ALTERATIONS IN

OXYGENATION

■ Eric B. Panopio, M.D.

The Red Blood Cell
The RBC

❖ a.k.a “erythrocytes”
❖ contain the O2 – carrying hemoglobin
❖ live only about 120 days
❖ healthy adult male – 5.4 million RBC
per (ml) of blood
❖ healthy adult female – 4.8 million
 RBC
■ function: to transport oxygen from lungs to
tissues
■ RBC production
☛ regulated by erythropoietin
☛ requires iron, vitamin B12, & folate
☛ occurs in the bone marrow
■ lifespan: 120 days
■ heme is converted to bilirubin & removed by
the liver through bile
 RBC ANATOMY
♥ RBC’s are biconcave discs with a diameter
of 7.8 mm
♥ RBC’s lack a nucleus
♥ can neither reproduce nor carry on
extensive metabolic activities
♥ are highly specialized for their O2 transport function
♥ lack mitochondria & generate ATP aerobically
♥ each RBC has 280 million hemoglobin molecules
♥ each hemoglobin can carry up to 4 O2 molecules

RBC
Physiology
 HEMOGLOBIN

Magnified Hemoglobin Crystals

➢ hemes – non-protein pigments

➢ globin – protein
➢ transport about 13% of the total CO2
➢ regulates blood flow & blood pressure
Erythropoiesis:
PRODUCTION OF RBC’s
Red Bone Marrow

Proerythroblast

Reticulocyte

Mature RBC
Main Stimulus
for
Erythropoeisis:
HYPOXIA
 Some stimulus disrupts
Homeostasis by
decreasing
O2 delivery to kidneys
(and other tissues)

Receptors
kidney cells detect low O2 level
Increased erythropoeitin
input secreted into blood
Control center
Proerythroblasts in red bone marrow mature
more quickly into reticulocytes
More reticulocytes enter
output circulating blood

Effectors
Larger # of RBC’s in circulation

Increased O2 delivery to tissues

 Anemia
■ a deficiency of red cells or hemoglobin
■ results from:
☛ excessive loss
☛ increased destruction
☛ impaired RBC production
■ blood loss anemia: loss of iron-containing
RBC’s from the body
■ hemolytic anemia: destruction of RBC with
iron being retained in the body
 Anemia
■ a condition of an abnormally low number of
circulating RBC or hemoglobin level, or both
■ manifestations – caused by:
☛ decreased hemoglobin in the blood
☛ tissue hypoxia due to ↓ oxygen transport
☛ recruitment of compensatory mechanisms

(tachycardia, palpitations) to increase oxygen

delivery to tissues
► An abnormally low # of circulating RBC’s or hemoglobin
level, or both, resulting in diminished O2 – carrying
capacity

►results from:
►excessive loss (blood loss anemia)
►increased destruction (hemolytic anemia)
►impaired production of RBC’s (IDA,
megaloblastic & aplastic anemia)
 Manifestations of ANEMIA:
✦ impaired O2 transport
✦ alterations in red cell
structure
✦ s/s associated with the
pathologic process

The background cells in this

micrograph are erythrocytes
(red blood cells). These
cells are non-nucleated,
biconcave discs that are filled
with hemoglobin.

Sickle cell anemia is an

inherited condition which
results in some erythrocytes
being malformed.
► iron & other components of the erythrocyte are lost
from the body
❖ ACUTE BLOOD LOSS
➢ carries a risk of hypovolemia & shock
➢red cells are normal in size and color

❖ CHRONIC BLOOD LOSS

➢ does not affect blood record volume but leads
to IDA when iron stores are depleted
 Blood Loss Anemia
■ may be acute or chronic
■ iron & other erythrocyte components are lost
from the body with bleeding
 premature destruction of red cells,
with retention in the body of iron & the
other products of red cells destruction
 Hemolytic Anemia
■ char by premature RBC destruction, with retention in
the body of iron & other products of RBC destruction
■ can be caused by:
☛ defects in RBC membrane
☛ hemoglobinopathies (sickle cell, thallasemia)
☛ inherited enzyme defects (G6PD def’cy)
■ acquired forms: due to extrinsic agents
drugs bacterial toxins
antibodies physical trauma
❖ INTRINSIC

➢defects of the red cell

membrane
➢various hemoglobinopathies
& inherited enzyme
defects

❖ EXTRINSIC
➢drugs
➢bacterial & other
toxins hemolytic anemia in the
➢ antibodies Microvasculature
physical trauma

❖ The person experiences :

➢ easy fatigability
➢ dyspnea
➢ mild jaundice
Hemolytic disease of the new born
 Iron-deficiency Anemia
■ char by ↓ Hb synthesis
■ can result from:
☛ dietary deficiency
☛ loss of iron through bleeding
☛ ↑ demands for RBC production
■ vitB12 & folic acid deficiency: impair cell
production by interfering with DNA synthesis
 IDA
❖ Common worldwide cause of anemia affecting persons
of all ages
❖ results from dietary deficiency, loss of iron through
bleeding or increased demands
❖ characterized by a low hemoglobin & Hct, decreased
iron stores, & low serum iron & fernitin

Manifestations:
❖ fatigability, palpitations, dyspnea, angina, &
tachycardia
iron deficiency anemia, atrophic glossitis
Treatment:
❖ increasing dietary intake of iron
❖administering supplemental iron
➢ ferrous sulfate
➢iron dextran

iron defeciency anemia,

peripheral smear
 Aplastic Anemia
■ is caused by bone marrow suppression
■ results in a reduction of white blood cells and
platelets, as well as RBC’s
 What is aplastic anemia?

Aplastic anemia occurs when the bone marrow

produces
too few of all three types of blood cells:
red blood cells,
white blood cells,
and platelets.
A reduced number of red blood cells causes
hemoglobin to drop
One fat cell. Aplastic anemia marrow
C ♦ history of specific infectious diseases such as
infectious hepatitis

A ♦ history of taking certain medications, such as

antibiotics and anticonvulsants

U ♦ exposure to certain toxins such as heavy metals

♦ exposure to radiation

S ♦ history of an autoimmune disease

E
♦ inherited condition

S
S ❖ headache
❖ dizziness

Y ❖ nausea
❖ shortness of breath

M
❖ bruising
❖ lack of energy or tiring easily (fatigue)
❖ abnormal paleness or lack of color of the skin
P ❖ blood in stool
❖ nosebleeds

T
❖ bleeding gums
❖ fevers
❖ sinus tenderness
O ❖ enlarged liver or spleen
❖ oral thrush - white patches on a red, moist,

M swollen surface, occurring anywhere in the

mouth.

S
 How is aplastic anemia diagnosed?

complete medical
history and physical
examination, diagnostic
procedures for anemia
include additional
blood tests and
a bone marrow
biopsy.

aplastic anemia,
bone marrow
Polycythemia is an increased volume of red blood cells.
The hematocrit is elevated by more than 55% in men or
more than 50% in women.

Symptoms:

✓Headache ✓blurred vision

✓tinnitus ✓angina
✓paresthesias ✓claudication
✓dizziness ✓dyspnea
✓fatigue ✓thrombophlebiatis
 Polycythemia
■ a condition in which the red cell mass is increased
■ types:
1. relative – due to loss of vascular fluid & is corrected
by replacing the fluid
2. primary/polycythemia vera – a proliferative bone
marrow disease with ↑ in total RBC mass and ↑
WBC & platelet counts
3. secondary – due to ↑ erythropoietin levels caused by
hypoxic conditions e.g. chronic heart & lung
diseases
 Hemoglobin
■ high concentrations at birth
■ gradually falls to minimal value at 2 mos.
■ during early neonatal life: shift from fetal to
adult hemoglobin
■ physiologic jaundice
☛ hyperbilirubinemia during 1st week of life
☛ related to: ↑ RBC breakdown
liver unable to conjugate bilirubin
 Kernicterus
■ due to elevated elvels of lipid-soluble,
unconjugated bilirubin, w/c can be toxic to
brain cells
■ treated with: phototherapy
exchange transfusion
 Hemolytic Disease of the
Newborn
■ occurs in Rh(+) infants of Rh(-) mothers who
have been sensitized
■ involves hemolysis of infant RBC in respose to
maternal Rh antibodies that have crossed the
placenta
■ sensitization prevented by: Rh immune
globulin administration to the mother 72 hours
of delivery of Rh+ infant, abortion, or
amniocentesis
 RBC Changes in Aging
■ decreased bone marrow cellularity
■ hemoglobin decrease
☛ decline is less in women
☛ orally administered iron is poorly used in the

elderly
■ underlying neoplasms: may contribute to
anemia
The Cardiovascular
System
 Gross Anatomy of the Heart
■ Borders of the Heart:
☛ right border: RA
☛ left border: LVpart of L auricle
☛ superior border: root of great vessels
☛ inferior border: RV, apical LV
■ Cardiac walls:
☛ endocardium
☛ myocardium
☛ epicardium
 Chambers of the Heart
■ RA
☛ receives blood from the SVC & the IVC
☛ coronary sinus: blood from walls of the heart
■ RV
☛ pumps blood via the pulmonic valve
☛ wall thicker than RA
☛ crescent-shaped
■ LA
☛ behind the RA
☛ drains into the LV guarded by the bicuspid or

mitral valve
■ LV
☛ circular in shape
☛ pumps blood into the systemic circulation

guarded by the aortic valve (semilunar valves)

