HEART FAILURE

Dr. Leslie Asuncion- Viado | August 14, 2019

_______________________________________________ heart failure in the future with the

OUTLINE OF TOPICS_____________________________ accumulation of chemotherapeutic drug.
But between systolic and diastolic failure,
A. Heart Failure those who are receiving chemotherapy
B. Cor Pulmonale will manifest first as a diastolic dysfunction
C. Cardiogenic Shock (relaxation abnormality).

HEART FAILURE » Duchenne’s, Becker’s, and limb-girdle

 Complex clinical syndrome muscular dystrophies
 Structural and functional impairment
 Diastolic and systolic function - High output failure (AV fistula) - those who
 Develop signs and symptoms undergo dialysis, their access for hemodialysis
o Hospitalization, poor quality of life and is the creation of AV fistula. At first, they have
short life span this catheter inserted in the jugular vein or in
 Inherited or acquired cardiac abnormality the femoral vein. Because these are temporary
depending on the risk factor access catheter, they will be subjected to have
 Heart failure preferred over CHF because not all an AV fistula creation in the future. Because
heart failures is in congestion this will be long lasting. However, sometime in
the future, the life of the patient who are having
Epidemiology dialysis then these patient will be exposed or
 Prevalence in developed country is 2%, but as prone to have heart failure in the failure.
population grows older up to 65%, the incidence
will increase up to 10% Other cause of high output HF would be
Thyrotoxicosis.
 Lower incidence among women, initially women
are not affected. Before menopause, women are
Another AV fistula for those who will undergo
protected by the hormones to have myocardial
catheter insertion like angiography. Once the
infarction and eventually heart failure. But as the
patient’s angiographer will poke both the artery
patient approaches her perimenopausal state,
and veins, it will create a fistula. And in the
there will be equal incidence of heart failure
future once it is not corrected, then it will cause
between men and women.
high output failure.
 Occur in low (HFrEF or systolic HF) and normal
ejection fraction (HFpEF or diastolic HF)
» 2 parts/types: the one that reduce ejection
fraction is also called as systolic heart failure.
And the other one is diastolic HF, wherein the
eject fraction is preserved and that is what we
call the relaxation abnormality. Almost no
congestion.

