ANATOMY

1. Basic anatomy of mediastinum

Thoracic cavity- consists of 2 lateral pleural cavities and a central mediastinum
MEDIASTINUM
● occupied by the mass of tissue between the two pulmonary cavities
● central compartment of the thoracic cavity
● Covered on each side by mediastinal pleura, contains all thoracic viscera and structures EXCEPT the lungs
● highly mobile region- consists of hollow visceral structures united by loose CT, often infiltrated with fat
● looseness of CT- allows to accommodate movement, pressure and volume changes in thoracic cavity
● Divided into SUPERIOR and INFERIOR mediastinum
SUPERIOR MEDIASTINUM: transverse thoracic plane (sternal angle to T4 vertebra)
Contents: Thymus, Trachea, Esophagus, Aortic arc, Brachiocephalic trunk, Left common carotid artery, Left subclavian artery,
Internal thoracic arteries, SVC, Left superior intercostal vein, Brachiocephalic veins, Phrenic & Vagus nerves, Left recurrent
laryngeal branch of the left vagus nerve
INFERIOR MEDIASTINUM: bet. transverse thoracic plane & diaphragm (larger than superior)
● WAnterior - posterior to body of sternum and anterior to pericardium
● Middle - pericardium, heart and its vessels (ascending aorta, pulmonary trunk, SVC)
● Posterior - posterior to pericardium and anterior to vertebrae, Esophagus and esophageal plexus, Thoracic aorta and its
branches, Azygos and hemiazygos venous systems, Thoracic duct
** WIDENING OF INFERIOR MEDIASTINUM- due to enlargement/hypertrophy of heart during congestive heart failure, viewed in chest
radiographs
2. Basic anatomy of pericardium and pericardial cavity
PERICARDIUM
● fibroserous membrane that covers the heart and beginning of great vessels
● closed sac,
● composed of two layers:
- Fibrous pericardium- tough external, inelastic, attached anteriorly and inferiorly to the sternum and diaphragm
- holds the heart in its middle mediastinal position and limits expansion of heart
- Serous pericardium-composed of mesothelium, lines the internal surface of fibrous p. and external surface of heart
- glistening lubricated surface allows heart free movement required for its “wringing out” motions during contraction
- Parietal layer - lines internal surface of fibrous p., sensitive
- pain impulses conducted from it by somatic phrenic nerves result in referred pain sensation
- Visceral layer- layer reflected onto the heart at greater vessels (aorta, pulmonary trunk and veins, SVC, IVC)
- Forms the epicardium (outermost of 3 layers of heart wall)
Arterial supply: pericardiophrenic artery (branch of internal thoracic artery)
- smaller contribution- musculophrenic a,bronchial, esophageal, superior phrenic a, coronary arteries
(visceral layer only)
Venous drainage: pericardiophrenic vein, azygos venous system
Nerve supply: phrenic nerves, vagus nerves, sympathetic trunk
PERICARDIAL CAVITY
● Potential space between opposing layers of parietal and visceral layers of serous pericardium
● Normally contains a thin film of fluid that enables heart to move and beat in a frictionless environment
● Contains 15 to 50 mL of ultrafiltrate of plasma- “if serous in its characteristic, cause is usually CHF”
3. Discuss the chambers of the heart and its borders
CHAMBERS OF THE HEART
● Right Atrium
○ Consists of 2 regions:
■ Auricle: Main concavity and small outpouching
■ At the region of the junction between these two parts, on the outer side, there is a vertical groove called the
sulcus​ terminalis​. The inner side forms a ridge called ​cristae terminalis
■ The main part of the Atrium lies posterior to crista terminalis and is derived embryologically from ​sinus
venosus​. The part of the atrium, which lies in front of crista terminalis, is roughened by bundles of muscle
fibers, ​musculi pectinati​. The anterior part is derived embryologically from ​primitive atrium.
○ Openings in the right atrium​:​ There are four openings in the right atrium that are described below:
● Opening for superior vena cava: It lies in the upper part and has no valves
 ● Opening for inferior vena cava: It lies in the lower part and is guarded by a rudimentary, and nonfunctioning
valve.
● Opening for the coronary sinus: It lies between the opening for inferior vena cava and the atrioventricular
orifice. It is also guarded by a rudimentary, nonfunctioning valve.
● Right atrioventricular orifice: It lies anterior to the opening for inferior vena cava and is guarded by the
tricuspid valve.
● Right Ventricle
○ Mas makapal ang walls ng right ventricle kaysa sa right atrium.
○ Have projecting ridges called ​trabeculae corneae​ and they give the walls spongy appearance. They have 3 types:
■ Type 1: consists of papillary muscles, which project inward. Their bases are attached to the ventricular wall
while their apices are attached as fibrous chords, known as ​chordae tendinae​, to the cusps of the tricuspis
valve
■ Type 2: same as type 1 except free sila sa middle. They have a ​moderator band that crosses the entire
ventricular cavity from septal to anterior wall.
■ Type 3: simply composed of ​prominent ridges
○ Openings in the right ventricle: There are ​two openings in the right ventricle​: the ​right atrioventricular orifice
(guarded by tricuspid valve) and the opening for the ​pulmonary trunk​ (guarded by pulmonary valve).
■ Tricuspid valve: It consists of three cusps each of which is formed by a fold of endocardium with a little
amount of connective tissue enclosed. The bases of all three cusps are attached to the fibrous ring of the
skeleton of heart and their free edges are attached to chordae tendineae. Chordae tendineae connect them
to the papillary muscles, which prevent the cusps from being forced into the atrium of turning inside out
during ventricular contraction.
■ Pulmonary valve: ​It guards the pulmonary orifice that leads to pulmonary trunk. It also consists of three
cusps with similar formation, however, in this case the cusps are semilunar in shape. The curved lower
margins and sides of each cusp are attached to the arterial wall and their open mouths are directed into the
pulmonary trunk. No chordae tendinae or papillary muscles are associated with this valve. External to each
cusp, the wall of pulmonary trunk bulges out to form a sinus.
● Left Atrium
○ Similar to right atrium, it consists of a main cavity and the left auricle. In anatomic position of the heart, it is situated
behind the right atrium and ​forms a greater part of the base of the heart. The interior of the left atrium is smooth
but the auricle possesses muscular ridges as was the case with right atrium.
○ Openings in the left atrium: There are a total of five openings in the left atrium​, four of which are for the
pulmonary veins and one is the left atrioventricular orifice. The ​openings of the pulmonary veins are not guarded
by any valve​, however, the ​left atrioventricular orifice is guarded by bicuspid valve.