Blood Flow Through the Heart
SVC, IVC, coronary sinus → RA → tricuspid
valve → RV → pulmonic valve → pulmonary
artery → lungs → pulmonary vein → LA →
bicuspid valve → LV → aortic valve → aorta
Flow of Blood to the Heart from Systemic Circulation
 Conductions System
1. SAN
☛ pacemaker of the heart, origin of excitation
☛ firing rate of 90 to 120 beats/min
2. AVN
3. Bundle of His or Atrioventricular bundle
4. Purkinje fibers
☛ possesses the highest conduction velocity
5. ventricles
 HR Determinants
■ Temperature
☛ intrinsic firing ↓ with cooling
■ Ions
☛ ↑intrinsic firing with ↑ potassium & ↓ calcium
■ Vagus nerve
☛ innervates SAN & liberate acetylcholine
■ Sympathetic nerves
 Heart Sounds
■ 1st heart sound
☛ closure of AV valves
■ 2nd heart sound
☛ closure of semilunar v.
■ atrial sound
☛ at the end of 1st diastole
☛ blood flow with a rumbling motion
 Arterial Coronary Circulation
■ Arterial circulation of the heart comes from the
right & left coronary arteries
■ Right coronary artery
☛ Nodal branch: SA node
☛ Marginal branch: RV, myocardium
☛ Posterior IV branch: RV/LV wall, IV septum
■ Left coronary artery
☛ Ant IV or L ant descending: RV/LV wall
☛ Marginal branch: IV septum
☛ Circumflex branch: LV & LA walls
 Coronary Arteries
Anterior View Posterior/Diaphragmatic View
 Venous Coronary Circulation
■ drains into three veins:
1. coronary sinus
2. anterior cardiac veins: IV septum, ant RV/LV
3. least cardiac veins: endocardium & myocardium
■ Coronary sinus
☛ great cardiac: IV septum, ant RV & LV
☛ lesser cardiac: marginal area, RA
☛ middle cardiac: IV septum, post RV & LV
■ Coronary sinus
☛ great cardiac: IV septum, ant RV & LV
☛ lesser cardiac: marginal area, RA
☛ middle cardiac: IV septum, post RV & LV
 Cardiac Innervation
■ Controlled by the ANS
■ Parasympathetic stimulation results in
decreased heart rate & stroke volume
■ Sympathetic stimulation results in increased
heart rate & stroke volume
 Preload
■ degree of tension on the cardiac muscle when it
begins to contract
■ is usually the end-diastolic pressure when the
ventricle is already filled with blood
 Afterload
■ the load against which the cardiac muscle
exerts its contractile force
■ is the pressure within the aorta and pulmonary
vein against which the ventricles have to
contract
 Frank Starling Mechanism
■ intrinsic ability of the heart to adapt to
changing volumes of inflowing blood
■ the greater the heart ms is stretched during
filling, the greater will be the force of
contraction and the greater the output to the
aorta
 Cardiac Output
■ amount of blood ejected by the LV into the
aorta per minute
■ equivalent to stroke volume X heart rate
 Stroke Volume
■ amount of blood ejected by the ventricle per
beat or systole
■ about 70 ml at rest
 Atherosclerosis
- characterized by irregularly distributed lipid
deposits in the intima of large and medium-sized
arteries; such deposits provoke fibrosis and
calcification. Set in motion when cells lining the
arteries are damaged as a result of high blood
pressure, smoking, toxic substances in the
environment, and other agents. Plaques develop
when high density lipoproteins accumulate at the
site of arterial damage and platelets act to form a
fibrous cap over this fatty core. Deposits impede
or eventually shut off blood flow.
 Myocardial Infarction

- infarction of an area of the heart

muscle, usually as a result of occlusion
of a coronary artery.
- Heart attack
 Distended Jugular Vein

- Indicates an abnormal increase in the

volume of the venous system.
- Usually associated with right-sided
Heart failure
 Aorta
- a large artery which is the main trunk of the
systemic arterial system, arising from the left
ventricle and ending at the left side of the body
of the 4th lumbar vertebra by dividing to form
the right and left common iliac arteries. The
aorta is made up of the ascending aorta, aortic
arch, and descending aorta, which is divided
into the thoracic aorta and the abdominal
aorta.
Origin
[Mod. L. fr. G. aortT, from aeirb, to
lift up]
 Aortic Aneurysm
- circumscribed dilation of an artery or a
cardiac chamber, a direct communication with
the lumen, usually due to an acquired or
congenital weakness of the wall of the artery
or chamber.
- circumscribed dilation of a cardiac chamber
usually due to an acquired or congenital
weakness of the wall of the heart.
Origin
[G. aneurysma (-mat-), a dilation, fr. eurys,
wide]
 Aortic Coarctation
- Severe narrowing of the aorta causing
the blood flow and blood pressure
downstream from the narrowing to be
reduced.
 Heart
Metastases
 Heart Myxoma
- a benign neoplasm derived from
connective tissue, consisting of
polyhedral and stellate cells embedded
in a soft mucoid matrix; occurs in bone,
skin, and muscle; when arising from
cardiac muscle may encroach on the
cavity of an atrium.
Origin
[myxo- + G. -bma, tumor]
 End:
Overview of Alterations in Oxygenation

Prepared by:
Eric B. Panopio, M.D.
ALTERATIONS IN
PULMONARY GAS
EXCHANGE

■ Eric B. Panopio, M.D.

Alteration in Ventilation &
Gas Exchange
 DISORDERS OF LUNG
INFLATION
■ Disorders of the pleura
■ Atelectasis
 PLEURAL PAIN
■ Pain is a frequent symptom of pleuritis, or inflammation of
the pleura.
■ Pleuritis is common in infectious processes such as viral
respiratory infections or pneumonia that extends to involve
the pleura.
■ It usually is unilateral and tends to be localized to the lower
and lateral part of the chest.
■ The pain is usually made worse by chest movement, such as
deep breathing and coughing.
 PLEURAL EFFUSION
■ Refers to an abnormal collection of
fluid in the pleural cavity.
Mechanisms that have been linked to the
abnormal collection of fluid in the pleural
cavity:

■ Increase capillary pressure

■ Increase capillary permeability
■ Decrease colloidal osmotic pressure
■ Increase negative intrapleural pressure
■ Impaired lymphatic drainage of the pleural
space
 Hydrothorax
■ Refers to the presence of fluid in one or
both pleural cavities, usually resulting from
cardiac failure.
 Empyema
■ Refers to pus in a body cavity; when used
without qualification, refers specifically to
pyothorax.
 CHYLOTHORAX
■ Refers to an accumulation of milky chylous
fluid in the pleural space, usually on the left.
 HEMOTHORAX
■ Refersto the presence of blood in
the thoracic cavity
 MANIFESTATIONS OF PLEURAL
EFFUSSION:
■ Signs of blood loss
■ fever
■ other signs of inflammations
 CHARACTERISTIC SIGNS OF
PLEURAL EFUSSION:
■ Dullness or flatness to percussion and
diminished breath sounds
■ Dyspnea
■ Pleuritic pain
■ Mild hypoxemia
 PNEUMOTHORAX
■ Refers to air in the pleural cavity
TYPES OF PNEUMOTHORAX
■ Spontaneous pneumothorax - occurs when an
air -filled bleb, or blister, on the lungs surface
ruptures.
■ Traumatic pneumothorax - maybe cause by a
penetrating or non penetrating injuries.
■ Tension pneumothorax - occurs when the
intrapleural pressure exceeds atmospheric
pressure.
 Collapse
Lung
Mediastinal
Shift
Absent Vascular
Markings

Pneumothorax
MANIFESTATIONS OF SPONTANEOUS
PNEUMOTHORAX

■ Ipsilateral chest pain

■ Increase respiratory rate
■ Dyspnea
■ Increased heart rate
■ Chest asymmetry
■ Hyperresonant sound upon chest percussion
■ Decreased breath sound or absent over the area of
pneumothorax.
 MANIFESTATIONS OF TENSION
PNEUMOTHORAX

