pathophysiologi ca dr. faesol

PATOFISIOLOGI KARDIOVASKULAR

DR.dr.Zaenal M. Sofro, AIFM, Sport & Circ. Med.

Bagian Ilmu Faal Fak.Kedokteran UGM

Na+

K+Na+

K+

-70 mV

RESTING

THRESHOLD

-0

Graduallyincreasing PNa

AUTOMATICITY

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

CV Risk Factors•Diabetes•Hypertension•Hyperlipidemia•Smoking

Atherosclerosis

MyocardialInfarction

Remodeling

CongestiveHeart Failure

End-StageHeart Disease

Death

VentricularDilation

Loss of contractility

CAD

Cardivascular Disease is a Continuum

Willem Einthoven(1860-1927)

Cardiac Physiology Electrocardiography Diagnosis

Cardiac Physiology Electrocardiography Diagnosis

Essential functions of the heart are secured Essential functions of the heart are secured by integration of electrical and mechanicalby integration of electrical and mechanical

functions of the heartfunctions of the heart

Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)

- - changes of the heart ratechanges of the heart rate- changes of stroke volume- changes of stroke volume

• Control of HR:Control of HR:- autonomic nervous system- autonomic nervous system

- - hormonal(humoral) controlhormonal(humoral) control • Control of SVControl of SV:: - preload- preload

- contractility- contractility- afterload- afterload

ST Elevation InfarctionHere’s 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 T- waves

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 V1 V4I

II

III

LATERAL

INFERIOR

ANTPOST ANT

SEPTAL

ANT

LAT

aVL

aVF

V2

V3

V5

V6

Figure 15-8

Blood Pressure

- - venous returnvenous return- extracellular fluid volume- extracellular fluid volume- myocardial contractility- myocardial contractility

- - vasoactive substancesvasoactive substances- thickening of arteriolarthickening of arteriolar wallwall

VEINS

CAPACITYVESSELS

HEART

80 mmHg 120 mmHg

SYSTOLE

DIASTOLE

ARTERIES (LOW COMPLIANCE)

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 R–A–A system

Causes leading to changes of number and size of cardiomyocytes

(Brown, 1997)(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 systemGambar 5

Blood PressureBlood Pressure

Diastolic pressure is measured when ventricles are at rest

Systolic pressure is measured as the ventricles contract

Based on: Harvard Family Health Guide

• 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 HgDiastolic – 70 - 80 (equilibration 60 - 89) mm Hg

Pressure Drops Within the Circulation

Art

erie

s

ArteriesA

rter

iole

s

ArteriolesC

apill

arie

s

Capillaries

Ven

ules

VenulesV

eins

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 (АP)by hemodynamic system

Formula: АP = CO · PRCO – cardiac output

PR – peripheral vascular resistance (depended to arterioles tone)

CO leads to PR and АP normalizes finally

PR leads to CO and АP normalizes finally

AP normal range:Systolic – 100 - 125 (equilibration 100 - 139) mm HgDiastolic – 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

Baroreceprotsin aorta & carotid bodies

Cardiovascular ctr in medulla oblongata

Vaso-constricti

on

Heart rate

Sym

p. +

Para

sym

p. -

pressure

NEURAL MECHANISMS

43

The Polyvagal TheoryBy 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)

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

Medulla oblongata (vessel’s active center)

Afferent impulses

Heart (CO increase at decreased АP)

Arterioles (spasm) Еfferent і 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

AP elevation (value above 139/89 mm Hg), which is resulted from rising of peripheral vessels resistance

(one of the most common cardiovascular disorders)

Arterial hypertension (АH)

Classification

Arterial hypotension

Arterial hypertension

AcuteChronic

Secondary

AP above 139/89 mm Hg

Primary

AP less than 100/60 mm Hg

Classification

Primary AH (essential, hypertonic disease)

Secondary AH (that is happened in 10 - 20 % cases).

It’s a symptom of some disease course

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.