● Left Ventricle
○ It is the ​strongest chamber of the heart​. Mas makapal ito . The reason for extra thick walls is that the left ventricle
has to deal with high pressures. The pressure inside the left ventricle is about six times higher than that inside the
right ventricle. In cross section, the right ventricle is circular and consequently the right ventricle is crescentic. It is
because of the bulging of the interventricular septum into the right ventricle.
○ Openings in the left ventricle: There are two openings in the left ventricle: the left atrioventricular orifice (guarded
by mitral valve, also known as bicuspid valve) and the aortic opening (guarded by aortic valve).
○ Mitral valve: ​It consists of two cusps, which have a structure similar to the cusps of the tricuspid valve. The anterior
of the two cusps is larger and intervenes between atrioventricular and aortic orifices. The attachment of chordae
tendinae and papillary muscles is also similar to that of tricuspid valve.
○ Aortic valve: It is precisely similar to the pulmonary valve. Behind each cusp the aortic wall bulges to form an aortic
sinus.

● BORDERS OF THE HEART

○ Right Border - Right Atrium
○ Inferior Border - Left Ventricle and Right Ventricle
○ Left Border - Left Ventricle (and some of the left atrium)
○ Superior Border - Right and Left atrium and the great vessels
3 LAYERS OF THE HEART

● SUPERFICIAL TO DEEP
○ Endocardium: lining that covers the internal layer, 2 layers: 1st layer
lines heart chamber, 2nd layer is subendocardial CT
○ Myocardium: thick helical middle layer composed of cardiac muscle,
cardiomyocytes= rich in glycogen deposits and mitochondria
○ Epicardium: thin mesothelial layer of serous pericardium, nerves and
BV are found here

Moore 7th ed pg136

HISTOLOGY
1. Discuss the changes in heart muscle during MI and hypertension

The histology of myocardial infarction changes over the time-course of the disease. At time 0, there are no microscopic
histologic changes. Under light microscopy, within 0.5 to 4 hours, waviness of fibers at the periphery of the tissue is seen.
Glycogen is depleted. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema.At 12 to 24 hours, the
gross specimen becomes dark and mottled. There are contraction band necrosis and neutrophil predominance on
histopathology. At 1 to 3 days, there is a loss of nuclei, and at 3 to 7 days, macrophages appear to remove apoptosis cells. At
7 to10 days, granulation tissue appears. At 10 days and onward, there is collagen one deposition. After 2 months, the
myocardium is scarred.

