SIDED
DISEASE HEART FAILURE

coronary atherosclerosis * usually SYSTOLIC

(pumping)

DAMAGE to
MYOCARDIUM

SCAR TISSUE

plaque
buildup
 LEFT-SIDED
LONG-STANDING HEART FAILURE
HYPERTENSION
* usually SYSTOLIC
(pumping)
ISCHEMIC HEART
DISEASE
 LEFT-SIDED
LONG-STANDING HEART FAILURE
Systemic HYPERTENSION
* usually SYSTOLIC
circulation
ARTERIAL PRESSURE +++ (pumping)
ISCHEMIC HEART
HARDER to PUMP DISEASE

HYPERTROPHY

WEAKER
CONTRACTIONS
 DILATED LEFT-SIDED
CARDIOMYOPATHY HEART FAILURE

* usually SYSTOLIC
(pumping)
ISCHEMIC HEART
DISEASE
LONG-STANDING
HYPERTENSION
 DILATED LEFT-SIDED
CARDIOMYOPATHY HEART FAILURE

* usually SYSTOLIC
(pumping)
ISCHEMIC HEART
DISEASE
LONG-STANDING
HYPERTENSION
 DILATED LEFT-SIDED
CARDIOMYOPATHY HEART FAILURE

* usually SYSTOLIC
(pumping)
ISCHEMIC HEART
DISEASE
LONG-STANDING
HYPERTENSION

SYSTOLIC HEART FAILURE

 LEFT-SIDED
HEART FAILURE

* usually SYSTOLIC
(pumping)
ISCHEMIC HEART
DISEASE
LONG-STANDING
WALLS
HYPERTENSION
DILATED
CHAMBER
CARDIOMYOPATHY
LONG-STANDING
LEFT-SIDED
HEART FAILURE
HYPERTENSION
 LONG-STANDING
LEFT-SIDED
HEART FAILURE
HYPERTENSION

DIASTOLIC
HEART FAILURE
 LEFT-SIDED
AORTIC STENOSIS HYPERTROPHIC HEART FAILURE
CARDIOMYOPATHY

LONG-STANDING
HYPERTENSION

DIASTOLIC
HEART FAILURE
 LEFT-SIDED
HEART FAILURE
RESTRICTIVE
CARDIOMYOPATHY
LONG-STANDING
HYPERTENSION
AORTIC STENOSIS
HYPERTROPHIC
CARDIOMYOPATHY

DIASTOLIC
HEART FAILURE
ETIOLOGY

23
ETIOLOGY

24
Sign and Symptoms
LEFT-SIDED
HEART FAILURE

LONG-STANDING
HYPERTENSION
AORTIC STENOSIS
HYPERTROPHIC
CARDIOMYOPATHY
RESTRICTIVE
CARDIOMYOPATHY
 LEFT-SIDED
HEART FAILURE

LONG-STANDING
HYPERTENSION
AORTIC STENOSIS
HYPERTROPHIC
CARDIOMYOPATHY
RESTRICTIVE
CARDIOMYOPATHY

Leaks from
BLOOD VESSELS FLUID BUILDUP
blood starts to back up
into the lungs
increase the pressure in the
pulmonary artery and can
also result in fluid moving
from the blood vessels to
the interstitial space causing
pulmonary edema, or
congestion
In the alveoli of the
lungs, all this extra fluid
makes oxygen and
carbon dioxide
exchange a lot harder,
since a wider layer of
fluid takes more time
for oxygen and carbon
dioxide to diffuse
through
Dyspnea
Orthopnea
Dyspnea
Orthopnea
Dyspnea
Orthopnea
Crackles (rales)
RV Failure
Sign and Symptoms
 Treatment
• Treat underlying condition
• ACEI, beta blockers for systolic dysfunction
• Diuretics to reduce water retention
• Right-sided HF will be treated similarly to left-sided HF,
especially because it’s often a result of left-sided HF; therefore,
medications like ACEI and diuretics may be prescribed
THANK YOU
Sign and Symptoms
 Etiology and Pathophysiology
↓RV contractility
•RV infarction
•Right sided
cardiomyopathy
•Perioperative RV injury

Pressure Decreased
overload contractility
•Severe sepsis
•Post cardiac
transplantation
•Adult
•PE
•Tricuspid congenital
•Left sided CM
regurgitation heart dis
•Pulmonary
•Pulmonic stenosis
regurgitation •Pericardial
RV volume disease
overload Volume •Valvular disease RV pressure
overload •Pulmonary overload
HTN

