PATOFISIOLOGI

KARDIOVASKULAR
DR.dr.Zaenal M. Sofro, AIFM, Sport & Circ. Med.
Bagian Ilmu Faal Fak.Kedokteran UGM

AUTOMATICITY

+
Na

K+

Gradually
increasing PNa
Na+

K+

-70 mV

THRESHOLD
RESTING

-0

Cardivascular Disease is
a Continuum
Myocardial
Infarction

CAD

Atherosclerosis

CV Risk Factors
Diabetes
Hypertension
Hyperlipidemia
Smoking

Loss of
contractility

Remodeling

Ventricular
Dilation
Congestive
Heart Failure

End-Stage
Heart Disease

Death

Adapted from Dzau V, Braunwald E. Am Heart J. 1991

Willem Einthoven
(1860-1927)

Cardiac Physiology

Electrocardiography Diagnosis

Cardiac Physiology

Electrocardiography Diagnosis

Essential functions of the heart are secured

by integration of electrical and mechanical
functions of the heart
Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)
- changes of the heart rate
- changes of stroke volume

Control of HR:
- autonomic nervous system

- hormonal(humoral) control
Control of SV: - preload
- contractility
- afterload

ST Elevation Infarction
Heres a diagram depicting an evolving infarction:
A. Normal ECG prior to MI
B. Ischemia from coronary artery
occlusion results in ST depression (not
shown) and peaked T-waves
C. Infarction from ongoing ischemia
results in marked ST elevation
D/E. Ongoing infarction with appearance of
pathologic Q-waves and T-wave
inversion
F. Fibrosis (months later) with persistent
Q- waves, but normal ST segment and Twaves

ST changes: axis + anatomy

Lateral:
I, aVL
LCA, CFX

Anterior:
V1, V2, V3, V4
LAD

Inferior:
-II, III and aVF
-RCA (or LCA)

Memorize this slide

Location of infarct
combinations

aVR

LATERAL
aVL

II

V1

ANT
POST
V2

V4

ANT
SEPTAL

V5
ANT

V3
III

INFERIOR

aVF

V6 LAT

Blood Pressure

Figure 15-8

- venous return

- extracellular fluid volume

- myocardial contractility

- vasoactive substances

- thickening of arteriolar

wall

ARTERIES (LOW COMPLIANCE)

HEART
DIASTOLE
VEINS

CAPACITY
VESSELS

80 mmHg

120 mmHg

SYSTOLE

CAPILLARIES

Cardiac Cycle
Ventricular Filling

Isovolumetric
Relaxation

Isovolumetric
Contraction
Ventricular
Ejection

Cardiac cycle everything that occurs from the start of 1

heartbeat to the start of the next.

-includes contraction (systole) and relaxation

(diastole) of all 4 chambers

Left
atrium

Left
ventricle

Aorta

Adaptive mechanisms of the heart

to increased load
Frank - Starling mechanism
Ventricular hypertrophy
increased mass of contractile elements strength
of contraction

Increased sympathetic adrenergic activity

increased HR, increased contractility

Incresed activity of RAA system

Causes leading to changes of number and size

of cardiomyocytes

(Brown, 1997)

Physiologic Requirements to
Perform Exercise

ERGOMETRY TEST

External to Internal environment

..a hint of integration?

Wellness Continuum

The Heart-Brain Connection

Vagus mammalia dan social engagement system

Gambar 5

Blood Pressure

Systolic pressure
is measured as the
ventricles contract

Based on: Harvard Family Health Guide

Diastolic pressure is
measured when
ventricles are at rest

The level of blood

pressure in the
healthy people is the
very stable value.
The stability of blood
pressure is supported
by regulative systems.
Hayton (1974) divided
them into two groups
hemodynamic
system and regulative
system.
Arterial blood pressure normal range:
Systolic 100 - 125 (equilibration 100 - 139) mm Hg

Diastolic 70 - 80 (equilibration 60 - 89) mm Hg

Veins

Venules

Capillaries

Arterioles

Arteries

Pressure Drops Within the Circulation

Arteries
Arterioles

Capillaries
Venules
Veins

 Blood pressure is one of the

most variable but best

regulated functions of the
body.
The purpose of the control of
blood pressure is to keep
blood flow constant to vital
organs such as the heart,
brain, and kidneys.
The continuous elevation of
blood pressure that occurs
with hypertension is a
contributor to premature death
and disability due to its effect
on the heart, blood vessels,
and kidneys.