Etiology
 Coronary artery disease major cause in developed
countries (60-75%) because of their diet or food
such as steak, burger and fries.
 Hypertension (75%)
 20-30% of depressed EF is unknown cause
- Non-ischemic (no vascular occlusion), dilated
or idiopathic
» Secondary factors: Viral infection, the
most common cause or toxin exposure
(alcohol/chemo) - So that’s why if the
patient will receive chemotherapy, we
should always assess the heart’s function.
We ask the patient to have baseline
echocardiogram because once the
patient is exposed to chemo, for example
those with breast cancer, when they are
exposed to Doxorubicin which is
cardiotoxic, then this patient might have » Infarction - complete or partial obstruction of flow
MED | HEART FAILURE
» Infection - because of the impairment of rhythm of
the hear, exposure to chronic tachycardia and
bradycardia can lead to HF
» Hypertension can be a cause of preload and
afterload HF.
» Note nutritional status of the patient.
Global Consideration
 Rheumatic heart disease - Africa and Asia -
because of the presence of tooth decay, dental
caries, people exposed to too much sweets without
proper oral hygiene can lead to RHD.
 Coronary Artery disease – Western Europe and
North America because of their diet.
 Chagas disease – South America
 Hypertension – African and African-American
population
 Anemia – developing countries because of poor
nutrition.
Prognosis
 Symptomatic HF still carries a poor prognosis
 30-40% of patients die within 1 year of diagnosis
 60-70% die within 5 years – worsening HF or
ventricular arrhythmia
 Patients with symptoms at rest have 30-70%
annual mortality rate
 Symptoms with moderate activity have annual
mortality rate of 5-10%
 Class II – 5-10% (dies within 1 year of diagnosis)
 Class IV - 30-70%
*** Functional status is an important predictor of patient
outcome
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
T1
» This is the pathogenesis of heart failure with low
ejection fraction. Take note that a patient will have
heart failure in the future when there is an index
event, whether MI, exposure to high output failure,
cor pulmonale or other cases such as chemo or
alcohol. This will lead to reduced EF. Initially the
patient’s heart is still small. At this time, during the
time of index event such as MI, there will be
activation of your hormonal system, which is
RAAS. There will be production of different
elements such ANP, BNP, aldosterone, renin,
vasopressin, those mechanisms will try to protect
the heart initially. So at that time, the patient’s heart
is not yet reorganized. Normal function and normal
structure but decreased blood flow. At that time,
patient will remain asymptomatic. As the years by,
there is chronic exposure to low blood flow to the
coronaries. There will be still impairment of the
nutrition of the heart. There is chronic exposure to
this elements. Initially, it is good because it will help
increase contractility and compensate for low
cardiac output. However, due to chronic exposure
to these elements, there will be reorganization of
the myofibrils. If the ER is reorganization of the
myofibrils, decrease ATP, the patient’s heart will be
exposure to lactic acidosis. There will be decrease
in the EF over time because of this chronic
exposure to RAAS, there will be reorganization of
myofibrils. Expulsion of calcium intracellular.
Presence of chronic aldosterone which can cause
fibrosis of myofibrils, this will lead to stiffening of the
heart. If there is stiffening of the heart, relaxation
will be impaired. There will be increased volume,
the myocardium will be stretched leading to
regurgitation. Symptoms will appear.
 Compensatory mechanism:
o Neurohormonal system
o Inc. Contractility
o ANP, BNP, PGE2, PGI2, NO
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MED | HEART FAILURE
ACTIVATION OF NEUROHORMONAL SYSTEM
BASIC MECHANISM OF HEART FAILURE
Left Ventricular Remodeling At Cellular Level:
 Myocyte hypertrophy because of pressure and
volume overload
 Alteration of contractile properties because of
disorganization of myofibrils
 Loss of myocyte – necrosis, autophagia, apoptosis
 Β adrenergic desensitization
 Abnormal myocardial energetics and metabolism
 Reorganization of extracellular matrix and
dissolution of organized collagen
Sustained Neurohormonal Activation And Mechanical
Overload
 Transcriptional and posttranscriptional changes in
the genes and proteins
 Regulate excitation-contraction coupling and
cross-bridge interaction
 Changes that regulate excitation-contraction:
- Decreased function of sarcoplasmic reticulum
Ca+2 adenosine triphosphatase (SERCA2A) –
resulting in decreased Ca+2 uptake into the
sarcoplasmic reticulum (SR), and
hyperphosphorylation of the ryanodine
receptor - Ca+2 leakage from the SR –
myocytolysis and disruption of
cytoskeletal links
Myocardial Relaxation Is An ATP-Dependent Process
 Regulated by uptake of cytoplasmic Ca+2 into the