Etiology (primary AH)

Contributing factors

Family history of hypertension

Age-related increases in blood pressure

Race

Diabetes mellitus

Risk Factors

Contributing factorsLifestyle Factors

Physical inactivity

High sodium intake

Stress

Excessive calorie intake and obesity

Excessive alcohol consumption

Oral contraceptive drugs

Emotional excitement (SNS activation)

Increase of circulative blood volume (CBV)

Cardiac output (CО) increase

Kidney functions violation

Peripheral vessels resistance increase

PathogenesisAP = СO х PR

Increase of circulative blood volume (CBV)

Pathogenesis

Reasons

NaCl (intake more 5 g/day)

Decrease Na excretion by kidney (kidney diseases)

1. CBV increase

Na retention in blood

Blood osmotic pressure increase

Hypervolemia

Cardiac output increase

AP elevation

Na accumulation in vessels smooth muscle wall and increase of its

osmotic pressure

Vessels wall edema

Vessels narrowing

Peripheral vessels resistance increase

Vessels smooth muscle sensitivity to

vasoconstrictive influences increase

(noradrenalin, adrenalin, endothelin, angiotensin)

Formula: АP = CO · PR

Pathogenesis

Vessels spasm

2. Cardiac output increase (CO)

Reasons

Circulative blood volume increase (CBV)

Physical (overload) stress

Emotional stress

Hyperthyroidism

Pathogenesis

2. Cardiac output increase

SAS activation

Adrenalin excretion

Increase of cardiac contractility force

Increase of cardiac output

Increase of heart beats

AP elevation

Pathogenesis

Formula: АP = CO · PR

3. SAS activation

Interaction adrenalin and alpha-adrenoreceptors

Arterioles smooth muscles spasm

Suprarenal glands activation

Venues smooth muscles spasm

Increase of circulative blood in big blood

circle adrenoreceptors of

heart

АdrenalinNoradrenalin

Increase of CBV

CO increaseArterioles

narrowing

alpha-adrenoreceptors of vessels

CO increase

AP increase

SAS activation

Arterioles narrowing

PR increase

Pathogenesis

Formula: АP = CO · PR

4. Kidney functions violation

Long time spasm of kidney arteries

AP increase

AP decrease in renal capillaries

Activation of JGA

Renin excretion

Angiotensin 2 synthesis

Angiotensin 2 effects

• 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)

Pathogenesis

Depressive function of kidney – synthesis of the substances for AP reduce

PG Е 2

Phospholipid Renin Inhibitor

Angiotensinase

Phosphatydilcholin alkali ethers

! ! !Exhaustion of kidney

depressive function leads to arterial

hypertension stabilization

dilates renal arteries, reduces renin synthesis and reduces Na

reabsorbing in kidney

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

1. Renal (resulted from kidney pathology)

Etiologysecondary АH

Acute renal failure

Kidney damage at collagenosis

Kidney amiloidosis

Diabetic nephropathy Nephropathy of the pregnant

Hereditary defect of renal vessels Renal vessels atherosclerosis,

embolism or thrombosis

Kidney tumor

Acute urinary tract obstruction

Glomerulonephritis Pyelonephritis

Polycystic kidney disease

4. Endocrinopathy (develops in the result of endocrine glands pathology)

Etiologysecondary АH

Cushing's disease (Adrenocorticotropin over

production by the pituitary gland anterior part)

Acromegaly (Somatotropin over production by

the pituitary gland anterior part)

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 endotheliocytesPheochromocytoma

5. Neurogene (is accompanying to nerves system pathology)

Etiologysecondary АH

Brain hemorrhage

Encephalitis

Brain tumor

Brain trauma

Brain ischemia

7. Drug-induced

6. Cardiac

Etiologysecondary АH

Heart failureHeart defect

Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives

1st period functional violations (heart hypertrophy)

2d periodPathological changes in arteries and arterioles (dystrophy):- Arterioles sclerosis- Arteriole’s wall infiltration by plasma (leads to dystrophy)- Arterioles necrosis (hypertonic crisis arises in clinic)- Vein’s wall thickening

Arterial hypertension after-effects

3d period Secondary changes in organs and systems

Kidney (nephrosclerosis and chronic

kidney insufficiency)

CNS – brain hypoxia – neurons destruction– apoplexy (because vessels destruction and rupture

leads to brain hemorrhages and brain destruction)

HeartDecompensate heart failure

Organs of vision- retinopathy (retina’s vessels injury)- hemorrhages and separation (exfoliation) of

retina, that leads to blindness

Endocrine systemGlands atrophy and sclerosis

Arterial hypertension after-effects

JAZAA KUMULLAH KHAIRAN KATSIRAN