Regulation of arterial pressure (P)

by hemodynamic system
Formula: P = CO PR
CO cardiac output
PR peripheral vascular resistance (depended to arterioles tone)

CO leads to

PR leads to

PR and P normalizes finally

CO and P normalizes finally

AP normal range:
Systolic 100 - 125 (equilibration 100 - 139) mm Hg
Diastolic 70 - 80 (equilibration 60 - 89) mm Hg

Mechanisms of Blood
Pressure Regulation

Short-term
regulation

neural mechanisms
hormonal mechanisms

Long-term
regulation

Gravity: role of baroreceptor reflex in orthostatic adjustment

Parasymp. -

Cardiovascular
ctr in medulla
oblongata
Baroreceprots
in aorta & carotid bodies
Vasoconstricti
on

Heart
rate

pressure

NEURAL MECHANISMS

The Polyvagal Theory

By Stephen Porges
The Vagus Nerve in three parts, all
working simultaneously:
Ventral Vagal System:
Is part of the Parasympathetic
Nervous System
(Social Engagement/frontal
cortex)
Sympathetic Nervous System:
(Fight/Flight, Freeze - Limbic
Brain)

43

Dorsal Vagal System:

Is part of the Parasympathetic
Nervous System
(Freeze/Immobility/Brainstem)

Location and innervation of the aortic arch and

carotid sinus baroreceptors and the carotid
body chemoreceptors.

Regulative systems
1. Barroreceptors of aorta
arch and sinus caroticus

Barroreceptors
of the vessels

Afferent impulses

Medulla oblongata
(vessels active center)
Heart (CO increase at
decreased P)
Arterioles (spasm)

fferent impulses

Pusat vagus bermielin dan yang tidak bermielin

di medulla oblongata. Sumber: Porges (2011)
Gambar 17

Regulative systems

Role of the vasopressin in

arterial hypertension
pathogenesis

Arterial hypertension (H)

AP elevation
(value above 139/89 mm Hg), which
is resulted from rising of peripheral
vessels resistance
(one of the most common cardiovascular disorders)

Classification
Arterial hypertension
Primary

AP above 139/89 mm Hg

Secondary

AP less than 100/60 mm Hg

Arterial hypotension

Acute

Chronic

Classification
Primary AH
(essential, hypertonic disease)

Secondary AH
(that is happened in 10 - 20 % cases).
Its a symptom of some disease course

Etiology (primary AH)

Reason is unknown.
AH is polyetiological disease.
AH arises on the ground of genetically
peculiarities of metabolism.
That is possible to have genetically defect of the
systems, which control relaxation of the
smooth muscle cells of the arterioles.

Contributing factors
Risk Factors

Family history of hypertension

Race

Age-related increases in blood

pressure
Diabetes mellitus

Contributing factors
Lifestyle Factors
Stress

Excessive calorie
intake and obesity

Excessive alcohol
consumption

High sodium
intake

Physical
inactivity

Oral contraceptive
drugs

Pathogenesis
AP = O PR

Increase of circulative blood volume

(CBV)
Emotional excitement
(SNS activation)
Cardiac output (C) increase
Peripheral vessels resistance
increase
Kidney functions violation

Pathogenesis
Increase of circulative blood volume (CBV)

NaCl (intake more 5 g/day)

Reasons
Decrease Na excretion by kidney
(kidney diseases)

Pathogenesis

1. CBV increase
Na accumulation in
vessels smooth muscle
wall and increase of its

Na retention in blood

osmotic pressure
Blood osmotic pressure
increase

Vessels smooth muscle

sensitivity to
vasoconstrictive
influences increase
(noradrenalin, adrenalin,
endothelin, angiotensin)

Hypervolemia

Vessels wall edema

Vessels
narrowing

Cardiac output increase

Vessels
spasm

AP elevation
Formula: P = CO PR

Peripheral vessels
resistance increase

Pathogenesis
2. Cardiac output increase (CO)

Circulative blood volume

increase (CBV)

