CARDIAC MECHANICS
HEART AS A PUMP
CARDIAC CYCLE
HEART FAILURE
CONTRACTILITY
Ability to contract
Depends on:……..
CARDIAC OUTPUT (CO)
CO
HR
SV
CO = HR x SV
CORONARY
FLOW
EDV
Venous return
Compliance
Aortal pressure
LV = RV SV = EDV - ESV
Ejection fraction
EF = EDV – ESV / EDV
5l/min
70ml
>60%
REGULATION
ANS
AUTOREGULATION of cardiac contraction
Heterometric: Starling law
Homeometric: Frequency effect
CARDIAC RESERVE = maximal CO / resting CO
CORONARY RESERVE = maximal CF / resting CF
CHRONOTROPIC RESERVE = maximal HR / resting HR
VOLUME RESERVE = maximal SV / resting SV
CARDIAC INDEX = CO / body surface
4 - 7
3,5
3 - 5
1,5
CF = coronary flow
CARDIAC RESERVE
CO (l/min)
WORKLOAD (W/kg)
ATHLETHS HEART
PHYSIOLOGICAL RESPONSE
HEART FAILURE
1 2 3 4
10
30
20
Cardiac
muscle
Skeletal, cardiac and smooth muscle – action potential and contraction
Skeletal
muscle
Smooth
muscle
Action potential (AP):
approx. 250 ms
Contraction: approx.
250 ms
0 200100 300 400
Time from AP
onset (ms)
AP: approx. 5 ms
Contraction:
approx. 20 ms
AP: approx. 50
ms
Contraction: approx. 1000 ms
Fluctuating resting membrane
potential
Long refractory time
AP duration depends on heart rate
Duration of the electro-mechanical
latency and contraction depends on the
fiber type (F or S)
spike
Passive tension, active tension, isometric contraction, isotonic contraction, auxotonic contraction
LENGTH – TENSION RELATIONSHIP
Fuyu Kobirumaki-Shimozawa et al., J Physiol Sci (2014) 64:221–232
STARLING LAW
Henry Pickering Bowditch
(1840 – 1911)
HOMEOMETRIC AUTOREGULATION
(FREQUENCY EFFECT)
During increasing HR (stimulation frequency) the force of developed contraction rises
Ratio between intra- and extracellular calcium concentrations increases
0,5 Hz 2 Hz1 Hz 3 Hz
AFTERLOADED CONTRACTION PRELOAD, AFTERLOAD
Length – tension relationship
EJEKČNÍ FRAKCE
LAPLACE LAW
T = P. r / h
P = T . h / r
HYPERTROPHY
1. T = VO2
2. h
AB –isovolumic contraction
BC – ejection
CD – isovolumic relaxation
DA – filling
PRELOAD AFTERLOAD
P = T . 2h . r –1 Ventricular filling: r and T rise, P first falls down, then rises up
(length/tension relationship)
P = T . 2h . r –1 Isovolumic contraction: T rises up, valves closed – increase in P
P = T . 2h . r –1 Ejection: r decreases, h rises, thus P increases (even at the same T)
P = T . 2h . r –1 Isovolumic relaxation: T decreases, valves closed – decrease in P
I. III.II. IV.
I. – mitral (+ tricuspidal) valve closure
II. - aortal (+ pulmonary) valve closure
III. - fast filling of ventricles - pathological
IV. - contraction of atria – mostly pathological
Caused by vibration of:
•Closure and stretching of
valves
•Izovolumic contraction of heart
muscle (papill. muscles, tendons)
•Turbulent blood flow
Vibration of ventricular wall
HEART SOUNDS
MURMURS – pathological phenomena
1. SYSTOLIC:
• Stenosis – aortal, pulmonary (1)
• Regurgitation – mitral, tricuspidal (2)
2. DIASTOLIC:
• Stenosis – mitral, tricuspidal (3)
• Regurgitation – aortal, pulmonary (4)
3. SUSTAINED:
• Defects of septum I. III.II. IV.
Splitting of I. or II. sound:
asynchronous closure of
M - T valve (I.)
or Ao - P valve (II.)
(inspiration,
hypertension….)
TURBULENT BLOOD FLOW
POLYGRAPHY (polygram)
HEART FAILURE
The heart is not able pump sufficient amount of blood into periphery at normal
venous return.
MOST OFTEN CAUSES:
• Severe arrhythmias
• Overload – volume (aortal insufficiency, a-v shunts) or pressure (hypertension
and aortal stenosis – left overload, pulmonary hypertension and stenosis of
pulmonary valve – right overload)
• Cardiomyopathy
SYMPTOMS: fatigue, oedemas, venostasis, dyspnoea, cyanosis
ACUTE x CHRONIC. COMPENSATED x DECOMPENSATED.
ACUTE FAILURE
CARDIOGENIC SHOCK
COMPENSATION
CHRONIC FAILURE
SUDDEN DEATH
DECOMPENSATION
GRADUAL LOSS OF
CARDIAC RESERVE
COMPENSATION
HEART FAILURE COMPENSATION
BAROREFLEX
Physiological role: compensation of decrease in minimal volume of circulating fluids
Signal: BP decrease (orthostase, work vasodilatation)
Sensor: baroreceptors
Response: activation of SAS (increased HR, inotropy, BP)
Pathological signal: long-lasting decrease of BP due to heart insufficiency
Results: increased energy outcome – vicious circle
ACTIVATION OF RAAS
Physiological role: compensation of loss of circulating fluids (bleeding)
Signal: decrease in renal perfusion
Sensor: juxtaglomerular system of kidney
Response: BP increase (angiotenzin II.), water retention (aldosteron)
Pathological signal: decrease in renal perfusion due to heart insufficiency
Results: increased preload and afterload, increased energy outcome – vicious circle
DILATATION (STARLING PRINCIPLE)
Physiological role: compensation of momentary right-left differences
Signal: orthostase, deep breathing, beginning of exercise
Pathological signal: continual blood stasis in the heart
Results: increased energy outcome – vicious circle
HYPERTROPHY
Physiological role: preservation of energetically demanding tension of
ventricular wall
Signal: P = s . 2 h / r, intermittent BP increase (athletes heart)
Response: concentric remodelling
Pathological signal: continual increase of preload or afterload
Results: worsening of oxygenation, fibrotisation – vicious circle