■ Mediastinal shift
■ Distention of the neck veins
■ Clinical signs of shock
 ATELECTASIS
■ Refers to reduction or absence of air in part or
all of a lung, with resulting loss of lung
volume.
■ Pulmonary collapse: secondary atelectasis due
to bronchial obstruction, pleural effusion or
pneumothorax, cardiac hypertrophy, or
enlargement of other structures adjacent to the
lungs.
 MANIFESTATIONS OF
ATELECTASIS
■ Tachypnea
■ Dyspnea
■ Cyanosis
■ Signs of hypoxemia
■ Diminished chest expansion
■ Absence of breath sounds
■ Intercostal retractions
■ Fever and other signs of infections
 HYPOXEMIA
■ Refers to a reduction in blood oxygen levels.
■ Subnormal oxygenation of arterial blood, short
of anoxia.
 Causes of Hypoxemia
■ Inadequate amount of oxygen in the air
■ disease of the respiratory system
■ alterations in circulatory function
MANIFESTATIONS OF HYPOXEMIA
SIGNS AND SYMPTOMS OF HYPOXIA
■ tachycardia ■ Loss of judgement
■ mild ­ BP ■ euphoria
■ cool, moist skin ■ unruly or combative behavior
■ confusion ■ sensory impairment
■ delirium ■ mental fatigue
■ difficulty problem solving ■ drowsiness
■ stupor,coma (late)
■ hypotension(late)
■ Bradycardia (late)
 TYPES OF HYPOXIA
■ HYPOXEMIC HYPOXIA
■ CIRCULAORY HYPOXIA
■ ANEMIC HYPOXIA
■ HISTOTOXIC HYPOXIA
 HYPOXEMIC HYPOXIA
■ Refers to decrease oxygen level in the blood
resulting in decrease oxygen diffusion into the
tissues.
■ Causes:
 CIRCULATORY HYPOXIA
■ Hypoxia resulting from inadequate capillary
circulation.
■ Causes:
 ANEMIC HYPOXIA
■ Result of decreased effective hemoglobin
concentration, which causes a decrease in the
oxygen-carrying capacity of the blood.
 HISTOTOXIC HYPOXIA

■ Occurs when a toxic substance, such as

cyanide, interferes with the ability of tissues to
use available oxygen.
Hypoxemia, Cyanosis &
Hypercapnia
Hypoxemia
 - decreased sensory function, such as impaired vision or fewer
complaints of pain, may be an early sign of worsening hypoxemia.

CYANOSIS
- refers to the bluish discoloration of the skin and mucous membranes
that results from excessive concentration of reduced or deoxygenated
hemoglobin in the small blood vessels.
MARKED: lips, nail beds, ears, cheeks.
DEGREES: modified by the amount of cutaneous pigment, skin thickness,
and the state of the cutaneous capillaries.
**Difficult to distinguish in person with dark skin and in areas of the body
with increased skin thickness.
TYPES:
Central Cyanosis – evident in the tongue and lips
- it is caused by an increased amount of deoxygenated
hgb or an abnormal hgb derivative in the arterial blood
Peripheral Cyanosis – occurs in the extremities and on the tip of the nose
or ears.
DIAGNOSIS is based on clinical observation and diagnostic measures of
oxygen level.
TWO NON-INVASIVE METHODS FOR OXYGEN ASSESSMENT
1. Transcutaneous Sensor Method
- uses an oxygen electrode
2. Pulse Oximeter
- cannot distinguish between oxygen-carrying hgb and CO-
carrying hgb.
Central Cyanosis
Peripheral CYANOSIS
Pulse Oximeter
Cyanosis
HYPERCAPNIA
- refers to an increased in the CO2 content of the blood.
- diagnosis is based on physiologic manifestations, arterial pH, and
blood gas levels.
- can occur in a number of disorders that cause hypoventilation or
mismatching of ventilation and perfusion.
- hypoventilation is a cause of hypercapnia in respiratory failure due
to depression of the respiratory.
- due to ventilation-perfusion inequalities is seen most commonly in
persons with COPD.
Hypercapnia
Respiratory Failure
 MECHANISM
■ Respiratory failure – is a condition in which the
lungs fall to oxygenate the blood adequately
and to prevent carbon dioxide retention.
■ It is the result of number of condition that
impair ventilation and perfusion, or disrupt
blood flow in the lungs
 COMMON MANIFESTATION OF
RESPIRATORY FAILURE:

1.HYPOXEMIA- it can occur as a result

of hypoventilation, diffusion impairment,
shunt, and ventilation-perfusion
impairment.
 2. HYPERCAPNIA- 4 factors:
■ alterations in CO2 prodxn.
■ disturbance in gas exchange fxn of the lungs.
■ abnormalities in resp. fxn of the chest wall and
resp. muscles.
■ changes in neural control of respiration.
Acute Respiratory Distress
Syndrome
 Acute Respiratory distress syndrome
(ARDS)
■ Is a potentially lethal form resp. failure that can
follow severe shock.
SYMPTOMS:
■ usually do not develop until 24-48 hrs. after the
initial trauma.
■ RR and effort of breathing=increases

■ ABG=present profound hypoxemia and

hypercapnia.
 ETIOLOGY:
■ Exact cause is unknown
■ Neutrophils= are thought to play a major role
in the pathogenesis of ARDS.

■ * A cytokine-mediated activation and

accumulation of neutrophil in the pulmonary
vasculature and subsequent endothelial injury
is thought to cause leaking of fluid and plasma
protiens into the interstitium and alveolar
spaces.
Infant Respiratory Distress
Syndrome
 IRDS
■ A.k.a Hyaline membrane disease; Infant respiratory
distress syndrome (IRDS); Neonatal respiratory distress
syndrome; RDS – infants.
■ The most common lung disorders in premature infants
and causes increasing difficulty in breathing.
■ Affects 10% of all premature infants and only rarely
affects those born at full-term.
■ Caused by a lack of lung surfactant. **
■ Risk factors: prematurity, diabetes in the mother, and
stress during delivery.
 IRDS
Symptoms:
■ Rapid breathing
■ Unusual breathing movement
■ Shortness of breath
■ Nasal flaring
■ Bluish color of the skin
■ Arms or legs puffy or swollen
Sudden Infant Death
Syndrome
 SIDS

■ A.K.A Crib death

■ The unexpected, sudden death of any infant or child
under one year old, in which an autopsy does not
show an explainable cause of death.

CAUSES:
▪ cause of SIDS is unknown
 SIDS
Factors increase the risk of SIDS:

■ Babies who sleep on their stomachs

■ Babies who have soft bedding in the crib
■ Multiple birth babies
■ Premature babies
■ Babies with a sibling who had SIDS
■ Mothers who smoke or use illegal drugs
■ Teen mothers
■ Short intervals between pregnancies
■ Late or no prenatal care
■ Situations of poverty
 SIDS
Symptoms:
■ There are no symptoms. Babies who die of SIDS do
not appear to suffer or struggle.
Tests :
■ Autopsy results are not able to confirm a cause of
death, but may help add to the existing knowledge
about SIDS.
Prevention :  
■ Put babies to sleep on their backs. DO NOT put
babies to sleep on their stomachs.
■ Also avoid soft bedding.
Chronic Obstructive
Pulmonary Diseases
 Chronic Obstructive Pulmonary Disease

-- An umbrella term encompassing a cluster of diseases in which recurrent

obstruction of airflow is a prominent feature.

-- A common disorder usually characterized by airflow limitation that is

not fully reversible and a history of inhalation of such irritants as
tobacco smoke.

 -- 5th leading cause of death in the US

 Chronic Obstructive
Pulmonary Disease

Causes and Incidence:

Smoking, air pollution, and industrial exposure are
major risk factors.This disease constellation is the
fifth leading cause of death in the United States, and
the incidence and death rate are increasing.
 Chronic Obstructive
Pulmonary Disease

CLINICAL SYNDROMES

 Type A COPD
-- Referred to as pink puffers
-- Predominant emphysema, progressive exertional dyspnea,
weight loss
-- Little improvement with bronchodilators
-- Symptoms show at a relatively old age (>60)
 Chronic Obstructive
Pulmonary Disease

Type B COPD

-- Referred to as blue bloaters

-- CLINICAL PICTURE:
predominant bronchitis chronic cough
expectoration episodic dyspnea
frequent wheezing/bronchi weight gain

DIAGNOSIS: Pt’s history, Signs and Symptoms, Spirometric Screening, PE:

hyperinflation, poor diaphragmatic movement, use of accessory muscles of
respiration, decreased breath sound and wheezing.
 Chronic Obstructive
Pulmonary Disease

TREATMENT: Bronchodilation: B-adrenergic agonists;

Corticosteroid therapy; Sputum mobilization; Management of
infection.
 
PREVENTION: Avoidance of smoking
 
COMPLICATIONS: Pneumonia, bronchogenic carcinoma,
polycythemia, respiratory failure, infection, general disability
 Emphysema
-- A chronic obstructive pulmonary disorder characterized by permanent
anatomic alteration of the airway spaces distal to the conducting
airways.

Causes and Incidence: Any factor that leads to chronic alveolar

inflammation can serve as a precursor for the formation of
emphysematous lesions. Common precursors are tobacco smoking;
air pollution, particularly in an occupational setting; underlying
respiratory disease; and severe respiratory infection in early
childhood. A rare congenital alpha1-antitrypsin deficiency also is a
precursor. Emphysema is the leading cause of death from respiratory
disease in the United States. The incidence increases with age and is
highest in white, male, blue-collar workers.
 Emphysema
Disease Process: Recurrent alveolar inflammation leads to
degradation of the elastin in the distal airways because of an
imbalance in the elastase-antielastase mechanism. As the
degradation proceeds, elastic recoil is lost, the alveolar walls are
destroyed, blood vessel density is reduced, the air spaces enlarge,
and the peripheral bronchioles collapse; this leads to air trapping
and impaired gas exchange.