SR by SERCA2A and extrusion of calcium by
sarcolemmal pumps
 Reduction in ATP concentration---- slowed
myocardial relaxation
 Hypertrophy or fibrosis ---- LV filling pressures
elevated at the end diastole
 Increase in HR ---- reduce filling time elevated LV
filling pressure
 Increase myocardial stiffness: LV hypertrophy and
increased myocardial collagen
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
T1
 Can occur alone or in combination with systolic
dysfunction with HF
Ventricular Remodeling
 Refers to the changes in LV mass, volume, and
shape and the composition of the heart
 Contribute independently to the progression of HF
 Increase in LV end-diastolic volume
 LV wall thinning occurs as the left ventricle begins
to dilate leads to afterload mismatch
decrease in stroke volume
High End-Diastolic Wall Stress
 Hypoperfusion of subendocardium worsening
of LV function
 Increased oxidative stress activation genes
sensitive to free radicals (TNF and interleukin 1B)
 Sustained expression of stretch-activated genes
(angiotensin II, endothelin, and TNF)
 Increasing LV dilatation also results in tethering of
the papillary muscles with resulting
incompetence of the mitral valve apparatus and
functional mitral regurgitation - systolic murmur
Clinical Manifestation
Cardinal symptoms: fatigue and shortness of breath
Mechanism are:
A. Pulmonary congestion – most important
mechanism
 Accumulation of interstitial or intra-
alveolar fluid---- activates juxtacapillary J
receptors---- rapid, shallow breathing.
B. Reductions in pulmonary compliance
C. Increased airway resistance
D. Respiratory muscles and/or diaphragm fatigue
E. Anemia
Symptoms
1. Othopnea
2. PND
3. Cheyne-stokes respiration
4. GI symptoms
5. Cerebral symptoms - due to apneic episode and
because of poor circulation to the brain
6. Nocturia
Physical Examination
 General appearance (agitates, restless, confused,
loss of consciousness) and vital signs (increased
BP, if hypertension is the cause, if LV is affected:
high or normal, if RV is affected: hypotensive;
» HR: tachycardia, due to compensation, RV:
bradycardia
» RR: increased not unless patient has apneic
episodes
» Temperature: cold clammy if MI, due to
vasoconstriction; IMPORTANT IN HEART
FAILURE because you want to know if the
patient is in febrile state or not. Why? Because
a very stable heart failure will not be
decompensated, meaning there will be no
symptoms, not unless the patient will have
infection.
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MED | HEART FAILURE
 Jugular veins - normal: <8cm H2O
 Pulmonary exam - Inspection: retractions,signs of
chronic hypoxia, barrel chest; Percussion: note for
dullness (effusion, consolidation); Palpation:
tactile fremitus; Auscultation: usual location of
pleural effusion - bilateral, but if unilateral, right
 Cardiac exam - Inspection: apex beat is displaced,
dynamic or adynamic precordium; Palpation:
check for thrills: PMI displaced, note for RVE;
Percussion: borders of the heart, if displaced,
enlargement; Auscultation; check if the patient is
in sinus or arrhythmia. Very important if the patient
is in sinus. Check for S1, S2, S3, S4. If there is S3
gallop, the heart is very stiff. Look for murmurs.
 Abdomen - globular because of the ascites; check
for umbilical veins, Sometimes it’s like cirrhotic
because of the chronic exposure to large volume
in the liver -- Ischemic hepatopathy which may lead
to liver cirrhosis causing prominent veins in the
abdomen. Palpate and percuss the liver, palpation
in the abdomen may cause epigastric pain; and
extremities - cold clammy, Decreased filling time,
pulmonary cause: clubbed fingers due to constant
or chronic exposure to alveolar hypoxia; check for
pulse, check BP for narrow pulse pressure, check
simultaneously the heart rate and pulse rate
because there is pulse difference especially in
patients with atrial fibrillation. Heart rate is greater
than pulse rate because we cannot detect with our
bare finger.
 Cardiac cachexia - most of them are cachectic; Fat
people are protected from symptoms and bad
prognosis of HF.
Diagnosis
 Routine Lab testing
» CBC- hemoglobin/hematocrit
» COPD/ Cor pulmonale- INC Hb/Hct
» Platelet count- one sign of liver dysfunction:
DECREASE plt
» WBC count: to look for infection
» Creatinine: since there is decrease blood flow
to the periphery, there is decrease blood flow
to the renal system, then there will be
impairment of the renal function, there will be
INC creatinine: causing CARDIO-RENAL
SYNDROME which will lead to inadequate
effect of diuretics sa kanila kailangan na mag
dialysis
» Electrolytes: to prevent arrythmia, kasi kung
may arryhthmia, can cause heart failure, it can
cause death
» SGPT/SGOT, liver function test: check sugar,
cholesterol for us to treat the secondary
causes of heart failure
 EKG
» Kailangan mong malaman kung sinus, dito mo
malalaman kung sinus so pag sinabi mong
sinus, T wave always follow the QRS, ditto mo