https://www.ncbi.nlm.nih.gov/books/NBK459269/

Hypertensive heart disease is a constellation of abnormalities that includes left ventricular hypertrophy (LVH), systolic and
diastolic dysfunction, and their clinical manifestations including arrhythmias and symptomatic heart failure. The classic
paradigm of hypertensive heart disease is that the left ventricular (LV) wall thickens in response to elevated blood pressure as
a compensatory mechanism to minimize wall stress. Subsequently, after a series of poorly characterized events (“transition to
failure”), the left ventricle dilates, and the LV ejection fraction (EF) declines (defined herein as “dilated cardiac failure”)

https://dacemirror.sci-hub.tw/journal-article/030c6f3137cb1be81201a0bdd1ab5880/drazner2011.pdf

PHYSIOLOGY
1. Discuss the baroreceptors role in control of arterial blood pressure

A rise in arterial pressure stretches the baroreceptors and causes them to transmit signals into the central nervous
system. “Feedback” signals are then sent back through the autonomic nervous system to the circulation to reduce
arterial pressure downward toward the normal level

After the baroreceptor signals have entered the tractus solitarius of the medulla, secondary signals inhibit the
vasoconstrictor center of the medulla and excite the vagal parasympathetic center. The net effects are (1)
vasodilation of veins and arterioles throughout the peripheral circulatory system and (2) decreased heart rate and
strength of heart contraction. Therefore, excitation of the baroreceptors by high pressure in the arteries reflexly
causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in
cardiac output. Conversely, low pressure has opposite effects, reflexly causing the pressure to rise back toward normal.

In summary, the primary purpose of the arterial baroreceptor system is to reduce the minute-by- minute variation in
arterial pressure to about one-third that which would occur if the baroreceptor system was not present
Guyton (205-207) pdf page(226-228)

2. Discuss the changes in the ventricles during periods of fluid overload and dehydration
According to Frank Starling Law, the greater the heart muscle is stretched during filling, the greater the force of contraction and greater
quantity of blood pumped into the aorta. The stretching in turn causes the muscle to contract with increased force because the actin
and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. Also included in this principle is that
an increase in volume also increases heart pumping. ​Stretch of right atrial wall directly increases heart rate by 10-20 percent. ​(p. 119
Guyton)

The heart has limits for the cardiac output it can achieve. ​The normal human heart can pump 2.5x (13.5L) than normal before the
heart itself becomes a limiting factor for the cardiac output. (p. 247 Guyton)

While in left ventricular remodelling, ​volume overload or isotonic exercise can lead to eccentric LV hypertrophy. Eccentric LV
hypertrophy is characterized by increased cardiac mass and chamber volume. Relative wall thickness may be normal, increased, or
decreased. With eccentric hypertrophy, sarcomeres are added in series, and individual cardiomyocytes grow longer. (UpToDate)
There is virtually no isovolumic diastolic phase because the ventricle is filling throughout diastole. The isovolumic phase of systole is
also brief because of low aortic diastolic pressure.

Eventually, however, progressive volume overload increases EDV to the point that compensatory hypertrophy is no longer
sufficient and a decline in systolic function occurs.

In decreased or fluid dehydration in the ventricle, this would result in decreased stroke volume and cardiac output. Basically just the
opposite of what happens in overload: decreased stretch, decreased pressure, decreased volume, decreased fiber length of the
myocardium which results in decreased contraction.

3. To understand the relevance of pressure changes in chambers of the heart during the cardiac cycle. (Guyton 114-115)
Pressure changes in atria (pressure elevations)

A wave​(Atrial Systole)= caused by atrial contractions

C wave ​(Isovolumic contraction) = occurs when the ventricles begin to contract; it is caused partly by slight backflow of blood into the
atria at the onset of ventricular contraction but mainly by bulging of the AV valves backward toward the atria because of increasing
pressure in the ventricles.
V wave ​(Isovolumic Relaxation) = occurs toward the end of ventricular contraction; results from slow flow of blood into the atria from the
veins while the AV valves are closed during ventricular contraction. When ventricular contraction is over AV valves open allowing stored
atrial blood to flow rapidly into the ventricles and causing the v eave to disappear.