Symptoms: Emphysema is thought to begin in early adulthood and

remain asymptomatic until middle age. Gradual progressive
exertional dyspnea is the most common presenting complaint.
Chronic productive coughing, wheezing, recurrent respiratory
infection, and fatigue may also be present. Severe dyspnea and
cyanosis are late signs.
 Emphysema

Potential Complications: Alveolar blebs and bullae may form and

rupture, leading to pneumothorax. Cor pulmonale and heart failure
may also occur.

Diagnostic Tests: Clinical evaluation: History of smoking,

occupational exposure; Radiology: Normal in early disease;
localized radiolucency with decreased vascular markings;
Pulmonary function: Total lung capacity, residual volume, and
functional residual capacity, increased compliance; decreased
forced vital capacity and forced expiratory volume; Arterial blood
gases: Decreased PaO2; normal PaCO2 until late in disease, when
it increases
 Emphysema
Treatments: Drugs: Bronchodilators to promote mucus clearance;
anti-infective drugs to treat secondary bacterial infection; flu and
pneumonia vaccines for prophylaxis; antitrypsin replacement
therapy for individuals with demonstrated deficiency
(experimental); General: Removal of irritants; chest
physiotherapy, vaporizer to loosen secretions; low-level oxygen
to treat hypoxemia, with careful monitoring of blood gases for
rise in PaO2 without rise in PaCO2; consistent exercise to
improve ventilatory and cardiac function; counseling for
depressive episodes.
 
 Normal lung

Centri-acinar emphysema
 Chronic Bronchitis
Symptoms: Chronic bronchitis may be asymptomatic for years. A
productive cough and exertional dyspnea are typical presenting
signs. The cough becomes increasingly progressive and the
sputum production copious; several attacks a year are common.
Chest retractions, wheezing, tachypnea, and cyanosis may also be
present.
 
Potential Complications: Cor pulmonale, pulmonary hypertension,
right ventricular hypertrophy, and respiratory failures are
common complications.
 Chronic Bronchitis
Diagnostic Tests: Clinical evaluation: History of chronic lung irritation (e.g.,
smoking, occupational exposure); Radiology: Increased markings,
hyperinflation; Pulmonary function: Residual volume increased, forced vital
capacity and forced expiratory volume decreased; compliance and diffusion
normal; Arterial blood gases: PaO2 decreased, PaCO2 increased; Sputum:
Culture of multiple microorganisms and neutrophils.

Treatments: Drugs: Anti-infective drugs for any infection; bronchodilators to

reduce dyspnea; corticosteroids to reduce inflammation; flu and pneumonia
vaccines for prophylaxis; General: Removal of irritant; chest physiotherapy to
loosen secretions; vaporizer and increased fluids to liquefy secretions;
oxygenation for hypoxia; consistent exercise to improve ventilatory and cardiac
function
 Chronic Bronchitis
-- An obstructive pulmonary disorder characterized by a
chronic and recurrent productive cough for at least 3
months during each of 2 successive years.
 
Causes and Incidence: Bronchial irritants (e.g., cigarette
smoke) in conjunction with a genetic predisposition
are thought to be the chief cause.
 
 Chronic Bronchitis
Disease Process: Chronic irritation leads to hypersecretion and
hypertrophy of the bronchial mucous glands and an increase in
the size and number of goblet cells. These cells invade the
terminal bronchioles, damaging cilia, increasing sputum and
bronchial congestion, and narrowing the bronchial lumen. As
the disease progresses, leukocytes invade the secretions,
aggravating the edema and eventually causing tissue necrosis.
Granulated squamous epithelium replaces ciliated epithelium
and fibroses, leading to tissue scarring, stenosis, and airway
obstruction and a severe ventilation-perfusion imbalance.
 Cor Pulmonale (Pulmonary Heart
Disease)
-- Acute right heart strain or chronic right ventricular hypertrophy with or
without heart failure resulting from disease states which affect the
function and/or structure of the lungs and cause pulmonary
hypertension.
-- Refers to a structural or functional alteration of the right ventricle as a
result of pulmonary disease.

CAUSES: Any disease affecting the lungs and accompanied by

hypoxemia may result in cor pulmonale. The most frequent is severe
COPD. Other causes are conditions that restrict or compromise
ventilatory function leading to hypoxemia or acidosis, or conditions
that reduce the pulmonary vascular bed. Certain disorders of the
nervous system, respiratory muscles, chest wall, and pulmonary
arterial tree may also be responsible for cor pulmonale.
 Cor Pulmonale (Pulmonary Heart
Disease)
CLINICAL PRESENTATION: Early in the course: symptoms
only occur in association with exercise. Physical findings:
peripheral edema, liver enlargement, and neck vein
engorgement.

DIAGNOSIS: X-ray: widened pulmonary arteries; ECG

 
TREATMENT: Supplemental oxygen, diuretics, and vasodilators
 
 Bronchiectasis

-- An irreversible dilation of the tracheobronchial tree, with destruction of

the bronchial walls.

Causes and Incidence: Bronchiectasis is caused by conditions that

repeatedly damage the bronchial walls and interfere with clearance of
bronchial secretions, such as cystic fibrosis, immune-deficiency
diseases, repeated respiratory tract infections, tuberculosis, inhalation
of noxious gases, repeated aspiration pneumonia, and complications of
measles and pertussis. Rare congenital anomalies may also be a cause.
The incidence has declined dramatically since the introduction of
antibiotics. Children are most vulnerable, and the incidence is highest
among Inuit and Maori populations.
 Bronchiectasis

Disease Process: Repeated inflammatory and infectious

processes slowly alter the structure of the bronchial walls,
diminishing cilia and impairing the ability to clear secretions,
increasing mucus production, reducing elasticity and muscular
response, and causing permanent dilation of various areas in
the tracheobronchial tree.

Symptoms: The individual is often asymptomatic early in the

disease. A chronic cough with sputum production is the most
common presenting sign. Hemoptysis and recurrent
pneumonia are also common, as are dyspnea, wheezing, and
fatigue.
 Bronchiectasis
Potential Complications: Pulmonary hypertension, right ventricular failure, and cor pulmonale
are common complications with long-standing disease.

Diagnostic Tests: Clinical examination: Chronic cough, mucopurulent sputum, hemoptysis,

moist rales, rhonchi; Sputum: Foamy with sediment; large number of WBCs; Radiology:
Chest x-ray shows increased markings, honeycombing, tram tracking; Bronchography:
Definitive diagnosis made with visualization of bronchiectatic areas

Treatments: Surgery: Bronchial resection for confined disease unresponsive to conservative

therapy; Drugs: Mucolytics to clear secretions; antibiotics to treat bacterial infection;
bronchodilators to reduce dyspnea; General: Chest physiotherapy with postural drainage to
clear secretions; increase fluids, use vaporizer to liquefy secretions; avoid respiratory
infections.
 End:
Alterations in Pulmonary Gas
Exchange

Prepared by:
Eric B. Panopio, M.D.
 Alterations in Cardiac
Output and Heart Failure

■ Eric B. Panopio, M.D.

HEART FAILURE
 Alternate Names:
■ Myocardial insufficiency, congestive heart failure, cardiac
insufficiency
Definition
■ The inadequacy of the heart to maintain the circulation of blood,
with the result that congestion and edema develop in the tissues
■ Insufficient cardiac output due to cardiac causes
■ Impaired ability of myocardial fibers to contract and relax
■ Excessive cardiac work load
Left-sided failure
■ the LV is the failing chamber e.g. MI
■ LVF may occur without RVF
Right-sided failure
■ the most common cause of RVF is LVF
■ in COPD, increased pulmonary vascular resistance occur due to
architectural changes in the lungs
 Causes of Heart Failure
Impaired Cardiac Fxn Excess Work Demand
Myocardial Dse
Cardiomyopathies Increased Pressure Work
Myocarditis Systemic HPN
Coronary Insufficiency
Pulmonary HPN
MI
Valvular Heart Dse Coarctation of the aorta
Stenotic Valvular Dse
Regurgitant Valvular Dse
Increased Volume Work
Congenital Heart Defects Arteriovenous shunt
Excessive administration
Constructive Pericarditis
of intravenous fluids
Increased Perfusion Work
Thyrotoxicosis
Anemia
 Signs & Symptoms