malalaman kung yung patient is in tachycardic
state, kasi sinus tachycardia pag more than
100bpm
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
T1
» Atrial flutter: sawtooth appearance
» Chamber enlargement: Malaki ang left atrium
dahil sa severe regurgitation, there will be
notching of your T wave so instead na curve
and smooth, meron siyang McDonalds sign sa
T wave sa lead 2 dahil siya ang pinaka stable
na lead
» Kung may right atrial enlargement: t wave
merong tenting of the T wave
» Left ventricular hypertrophy: V1 to V6
» Right ventricular enlargement
» STEMI: t wave inversion, ST depression
 CXR
» Cadiomegaly: know the borders of the heart
» Right border: right atrium
» Inferior border: left ventricle and right ventricle
» Superior border: right and left atrium and the
great vessels
» Left border: left ventricle
» In chest xray: both AP view and Lateral view:
to see left atrial enlargement and right ventricle
enlargement
» RV enlargement lateral view, between sternum
and right atrium its obscured walang space
» LA enlargement: Between vertebra and left
atrium: dapat may space
» Presence of congestion, infection, pleural
effusion
 Assessment of LV function (2D echo/MRI)
» Eto malalaman mo yung function ng heart,
ejection fraction, CO, the size of the chambers,
kung merong regurgitation, ruptured papillary
muscles, presence of pulmonary hypertension,
assessment of the ventricle, ruptured ventricle,
MI, atrial fib, presence of clot or thrombus
» Sa MRI mas maganda na nakikita ang right
side of the heart, right ventricle
 Biomarkers (BNP, NTBP, soluble ST2, galectin-3)
 Exercise testing – peak oxygen uptake (<14ml/kg)
» Only used if the patient will undergo bypass
» Mas maganda if MORE than 14ml/kg
Differential Diagnosis
Heart failure in general can be mistaken with other
disease entity in or body
 Renal
 Pulmonary
 Varicose- paa lang not extending upward wala ng
ibang sysmptoms
 Hepatic
Management
HFpEF (Heart failure with preserved ejection fraction)
 Control congestion- by diuretics
 Stabilize heart rate and blood pressure
 Improve exercise tolerance
 Volume management
4
MED | HEART FAILURE
o Diuretics- loop, K sparing, osmotic
diuretics, acetazolamide, furosemide,
spironolactone – most important
» Be careful when you diuresis a
patient because when overdiurese,
magkaka acute kidney injury so
check for creatinine baseline
» If INC creatinine: the most powerful
diuretics to use is LOOP diuretics
(furosemide), kung di na kaya mag
dialysis na slow low efficient (SLED)-
normally 3-4 hrs lang ang dialysis sa
SLED 6hrs and konting volume lang
then repeat na naman the following
day para hindi magkaroon ng abrut
change in volume status of the
patient to avoid hypotension
o Cardiorenal syndrome
o Ultrafiltration
 Vascular therapy
o Vasodilators- ACE inhibitors, ARBs, CCB
(be cautious in giving this to patients with
low ejection fractions because can cause
depressed Ca); Ang pre-venodilators will
be nitrates
 Inotropic therapy
o Dobutamine- 1st to give
Inotropic: for contraction
Cronotropic: heart rate
What we want to have is INC force of
contraction and DEC heart rate
2nd line: norepinephrine almost same
effect with dobutamine
o Milrinone (PDE3I)
o Levosimendan, omecamtiv
 Neurohormonal antagonist – Tolvaptam- given
when decrease ang Sodium dahil sa dilutional
hyponatremia, this will increase the sodium
ADHF (Acute decompensated heart failure)
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
T1
HFpEF
Treatment
HFrEF
 Neurohormonal antagonist
o ACEI and BB
 Mineralocorticoid antagonists- prevent fibrosis and
remodeling of the heart
o Eplerenone or spironolactone (has an
effect in the endocrine system causing
gynecomastia)
 RAAS therapy and neurohormonal escape
 Vasodilators
o Hydralazine (kung meron emergency or
hypertensive crisis and if the
PREGNANT), nitrates
 Heart rate modification
o Ivabradine- meron stop clock kung na
reach na ang normal heart rate di na niya
i-further reduced pa, but the drawback
based on my personal experience, it can
cause arrythmia and atrial fibrillation
o Digoxin
 Diuretics
 CCB
 Inflammatory cytokines (infliximab, etanercept)-
kung mayaman ang pasyente
 Statins
 Anticoagulants/Antiplatelet- if caused by MI and to
prevent stroke
 Fish oil- subs to statins if they have liver disease
 Micronutrients – thiamine and selenium-
antioxidant property
 Enhanced external counter pulsation
 Exercise (minimum lang)
Management of selected co-morbidity
 Sleep disordered breathing (give CPAP)
 Anemia
 Depression – sertraline
 Atrial arrhythmias – amiodarone, dofetilide
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MED | HEART FAILURE T1
 Cardiac resynchronization therapy
o Ventricular dyssynchrony
 Sudden cardiac death prevention
o ICD
 Surgical therapy
o CABG, SVR
 Mitral regurgitation repair
 Gene therapy
 Vaccine (dahil one cause na nagiging unstable ang
stable patient ay dahil sa infection so give
pneumococcal vaccine)

