Cardio Formulas and Cardiology Flashcards
Velocity of blood flow
v = volume of blood flow/cross sectional area
Blood flow is also the
Ohm’s law
Blood flow formula
Flow rate = P1 - P2/Resistance
Tendnecy for turbulent flow =
Reynolds number = (velocity of blood flow x diameter x density) / viscosity
Re = vdp/n
cm/sec, cm
Greatest in proximal aorta and pulmonary artery
Resistance of the entire peripheral circulation =
TPR = 100mmHg (Pa - Pv)/ 100ml/sec (CO or blood flow)
Total pulmonary vascular resistance =
TPVR = (16 - 2)/100
(Pulmo artery pressure - left atrial pressure)/ 100 (CO, blood flow)
Total pulmo vascular resistance = 0.14 PRU
Conductace =
Conductance = 1/ resistance
Conduntance of vessel
inc in proportion to fourth power of diameter
C inc in proportion to fourth power of diameter
The great inc in conductance when diameter inc is exemplified by
Poiseuille’s law
Velocities of all concentric rings of flowing blood x areas of the ring
Poiseuille’s law
Poiseuille’s law =
Rate of Flow = pie(pressure difference between ends of vessels)radius raised to the 4th power / 8(viscosity)(length=1)
The greatest role of all factors in determining rate of blood flow
Diameter
2/3 of total systemic resistance to blood flow comes fr
arterioles
Arterioles regulate blood flow by
Turning off blood flow (arterioloconstriction) and inc flow by 256fold by arteriolodilation
The flow through artery, arteriole, cap, venule and vein are arranged in
Series
Rtotal = R1 + R2 + R3
Blood flow to organs are arranged in
Parallel
1/Rtotal = 1/R1 + 1/R2
Total conductance = C1 + C2
Amputation of limb or removal of kidney reduces total vascular conductance and total blood flow (CO) inc total peripheral vasc resistance
Viscosity of blood is
3x as great as water
Vascular distensibility =
Vascular distensibility = inc in volume / inc in pressure x original volume
fractional inc in volume for each millimeter of mercury rise in pressure
Vascular compliance =
VC = inc in volume/inc in pressure
Compliance = distensibility x volume
So a highly distensible vessel may have far less complaince than a vessel with large volume
Pulse pressure =
pulse pressure = stroke volume/arterial compliance
Damping =
Damping = resistance x compliance
MAP is not just average of systolic and diastolic pressure bec
Bec greater fraction of cardiac cycle is spent in diastole
60 Diastolic
40 Systolic
MAP =
Averahe arterial pressure with respect to time
MAP = (SBP + 2DBP)/3
Diastolic pressure + 1/3 of pulse pressure
Four primary forces determining fluid movement in capillary membrane:
Starling forces
1 Capillary pressure
2 Interstitial fluid pressure
3 Capillary plasma colloid osmotic pressure
4 Interstitial fluid colloid osmotic pressure
Net Filtration Pressure =
NFP = (Pc-Pif)-(Plasmacoll+Ifcolloid)
Filtration=
Filtration= capillary filtration coeff x NFP
Plasma colloid osmotic pressure is 28 mmHg; 19 by proteins and 9 by Na, potassium and cations. Extra osmotic pressure is called
Donnan effect
Physiologic properties of the heart:
All or none principle
No fatigue, no tetany
Duration of cardiac muscle contraction is a function of the duration of the action potential
Is the principle that the strength by which a nerve or muscle fiber responds to a stimulus is not dependent on the strength of the stimulus
All-or-none Law
If the stimulus is any strength above threshold, the nerve or muscle fiber will give a complete response or otherwise no response at all
All-or-none law
Increase in contractility
Positive inotropic effect
Decrease in contractility
Negative inotropic effect
Ability to initiate its own beat
Ability to generate spontaneous action potential
Automaticity
Regularity of such pacemaking activity
Rhythmicity
Fibers of SA node connect with surrounding atrial muscles
Conductivity
Conduction velocity in atrial muscle
0.3-0.5 m/sec
Ability of the heart to initiate an action potential in response to an inward depolarizing current
Excitability
Smallest branches of the arteries
Arterioles
The site of highest resistance in the cardiovascular system
Alpha 1 and beta 2 adrenergic