■ Dyspnea
➢ most frequently encountered symptom of CHF
➢ the feeling of breathlessness is due to vascular congestion w/c reduces
pulmonary oxygenation
■ Orthopnea
➢ dyspnea that occurs in the recumbent position and is relieved by
elevation of the head
➢ results from volume pooling in the central vasculature during
recumbency
■ Paroxysmal nocturnal dyspnea
➢ sudden dyspnea that awakens the patient from sleep
■ Nocturia
➢ due to ↑ renal blood flow in recumbency during sleep
■ Edema
■ Anorexia
■ Tachycardia
➢ A compensatory mechanism for maintaining cardiac output
in the presence of decreased stroke volume
■ Pulmonary rales
➢ The increased left ventricular filling pressure is referred to
the left atrium and pulmonary veins and the increased
hydrostatic pressure produces transudation of fluid into the
alveoli
■ Ascites
➢ Transudation of fluid into the peritoneal space
■ Cardiac enlargement
■ Ventricular gallop
■ Neck vein distension
■ Edema
 Right-Sided Heart Failure
■RH pumps de-O2ated bld from the systemic
circ into the pulmo circ
■ RH Failure: accumulation/damming back of

bld in the systemic venous sys

■ Increase in RA, RV end-diastolic, and

systemic venous pressures

 Manifestations of Right-Sided Heart
Failure
■ Fatigue
■ Dependent edema
■ Distention of the jugular veins
■ Liver engorgement
■ Ascites
■ Anorexia and complaints of gastrointestinal

distress
■ Cyanosis
■ Elevation in peripheral venous pressure
 Left-Sided Heart Failure
■ LH pumps bld from the low-pressure
pulmonary circ into the high-pressure arterial
side of the systemic circ
■ LH failure: Dec in CO; Inc in LA and LV
end-diastole pressures; congestion in the
pulmonary circulation
 Manifestations of Left-Sided Heart
Failure
■ Exertional dyspnea
■ Orthopnea
■ Paroxysmal nocturnal dyspnea
■ Cough
■ Blood-tinged sputum
■ Cyanosis
■ Elevation in pulmonary capillary wedge

pressure
 RIGHT-SIDED vs. LEFT-SIDED HEART
FAILURE
RIGHT-SIDED HEART FAILURE
■ represents failure of the right heart
to pump blood forward into the
pulmonary circulation; blood
backs up in the systemic
circulation, causing peripheral
edema & congestion of the
abdominal organs
■ Damming back of blood in
systemic venous system which
causes an increase in ® atrial, ®
ventricular end-diastolic &
systemic venous pressure
■ Accumulation of edema is
evidenced by weight gain
LEFT-SIDED HEART FAILURE
■ represents failure of of the left
heart to move blood from the
pulmonary circulation into the
system circulation, blood backs up
in the pulmonary circulation
■ Decrease in cardiac output,
increase in left atrial and left
ventricular end –diastolic pressures
& congestion in the pulmonary
circulation
 SYSTOLIC vs. DIASTOLIC FAILURE
SYSTOLIC
■ Forward Failure –
characterized by impaired
forward movement of blood
into the arterial system
emerging from the heart
■ Involves a decrease in
cardiac contractility &
ejection fraction
■ Produces volume overload
or generate a pressure
overload on the heart
■ Ejection fraction declines
progressively with increasing
degrees of myocardial
dysfunction.
DIASTOLIC
■ Backward Failure – failure of
one ventricles to effectively
empty the heart during
diastole
■ Characterized by smaller
ventricular chamber size,
ventricular hypertrophy &
poor ventricular compliance
(ability to stretch during
filling
■ Causes: mitral stenosis,
myocardial hypertrophy,
hypertrophic
cardiomyopathy, aging,
ischemic heart disease
 Systolic Dysfunction

Can’t contract normally

Can’t pump out as much
of the blood it contains
because musc is weaker
Result: the amt pumped to
the body and to the lungs
is reduced
Left ventricle usually
enlarges
 Diastolic Dysfunction

It’s walls stiffen and may

thicken
Can’t fill normally with
blood
blood backs up in the left
atrium and pulmonary
blood vessels
Result: congestion
may be able to pump out a
normal percentage of the
blood it receives.
 Respiratory Manifestations

■ Dyspnea / Exertional dyspnea

■ Orthopnea
■ Cardiac asthma
■ Cheyne-Stokes Respiration
 Cachexia and Malnutrition

■ Cardiac cachexia: condition of malnutrition

and tissue wasting that occurs in persons with
end-stage HF
 Cyanosis

■ Central cyanosis: arterial desaturation

resulting from impaired pulmonary gas
exchange
■ Peripheral cyanosis: venous desaturation
resulting from extensive extraction of oxygen
at the capillary level
 Diagnosis & Tests

■ History and physical examination

■ ECG
■ Chest x-ray
■ Echo cardiography
■ Invasive Hemodynamic monitoring
➢ CVP
➢ Pulmonary capillary wedge pressure
 Treatment

■ Directed toward relieving the symptoms and

improving the quality of life
■ Restriction of salt intake and diuretic therapy
■ Pharmacologic therapy
➢ Diuretics
➢ Cardiac glycosides e.g. digoxin
➢ Beta adrenergic agonists e.g. catecholamines
➢ Reducing afterload e.g. vasodilators captopril, prazosin,
nitrates, diuretics
■ Modification of activities and lifestyle
■ Carefully designed and managed exercise programs
 CORONARY
ARTERY DISEASE
 Coronary Artery Disease
Alternate Names:
■ Atherosclerotic coronary artery disease
Definition
■ the focal narrowing of the large and medium-
sized coronary arteries due to proliferation of
smooth ms cells and the deposition of lipids
Myocardial infarction
■ also known as heart attack or coronary
■ the development of ischemia with resultant
necrosis of myocardial tissue
 Thrombus formation
FATTY ACTIVATE
DEPOSITS D
PLATELETS

LDL
 Pathophysiology

■ Caused by the narrowing of the coronary

arteries usually because of atherosclerosis
■ Factors associated with anginal pain:
➢ Physical exertion
➢ Exposure to cold
➢ Eating a heavy meal
➢ Stress or emotionally provoked situation
 Causes & Risk Factors

■ Type A personality
■ Obesity
■ Hypertriglyceridemia
■ Serum cholesterol - higher LDL and VLDL
■ Age
■ Sex
■ Smoking
■ Hypertension
■ Diabetes mellitus
■ (+) family history
■ Oral contraceptives
 Signs & Symptoms

Angina Pectoris
■ related to exertion, the single most impt feature of
angina is precipitation by exertion
■ symptom quality: feeling a pressure sensation in their
chest
■ radiation of pain: left arm, right arm, jaw, teeth, or
throat
Unstable angina
■ a change in the status of a px’s angina e.g. new-onset
angina, increasing severity, duration or frequency
Variant or Prinzmetal’s Angina
■ usually occurs at rest instead of during exercise
 Angina Pectoris

■ Literally means “pain in the chest”

■ Oxygen demand > than Oxygen Supply in Heart
Muscles
■ Heart arteries are spastic
■ 80% men form 50-60 years old
■ Reversible and no permanent damage to the heart
■ Pain relieved at rest and with nitroglycerin drug
■ Variant or Prinzmetal’s Angina: characterized by pain
that is not precipitated by cardiac work; aka angina
inversa
 Myocardial Infarction

■ “Heart Attack”
■ Means “ death of the myocardium”
■ Blood supply to the heart is significantly reduced
or blocked
■ Part of heart dies
■ Most die 2 hours after signs and symptoms
■ Death due to Cardiogenic Shock , Congestive
Heart Failure – 3-7 days post attack,
Dysrhythmias – irritable heart/problems of
electrical conduction of the heart.
 Angina Pectoris Myocardial Infarction
Location Substernal or across Same
of Pain the chest

Radiation Neck , Jaw , Arms Same, usually radiates

of the Pain
Nature of Dull or heavy
the Pain discomfort with a
pressure squeezing
sensation
Duration 2-10 minutes
to left shoulder and left
arm
Same, but maybe more
intense (crushing pain)
Note: 25% of MI have
no pain at all
Longer, > 30 minutes
 Angina Pectoris Myocardial Infarction

Other Usually none ➢      Perspiration

symptoms ➢      Weakness
➢      Nausea
➢      Pale gray color
➢      Feeling of
impending doom
➢      Syncope
➢      Dyspnea
➢      Signs of Shock
 Angina Pectoris Myocardial Infarction
Precipitating Extremes in Often None
Factors weather, exertion,
stress, meals

Factors Stopping physical No relief or incomplete

Giving Relief activity, reducing relief from nitroglycerin
stress,
Nitroglycerin
 What to do in MI/Angina Pectoris?