COR PULMONALE
(problema sa lungs na nag lead sa Right-sided HF)
 Pulmonary heart disease
 Altered RV structure and/or function in chronic lung
disease
 Triggered by the onset of pulmonary hypertension
 Exclude congenital heart disease and those
diseases in which the right heart fails secondary to
dysfunction of the left or right side of the heart

Etiology and Epidemiology

 Develops in response to acute or chronic changes
in the pulmonary vasculature and/or the lung
parenchyma
 Cause pulmonary hypertension
» Kung mataas ang pressure sa pulmonary, it
will reflect in the RV which will be reflected
back to the RA
» Lahat ng pressure sa lungs it will be reflected
backward
» Acute cause: DVT
» Chronic cause: COPD, chronic infection
 True prevalence difficult to ascertain:
o Not all patients with chronic lung disease
will develop cor pulmonale
o Diagnosis routine physical examination
and laboratory testing is relatively
insensitive
*** Advances in 2D echo/Doppler imaging and biomarkers
(BNP) make it easier to screen for and detect cor
pulmonale
Symptoms
Pathophysiology
 Pulmonary hypertension – common mechanism
 PAP – >15mmHg
Parenchymal Dse, 1 pulmonary vascular d/o, Chronic
Alveolar Hypoxia
Vascular remodeling, Vasoconstriction and Destruction
» Symptoms just like Right-sided HF, the most
common is DYSPNEA. Difference? Makikita sa 2D
echo na maganda ng RV function but the LV
function is bad.
» ACZ wave sa Jugular vein
» A wave- atrial contraction
» C wave- caused by bulging of the tricuspid valve
(lesser compliance) during the attempt of
ventricular contraction
» Z wave- tricuspid regurgitation, 3rd possible bump
 Related to the underlying pulmonary disorder
 Dyspnea – the most common symptoms:
o Increased work of breathing ------ changes
in elastic recoiled
o Altered respiratory mechanics---- vascular
disease
 Orthopnea and PND
 Abdominal pain and ascites
 Lower-extremity edema

Signs
PAP and RV afterload increase  Tachypnea
 Elevated jugular venous pressure
 Hepatomegaly and lower-extermity edema
COR PULMONALE  Prominent V waves
 RV heave
 Carvallo’s sign- holosystolic murmur, present when
you ask the px to inhale, there will increase venous
6
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
MED | HEART FAILURE T1
return and will add up to the volume present in RA o Tamponade
and RV so ang mangyayari is there will be louder
murmur bec mas marami ang vol sa RA na bumalik;
pathognomotic of RV failure
 Cyanosis is a late finding
o Secondary to a low cardiac output
o Systemic vasoconstriction and VQ
mismatch

Diagnosis
 EKG- tending of P wave, tall R wave, deep S
 Chest Ct scan- dun malalaman kung may
pulmonary embolism sa bifurcation ng pulmonary
artery
 MRI- better to see RV
 2D echo with Doppler study
 Right heart catheterization- to know the pressure
sa right side ng heart
 BNP- increase when there is RV overload

Treatment
 The primary treatment goal of cor pulmonale is to
target the underlying pulmonary disease
 General principles of treatment include noninvasive
mechanical ventilation and bronchodilators
 Treat infection
 Adequate oxygenation (oxygen saturation 90-92%)
and correcting respiratory acidosis are vital for
decreasing pulmonary vascular resistance and
reducing demands on the RV
 Transfused if they are anemic