Gregory piazza, Chest 2005; 128 : 1836-1852

 DIAGNOSTIC
Physical examination

Electrocardiography

Chest X-ray

Echocardiography

Cardiac MRI

Right-Heart Catheterization

Biomarkers
 Physical Examination
Symptoms of RV Failure Signs of RV Failure
Acute Acute
Dyspnea Hypotension
Lightheadedness Tachycardia
Syncope Tachypnea
Chest discomfort Cyanosis
Chronic Elevated JVP
Acute symptoms Parasternal heave
Right-upper-quadrant abdominal pain RV third-heart sound
Lower-extremity swelling Tricuspid regurgitation
Accentuated sound of PVclosure
Chronic
Acute signs
Hepatic enlargement and ascites
Lower-extremity edema

Gregory piazza, Chest 2005; 128 : 1836-1852

 DiagnosticECG
Testing
• Depending on the cause of RV failure, patients may have ECG evidence of right-heart
dysfunction with or without evidence of RV infarction
 ECG

• Loss of the
R wave

• ST segment
elevation

• in V1 and
right-sided
leads
 Chest Radiography
Chest X Ray
• RV is poorly visualized on a conventional chest radiograph because of its anatomic
location
 Echocardiography
ECHOCARDIOGRAPHY
a rapid and effective means for diagnosing RV failure & several associated
conditions

RV dilatation = ratio of RV end-diastolic area to LV end-diastolic area of > 0.6

Severe RV dilatation = ratio is >1.0

In RV failure secondary to acute PE  McConnell sign

(a distinct regional pattern of dysfunction with
diffuse hypokinesis of the RV-free wall sparing the apex)
 ECHOCARDIOGRAPHY
 To confirm the diagnosis of RV failure.
 To triage patients into the following four groups:

RV failure without
elevated
LV failure
pulmonary artery
pressures

RV failure with
elevated
pericardial disease
pulmonary artery
pressures
 ECHOCARDIOGRAPHY
Echocardiographic findings in RV failure
 Cardiac MRIMRI
Cardiac
• a direct evaluation of RV size, mass, morphology, and function
• Gadolinium-enhanced cardiac MRI  can detect ischemic myocardium
• delayed contrast-enhanced MRI  can differentiate ischemia from infarction.

Cardiac MRI findings in RV failure :

• RV dilatation
• tricuspid regurgitation
• Hypertrophy
• Interventricular septal flattening
• paradoxical motion
• change
• in chamber morphology (crescent shape to a more
concentric form )
 Cardiac MRI
• Minimal change in
chamber size from
diastole (A) to
systole (B)

• Marked RV dilatation
( C)

• Area of infarction
indicated by
increased signal
intensity along the
RV wall (D)
 Cardiac troponins
Cardiac Marker
• Have well-established diagnostic and prognostic roles in ischemic heart
disease

increased wall
tension, metabolic RV ischemia
Troponin elevation
demand, and reduced or microinfarction
coronary perfusion
 Right Heart Catheterization

 Right heart catheterization is an important part of the

evaluation of right heart disease
 Indications:
→ assessment of pulmonary vascular resistance or impedance,
pulmonary pressures, cardiac output shunt fraction, and
pulmonary vasoreactivity

Mehdi Skhiri, Rev Esp Cardiol., 2010; 63(4): 451-471

 History and PD suggestive of RHF

ECG
Chest X-ray
Cardiac biomarker

Transthoracic echocardiogram

RV failure with RV failure without

LV failure Pericardial disease
↑ PA pressure ↑ PA pressure

Acute MI PE RV infarction
Left sided-CM Pulmonary HTN Valvular disease
Valvular disease CHD Right sided CM

Right heart cath Right heart cath

Left/right heart Left/right heart cath
Chest CT Chest CT
catheterization Cardiac MRI Cardiac MRI
Cardiac MRI

Gregory piazza, Chest 2005; 128 : 1836-1852

 BNPBNP
• To evaluate of acute dyspnea
• To assess risk for mortality and cardiovascular events
• correlate with the degree of RV dysfunction and adverse outcomes

• The increasing BNP levels were positively correlated with :

– mean pulmonary artery pressure,
– pulmonary vascular resistance,
– mean right atrial pressure,
– RV end-diastolic pressure, and
– RV mass

• The increasing BNP levels were inversely correlated with :

– cardiac output
– RV systolic function
 Management of RV Failure

• requires treatment of the underlying causes and

• hemodynamic support based on pathophysiology

Tx for Patients Patients with Patients with RV Neither

with elevated pulmonary volume overload pulmonary
pulmonary arterial hypertension and hypertension nor
pressures and RV without RV normal pulmonary RV volume
volume overload volume overload artery pressures overload

• inotropes, • volume • inotropic support • volume

• vasodilators, administration • mechanical assist administration
• mechanical assist • pulmonary devices
devices, vasodilators • or surgery
• surgery
PATOPHYSIOLOGY