■ Assume its MI
■ Make patient comfortable, Semi-Fowlers often best
■ Have the patient cease ALL movement, Do not allow to
help self position
■ Loosen clothing
■ Reassure and calm the patient
■ Assist and administer medication (Nitroglycerin) – if not
relieved, chances are suffering from MI
■ Call for assistance, Monitor and record Vital Signs
■ If arrests, do CPR
 Diagnosis & Tests

■ History & PE: mitral regurgitation, systolic

murmur
■ ECG
 Treatment

■ Nitrates: produces venodilatation to reduce

blood pressure & cardiac size
■ Beta-adrenergic blocking agents: stimulation of
this receptor results in increase inotropic &
chronotropic effect
■ Calcium antagonists: prevents coronary spasm
since calcium regulates the contraction of
smooth muscle
■ Coronary artery bypass surgery
 COR
PULMONALE
 COR PULMONALE
■ refers to right heart failure resulting from
primary lung disease & long-standing primary
or secondary pulmonary hypertension
■
 Cor Pulmonale
Definition
■ Refers to a structural or functional alteration of the
right ventricle as a result of pulmonary disease
■ Chronic cor pulmonale is characterized by
hypertrophy of the right ventricle resulting from
disease of the lungs
■ Acute cor pulmonale is characterized by dilation and
failure of the right side of the heart due to pulmonary
embolism.
■ It involves hypertrophy & eventual failure of the right
ventricle
■ Causes
➢ Acute or chronic pulmonary disease such as severe
pneumonia, pulmonary embolus, pulmonary hypertension
leading to pulmonary hypertension which may cause RV
dilatation, hypertrophy, & failure
■ Manifestation
➢ Early in the course: symptoms only occur with exercise
➢ Peripheral edema
➢ Liver enlargement
➢ Neck vein engorgement
■ Management
➢ Focuses on the treatment of the lung disease & the heart
failure.
➢ Supplemental O2, diuretics, vasodilators
ORTHOSTATIC
HYPOTENSION
 Definition
■ A decrease of 20 mm Hg or greater of both systolic &
diastolic arterial pressure with a concomitant pulse
increase of 15 bpm or more on standing from a supine
or sitting position
■ Represents an abnormal decrease in blood pressure on
assumption of the upright position
■ Accompanied by a decrease in cerebral perfusion that
causes a feeling of dizziness, light-headedness, & in
some case fainting
■ Poses a threat for elderly
■ Caused by decrease vascular volume, impair muscle
pump function, interfere with cardiovascular reflexes
 Causes & Risk Factors

■ Slowing of the postural reflex with aging

■ Reduced blood volume
■ Drug-induced hypotension
■ Aging
■ Bed rest
 Functional Classification of Orthostatic
Hypotension
CLASS 1 - asymptomatic postural hypotension
(decrease in either systolic or diastolic blood pressure ≥ 20mmHg)

CLASS 2 - light headedness (dizziness, giddiness) associated with

postural hypotension but no history of syncope
CLASS 3 - history of syncope (fainting) accompanied with
postural hypotension
CLASS 4 - incapacitated because of severe dizziness or
frequent syncope due to documented postural hypotension
 Signs & Symptoms

■ Dizziness
■ Syncope
➢ Loss of consciousness and postural tone caused by
diminished cerebral blood flow
 Diagnosis & Tests

■ BP measurement in the supine, sitting and

upright position
■ History of symptomatology
■ Medication use
■ Assess for conditions that may contribute to a
postural drop in blood pressure
 Treatment

■ Non-medical intervention
■ Aimed at correcting the reversible causes
■ Assist the client in compensating for the
disorder
■ Prevent falls and injuries
PERICARDITIS
 Definition
■ Inflammation of the pericardium
■ Pain occurs as a result of the inflamed pericardium
rubbing against the heart
■ Fluid may accumulate in the pericardial sac
■ Most often affects men ages 20 to 50, usually
following respiratory infections
Classification
■ Bacterial pericarditis: purulent or infectious
pericarditis
■ Constrictive pericarditis
■ Post-MI pericarditis
 Causes & Risk Factors

■ Can be caused by bacteria, fungal or viral such as

polio, influenza, rubella, RF and TB, adenovirus,
coxsackie
■ May be a result of injury or trauma to the chest,
esophagus, or heart
■ May be caused by systemic diseases such as
cancer, kidney failure, leukemia, HIV or aids
■ Caused by treatments such as radiation therapy to
the chest and use of medications that suppress the
immune system
 Signs & Symptoms
■ Chest pain ■ Anxiety
➢ usually relieved with sitting, ■ Fatigue
pleuritic type described as
sharp, stabbing
■ Fever
➢ may radiate to the neck , ■ Chills
shoulder, back, or abdomen ■ Sweating
➢ increased with deep ■ Auscultation: pericardial
breathing
rubbing sound and heart
■ Orthopnea sounds may be faint
■ Dry cough ■ Signs of pericardial effusion
■ Overall swelling ■ Decreased breath sounds,
crackles in the lungs
 Diagnosis & Tests

■ ECG: (+) ischemic changes due to ↓ oxygen

■ CBC: ↑ WBC count
 Treatment

■ Prevention: treat respiratory infections and other disorders

promptly
■ Goal: improvement of heart function
■ Analgesics: to relieve pain
■ Diuretics: to remove excess fluid
■ NSAIDS, corticosteroids: to relieve inflammation of the
pericardium
■ Activity restricted to bed rest with the head of the bed up to
reduce heart workload
■ Pericardiocentesis: removal of excess fluid from the
pericardial sac is recommended if enough fluid collects in
the pericardial sac to compromise heart function
■ Surgical pericardiectomy (cutting or removal of part of the
pericardium) if the disorder is chronic or recurrent
 Complications

■ Heart failure
■ Pulmonary edema
VALVULAR HEART
DISEASE
 Definition
■ A defect or disease in any of the 4 valves that
control the flow of blood will disrupt normal
blood flow
■ 2 types:
➢ stenosis – the valve fails to open fully
➢ insufficiency or regurgitation – the valve does not

close properly
■ HEART VALVES – determines the direction of the blood flow
through the heart chambers
■ VALVULAR HEART DEFECTS – exert their effects by
obstructing flow of blood (stenotic valve disorder) or
allowing backward flow of blood (regurgitant valve disorder)
■ STENOTIC VALVULAR DEFECTS – produce distention of
the heart chamber that empties blood through the diseased valve
& impaired filling of the chamber that receives blood that
moves through the valve
■ REGURGITANT VALVES – allow blood to move back through
the valve when it should be closed . This produce distention and
places increase work demands on the chamber ejecting blood
through the diseased valve
 Causes & Risk Factors

■ Congenital heart defects

■ Rheumatic heart disease
■ Hypertension
Mitral Valve Stenosis
 Signs & Symptoms
Stenosis Regurgitation
■ Angina ■ L ventricular failure:
■ Hoarseness dyspnea, orthopnea,
■ Syncope PND, angina, murmur
■ Hemoptysis
■ R sided failure
■ L sided failure: dyspnea,
orthopnea, PND
 Diagnosis & Tests

■ ECG
■ Echocardiography
■ Cardiac catheterization
➢ measure pressure gradient
 Abnormal Heart Sounds

rheumatic fever loud 1st heart sound

Mitral Stenosis

Crescendo type in Mitral Stenosis

High pitch blowing systolic murmur in Mitral Stenosis

Third heart sound in Mitral Stenosis

Opening snap in Mitral Stenosis

Presystolic murmur in Mitral Stenosis

 Abnormal Heart Sound Aortic Origin

Aortic stenosis loud systolic ejection murmur

Aortic stenosis Opening snap of aortic valve early systolic

ejection sound
 Treatment

Medical
■ Diuretics
■ Digitalis
■ Anticoagulants

Surgical
■ Commissurotomy
➢ allows relief of stenosis without valve replacement
■ Valve Replacement
➢ if commissurotomy cannot be performed
 End:
Alterations in Cardiac Output and Heart
Failure

Prepared by:
Eric B. Panopio, M.D.
 ALTERATIONS IN
CIRCULATION & TISSUE
PERFUSION

■ Eric B. Panopio, M.D.

PERIPHERAL VASCULAR
DISEASES
Vascular system
 PERIPHERAL VASCULAR DISEASE

■ A. Occlusive arterial diseases

1. Chronic
a. Thromboangiitis Obliterans
b. Arteriosclerosis Obliterans
2. Acute
a. Arterial Embolism
b. Arterial Thrombosis
c. Vasospastic Disease

• B. Venous diseases
1. Chronic venous insufficiency
2. Varicose veins
3. Acute Venous diseases
4. Thrombophlebitis
5. Thromboembolism

• C. Arteriovenous fistula
• D. Lymphedema
 Arteriosclerosis Obliterans (ASO)

■ A.k.a. – Atherosclerotic occlusive dse Clinical Presentation:

Chronic occlusive arterial dse 1. Aorta & Iliac @ies
Obliterative arteriosclerosis - bilateral claudication of calf muscles
Peripheral Arterial Dse - sense of weakness or tiredness
- relieved by rest
• Most chronic arterial d/o
• Most common Occlusive arterial dse. 2. Femoral & popliteal @ies]
• A progressive, obstructive, arterial dse of LARGE - intermittent claudication of calf muscles may radiate
& MEDIUM Sized @ies. to ipsilateral popliteal region or lower thigh.
• Men 50-70 y/o 3. Tibial & Common peroneal @ies
• Deposition of fatty streaks HARDENS - Insidious type
(Atheroma) - occurs more slowly over months or years
• Commonly seen in sites with: - pain at rest (indicates more severe involvement)
1. Sites of acute vessel angulation - (-) pedal pulse with exercise
2. Major @ial Bifurcation
Arteries most commonly affected:
1. Femoral @ & popliteal @ (MOST COMMON)
2. Femoral @ - MOST COMMON in DM & Non-DM
- in HUNTER’S CANAL aotoiliac jxn
3. SECOND MOST COMMON:
DM – Popliteal @ & Tibial @
non-DM – Aortoiliac @
Common risk factors:
1. Smoking 4. Hypertension
2. Hyperlipidemia 5. Obesity
3. Elderly 6. DM
DIAGNOSIS:
History
PE – Capillary refill, skin color, hair distribution
Doppler Ultrasonography
*Ankle-Brachial Index
Air plethysmography
Impedance plethysmography

