Module 6: Cardiovascular Flashcards
CARDIAC CYCLE: PHASES
- Period of Atrial Systole/Pre-systole
- Isovolumic contraction period
- Rapid/Maximum Ejection
- Reduced Ejection
- Protodiastole
- Isovolumic Relaxation
- Rapid Filling
- Reduced filling/Diastasis
TIMING (Events on the 2 sides of the heart are similar
but somewhat asynchronous.)
- Right atrial systole precedes left atrial systole
- Contraction of right ventricle starts after that of left ventricle
- Right ventricle ejection begins before the left. Because pulmonary pressure is lower than aortic pressure.
- During inspiration, aortic valve closes slightly before the pulmonary valve. Due to the lower impedance and distensibility of the pulmonary vascular bed
- Normally between 0-4 mmHg
- PEAKS
A Wave - A TRIAL CONTRACTION
C Wave - C ONRACTION OF VENTRICLES – OVERBULGING OF AV VALVES
V Wave – V ENOUS BLOOD GOING TO THE ATRIUM
ATRIAL PRESSURE PULSE
We plot this curve at 80 mm Hg level because aortic pressure is always high. Remember that:
- Blood Vessels are always in a condition or state of being slightly filled with blood
- Aorta made up of elastic tissues therefore can be stretched within limits
- If remove stretch — recoils
The rise and fall of Aortic Pressure Pulse reflects the balance between:
- The volume of blood entering the aorta from the heart
2. The volume of blood leaving the aorta and draining into the periphery, called ‘PERIPHERAL RUN-OFF”
- When ejection exceeds run-off, Aortic Pressure increases
- When run-off exceeds ejection, Aortic Pressure __
goes down or decreases
- Occurs during the distal third of diastole
- Preceded by p-wave in the ECG
- Slight increase in atrial pressure, ventricular pressure and ventricular volume
- NOT essential for ventricular filling
Atrial Contraction
- Preceded by QRS complex in the ECG
- First Heart Sound (S1) is heard
- Increase in ventricular pressure BUT ventricular volume remains the same
- Ventricular Pressure
Isovolumic Contraction
- Ventricular Pressure > Aortic Pressure
- *Semilunar valves open
- Rapid Increase in Ventricular Pressure, Decrease in Ventricular Volume
Rapid Ventricular Ejection
- T-wave occurs in the ECG
- Decrease in ventricular pressure, decrease in ventricular volume
Reduced Ventricular Ejection
- Ventricular Pressure Atrial Pressure
- *AV valves are still closed
- Decrease in ventricular pressure BUT ventricular volume remains the same
- Second Heart Sound Heard (S2)
Isovolumic Relaxation
- Ventricular Pressure
Rapid Ventricular Filling
- Reduced increase in ventricular volume
- Middle 1/3 of diastole
Reduced Ventricular Filling
- are vibrations caused by turbulent flow of blood and contraction of ventricular muscle, which are transmitted through the supporting tissues and to the chest wall
HEART SOUNDS
- associated with the closure of the AV valves at the onset of systole and isovolumetric ventricular contraction
- Soft closure
- slightly prolonged, soft, low-pitched
- duration of 0.15 seconds
- splitting when mitral valve closes before tricuspid valve
- heard best at MITRAL AND TRICUSPID AREA
FIRST HEART SOUND (S1)– “LUB”
- occurs at the end of systole as the pulmonary and aortic valves closed
- Snapping closure
- shorter, louder, high-pitched
- duration of 0.12 secs
- inspiration causes splitting of 2nd HS because aortic valve closes slightly before pulmonary valve
- heard best at PULMONIC AND AORTIC AREA
SECOND HEART SOUND (S2)–“DUP”
- associated with the rapid in rush of blood during rapid ventricular filling
- soft, low-pitched, duration of 0.1 sec
- recordable in from 26 to 85% of normal person
- maybe present 0.04 to 0.12 seconds after the onset of the second sound
- is most common in the presence of mitral stenosis
- normal in children
THIRD HEART SOUND (S3)
- associated with the atrial systole / contraction of the atrium – filling of ventricle
- recorded in 25% of normal person
- sometimes heard immediately before 1st heart sound
- not audible in normal adults
- audible in persons with left ventricular hypertrophy associated with hypertension
- present also when atrial pressure is high
FOURTH HEART SOUND (S4)
- are abnormal heart sounds which can be produced by:
1. blood flowing rapidly in the usual direction through an abnormally narrowed valve (STENOSIS)
2. blood flowing backward through a damaged, leaky valve (INSUFFICIENCY)
3. blood flowing between the 2 atria or 2 ventricles through a small hole in the wall separating them.