Leonard S Lilly. 2016

Patophyiology of Heart Disease
71
PATOPHYSIOLOGY
Patofisiologi

Leonard S Lilly. 2016. Patophyiology of Heart Disease

72
 Symptoms and Sign
Gejala Tanda
Tipikal Lebih spesifik
Sesak nafas Meningkatnya tekanan vena jugularis
Orthopnoea Reflux hepatojugular
Suara jantung ketiga (gallop rhythm)
Paroxysmal nocturnal dyspnoea
Impuls apikal berpindah ke lateral
Kurangnya toleransi olahraga
Fatique, kelelahan,
bertambahnya waktu untuk
pulih setelah berolahraga
Bengkak pergelangan kaki
Kurang tipikal Kurang spesifik
Batuk malam Kenaikan berat badan (> 2 kg / minggu)
Wheezing Pengurangan berat badan (pada HF lanjut)
Cachexia
Perasaan gemuk/bengkak
Murmur jantung
Kehilangan selera makan Edema perifer (pergelangan kaki, sakrum, skrotum)
Kebingungan (terutama pada Krepitasi paru
lanjut usia) Efusi pleura
Depresi Takikardia
Pulse Irregular
Palpitasi
Takipneu
Dizziness Pernafasan Cheyne Stokes
Syncope Hepatomegali
Bendopnea53 Asites
Ekstremitas dingin
Oliguria
Tekanan nadi sempit
73
2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Diagnostic
Algorithm

74
2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Framingham Criteria

75
 Forester Criteria

76
2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
 Diagnostic Modality
CXR – pembesaran ukuran jantung,
interstitial lung edema,
efusi pleura

Echocardiography
– dilatasi ventrikel kiri, dilatasi ventrikel kanan, dilatasi atrium,
disfungsi diastolik, disfungi sistolik ventrikel kiri dengan atau
tanpa regurgitasi katup mitral
– Exercise atau pharmacological stress echocardiography untuk
menilai iskemia yang diinduksi & viabilitas miokard

MRI
– melihat struktur dan fungsi ventrikel, inflamasi & jaringan
parut
– menilai iskemia miokard & tes viabilitas pada gagal jantung
dengan penyakit arteri koroner

2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
13. Katritsis DG., Gersh BJ., Camm AJ. Clinical Cardiology: Current Practice Guidelines. Oxford University press. 2013.361-363.
 Diagnostic Modality
Single–photon emission computed tomography dan
radionuclide ventriculography (SPECT)

Angiografi koroner
pada pasien gagal jantung dengan penyakit arteri
koroner

CT Cardiac
- memvisualisasikan anatomi koroner secara non
invasif
- mengeksklusi diagnosis penyakit arteri koroner

Tes diagnostik lain

ST2, galectin 3, copeptin, adrenomedulin
Genetic testing

2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
13. Katritsis DG., Gersh BJ., Camm AJ. Clinical Cardiology: Current Practice Guidelines. Oxford University press. 2013.361-363.
 Management
• Tujuan: memperbaiki gejala, kapasitas fungsional, kualitas hidup, angka readmisi,
dan mortalitas
• Terapi non farmakologis (modifikasi pola hidup)
• Terapi farmakologis dan device therapy
• Pembedahan (transplantasi jantung)

2. Ponikowski P, Voors AA, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
13. Katritsis DG., Gersh BJ., Camm AJ. Clinical Cardiology: Current Practice Guidelines. Oxford University press. 2013.361-363. 79
80
Management