TREATMENT:
1. Conservative Program Approach:
- cessation of smoking
- dietary mngt
- Pain control
- Daily walking
2. Medical:
- Low-dose aspirin
3. Bypass graft or Angioplasty
 Doppler Sonography
■ US enhanced with Doppler
measurements, which employ
the Doppler effect to assess
whether structures (usually
blood) are moving towards or
away from the probe, and its
relative velocity
■ By calculating the frequency
shift of a particular sample
volume, for example a jet of
blood flow over a heart valve,
its speed and direction can be
determined and visualised
 Impedance Plethysmography
■ An instrument for measuring
changes in volume within an
organ or whole body (usually
resulting from fluctuations in
the amount of blood or air it
contains)
■ Air plethysmography
uses a similar principle
but based on an air-filled
long cuff, which is more
convenient but less
accurate
 Thromboangiitis Obliterans
• Idiopathic diffuse inflammation in both arteries
and veins and surrounding CT.
• SECOND MOST COMMON chronic @ial d/o 4. Cold sensitivity
• Can affect arteries & veins ( most common in 5. cyanosis
Arteries) 6. decreased/absent posterior tibial &
• MEDIUM sized arteries of legs dorsalis pedis artery
• Syn: BUERGER’S Disease 7. ulceration & gangrene
• 40 y/o men who smoke heavily 8. thin, shiny, hairless skin

• SSx:
pain and tenderness Diagnosis:
Symptoms: Episodic and Segmental Arteriography
Intermittent claudication Histologic exam

Most common areas affected are:

1. LE: plantar, tibial & digital arteries
Treatment:
2. UE: digital, palmar & ulnar @ies
1. Cessation of smoking
2. Medications – Vasodilators & analgesics
1. Edema 3. Wound care for ulcers & gangrene
2. Rubor 4. Regional sympathetic ganglionectomy
3. paresthesia: An abnormal sensation, such as of 5. Amputation – when conservative
burning, pricking, tickling, or tingling intervention fails
Buerger’s Disease
Buerger’s Disease
Buerger’s Disease
 Acute Occlusive arterial diseases
A. Arterial Embolism: - SSx:
- MOST COMMON form of Acute arterial dse - 1. Paresthesia
arise within the heart in 60-65% 2. pallor
- arise within the LV secondary to MI 3. pulselessness
- arise from ATRIUM in 5-10% in RHD 4. paralysis
- occurs as a dislodged thrombus from the 5. pain in foot and hand
heart migrate to a peripheral arterial vessel. 6. numbness
- MAJOR SITES of lodgment of emboli:
1. LE – superficial femoral @ &
popliteal @ - Dx:
2. UE – 7-8% DOPPLER US
3. Brain – 10%
4. Viscera - Treatment:
Heparin
B. Arterial Thrombosis: Thromboembolectomy
- common in patients with: prevent pressure, monitor pulse & temp,
enhance venous return
1. MI
protection of limb
2. RHD
head of bed raised to 6-8 inches
3. Atherosclerosis
4. Aneurysm of the aorta
C. Vasospastic disease
1. Raynauds dse &
2. Raynauds Phenomenon
■ Unknown etiology; manifests as an episodic 2. Raynauds phenomenon:
arterial vasospasm in cold or emotional stress
- secondary to another dse.or underlying cause
■ Fingers affected more
- women 20%; 15-40 y/o
- may also occur with temperature changes &
■ TRIAD (FRENCH FLAG SIGN): occlusive arterial dse.
1ST - pallor
2ND - cyanosis Clinical presentation:
3RD - hyperemia or rubor 1. 6 P’s
2. stiffness
• CRITERIA for Diagnosis: 3. thickened fingertips
1. precipitated by cold or emotion 4. brittle fingernails
2. bilateral involvement RD: bilateral, distally to proximally along the digits.
3. absence of gangrene RP: unilateral involving only 1-2 fingers
4. absence of underlying dse
Diagnosis:
1. Raynauds dse: Hx & PE
- a primary vasospastic d/o Hx of symptoms for at least 2 yrs with no progression
- 80% are women 20-49 y/o & no underlying cause
- hypersensitivity of digital arteries to cold Treatment:
- secondary to cold intolerance 1. Prevention of vasospasm
- MC form of idiopathic cold intolerance 2. Avoidance of attack triggering stimulus
- cold temp
- emotional stress
- nicotine (causes vasospasm)
 B. Venous diseases
1. Chronic venous insufficiency:
- syn: Postphlebitic syndrome
- dec. venous return over a long period of time
- more prevalent than arterial dse.
- Common precipitating conditions:
1. varicose veins
2. Deep venous valvular insufficiency
3. Deep vein obstruction or compression
4. immobility
5. prolonged leg dependency
- Clinical presentation:
1. pain thru/out the leg
2. increasing heaviness cc is relieved by overnight rest
3. edema 6. subcutaneous fibrosis
4. varicosities 7. skin pigmentation
5. dermatitis 8. ulceration

- Client instructions:
Avoid: 1. prolonged sitting & standing
2. crossing the legs
3. sitting too high
4. wearing tight clothing above the knee
 2. Acute venous diseases
A. Varicose veins:
- abnormal dilation of veins leading to tortuosity of the vessels, incompetence of the valves & propensity
for thrombosis
- in 15% of adults; in women (in pregnancy)
- Etiology & Risk factors:
1. Heavy lifting 4. Obesity
2. heart failure 5. hemorrhoids
3. constipation
Clinical Presentation:
1. Gradual, dull aching heaviness (MOST COMMON Sx)
2. Feeling of fatigue on long standing
3. Lower leg cramps
4. Lower leg ulceration
5. Relieved by leg elevation
6. Dilated tortuous, elongated veins under the skin
(MOST VISIBLE sign)
Diagnosis:
Visual inspection & palpation
Doppler US – used to localize incompetent valves
Treatment:
1. periodic rest; feet elevated
2. Client education in:
1. promoting circulation
2. frequent posture changes
3. performance of simple exercises
4. use of properly fitting elastic stockings
3. Surgery – vein stripping
Thrombophlebitis:
■ Inflammation of a vein with thrombus formation
■ Damage to endothelial lining on which platelets are deposited leading to thrombus formation
■ May affect:
1. deep veins (pelvis & LE)
2. superficial veins (saphenous veins)
• Etiology:
*1. venous stasis
2. hypercoagulability
3. vein wall trauma – direct blow, IV injection, fractures, dislocation
• Clinical presentation:
- asymptomatic during the early stage
- Dull ache, tightness and pain in the calf
- Affected side is warmer
- Cyanotic skin
• Diagnosis: Doppler US
• Treatment:
1. anticoagulants
2. bed rest
3. heat application
4. ambulation with elastic stockings

• Most important complication after surgery

• Venous thrombosis secondary to stasis in UNINFLAMED veins usually the calf
• MOST COMMON on the LEFT side
Thrombophlebitis
 Thrombophlebitis: Phlebothrombosis:

Major cause: Vein wall inflammation Stasis

Clot: Short, well anchored Long, poorly anchored

Emboli: Rare except in infected 1. Pulmonary emboli

areas. common
(Pyemic emboli) 2. Massive sterile emboli

Site involved: anywhere Usually calf veins

Clinical feature: Pain & signs of acute Silent with few SSx.
inflam.
 Arteriovenous Fistula
• Abnormal communication of artery & vein ■ Anatomic changes:
• TYPES:
1. Congenital or A-V malformation
1. elongated & distended
2. Acquired arterio-venous fistula 2. smooth muscle atrophy
• Etiology: 3. dec. elastic tse
1. penetrating injury 4. atheromatous plaque
2. aneurysmal erosion formation
3. infection & neoplasm
4. surgical construction in dialysis 5. distal vein dilates &
• Clinical presentation: elongates with incompetent
valves
A. Acute phase:
1. (+) pulsating hematoma
2. (+) palpable thrill
3. (+) bruit

B. Chronic phase:
1. heart failure
2. peripheral ischemia
3. gangrene
Arteriovenous Fistula
 Lymphedema

■ Abnormal accumulation of water and protein in skin and subcutaneous tse. d/t disruption or occlusion of
lymph channels.
■ TYPES:
A. Primary Lymphedema
- impaired lymphatic flow owing to Congenital malfunction of the lymphatic vessels

1. Congenital lymphedema:
*Agenesis – no formation of lymph sys.
*Aplasia – poorly developed lymph sys.

2. Hereditary lymphedema:
* Milroy’s dse (AD) – lymphedema of 1 or more ext right after
birth.
` - will not impair dev’t & act.
3. Lymphedema Praecox:
- in 2nd & 3rd decade
- pitting & soft edema to non-pitting & firm edema
- no pain, ulceration
- with recurrent infections
4. Lymphedema Tarda:
- Tarda (“late”)
- >35 y/o
- non-pitting & firm edema
- no pain, ulceration
- with recurrent infections
Secondary Lymphedema