Reasons

Emotional stress

Physical (overload) stress

Hyperthyroidism

Pathogenesis

2. Cardiac output increase

SAS activation

Adrenalin excretion

Increase of cardiac
contractility force

Increase of heart beats

Increase of cardiac
output

AP elevation
Formula: P = CO PR

Pathogenesis

3. SAS activation

SAS activation

Interaction adrenalin and

alpha-adrenoreceptors

Arterioles smooth
muscles spasm
Arterioles narrowing

Suprarenal glands
activation

Venues smooth
muscles spasm
Increase of circulative
blood in big blood
circle

Increase of CBV

PR increase
CO increase

Formula: P = CO PR

Noradrenalin
adrenoreceptors of
heart

CO increase

AP increase

drenalin

alpha-adrenoreceptors
of vessels

Arterioles
narrowing

Pathogenesis

4. Kidney functions violation

Long time spasm of

kidney arteries
AP decrease in renal
capillaries
Activation of JGA

Angiotensin 2 effects

Renin excretion

Angiotensin 2
synthesis

AP increase

Smooth muscles contraction in the

vessels
Stimulation of the vasoactive center
in brain
Noradrenalin excretion increase
Adrenalin excretion increase from
suprarenal glands
Aldosteron excretion increase from
suprarenal glands (Na retention due
to kidney)

Depressive function of kidney synthesis of the

substances for AP reduce

PG 2

dilates renal arteries, reduces renin

synthesis and reduces Na
reabsorbing in kidney

Phospholipid Renin
Inhibitor

Angiotensinase

Phosphatydilcholin
alkali ethers

! ! !
Exhaustion of kidney
depressive function
leads to arterial
hypertension
stabilization

Increase of vesseles
resistance
It is the defining
mechanism. Irrespective
of first reason, in the
patients with hypertonic
disease almost always
increases peripheral
resistance.
It is considered, that the
essence hypertonic
disease just is in
increase of peripheral
vessels tonus.
Hyperkinetic phase,
which is connected to
increase of cardiac
output, happens only at
early stages of disease
and not in all patients.

The hereditary predisposition

Etiology
secondary H
1. Renal
(resulted from kidney pathology)
Pyelonephritis

Glomerulonephritis

Kidney damage at
collagenosis

Acute renal failure

Acute urinary tract
obstruction

Kidney amiloidosis

Kidney tumor

Diabetic nephropathy

Nephropathy of the pregnant

Hereditary defect of renal

vessels
Polycystic kidney disease

Renal vessels atherosclerosis,

embolism or thrombosis

Etiology
secondary H
4. Endocrinopathy
(develops in the result of endocrine glands pathology)
Acromegaly
(Somatotropin over production by
the pituitary gland anterior
part)

Cushing's disease
(Adrenocorticotropin over
production by the pituitary gland
anterior part)

Pheochromocytoma

Hyperaldosteronism (aldosteron
over excretion by suprarenal
glands)

Menopause
(age-depended decrease of female
gonads activity estrogens
excretion decrease)
Possible mechanism deficit of
NO synthesis by
endotheliocytes

Etiology
secondary H
5. Neurogene
(is accompanying to nerves system pathology)
Encephalitis
Brain tumor

Brain trauma
Brain ischemia

Brain hemorrhage

Etiology
secondary H

6. Cardiac
Heart defect

Heart failure

7. Drug-induced
Drugs, which cause vessels spasm (influent
on kidney), hormonal contraceptives

Arterial hypertension after-effects

1st period
functional violations
(heart hypertrophy)

2d period
Pathological changes in arteries and arterioles (dystrophy):
-

Arterioles sclerosis
Arterioles wall infiltration by plasma (leads to dystrophy)
Arterioles necrosis (hypertonic crisis arises in clinic)

Veins wall thickening

Arterial hypertension after-effects

3d period
Secondary changes in organs and systems
CNS

Kidney
(nephrosclerosis and chronic
kidney insufficiency)

brain hypoxia
neurons destruction
apoplexy (because vessels destruction and rupture
leads to brain hemorrhages and brain
destruction)

Heart
Decompensate heart failure

Organs of vision
retinopathy (retinas vessels injury)
hemorrhages and separation (exfoliation) of
retina, that leads to blindness

Endocrine system
Glands atrophy and sclerosis

JAZAA KUMULLAH KHAIRAN

KATSIRAN