Pressure changes in ventricle

In ventricular systole large amount of blood in both atria because of closed AV valves so may mataas na pressure sa atria. After systole
ventricular pressure falls to their low diastolic values kasi walang blood sa ventricles (refer to pic). So habang nag iincrease pressure sa
atria napupush yung valve to open and allow blood to flow rapidly into the ventricles kaya tumaas biglas pressure sa ventricles. Tawag
jan rapid filling of the ventricles. Pag mataas na yung pressure sa ventricles ma close niya yung AV valve to prevent backflow then
aortic valves naman mag open hence ventricle pressure will decrease so mag close aortic valve. Repeat

4. To discuss the fundamental properties of the heart (Autorhythmicity, Conductivity, Excitability and Contractility) and
changes during diseased state
Autorhythmicity (Chronotropism) ​- Ability of the heart of self-excitation W/O ANY EXTERNAL STIMULUS.
- Generated by ​SA Node
- Produce changes in HR through firing rate of the SA Node
- Directly proportional to HR
 - Positive Chronotrophic Effect​ = INC HR
- Negative Chronotropic Effect​ = DEC HR
- 3 Phases
- Phase 4 (​Pacemaker Potential​)
- MAXIMUM Diastolic Potential
- Automaticity of Nodal Cells
- SLOW DEPOLARIZATION produced by ​Opening of Sodium Funny Channel
- = Sodium INFLUX
- TURNED ON ​by Repolarization from the preceding AP
- ENDS ​when it reaches ​-40mV​, the Threshold.
- Leakiness of the membrane to Sodium ​ that make it more positive
- Phase 0 (​Upstroke)
- DEPOLARIZATION
- TURNED ON ​when Threshold is met (​-40 mV​)
- Opening of the​ ​L-type Calcium Channel​ causing an ​UPSTROKE (DEPOLARIZATION)
- = Calcium INFLUX
- Phase 3 (​Repolarization​)
- Opening of the​ ​Potassium Channel ​and Closing of L-type Calcium Channel
- = Potassium Efflux
- = Cease Sodium and Potassium Influx
- So bakit sustained yung Action Potential?
- Due to continuous inward-leaking of Sodium and Calcium Ion
- This is also the reason why Hyperpolarization is not maintained FOREVER and NO RESTING MEMBRANE
POTENTIAL because sustained lang at -55 to -60 mV
READ GUYTON page 123-124 for more knowledge! :))

Conductivity ​(​Dromotropism​)
- Ability to ​CONDUCT IMPULSE
- Produce changes in Conduction Velocity.
- Relative to the PR interval
- Conduction of IMPULSE from SA Node to AV Node
- Positive Dromotropic Effect ​= Fast Conduction of Impulse from SA to AV = Fast Conduction of AP from Atria to Ventricle =
DEC. PR Interval
- Negative Dromotropic Effect ​= Slow Conduction of Impulse from SA to AV = Slow Conduction of AP from Atria to Ventricle =
INC. PR Interval
- HOW IMPULSE TRAVEL
- Impulse, after traveling the Internodal pathway, reaches the AV node about ​0.03s​ after its origin in the Sinus Node
- There is a delay of ​0.09s ​in the AV Node before it enters the penetrating portion of AV Bundle, where it passes the
Ventricles
- Another delay of ​0.04s​ occurs in the penetrating AV Bundle before entering the Left and RIght Bundle Branch
- There’s a total of ​0.16s ​delay from the Sinus Node to the AV Node before the excitatory signal (Impulse) reaches the ventricle
to elicit contraction
- 0.13s ​total delay in the AV Node and AV Bundle system.
- SIGNIFICANCE? ​Conduction delay is important cardiac impulse does not travel from the ATRIA into the VENTRICLES TOO
RAPIDLY. Thus, allowing more time for VENTRICULAR REFILL
- BAKIT MAY SLOW CONDUCTION? ​This is due to diminished number of GAP JUNCTIONS b/n successive cells in the
conduction pathways
- SA Node ​= 0.8m/s ; ​AV Node​ = 0.05m/s ; ​Purkinje System ​= 1.5-4m/s
- Purkinje System ​fast conduction velocity is helpful for the instantaneous transmission of the Cardiac Impulse throughout the
entire remainder of the Ventricular Muscle
READ GUYTON page 125-126 for more knowledge! :))