■ With clear cause ■ Clinical presentation:

■ Acquired; most common type 1. swelling 4. paresthesia
2. pain 5. LOM
■ Etiology: 3. dec coordination 6. ROM
1. Excessive lymphatic load
2. fibrosis TREATMENT:
3. filariasis 1. Diuretics
4. trauma 2. Benzo-alpha-pyrones
5. surgical removal of lymph nodes 3. Elevation
- in radical mastectomy 4. ROM exer
■ TYPES: 5. Manual lymphatic drainage
1. Infectious – common in 3rd world
countries 6. Compressive garments
2. Malignancies – common in western 7. Isometric exer.
countries
A. Obliterative edema (obstructive)
- caused by malignancies
(breast Ca & lymphoma- female)
(prostate Ca – male)
B. Inflammatory
- TB, elephantiasis,
filariasis
SHOCK
■ a life-threatening condition that occurs when
the body is not getting enough blood flow
■ major classes of shock:
☛ cardiogenic
☛ hypovolemic
☛ anaphylactic
☛ septic
☛ neurogenic
■ caused by any condition that dangerously
reduces blood flow, including:
1. heart problems (such as heart attack or
heart failure)
2. low blood volume (as with heavy bleeding or
dehydration)
3. changes in blood vessels (as with infection or
severe allergic reactions)
 SSx of Shock
anxiety/agitation confusion
pale, clammy skin ↓/- urine output
bluish lips/fingernails dizziness/faintness
profuse sweating rapid, weak pulse
shallow breathing chest pain
unconsciousness
 Hypovolemic Shock
■ a condition where the heart is unable to supply
enough blood to the body because of blood
loss, or inadequate blood volume
■ in blood loss 1/5 or more of N blood vol
 Anaphylactic Shock
■ an acute systemic type of allergic reaction
■ histamine secretion causes constriction of the airways
■ SSx

dyspnea wheezing
confusion slurred speech
gen. itching nausea, vomiting
abdominal pain skin redness
nasal congesion cough
 Septic Shock
■ a serious, abnormal condition that occurs when an
overwhelming infection leads to low blood pressure
and low blood flow
■ SSx:

fever, chills light-headedness

dyspnea palpitations
cool, pale limbs elevated temperature
restlessness agitation
lethargy confusion
 Cardiogenic Shock
■ a disease state where the heart is damaged
enough that it is unable to supply sufficient
blood to the body
■ can be caused by disorders of the heart muscle,
the valves, or the heart's electrical conduction
system
 Cardiogenic Shock SSx
rapid, weak pulse rapid breathing
anxiety, nervousness cool skin
weakness, lethargy fatigue
loss of alertness ↓ concentration
agitation, confusion coma
pale skin color profuse sweating
poor capillary refill ↓/- urine output
 Diagnosis & Tests
■ BP: less than 90 systolic
■ ECG
■ coronary angiography
■ echocardiogram
■ CBC
■ arterial blood gas
 Treatment
■ treat underlying cause of shock
■ epinephrine, amrinone: to ↑ BP
■ oxygen: to reduce heart workload
■ IV fluids, blood & blood products
■ cardiac pacing
■ intra-aortic balloon counterpulsation (IABP): to
improve CV function
 STAGES OF SHOCK
■ Initial nonprogressive stage
(Early Shock)

The body attempts to compensate for

the decreased flow of fluids and oxygen
to the tissues. 
 SIGNS OF EARLY SHOCK

■ Increased heart rate

■ Normal to increased intensity of pulses (may feel like
they are "pounding"). 
■ Mucous membranes may look redder than normal
(this is common with septic shock). 
■ Capillary refill time of one to two seconds
■ Body temperature may be low or, in the case of septic
shock, may be elevated. 
■ Progressive stage
(Middle Stages of Shock)

The body begins to have difficulty

compensating for the lack of blood flow and
oxygen. 
 SIGNS OF MIDDLE STAGE

■ Hypothermia (low body temperature).  Hairless areas

may feel cool to the touch. 
■ Weak pulse. 
■ Capillary refill time is prolonged.
■ Heart rate is increased.
■ Mucous membranes are pale. 
■ Depressed mental state.
■ Cool limbs. 
■ Irreversible stage
(End Stage or Terminal Shock)

Occurs when the body can no longer

compensate for the lack of oxygen and
blood flow to its vital organs. 
 SIGNS OF END STAGE

■ Slow respiratory rate. 

■ Slow heart rate.
■ Depressed mental state or unconsciousness.
■ Prolonged capillary refill time.
■ Weak or absent pulse. 
 TYPES OF SHOCK
■ HYPOVOLEMIC SHOCK
characteristics:
loss of whole blood
loss of plasma
loss of extracellular fluid
 STAGES OF HYPOVOLEMIC
SHOCK
■ INITIAL STAGE
- the circulatory blood volume is decreased
■ SECOND STAGE
- compensatory stage
■ THIRD STAGE
- progressive stage (favorable signs begin to appear)
■ FOURTH AND FINAL STAGE
- irreversible stage
 MANIFESTATION

■ Thirst
■ Increased heart rate
■ Cool and clammy skin
■ Decreased in arterial blood pressure
■ Decreased in urine output
■ Changes in mentation
 TREATMENT
■ Supine position
■ Administer oxygen

Goal of treatment: to restore vascular volume

HOW?
- IV administration of fluids and blood

- Crystalloids

- Plasma expanders (dextrans & colloidal albumin

solutions)
- Vasoactive drugs (adrenergic drugs)
 
 
 
■ OBSTRUCTIVE SHOCK
- the term is used to describe circulatory shock that
results from mechanical obstruction of the flow of
the blood through the central circulation

CAUSE: dissecting aortic aneurysm, cardiac

tamponade, pneumothorax, atrial myxoma
* pulmonary embolism (most common cause)
■ PRIMARY PHYSIOLOGIC RESULTS
- elevated heart pressure
- impaired venous return to the heart

■ TREATMENT modalities
- surgical intervention
* pulmonary embolectomy
* pericardiocentesis ( removal of fluid from the
pericardial sac) for cardial tamponade
* the insertion of a chest tube
■ DISTRIBUTIVE SHOCK
characteristics
- loss of sympathetic vasomotor tone
- presence of vasodilating substances in
the blood
- presence of inflammatory mediators
 KINDS OF DISTRIBUTIVE
SHOCK
■ NEUROGENIC SHOCK
- caused by decreased sympathetic control of
blood vessels tone due to a defect in the
vasomotor center in the brain stem or the
sympathetic outflow to the blood vessels.
■ Fainting due to emotional causes is a
transient form of neurogenic shock
■ The term spinal shock is used to describe
the neurogenic shock that occurs in persons
with spinal cord injury.
■ Neurogenic shock often slower than normal,
and the skin is dry and warm.
■ This is rare and usually transitory.
■ ANAPHYLACTIC SHOCK
- characterized by massive vasodilatation,
pooling of blood in the peripheral blood
vessels, and increased permeability
- caused by an immunologically mediated
reaction in which vasodilator substances
such as histamine are released into the
blood.
- frequent causes of anaphylactic shock are
reactions to drugs (penicillin); foods (nuts); and
insect venoms.

- the most common cause is stings from insects

of the order Hymenoptera (bees, and fire ants)
 TREATMENT
■ Immediate discontinuance of the inciting
agent or institution of measures to decrease
its adsorption (application of ice)
■ Close monitoring of the cardiovascular and
respiratory function
■ Maintenance of adequate respiratory gas
exchange, cardiac output and tissue
perfusion.
■ SEPSIS AND SEPTIC SHOCK
- septic shock is associated with severe
infection and the systemic response to
infection.
- commonly associated with pathologic
complications, such as pulmonary
insufficiency, disseminated intravascular
coagulation and multiple organ dysfunction
syndrome
 MANIFESTATIONS

■ Fever
■ Vasodilatation
■ Warm, flush skin

■ * most common type of distributive shock

 •SEPSIS AND SEPTIC SHOCK

- is a disease state where the heart is damaged

enough that it is unable to supply sufficient
blood to the body.

- It is usually caused by myocardial infarction.

 SIGNS AND SYMPTOMS
■ rapid pulse        
■ pulse may be weak (thready)     
■ rapid breathing▪         
■ anxiety, nervousness       
■ skin may feel cool to touchweakness,
lethargy, fatigue
■ decreased mental status
■ loss of alertness
■ loss of ability to concentrate
■ restlessness, agitation,confusion        
■ coma      
■ skin color pale or mottled         
■ profuse sweating, moist skin       
■ decreased urine output (or none)        
■ poor capillary refill
 MANAGEMENT
■ Early assessment and treatment
■ Volume status must be establish
■ Insertion of pulmonary artery catheter
■ Dobutamine
■ Vasodilators
■ Intra-aortic balloon pump
■ Coronary cardiac catheterization
 End:
Alterations in Circulation & Tissue
Perfusion

Prepared by:
Eric B. Panopio, M.D.