Arterioles
Arteriole SNS receptors
Alpha 1 and beta 2 adrenergic
Contains the highest proportion of blood in the cardiovascular system
Largest total unstressed blood volume
Thin walled
Low pressure
Alpha 1 adrenergic
Veins
Gas and nutrients exchange in the cardiovascular system
Largest total cross sectional and surface area
Capillaries
A collapsed larger lumen
Thin wall
No Internal elastic lamina
Tunica media has large quantity of collagen (few smooth muscles and less elastic fibers) that is the reason they are easily compressed
Tunica adventitia is thicker than tunica media in large veins
Presence of valves to prevent back flow
Medium sized vein
Thick wall
Arteries retain their patency
Internal elastic lamina is present only in arteries
Tunica media is thicker than adventitia
Medium sized artery
Inotropic drugs
Dopamine
Dobutamine
Pacemaker of heart
Located near:
SA Node
Sulcus terminalis and SVC as it enters the right atrium
Formed bt the left and right brachiocephalic/innominate vein
SVC
Level at which the SVC is formed
1st right costal cartilage
Send blood from the heart
High pressure
Narrow lumen diameter
Thick walled
Wall layers:
T. Adventiria
T. Media
T. Intima
Large amounts of muscle and elastic fibers
No valves
Arteries
Change in HR
Chronotropic
Change in conduction velocity
Dromotropic
Send blood to the heart
Low pressure
Wide lumen diameter
Thin walled
Wall layers:
T. Adventitia
T. Media
T. Intima
Small amounts of muscle and elastic fibers
With valves
Veins
Thick walled
Extensive elastic tissue and muscles
Artery
Material exchange with tissues
Low pressure
Extremely narrow lumen diameter
Extremely thin walled
Wall layers:
T. Intima
No muscle and elastic fibers
No valves
Capillaries
Receives blood from left ventricle
Aorta
Transport under high pressure, strong vascular walls
Arteries
Control conduits, last branch of arterial system, strong muscular walls that can strongly constrict or dilate
Arteriole
Exchange substances through pores
Capillaries
Collect blood from capillaries
Venules
Low pressure, transport blood back to the heart, controllable reservoir of extra blood
Veins
Means blood flows crosswise in the vessel and along the vessel
Forms whorls in the blood called
Turbulence
Eddy currents
Normal blood flow is
Laminar
Turbulence occurs when
Radius is large (aorta) Velocity is large (cardiac output) Vessel diameter (arterial stenosis) Low viscosity (anemia) Density of blood
Reynolds number of 2000 or less is
Laminar
Reynolds number is inversely proportional to the
viscosity
Pressure gradient and blood flow
directly proportional
Pressure gradient and viscosity
Directly proportional
A high Reynolds number meant
A high possibility of turbulence
Pressure gradient and length
Directly proportional
Pressure gradient and fourth power of radius
Inversely proportional
Pressure gradient and flow rate
Directly proportional
Flow rate and vascular resistance
Inversely proportional
Volume of blood passing through per unit of time
Flow rate
Difference between the systolic and diastolic pressures
SBP-DBP
Pulse pressure
Most inportant determinant of pulse pressure
Stroke volume
Pulse pressure is increased in aging population because of
Decreased capacitance
MAP is maintained at
110-130
MAP also =
CO x SVR + CVP
The highest arterjal pressure during a cardiac cycle
Occurs when the heart contracts and blood is ejected into the arterial system
Systolic pressure
Lowest arterial pressure in the cardiac cycle
Occurs when the heart is relaxed and blood is being returned to the heart via the veins
Diastole
Fall in the pressure by 20mmHg and or >10 mmHg diastolic in resposne to moving from supine to standing
Orthostatic hypotension
At least 2 separate clinic-based measurements
> 140/90 mmHg
and at least 2 non clinic measurements <140/90 mmHg in the absence of end organ damage
White coat hypertension
PD
Rigidity, tremors
Dysautonomia
Hypotension
Shy-Drager syndrome
Multiple Systems Atrophy
Cardiac Output =
CO = HR x SV
Cardiac reserve
If resting, CO is
After exercise,
6L/min
Inc to 21 L/min
Cardiac reserve?