ESC Guidelines of Acute and

Chronic Heart Failure 2016

81
 Management

ESC Guidelines of Acute and Chronic Heart

Failure 2016

82
 Embriology
Ventricular Properties

Circulation. 2014;129:1033-1044.
SYSTOLIC HEART FAILURE
* can’t pump hard enough
 SYSTOLIC HF
• Kind of a mathematical way to think this one is that the heart
needs to squeeze out a certain volume of blood each minute,
called cardiac output, which can be rephrased as the heart rate
(or the number of beats in a minute) multiplied by the stroke
volume (the volume of blood squeezed out with each heart
beat).
SYSTOLIC HEART FAILURE
* can’t pump hard enough
 SYSTOLIC HF
• The heart rate is pretty intuitive, but the stroke volume’s a little tricky.
• For example, in an adult the heart might beat 70 times per minute and the LV
might squeeze out 70ml per beat, so 70 x 70 equals a cardiac output of 4900 ml
per minute, which is almost 5 liters per minute.
• So notice that not all the blood was pumped out
• And the SV is a fraction of the total volume.
• The total volume may be closer to 110 ml, and 70 ml is the fraction that got
ejected out with each beat, the other 40 ml kind of lingers in the LV until the
next beat
• In this example, the EF would be 70 ml divided by 110 ml or about 64%, a normal
EF is around 50-70%, between 40-50% would be borderline,
• and anything about 40% or less would indicate systolic HF because the heart is
only squeezing out a little blood each beat.
 Diastolic Heart Failure
• Where the heart’s squeezing hard enough but not filling quite
enough
• In this case again the stroke volume is low, but the EF is normal
• It’s not filling enough so there’s a low total volume
• In this situation, the failure’s caused by abnormal filling of the
ventricle so that the chamber doesn’t get fully loaded or stretched
out in the first place
• Another term for this is having a reduced “preload” which is the
volume of blood that’s in the ventricle right before the ventricular
muscle contracts.
 Frank-Starling mechanism
• An important relationship between systolic and diastolic
function is the Frank-Starling mechanism, which basically
shows that loading up the ventricle with blood during diastole
and stretching out the cardiac muscle makes it contract with
more force, which increases SV during systole.
• This is kinda like how stretching out a rubber band makes it
snap back even harder, except that cardiac muscle is actively
contracting whereas the rubber band is passively going back to
its relaxed state.
Dyspnea
Orthopnea
Crackles (rales)
Dyspnea
Orthopnea
Crackles (rales)
• If enough fluid fills some of these capillaries in the lungs, they
can rupture, leaking blood into the alveoli.
• Alveolar macrophages then eat up these red blood cells, which
causes them to take on this brownish color from iron build-up.
And then they’re then called “hemosiderin-laden
machrophages”, also known as “heart failure cells”.
MEDICATIONS improve blood flow
ACE Inhibitors

DIURETICS
 Treatment
• For left-sided HF, certain medications can be prescribed to help
improve blood flow, like ACEI which help dilate blood vessels,
as well as diuretics to help reduce the overall fluid buildup in
the body which helps prevent hypertension from worsening
the HF
• Someone can also have isolated right-sided HF, though, and an
example of this would be a left-to-right cardiac shunt.
• In these cases, there might be a cardiac shunt like an ASD or a
VSD, that allows blood to flow from the higher-pressure left-
side to the lower pressure right side, which increases fluid
volume on the right side and can eventually lead to concentric
hypertrophy of the RV, making it more prone to ischemia –
which is a systolic dysfunction, and have a smaller volume and
become less compliant – which is a diastolic dysfunction.
• Another potential cause of isolated right-sided failure is chronic
lung disease.
• Lung diseases often make it harder to exchange oxygen
• Well in response to low oxygen levels, or hypoxia, the pulmonary
arterioles constrict, which raises the pulmonary blood pressure.
• This just like before, makes it harder for the right side of the heart
to pump against and can lead to right-sided hypertrophy and HF.
• When chronic lung disease leads to right-sided hypertrophy and
failure, it’s known as cor pulmonale.
• Also in the body, when blood backs up to the liver and spleen, fluid
can move into the interstitial spaces within those organs and they
can both become enlarged, called hepatosplenomegaly, which can
be painful, and if the liver is congested for long periods of time,
patients can eventually develop cirrhosis and liver failure, which
would be called cardiac cirrhosis.
• Excess interstitial fluid near the surface of the liver and spleen can
also move right out into the peritoneal space as well, and since that
cavity can take a lot of fluid before there is any increase in pressure,
a lot of fluid can build up in the peritoneal space which is called
ascites.
• Finally, fluid that backs up into the interstitial space in the soft
tissues in the legs causes pitting edema, where the tissue is
visibly swollen and when you apply pressure to it, it leaves a
“pit” and takes awhile to come back to its original place.
• This generally affects the legs in most people, because gravity
generally causes the majority of fluid to “pool” in the
dependent parts of the body, which is the legs when you’re
standing and the sacrum, essentially the lower back, when
you’re lying down.
• With HF, we saw that sometimes the muscle wall can stretch
and thin out, or sometimes thicken and become ischemic
• In either case, those heart cells get irritated, in both scenarios
the cells get irritated, and this can lead to heart arrhythmias
• With an arrhythmia, the ventricles don’t contract in sync
anymore making them less able to pump out blood and
worsening the whole situation.
• In some cases, patients might be treated with cardiac
resynchronization therapy pacemakers, which can stimulate
the ventricles to contract at the same time and potentially
improve the blood pumped out.
• Alternatively, for HF in general, some people might have
ventricular assist devices implanted, or VADs, which literally
assist or help the heart pump blood may also be implanted.
• In end-stage situations where other forms of treatment have
failed, patients might have a heart transplant.