MURMURS
A murmur heard throughout systole suggest __
stenotic semilunar valve or insufficient AV valve
A murmur heard during diastole suggests __
stenotic AV valve or an insufficient semilunar valve
Occasionally, a 3rd heart sound is heard which give rise to a triple beat that resembles the hoof beats of a galloping horse, called __. Most frequently associated with congestive heart failure.
GALLOP RHYTHM
The function of the ventricles is described by three parameters
- Stroke volume
- Ejection Fraction
- Cardiac output
CARDIODYNAMICS
- The volume of blood ejected on one ventricular contraction or the volume ejected on one beat (ml/beat)
- The difference between the volume of blood in the ventricle before each ejection and the volume remaining in the ventricle after each ejection
- SV = EDV – ESV
STROKE VOLUME
- The fraction (percent) of the EDV that is ejected in each stroke volume
- The ratio of SV to EDV and normally 60% to 65%
- Expressed by the ff equation:
EF = SV/EDV - A valuable index of ventricular function (contractility)
- Increases in EF reflects an increase in contractility
- Decreases in EF reflects a decrease in contractility
EJECTION FRACTION
When strength of contraction increases without an increase in fiber length, more blood in the ventricle is expelled, thus, __
EF increases and ESV decreases
- The total volume of blood ejected per minute
- CO (ml/min) = SV (ml/beat) x HR (beats/min)
- Direct proportionality true within limits
- If HR remains constant, CO increases in proportion to Stroke Volume (SV). Thus factors that increases SV can increase CO
- If SV remains constant, CO increase in proportion to HR up to about 180 beats/min
- HR and SV do not always change in the same direction
Cardiac Output
Cardiac Output
CO = Stroke Volume (EDV-ESV) x Heart Rate
Factors that affect cardiac output: Heart Rate (100 beats/min) – 70 beats/min
- respiration
- body temp.
- electrolyte concentration
- exercise
- emotions
- is the quantity of blood flowing from the veins into the right atrium each minute. The __ and the cardiac output must equal each other except for a few heartbeats at a time when blood is temporarily stored in or removed from the heart and lungs.
Venous return
EFFECT OF RESPIRATION ON HEART RATE
Inspiration → ↑ heart rate
Expiration → ↓ heart rate
Inspiration → ↓ Intrathoracic Pressure → ↑ venous return (right atrium) → ↑atrial volume → (+) atrial stretch receptors → ↑ heart rate
- the stretched right atrium initiates a nervous reflex called the __, passing first to the vasomotor center of the brain and then back to the heart by way of the sympathetic nerves and vagi, also to increase the heart rate.
Bainbridge Reflex
This law states that when increased quantities of blood flow into the heart, the increased blood stretches the walls of the heart chambers. As a result of the stretch, the cardiac muscle contracts with increased force, and this empties the extra blood that has entered from the systemic circulation. Therefore, the blood that flows into the heart is automatically pumped without delay into the aorta and flows again through the circulation.
Frank-Starling law of the heart
Factors Affecting Stroke Volume
- PRELOAD
- The load that stretches the cardiac muscle before contraction
- The degree of tension on the muscle when it begins to contract.
- Considered to be the end diastolic pressure, when the ventricle has been filled - AFTERLOAD
- Degree of vascular resistance to ventricular contraction
- The load against which the muscle exerts its contractile force - Inotropic State – Myocardial Contractility
FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM)
Increased heart rate
- more Action Potential per unit time
- more Ca++ enters myocardial cell during plateau of Action Potential
- more Ca++ released from Sarcoplasmic Reticulum
- greater tension produced during contraction
Control of Stroke Volume
A) HETEROMETRIC
- regulation of Stroke Volume as a result of changes in cardiac muscle fiber length (Frank Starlings Principle)
B) HOMEOMETRIC (includes nervous and hormonal control)
- not dependent on muscle length
HOMEOMETRIC REGULATION: Nervous Control (autonomic nervous system)
sympathetic → ↑ distensibility and force of ventricular contraction
parasympathetic → ↓ atrial force of contraction
HOMEOMETRIC REGULATION: Hormonal Control
- catecholamines → ↑ distensibility and force of ventricular contraction (cAMP on B1 adrenergic receptors)
- acetylcholine → ↓ atrial force of contraction (acting on muscarinic receptors )
- thyroxine
- glucagon → increases cAMP
Other Factors that increases stroke volume
- respiration agents
- caffeine
- theophylline (↑ cAMP)
- digitalis
- temperature
Factors that determine an adequate End Diastolic Volume:
- Filling time of Ventricle - dependent on cardiac rate
- Distensibility of Ventricle (Vent Compliance)
- Stronger Atrial Contraction
- INTRAPERICARDIAL PRESSURE
- Adequate Venous Return
- Increase in ventricular stiffness produced by Myocardial Infarction
- in heart failure, there must be a greater stretch of myocardium to achieve the needed Cardiac Ouput
- attained by administration of + inotropes