CR = 21-6 L/Min
Atrial contraction forces blood into ventricles
P wave
Atrial depolarization
Atrial systole
Ventricular contraction pushes AV valves closed
AV Closure
QRS Complex
Ventricle depolarization
Ventricular systole (first phase) Atrial Diastole
Semilunar valves open and blood is ejected
T wave ventricular repolarization
Ventricular systole second phase
Atrial diastole
Absence of p wave is seen in
atrial fibrillation
Preceded by the p wave Activation of stria Contributes to ventricular filling Increase in atrial pressure (A wave) Ventricular hypertrophy Fourth heart sound
Atrial systole
Begins at QRS complex
Activation of ventricles
AV valves close when V pressure is greater than A pressure
Closure of AV valves -> S1, ventricular pressure increases, no blood leaves yet because aortic valve is CLOSED
constant ventricular volume
Isovolumetric ventricular contraction
Max V pressure
C wave on venous pulse curve due to bulging of tricuspid valve intro right atrium, aortic valve opens
Ventricular volume decreases dramatically
Atrial filling begins
Onset of T wave (repolarization)
Rapid ventricular ejection
Slower ejection of blood
Ventricular pressure decrease
Aortic pressure decreases
Runoff of blood from large arteries to smaller arteries
Atrial filling
V wave (blood flow into right atrium, rising phase)
Flow to right atrium into right ventricle (falling phase)
Reduced ventricular ejection
Chambers relax and blood fills ventricles passively
Ventricular diastole (late) Atrial diastole
SV =
SV = EDV - ESV Normal = 120-50 = 70ml
Ejection fraction =
EF = SV/EDV
Normal is 70/120 = 58%
Extrinsic control of Stroke Volume: SNS
Arterial muscle (increases contractility) Ventricular muscle (increases contractility) Adrenal medulla (increase epinephrine augments the sympathetic actions on the heart) Veins (increase venous return)
Contraction of atria
Absent in atrial fibrillation
A wave
Ventricular contraction (tricuspid bulges) Won’t see
C wave
There are two positive waves
One occuring just before the first heart sound or the carotid impulse
One just after
When HR is 80 or less, they are fairly easy to time. But if the heart rate is fast, you may need to asucultate while you observe.
