PATHOPHYSIOLOGY

ETIOLOGY RISK FACTORS

 CAD  Age(over 75
 HPN years old)
 Vulvar Disorders
 Renal Dysfunction  Male
 Diabetes  Heredity
 Atherosclerosis  HPN
 Physical
inactivity
 Obesity

Digestion Process

Food taken in is broken down by our Digestive

System into NUTRIENT MOLECULE

Absorbed by our Digestive Tract through the Small

Intestines for the use of the body

Food containing carbohydrates and various sugars are

broken down into GLUCOSE

In order for glucose to be use as fuel by the cells it must

first enter cells initiated by INSULIN that is secreted in
the PANCREAS

INSULIN triggers cells to open up to let glucose move in

to be used as fuel/energy

Type 2 Diabetes

Body does not respond properly to INSULIN produced

by pancreas

Cells are INSULIN RESISTANT Insufficient INSULIN PRODUCTION by

the pancreas

Glucose builds up in the

bloodstream
 OVERTIME

MICRO BLOODVESSELS MACRO BLOODVESSELS

Can damage eyes, nerves Myocardial Dysfunction,

and kidneys Stroke, Poor Circulation,
Hypertension

MYOCARDIAL DYSFUNCTION
 Ischemic Heart Dse
 Hyperthyroidism
 Myocardial Infarction
 Valve Disease
 History of Alcohol and Cigarette
use
 Hypertension
 Diabetes

Left Ventricle cannot effectively pump blood out of

the ventricle into aorta and the systemic
circulation.

Causes an INCREASED left ventricular

blood volume

INCREASSES left ventricular pressure

Decreases blood flow from the left

ventricles

Blood volume and pressure builds-up in the

LA causing a decreased flow through the
pulmonary veins into the LA

Pulmonary venous blood volume and

pressure increases in the Lungs

Forces fluid from pulmonary capillaries into

the pulmonary tissues and alveoli causing
interstitial edema and impaired gas
exchange
 Signs and Symptoms
 Dyspnea
 Cough
 Pulmonary Crackles
 Low Saturation
Levels

AS HF DEVELOPS Body activates neurohormonal compensatory mechanism

 Decreased Cardiac Output

Activation of baroreceptors
 Decreased Systemic blood
pressure

 Decreased Perfusion to Stimulation of vasomotor regulatory centers in

Kidneys Medulla

Activation of RAAS Activation of Symphatetic nervous System

to release CATECHOLAMINES
(Epinephrine and Norepinephrine)
Causes a release of RENIN by the
KIDNEYS

Causes the conversion of Plasma Protein Increases Heart rate and contractility
Angiotensin to Angiotensin I that increases
Blood Pressure

Which then circulates to the Lungs that is

responsible for the conversion of
Angiotensin I to Angiotensin II

Angiotensin II stimulates the release of

ALDOSTERONE from the Adrenal Cortex

Na and Fluid Retention by the

renal tubules

Lead fluid volume

Increases Blood overload that is
Pressure and afterload commonly seen in
HF
 Angiotensin and
Aldosterone

Leads to increased preload

and afterload

Causes an increase stress

on the ventricular wall

Increase in cardiac
workload

Counter regulatory
mechanism is attempted

Release of Natriuretic
Peptides
(ANP and BNP)

Promotes vasodilation and Diuresis

(but not strong enough to overcome
negative effects of the other
mechanisms)

OVER TIME

As the Heart’s workload

continuously increases,
contractility of the myocardial
fibers decreases

Results in an increases blood volume

in the ventricle, stretching the
myocardial ms. Fibers and increasing
the size of the ventricle
(ventricular Dilation)

The heart compensates for the

increase workload is to
increase the thickness of heart Ventricular
muscle Remodeling
(Ventricular Hypertrophy)
 Signs and Symptoms
1. Dyspnea
2. Cough
3. Pulmonary Crackles
4. Low Saturation Levels

AS HF DEVELOPS Body activates neurohormonal compensatory mechanism

 Decreased Cardiac Output

Activation of baroreceptors
 Decreased Systemic blood
pressure

 Decreased Perfusion Stimulation of vasomotor regulatory centers in

to Kidneys Medulla

Activation of RAAS Activation of Symphatetic nervous System

To release CATECHOLAMINES
(Epinephrine and Norepinephrine)
Causes a release of RENIN by the
KIDNEYS

Causes the conversion of Plasma Protein Increases Heart rate and contractility
Angiotensin to Angiotensin I that increases
Blood Pressure

Which then circulates to the Lungs that is Increases Blood

responsible for the conversion of Increases
PressureBlood
Angiotensin I to Angiotensin II Increases
PressureBlood
Increases
PressureBlood
Increases
Pressure Blood
Increases
PressureBlood
Pressure
Angiotensin II stimulates the release of
ALDOSTERONE from the Adrenal Cortex

Na and Fluid Retention by the

renal tubules

Increases Blood
Pressure and afterload