Cardiac physiology, Topnotch Flashcards
Blood flow velocty in the aorta
11cm/sec
Blood flow velocity in the capillaries
0.03cm/sec
Control conduits for blood flow
Arterioles
Receptor for venous and arteriolar vasoconstriction in the skin, splanchnic, and renal circulation
a1
Receptor for arteriolar vasodilation in the skeletal muscles
b2
T/F: Capillaries undergo vasoconstriction and vasodilation
F
Law: Blood flow is proportional to pressure difference and inversely proportional to resistance
Ohm’s law
Law: Resistance is proportional to blood viscosity and length of vessel and inversely proportional to radius of vessel raised to the fourth power
Poiseuille’s law
Factors that affect Reynold’s number
1) Blood density
2) Blood viscosity
3) Blood flow velocity
4) Blood vessel diameter
Laminar vs turbulent: High Reynold’s number
Turbulent
Highest arterial BP
SBP
Lowest arterial BP
DBP
Systolic pressure-diastolic pressure
Pulse pressure
Central venous pressure is synonymous to ___ atrial pressure
Right
Pulmonary capillary wedge pressure estimates ___ atrial pressure
Left
Mean aortic pressure
100mmHg
Mean arteriolar pressure
50mmHg
Mean capillary pressure
20mmHg
Pressure in vena cava
4mmHg
Glomerular hydrostatic pressure
60mmHg
ECG: AV node conduction
PR segment
ECG: Conduction time through AV node
PR interval
ECG: Ventricular repolarization
T wave
ECG: Depolarization + repolarization of ventricles
QT interval
ECG: Plateau of ventricular action potential
ST segment
Effect on ECG: Flat/inverted T wave
Hypokalemia
Effect on ECG: Low P wave, tall T wave
Hyperkalemia
Effect on ECG: Prolonged QT interval
Hypocalcemia
Effect on ECG: Shortened QT interval
Hypercalcemia
PR segment
End of P wave, start of QRS complex
PR interval
Start of P wave, start of QRS complex
QT interval
Start of QRS complex, end of T wave
ST segment
End of QRS complex, start of T wave
Ventricular action potential: Phases
0-4
Ventricular action potential: Phase 0
Na influx (depolarization)
Ventricular action potential: Phase 1
K efflux (partial repolarization)
Ventricular action potential: Phase 2
Ca influx (plateau)
Ventricular action potential: Phase 3
K efflux (complete repolarization)
Ventricular action potential: Phase 4
RMP
SA node action potential: Phases
0,3,4
SA node action potential: Phase 0
Ca influx (depolarization)
SA node action potential: Phase 3
K efflux
SA node action potential: Phase 4
Slow Na influx towards threshold
Rate of phase 4 depolarization (fastest to slowest)
SA node > AV node > His-Purkinje system
Master pacemaker of the heart
SA node
Cardiac pacemaker with the slowest conduction velocity of 0.01-0.05m/sec
AV node
Cardiac pacemaker with the fastest conduction velocity of 2-4m/sec
His-Purkinje system
Intrinsic firing rate: SA node
70-80bpm
Intrinsic firing rate: AV node
40-60bpm
Intrinsic firing rate: Bundle of His
40bpm
Intrinsic firing rate: Purkinje fibers
15-20bpm
Stable vs unstable: RMP of SA node
Unstable
Stable vs unstable: RMP of latent pacemakers
Stable
RMP of latent pacemakers
-90mV
Time required for excitation to spread throughout cardiac tissue
Conduction velocity
Conduction velocity is proportional to
Inward current during upstroke
RMP of cardiac muscle is determined by
Conductance to K
Accounts for SA node automaticity
If/slow funny Na channels
Phase of cardiac AP responsible for setting the heart rate
Phase 4
Propagation of AP around the ventricles wherein the sign never reaches an area with ARP
Circus movements
Circus movements are the basis for
Vfib
Causes for circus movements (3)
1) Long conduction pathway
2) Decreased conduction velocity
3) Short refractory period
Condition wherein there is a long conduction pathway
Dilated cardiomyopathy
Conditions wherein there is decreased conduction velocity (3)
1) Ischemic heart
2) Hyperkalemia
3) Blocked Purkinje
Condition wherein there is a short refractory period
1) Epinephrine
2) Electrical stimulation
All Na inactivation gates closed
Absolute refractory period