Excitability ​(​Bathmotropism​)
- Response to stimulus
- Ability of the Cardiac Cells to initiate AP in response to INWARD, DEPOLARIZING CURRENT
- Myocardial Cells
 - Excitable cells that responds to Stimulus
- STIMULUS
- Electrical Energy
- Mechanical Energy
- Chemical Energy
- RESPONSE
- Generates AP
- Conduct Impulses
- Contract
- CONTRACTION REQUIRES
- AP generated from SA Node
- ATP
- Calcium from ECF and SR
- Myocardial Cell Structure
- Have Striations of Dark and Light Bands
- Has ​Sarcomere ​as Contractile
- Has ​Sarcotubular System
- Cardiac SR is less developed compared to that of the Skeletal Muscles
- Has ​Intercalated disks
- Maintain Cell-to-cell adhesion bec of ​Junction Complex
- Desmosomes ​- Holds cell together
- Gap Junction ​- Allow rapid spread of APs and permeable to ions
Contractility ​(​Inotropism​)
- Intrinsic ability of Cardiac Muscle to develop force at a given muscle length
- Related to ​Intracellular Calcium Conc.
- Can be estimated by ​EJECTION FRACTION ​[ (​SV/EDV​) X 100 ]
- Positive Inotropic Agents ​= INC. Contractility
- Negative Inotropic Agents ​= DEC. Contractility

BIOCHEM

To discuss the role of Renin, Angiotensin and Aldosterone in fluid retention or excretion
- The RAAS is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as vascular
resistance. When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already
present in the blood) into renin and secrete it directly into circulation. Plasma renin then carries out the conversion of
angiotensinogen, released by the liver, to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the
angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.
Angiotensin II is a potent vasoconstrictor peptide that causes blood vessels to narrow, resulting in increased blood pressure.
Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the renal
tubules to increase the reabsorption of sodium and water into the blood, while at the same time causing the excretion of
potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases
blood pressure.

If the RAS is abnormally active, blood pressure will be too high. There are many drugs that interrupt different steps in this
system to lower blood pressure. These drugs are one of the primary ways to control high blood pressure, heart failure, kidney
failure, and harmful effects of diabetes.Renin activates the renin–angiotensin system by cleaving angiotensinogen, produced
by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin–converting enzyme
primarily within the capillaries of the lungs.

- RAAS helps regulate long-term blood pressure and extracellular volume in the body. Liver releases Angiotensinogen into the
circulation in response to low BP and adverse changes in sodium conc. Renin is an enzyme secreted by the kidney, it cleaves
angiotensinogen to form the inactive decapeptide Angiotensin I. Angiotensin Converting Enzyme (ACE), predominantly found
in the pulmonary circulation but is also produced in the vascular endothelium tissues (of kidney, adrenal gland, brain and
heart), carries out further transformation of Angiotensin I. ACE converts Angiotensin I into the vasoactive peptide Angiotensin
II. ACE also degrades bradykinin which is required for synthesis of a major vasodilator, nitric oxide. Angiotensin II binds AT1
receptors expressed on the surface of vascular endothelium and impairs nitric oxide synthesis as well, this causes
 vasoconstriction. Stimulation of AT1 receptor causes adrenal gland to release aldosterone resulting in sodium retention.
Sodium retention combined with vasoconstriction leads to increase in BP. Increase in BP signals kidney to reduce renin. AT2
receptors counteract the effect of AT1 receptor stimulation.
Source: ​https://youtu.be/bY6IWVgFCrQ

CASE QUESTIONS
1. Salient features and explain why
This is a case of a 65 year old male hypertensive patient presenting with the signs and symptoms of :

Pertinent Positives (+)

Pulmonary congestion as evidenced by exertional dyspnea and orthopnea, presence of bibasal rales on
auscultation
● Orthopnea
- Defined as dyspnea (difficult respiration) occurring in recumbent (leaning/resting) position
- Results from redistribution of fluid from splanchnic circulation and lower extremities into the
central circulation during recumbency. This results in an increase in pulmonary capillary
pressure.
● Exertional Dyspnea
- Early stages of HF: exertional dyspnea
- Mechanism is pulmonary congestion with accumulation of interstitial or intra-alveolar fluid.
- Other factors that contribute to exertional dyspnea: reductions in pulmonary compliance,
increased airway resistance, respiratory muscle and/or diaphragm fatigue and anemia.
● Bibasal rales
- Pulmonary crackles (rales or crepitations) result from the transudation of fluid from the
intravascular space into the alveoli.
- When present in patients without concomitant lung disease, rales are specific for HF. Pleural
effusions result from the elevation of pleural capillary pressure and the resulting transudation of
fluid into the pleural cavities.