CARDIOGENIC SHOCK
 Most common etiology – severe left ventricular
dysfunction
 Leads to pulmonary congestion and/or systemic
hypoperfusion
 Characterized by systemic hypoperfusion
o Severe depression of the cardiac index
(<2.2 [L/min]/m2) thru 2D echo
o Sustained systolic arterial hypotension
(<90 mmHg) despite an elevated filling
pressure [PCWP] >18mmHg
 Caused by primarily myocardial failure
 Most commonly secondary to acute myocardial
infarction
 Less frequently by cardiomyopathy or myocarditis,
cardiac tamponade (>50ml fluid in the pericardial
cavity decreases relaxation of the heart), or critical
valvular heart disease
 50% - mortality
 Rate complicating acute MI was 20%
 But decrased to 5-7% due to increasing use of early
repurfusion therapy like streptokinase and early
angioplasty
 Most common with STEMI
 LV failure accounts account for ~80% of cases of
CS complicating acute MI
o Acute severe mitral regurgitation- most
common
o Ventricular septal rupture
o Predominant right ventricular (RV) failure,
and free wall rupture
7
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
MED | HEART FAILURE T1
 Release of inflammatory cytokines, inducible nitric  Reduction of preload
oxide synthase, and excess nitric oxide and o Diuretics, nitrates, morphine, ACEI,
peroxynitrite natriuretic peptide
 Lactic acidosis and hypoxemia worsen myocardial  Dangling legs (wag itaas ang paa, lalong mag HF,
ischemia and hypotension ayaw mo mag cause ng venous return)
o Severe acidosis reduces the efficacy of  Inotropic agents- best dobutamine
endogenous and exogenous  Digitalis
catecholamines  IABP
 Refractory sustained ventricular or atrial  Antiarrhythmic
tachyarrhythmias

ABG of CS px: metabolic acidosis REFERENCES:

1. Dr. Asuncion- Viado’s PPT
Patient profile 2. Recordings
TRANSCRIBED BY:
 Age, sex (female mas prone sa CS), co-
1. AGBAYANI, John Mark Kenneth N.
morbidities, early MI state, non-obstructing 2. ALSONG, Fides Angeli C.
myopathy, location of MI (anterior LV- 3. CAJIGAL, Haidee Jane L.
magshoshock mgt: volume, RV- magshoshock din 4. CAMPOL, Irene P.
mgt: inotropic agents) 5. CANUTO, Guiller Ivo E.
 Early MI or late of first day 6. CASTRO, Maricris T.
 Due reinfarction, expansion of MI or its 7. CEÑIDOZA, Daryl Anne I.
complications

Clinical Findings
Pulse is weak, mababa and BP, if the px is having severe
bradycardia it is due to RV infarction
 Dyspnea and appear pale, apprehensive,
diaphoretic and maternal status may be altered
 Pulse weak and rapid (90-110 bpm)
 Severe bradycardia due to high-grade block
 Systolic BP reduced (<90mmHg or > 30mmHg
below baseline)
 Narrow pulse pressure (<30mmHg)
 Tachypnea, chyne-stokes respirations
 Jugular venous distention
 Weak apical pules
 Soft S1 and S3 gallop
 Systolic murmurs
 Rales
 Oliguria

Diagnostics
 Laboratory
o WBCm Crea, liver enzymes, lactic acid,
ABG, cardiac markers
 ECG – ST elevation, Q waves, arrhythmias
 CXR – size of heart, congestion, effusion, kerley B
lines
 ECHO
 Swan ganz
 Cardiac catheterization

Treatment
 Vasopressors
 Mechanical ventricular support
o VA ECMO (parang dialysis machine for
the heart) or IABP (intra-aortic balloon
pump- we want to inflate the balloon
during DIASTOLE, pag na inflate during
systole magkaka HF dahil mataas ang
BP)
 O2 therapy with or without mechanical ventilation

8
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”
MED | HEART FAILURE T1

9
AGBAYANI | ALSONG| CAJIGAL | CAMPOL | CANUTO | CASTRO | CEÑIDOZA
“Stab the body and it heals, but injure the heart and the wound lasts a lifetime.”