Some Na inactivation gates start to open
Effective refractory period
T/F: AP can be conducted during ERP
F
AP can be conducted with a higher than normal stimulus
RRP
All Na inactivation gates open; membrane potential is higher than RMP
Supranormal period, cell is more excitable than normal
Drugs that change heart rate
Chronotropic
Drugs that change conduction velocity
Dromotropic
Drugs that change contractility
Inotropic
Drugs that change rate of relaxation
Lusitropic
Affected by chronotropes
SA node
Affected by dromotropes
AV node
Affected by inotropes
Stroke volume
Preload of the heart
Left ventricular end-diastolic volume
Afterload of the heart
Aortic pressure
Increase in preload will increase stroke volume within certain PHYSIOLOGIC LIMITS
Frank-Starling mechanism
Frank-Starling mechanism is due to (2)
1) Maximum degree of overlap between actin and myosin
2) Reduction of space between thick and thin filaments
Proportional vs inverse: LVEDV and venous return
Proportional
Proportional vs inverse: LVEDV and right atrial pressure
Proportional
Blood ejected by the ventricle per heart beat
Stroke volume
Percentage of EDV ejected by the ventricle per heart beat
EF
Total blood volume ejected per unit time
Cardiac output
Formula: Stroke volume
EDV-ESV
Formula: EF
SV/EDV
Formula: CO
HR x SV
Normal stroke volume
70mL
Normal EF
55%
Normal CO
5L/min
Work the heart performs with each beat
Stroke work
Work per unit time
Cardiac minute work
Ratio of work output to total chemical energy expenditure
Maximum efficiency of cardiac contraction
Stroke work is equal to
SV x aortic pressure
Primary source of energy for stroke work
Fatty acids
Cardiac minute work is equal to
CO x aortic pressure
Myocardial O2 consumption is increased by (4)
1) Afterload
2) Size of heart
3) Contractility
4) Heart rate
Normal maximum efficiency of cardiac contraction
20-25%
Phases of the cardiac cycle
1) Atrial contraction/systole
2) Isovolumetric contraction
3) Rapid ventricular ejection
4) Slow ventricular ejection
5) Isovolumetric relaxation
6) Rapid ventricular filling
7) Slow ventricular filling
Occurs during distal 3rd of systole
Atrial contraction
T/F: Atrial contraction is essential for ventricular filling
F
Atrial pressure wave seen with atrial contraction
a wave
Abnormal heart sound heard with atrial contraction against a stiff ventricle
S4
Atrial wave seen in isovolumetric contraction
c wave
Heart sound heard during isovolumetric contraction
S1 (AV valves close)
Atrial filling begins at this phase
Rapid ventricular ejection
ECG wave seen in reduced ventricular ejection
T wave
Phase of cardiac cycle where incisura of aortic pressure is seen
Isovolumetric relaxation
Atrial pressure wave seen in isovolumetric relaxation
v wave
Heart sound heard with isovolumetric relaxation
S2
Heart sound heard during rapid ventricular filling
S3
Rapid ventricular filling takes place in which part of diastole
First 1/3
Longest phase of the cardiac cycle
Reduced ventricular filling
Reduced ventricular filling is aka
Diastasis
Length of reduced ventricular filling is dependent on
Heart rate
Reduced ventricular filling occurs during
Middle 3rd of diastole
Increase vs decrease in aortic pressure: Incisura
Increase
BP control (3)
1) Central
2) Acute
3) Long-term
Central control of heart rate and BP
Vasomotor area of medulla
Portion of medulla: Excitatory to the CV system
Lateral
Portion of medulla: Inhibitory to the CV system
Medial
Acute controllers of BP
1) ANS
2) CNS ischemic response
3) Baroreceptors
4) Chemoreceptors
5) Lower pressure receptors
Long-term control of BP
RAAS
SY vs PSY: Greater control of the BP
SY
Buffers minute-to-minute changes in BP
Baroreceptors
Location of baroreceptors (2)
1) Carotid sinus
2) Aortic arch
Carotid baroreceptors respond to increase/decrease in pressures from
50-180mmHg
Aortic baroreceptors respond to pressure ___mmHg
> 80
Chemoreceptors respond to (2)
1) Low O2
2) High CO2
3) GIVEN BP less than 80mmHg