Distensibility of Ventricle (Vent Compliance)
- a minor factor
- not very essential for ventricular filling WHY:
- adequate filling is often observed in patients with atrial fibrillation, despite absence of atrial contraction
- severe Tachycardia period of ventricular systole becomes markedly shortened ventricular filling is seriously impaired despite the contribution of atrial contraction
Stronger Atrial Contraction
Contribution of Atrial Contraction is governed by:
- Heart rate - Moderate Tachy diastasis shortened therefore atrial contraction becomes substantial
- Stenotic AV Valve - Atrial contraction is important in ventricular filling
- when increased, limits the extent in which the ventricle can fill»_space; decreased EDV»_space; decreased CO
ex. Pericardial effusion – heart muscle - cannot stretch enough to receive blood from the atrium
INTRAPERICARDIAL PRESSURE
- flow of blood from periphery back to right atrium
- main determinant of cardiac output
- The degree of myocardial stretch created by venous return is called the PRE-LOAD on the heart
Adequate Venous Return (VR)
Factors that influences Venous Return
- Total Blood Volume
- Increased Venous Tone (constriction of veins)(Sympathetic Tone)
- venoconstriction
- reduces the size of venous reservoir
- decreases venous pooling
- increases VR - Posture
- gravitational force causes pooling of blood in the legs (venous pooling)
- standing decreases VR
- decrease CO because of pooling of blood in lower limbs - Skeletal Muscle Pump
- Respiratory / Thoraco – Abdominal Pump Practical Application : Cardiac patients refrain from Valsalva’s maneuver
- determined primarily by the balance between the force of contraction of the ventricle and aortic pressure.
a) force of myocardial contraction
b) aortic pressure load ( afterload )
END SYSTOLIC VOLUME
End Systolic Volume Determined by:
- AFTER LOAD
- In the left ventricle, afterload is equal to all the forces the muscle must overcome to eject at given volume of blood
- Dependent upon:
* Aortic pressure – the major contributor to afterload in the heart
* State of semilunar valves - CONTRACTILITY
- Increased myocardial contraction – decreased ESV
- Severely dilated heart (heart failure) – ESV can become much greater than SV
- Decreased by increases in myocardial contractility and heart rate
- Increased whenever heart is weakened (heart failure)
- Increased with increased outflow resistance (aortic valve stenosis, increased aortic pressure)
- Examination of ESV is clinically useful as an indicator of conditions affecting the heart
END SYSTOLIC VOLUME
Cardiac Output Varies According to:
- Level of activity of the body
- Strenuous exercise: Cardiac Outpu = 35 L/min
- Entire blood volume pumped around the circuit seven times per minute
- Cardiac Reserve - Size of Body (Surface Area)
- Cardiac Output increases in proportion to the surface area of the body, stated in terms of CARDIAC INDEX
- The amount of blood pumped out of the ventricle per minute per square meter of body surface area
- Cardiac Index = CO divided by body surface area
* Normal adults = 3 L/min/ sq.m.
* 10 yrs age = 4 L/min/ sq.m.
* 80 yrs age = 2.4 L/min/ sq.m.
- the difference between Cardiac Ouput at rest and the maximum volume of blood the heart is capable of pumping per minute
- The maximum amount of blood that can be pumped out by the heart above normal value
- Essential to withstand the stress of exercise
- Expressed in percentage
- Normal Young Adult = 300 - 400%
- Old Age = 200 – 250%
- Athletes = 500 – 600%
- Cardiac diseases = minimum or nil
CARDIAC RESERVE
- Work the heart performs on each beat
- Is equal force (aortic pressure) x Distance (SV)
- SW = AP x SV
- Cardiac work = ABP x SV
- amount of work done by right heart
STROKE WORK
Variations in Cardiac Output: Physiological Variations
- Sleep- no change
- Age
- Sex
- Body build
- Diurnal condition – low early morning
- Environmental conditions - Temperature above 37 degrees centigrade raises CO
- Emotional conditions – anxiety, excitement increases CO to 50%
- After meals – increased during first hour after meal to 30%
- Exercise – increases up to 700%
- Pregnancy – increased by 45 to 60 % during later pregnancy
- Posture – recumbent to upright, decreases CO because of pooling of blood in the lower limb
PATHOLOGICAL VARIATIONS: Cardiac Output increased in
- Fever due to oxidative process
- Anemia due to hypoxia
- Hyperthyroidism – increased basal metab
PATHOLOGICAL VARIATIONS: Cardiac Output decreased in
- Hypothyroidism
- Atrial fibrillation
- Congestive heart failure
- Heart block
- Hemorrhage
- Valvular lesions (insufficiency)
Measurement of Cardiac Output
- Direct Method
a. Use of cardiometer
b. Use of flowmeter
- Mechanical flowmeter
- Electromagnetic flowmeter
- Ultrasonic doppler flowmeter - Indirect Method
- Using FICK’s principle
- CO = O² consumed (in ml/min) / Arteriovenous O² difference
The heart rests upon the diaphragm and its apex is directed downward, forward and to the left. Strictly speaking, it is only the apical portion of the heart that goes beyond the sternum and occupies the left side of the chest.