Hepatic congestion as manifested in the liver edge being slightly tender on palpation and the presence of
fluid in the peritoneal cavity because of the (+) shifting dullness on PE.
● Flabby abdomen, liver slightly tender on palpation
- Hepatomegaly is an important sign in HF
- Enlarged liver is frequently tender and may pulsate during systole if tricuspid regurgitation is
present

Cardiomegaly because the ​apex beat is at the level of the 6th ICS​, left anterior axillary line when normally, it is
at the level of the 5th ICS, left midclavicular line.

(+) S3 at the apex

- Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure,
which is the most common cause of a S3. Associated dilated cardiomyopathy with dilated ventricles also
contribute to the sound
- S3 gallop is most commonly present in patients with volume overload (hypertension) who have
tachycardia and tachypnea and it often signifies severe hemodynamic compromise.

Venous congestion as seen in the development of ​(+) grade 2 bipedal edema with hyperpigmentation and
scaling predominantly on the medial aspect of the Ankles
- It is typically caused by one of two mechanisms. The first is venous edema, caused by increased
capillary filtration and retention of protein-poor fluid from the venous system into the interstitial space. The
other mechanism is lymphatic edema, caused by obstruction or dysfunction of lymphatic outflow from the
legs resulting in accumulation of protein-rich interstitial fluid. These two mechanisms can operate
independently or together.

Hypertensive ​(for 10 years)

Bilateral knee pain ​(worse on prolonged standing and walking long distance)
 Urinary urgency, urinary straining, and intermittency

(+) hard, nodular and enlarged prostate ​(may suggest prostate cancer)

(+) brown stool per examining finger, no blood

Pertinent Negatives (-)

(-) Diabetes mellitus, (-) bronchial asthma, (-) goiter, (-) headache, (-) chest pain, (-) palpitations, (-) epigastric
pain, (-) melena, (-) bowel movement changes, (-) dysuria, (-) tea colored urine, (-) ulcers, (-) lymphadenopathy, (-)
spider angiomata, (-) gynecomastia, Good S1 and S2, normal rate, regular rhythm, (-) no murmurs, full and equal
pulses, no cyanosis,, (-) warmth, tenderness, (-) bulge sign,. DRE: good sphincter tone, no masses, no
tenderness,

2. Primary diagnosis/diagnoses

- Congestive heart failure secondary to hypertensive heart disease with prostate cancer

3. Clues in the history and PE that helped you arrive at your diagnosis

- Patient is a known hypertensive for 10 years but not well controlled even on medication. He presented with exertional
dyspnea​, ​orthopnea​, ​bibasal rales, cardiomegaly, ascites ​and ​bipedal edema​.
- The patient is a 64 y/o male, which puts him at high risk in developing prostate cancer. And upon examination, a hard and
nodular enlarged prostate was observed.

4. In your diagnosis what would the expected finding in a chest radiograph and 12L ECG be
Main answer:
Chest Xray, we expect to see Cardiomegaly with the apex of the heart displaced to the left. There would also be prominent
bronchovascular markings because of the presence of pulmonary congestion. The costophrenic sulcus may also possibly be blunted if
there is pleural effusion.

A ​12-lead ECG​ will show left axis deviation to mean left ventricular enlargement as a result of poorly controlled hypertension​.

Congestive Heart Failure

- Result of insufficient output because of cardiac failure, high resistance in the circulation or fluid overload.
Stages of Congestive Heart Failure:

STAGE 1 Redistribution PCEP 13-18mmHg

- redistribution pulmonary vessels
- Cardiomegaly
- Broad vascular pedicle (non acute CHF)
- In a normal chest film with the patient standing erect, the pulmonary vessels supplying the upper lung fields are smaller and
fewer in number than those supplying the lung bases.The pulmonary vascular bed has a significant reserve capacity and
recruitment may open previously non-perfused vessels and causes distension of already perfused vessels. This results in
 redistribution of pulmonary blood flow. First there is equalisation of blood flow and subsequently redistribution of flow from the
lower to the upper lobes.