Location of low pressure receptors (2)
1) Atria
2) Pulmonary arteries
Low pressure receptors respond to
Increased intravascular volume
Responses of low pressure receptors
1) Increase ANP
2) Decrease ADH
3) Renal vasodilation
4) Increase heart rate
Increase in heart rate to match vascular resistance with cardiac output
Brainbridge reflex
CNS ischemic response starts at ___mmHg
Less than 60
CNS ischemic response is optimal at ___mmHg
15-20
In CNS ischemic response, all systemic arterioles vasoconstrict EXCEPT (2)
1) Cerebral vessels
2) Coronary vessels
Cushing reflex/reaction is a response to
Increased ICP
Cushing reflex/reaction: Triad
1) Htn
2) Bradycardia
3) Irregular respirations
Responsible in maintaining normal BP despite wide variation in salt intake
RAAS
RAAS takes ___ to take effect
20 minutes
Normal capillary hydrostatic pressure
25mmHg
Normal capillary oncotic pressure
28mmHg
Normal interstitial hydrostatic pressure
-3mmHg
Causes interstitial hydrostatic pressure to be negative
Lymphatic pump
Normal interstitial oncotic pressure
8mmHg
Hydraulic conductance of capillary wall
Filtration coefficient
Normal net filtration in capillaries
2mL/min
Net filtration pressure in kidneys
10mmHg
Amount of lymph produced per day
2-3L
T/F: Lymphatic vessels have valves
T
Cause of edema in burns and inflammation
Increased filtration coefficient
Mechanisms for control of local blood flow
1) Acute control
2) Long-term control
Mechanisms for ACUTE control of LOCAL blood flow
1) Myogenic theory
2) Metabolic theory
3) Autoregulation
Myogenic theory of BP control
Stretching of vascular smooth muscle causes a reflex contraction and vice verse
Metabolic theory of BP control
Metabolic activity causes release of vasodilator substances
Mechanisms under metabolic theory of BP control
1) O2/nutrient lack theory
2) Vasodilator theory
O2 lack theory of BP control
O2 is needed for smooth muscle contraction and lack of O2 leads to vasodilation
Nutrient lack theory of BP control
Thiamine, niacin, riboflavin, and glucose are needed for smooth muscle contraction and lack of these leads to vasodilation
Vasodilator theory of BP control
Metabolism releases adenosine, CO2, K, and hydrogen, which are vasodilators
Metabolic theory: Increase in blood flow in response to brief periods of decreased blood flow
Reactive hyperemia
Metabolic theory: Increase in blood flow to meet increased metabolic demand
Active hyperemia
Autoregulatory mechanism: Kidneys
Tubuloglomerular feedback
Autoregulatory mechanism: Brain
Response to CO2 and H levels
Autoregulatory mechanism: Heart
Response to perfusion pressure
Mechanism for long-term control of LOCAL blood flow
Angiogenesis
Susbtances that cause angiogenesis (3)
1) VEGF
2) FGF
3) Angiogenin
Angiogenesis occurs in response to
Hypoxia
Vascularity is determined by
MAXIMUM blood flow need
Most potent vasoconstrictor
ET-1
Vasodilator substance that counteracts TXA2
PGI2
Vasodilator vs vasoconstrictor: NE
Vasoconstrictor
Vasodilator vs vasoconstrictor: Epi
Vasoconstrictor
Vasodilator vs vasoconstrictor: ANP
Vasodilator
Vasodilator vs vasoconstrictor: H
Vasodilator
Vasodilator vs vasoconstrictor: CO2
Vasodilator EXCEPT at pulmonary vascular bed
Vasodilator vs vasoconstrictor: PGF
Vasoconstrictor
Vasodilator vs vasoconstrictor: K
Vasodilator
Vasodilator vs vasoconstrictor: TXA2
Vasoconstrictor
Vasodilator vs vasoconstrictor: ATII
Vasoconstrictor
Vasodilator vs vasoconstrictor: PGE
Vasodilator
Vasodilator vs vasoconstrictor: Lactate
Vasodilator
Vasodilator vs vasoconstrictor: Adenosine
Vasodilator
Vasodilator vs vasoconstrictor: Bradykinin
Arteriolar vasodilator, venous vasoconstrictor
Vasodilator vs vasoconstrictor: Histamine
Arteriolar vasodilator, venous vasoconstrictor
Special circulation/s whose major metabolic control is local rather than central
1) Cerebral
2) Coronary
3) Pulmonary
4) Renal
5) Skeletal during exercise
Special circulation/s whose major metabolic control is central (ANS) rather than local
Skin