A (atrial contraction, absent in atrial fibrillation)
V waves
Descent
Atrial relaxation
X wave
Atrial venous filling
Occurs at the same time of ventricular contraction
V wave
Descent
Ventricular filling
Tricuspid opens
Y descent
Intrinsic control of SV
Inc strength of cardiac contraction
Inc EDV
Inc venous return
Conditions with elevated a wave
Resistance to atrial emptying may occur at or beyond the tricuspid valve
Pulmonary hypertension
Rheumatic tricuspid stenosis
Right atrial mass or thrombus
Large positive venous pulse during a wave
It occurs when an atrium contracts against a closed tricuspid valve during AV dissociation
Premature atrial/junctional/ventricular beats
Complete atrio-ventricular (AV) block
Ventricular tachycardia
Most common cause of elevated v wave
Tricuspid regurgitation
Lancisi sign
The ventricle contracts and if the tricuspid valve does not close well, a jet of blood shoots into the right atrium
Tricuspid regurgitation if significant will be accompanied by a pulsatile liver (feel over the lower costal margin)
You will also hear the murmur of tricuspid regurgitation - a pansystolic murmur that increases on inspiration
Elevated v wave
Neck veins rise in inspiration rather than fall
Seen in pericardial tamponade
Right heart failure
Acute right ventricular MI
Kussmaul’s sign
Exaggerated x wave or diastolic collapse of the neck veins
From constrictive pericarditis
Friedrich’s sign
Initial depolarization of ventricle
Conduction velocity through AV node
PR interval
Ventricular depolarization
QRS Complex
Entire ventricular depolarization and repolarization
QT interval
Muscle length prior to contractility
It is dependent of ventricular filling or EDV
Preload
Period when ventricles are depolarized
ST segment
Ventricular repolarization
T wave
Preload =
EDV
RMP of ventricle, atria and Purkine
-90mV
Upstroke
Increase in Na conductance
Phase 0
Initial repolarization
Brief
K ions move out
Na decrease conductance
Phase 1
Plateau
Transient increase in calcium conductance, inward Ca
Phase 2
Calcium conductance decrease
K increase
Membrane hyperpolarizes
Phase 3
Resting membrane potential
Phase 4
This value is related to right atrial pressure
Preload
Most important determining factor for preload is
venous return
Conduction system
SAN -> AVN -> AV bundle -> Bundle branches -> Purkinje fibers
The tension or arterial pressure against which the ventricle must contract
If arterial pressure increases,
this also increases
Afterload
Provides direct flow of current from the atrium to ventricle
Cardiac skeleton
Slowest velocity of conduction is in the
AV Node
Fastest conduction of velocity in the
Purkinje fiber
Afterload =
End systolic wall stress
Resistance
AV Node is in
Triangle of Koch
Boundaries of Triangle of Koch
Septal leaflet of tricuspid valve
Opening of coronary sinus
Tendon of Todaro
SA NODE aka
Node of Keith and Flack
Lies in the sulcus between superior vena cava and right atrium
Exhibits self excitation
SA Node
RMP of SA Node
-55 mv to -60 mv
Volume of blood pumped per minute
CO = HR (75) x SV (70)
About 5.25 L/min
Cardiac output
Difference between resting and maximal cardiac output
Cardiac reserve
Volume of blood that filles the ventricle during diastole or relaxation
EDV
120 ml
Anterior internodal pathway
Bachmann
Middle internodal pathway
Wenkebach
Posterior internodal tract
Thorel
Volume of blood remaining in ventricle after systole
ESV
50 ml
Difference between EDV and ESV
Stroke volume
Found in the posterior wall of the right atrium
Behind the tricuspid valve near the opening of the coronary sinus
Delay of impulse transmission
Small bundle fibers
Less number of gap junctions
Atrio-Ventricular Node
Divides into one single right bundle branch and 2 branches of left bundle (anterior and posterior fascicles)
His Bundle
Merges with myocardial fibers
Conduction velocity is rapid
Higjly permeable gap junctions
Large fibers
Purkinje system
CV Response to exercise
Central command
Inc Sympathetic outflow
Dec Parasympathetic outflow
Inc heart rate Inc contractility Inc cardiac output Constriction of arterioles (splanchnic and renal) Constriction of veins Inc venous return
Inc blood flow to skeletal muscle
Exercise
Local responses
Inc vasodilator metabolites
Dilation of skeletal muscle arterioles
Dec TPR
Inc blood flow to skeletal muscles
Long QT syndrome pathogenecity genes
HERG gene (K channel gene chromosome 7)
SCN5A gene (Na gene chromosome 3) Brugada
syncope
Polymorphic ventricular tachycardia
Hypokalemia
with long QT interval
Torsade de pointes
Lead II, III, aVF
Inferior
Lead I and aVL
V5, V6
Lateral
Lead VI, V2
Septal
V3, V4
Anterior