Source:​https://radiologyassistant.nl/chest/chest-x-ray-heart-failure

ECG - ​graphic representation of the electrical activity of the heart. It records only the depolarization (stimulation) and repolarization
(recovery) potentials generated by the “working” atrial and ventricular myocardium

ECG is from a 32-year-old female with recent-onset congestive heart failure and syncope. The ECG demonstrates a tachycardia with a
1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the
ventricles are driving the atria (ventricular tachycardia).At first glance, sinus tachycardia in this ECG might be considered with severe
conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely,
electrocardiographic morphology gives clues to the actual diagnosis of VT. These clues include the absence of RS complexes in the
precordial leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated
cardiomyopathy.
Source:
https://www.medscape.com/answers/163062-86279/what-are-the-possible-presentations-of-heart-failure-on-electrocardiography

This ECG was obtained from an elderly man with a history of congestive heart failure. He is hypertensive at 180/102, and short of
breath with bibasilar rales.

What is happening in left bundle branch block?

The bundle branch system in the left ventricle is not functioning, either permanently, temporarily or even intermittently. LBBB can even
be rate-related, occurring during fast rates or in premature beats. The septum is depolarized from right to left (which is opposite of
normal), and the right ventricle is depolarized quickly.

The wave of depolarization then travels from the right ventricle to and across the left ventricle. This cell-to-cell depolarization is much
slower than conduction that proceeds by way of the bundle branches. It causes a loss of synchronization between the right ventricle,
septum and left ventricle.
Source:
https://www.ems1.com/ems-education/articles/12-lead-ecg-case-elderly-man-presents-with-chf-hypertension-and-dyspnea-EVTX1x1Ttv
8aIoS5/

5. What other lab procedures would you request and what are your expected findings
Echocardiogram/Doppler – a non-invasive cardiac imaging that is essential for diagnosis, evaluation, and
management of heart failure. This test could help spot blood clots, pericardial fluid, and problems with the aorta, and detect
abnormalities such as heart muscle damage, heart defects, heart size, pumping strength, and valve problems.

The LV chamber dimensions, volume, and ejection fraction vary by gender. Normal EF in men 53%-73% and
54%-74% in women. EF of <30%-40% could be indicative of heart failure. The presence of left atrial dilation and LV
hypertrophy, together with LV diastolic filling is useful for the assessment of HF using 2D Echocardiogram.
 Parasternal long axis view from a middle-aged man with heart failure. It shows normal left ventricular cavity
dimension with increased wall thickness and enlarged left atrium. The left ventricular systolic function was well preserved.
There was a small amount of pericardial effusion (*) circumferentially and large pleural effusion (PL). LA=left atrium, RV=right
ventricle, VS=ventricular septum.
Source: ​https://academic.oup.com/ehjcimaging/article/8/1/4/2397854

Routine Laboratory Testing ​- patients with new-onset HF and those with chronic HF and acute decompensation should have
a complete blood count, a panel of electrolytes, blood urea nitrogen, serum creatinine, hepatic enzymes, and a urinalysis. Selected
patients should have assessment for diabetes mellitus (fasting serum glucose or oral glucose tolerance test), dyslipidemia (fasting lipid
panel), and thyroid abnormalities (thyroid-stimulating hormone level).

Biomarkers ​- Circulating levels of natriuretic peptides are useful and important adjunctive tools in the diagnosis of patients
with HF. Both B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP), which are released from the failing heart, are
relatively sensitive markers for the presence of HF with depressed EF; they also are elevated in HF patients with preserved EF, albeit to
a lesser degree.

6. As a 5 star bedan physician, how are you going to help the px after his treatment
General Practitioner – recognizing the severity of cardiovascular diseases; encouraging the patient of behavioral change for
prevention by establishing the patient’s drive for lifestyle change; overmedication is avoided for medication maintenance to prevent
false sense of security
Researcher – ​working towards the improvement of healthcare outcome in cardiovascular medicine lol what else
Leader ​- establishing goals with the patient about maintenance after treatment and assuring ethical and cost-effective
technology and health care for the patient; working with multidisciplinary team for health and social development
Educator ​- educating the people how heart disease is still the leading cause of death and how they can lower the risk of heart
disease by something as simple as a lifestyle change, such as maintaining a healthy diet and regular exercise
Social advocator ​- being an advocator of barangay health program wherein people who cannot access proper healthcare
could receive free blood pressure, blood glucose tests, vaccinations, and etc. idk tama ba ‘to