Physiologic Anatomy of the Heart
- Normally heard / palpated at the the 5th ICS, LMCL
- Caused by ventricular contraction which rotates the heart, giving rise to a tap by the tip of the ventricle
Apex Beat
Enclosed in a 2-layered serous membrane, the PERICARDIUM, forming the pericardial sac
Visceral Layer - adheres to the surface of heart
Parietal Layer - attached to heart only at point of entrance of big vessels
Sac composed of fibrous connective tissue, not very distensible
- Helps prevent sudden overdistention of the heart chambers
- Congenital absence is NOT fatal
- Contains thin layer of serous fluid (30 mL) for lubrication
a progressive and sustained enlargement of the heart
Cardiac Hypertrophy
- an acute change in cardiac pressure
- Condition in which bleeding occurs between ventricle and pericardium due to puncture of coronary vessels during cardiac catheterization
- Bleeding compresses ventricles
Cardiac Tamponade
a slow progressive increase in pericardial fluid
Pericardial Effusion
scar tissue following __ in which inflamed pericardium eventually adheres to the epicardial tissues
Pericarditis
- condition that leads to irreversible changes and death of cardiac muscle cells.
- occurs when the blood supply to the myocardium is interrupted.
- manifested by chest pain that usually radiates to the lower jaw and shoulder.
Myocardial Infarction
FOR CONTRACTION
- normally non automatic
- main bulk of cardiac muscle
- examples: atrial muscle fiber; ventricular muscle fiber
FOR IMPULSE CONDUCTION
- automatic cells
- less abundant
- examples: SA node; AV node; Bundle of His; Purkinje fibers
Myocardial Cells
Physiologic Properties of the Heart
- Chronotropism / Autorhythmicity
- Dromotropism / Conductivity
- Bathmotropism / Excitability
- Inotropism / Contractility
- Spontaneously generates impulse without neural input
- Has an unstable RMP
- Has no sustained plateau
Action Potential of SA and AV Node
- Aka maximum diastolic potential
- The longest portion of the nodal Action Potential (AP)
- Accounts for the automaticity of nodal cells
- Slow depolarization produced by the opening of sodium channels → inward Na current
- Sodium current called If – f stands for funny
- Turned ON by repolarization from the preceding AP, ensuring that each AP is followed by another AP
- As threshold is reached (-40 mV), the T-type calcium channels open for the upstroke
Phase 4 (Pacemaker Potential)
- Increased calcium conductance
- Increased inward calcium current
- Calcium influx is carried by T-type calcium channels
- Not inhibited by calcium channel blockers like verapamil
Phase 0 (Upstroke)
Specialized Conduction System of the Heart
- SA Node (Node of Keith and Flack)
- AV Node
- Bundle of His: 0.12 m/s
- Bundle branches – right and left
- Purkinje system – spread throughout subendocardial region of ventricle
- Conduction velocity is 1.5 – 4 m/s
- Ventricular muscle fibers: 0.5 m/s
- 0.8 m/s
- Anterior interatrial tract
- Atrial muscle fiber: 0.3 m/s
- Internodal tracts
*Preferential pathway: 1.0 m/s
Anterior internodal tract of Bachman
Middle internodal tract of Wenckebach
Posterior internodal tract of Thorel
SA Node (Node of Keith and Flack)
- Node of Kent and Tawara: 0.05 m/s
- AN region (atrionodal) – site of principal delay
- N region (nodal/middle nodal) - where AV block most likely to occur
- NH (nodal His) – assumes pacemaker function is SA node is depressed
- Ensures that ventricles have sufficient to fill with blood before they are activated and eventually contract
- Slow conducting velocity is attributed to the small diameter of the nodal cells
AV Node
- Are irritable/excitable cells (able to respond to stimulus)
- Can be stimulated by:
Electrical energy – electrical current, defibrillator
Mechanical energy – blood stretching the heart
Chemical energy – epinephrine and norepinephrine - Can respond by:
Generating impulses / AP
Conducting impulses
Contracting - Their contraction requires
AP generated from SA node
ATP
Ca2+ from ECF (main source) and ICF/sarcoplasmic reticulum
Excitability: Myocardial cells
- Presents striations of dark and light bands
- Has the sarcomere as contractile
- Runs from Z line to Z line
- Contains thick filament (myosin) and thin filaments (actin, troponin & tropomyosin)
- Has sarcotubular system
THE MYOCARDIAL CELL STRUCTURE
Shortening occurs according to sliding filament model
- Skeletal Muscles – one sarcomere has 2 T-tubule system
- Cardiac Muscles – a sarcomere has only 1 T-tubule, located at Z line rather than at junction of A and I band
- T-tubule in cardiac muscle well developed, wider diameter, stores calcium also, form DIADS with the SR
- SR in cardiac muscle less developed, store less calcium, small diameter
- T-tubule have a diameter 5x as great as that of the skeletal muscles T-tubule (volume of 25x as great)
- Inside the T-tubules are mucopolysaccharides which are electronegatively charged and bind an abundant store of calcium
- Cardiac muscle functions as a __
- A stimulus applied to any one part of the cardiac muscle results in the contraction of the entire muscles
- 2 Syncytiums
1. Atrial Syncytium
2. Ventricular Syncytium
SYNCYTIUM
Other features of cardiac muscles
- Slow muscle - Cardiac muscle contracts repetitively for a lifetime thus requires continuous oxygen supply and so dependent on oxidative metabolism
- Very rich in mitochondria which contain the enzymes needed for oxidative Phosphorylation (sustains the myocardial energy requirements)
- Endowed with a rich capillary supply (one capillary per fiber) to provide adequate oxygen
- High content of MYOGLOBIN – a pigment which functions as an oxygen storage mechanism
Two different proteins are phosphorylated to produce the increase in contractility
- Phosphorylation of the sarcolemmal calcium channels that carry inward calcium current during Plateau phase.
- Phosphorylation of Phospholamban – a protein that stimulates calcium ATPase, resulting in greater uptake and storage of calcium by the SR.
Two factors determine how much calcium is released from the Sarcoplasmic Reticulum
- The size of the inward calcium current during the plateau of AP (size of the Trigger calcium)
- The amount of calcium previously stored in the SR for release.
**The larger the inward calcium current and the larger the intracellular stores, the greater the increase in intracellular calcium concentration and the greater the contractility.
The amount of extracellular calcium entering the cell during phase 2 (Plateau) is directly proportional to the:
- Extracellular calcium concentration
- Number of open calcium channels
- Duration of Action Potential
- Number of action potentials
FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM)
- Increased heart rate
- more Action Potential per unit time
- more Ca++ enters myocardial cell during plateau of AP
- more Ca++ released from SR
- greater tension produced during contraction - Sympathetic Stimulation (Catecholamines) via B1 receptors increase force of contraction by 2 mechanisms:
- increases the inward Ca++ current during plateau phase
- increases the activity of Ca++ pump of SR by Phosphorylation of Phospholamban. Result is more Ca++ accumulated by SR, thus more Ca++ available in subsequent beats. - Xanthines (caffeine & theophylline)
- inhibit breakdown of cAMP
FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM) 2
- Glucagon
- increases formation of cAMP used in some heart disease - Cardiac Glycosides (Digitalis)
- Increase force of contraction by inhibiting Na+, K+ - ATPase in the myocardial cell membrane. This increases intracellular Na+ which leads to increased availability of Ca++ - Length
- tension relationship in the ventricle Frank Starling’s Law of the Heart)
- direct relationship between initial fiber length and total tension developed
- at high degrees of stretch, the developed tension decreases. Not due to a decrease in the number of crossbridges between actin and myosin (skeletal muscle) because cardiac muscles do not reach this state. Severely dilated hearts not stretched to this degree
This enhanced contractility helps the heart eject more blood with each contraction and helps compensate for reduced filling time that is associated with tachycardia
a. positive staircase or BODWITCH STAIRCASE
- Increased HR increase the force of contraction in a stepwise fashion as the intracellular calcium increases cumulatively over several beats
- Force-frequency relationship
b. Post - extra systolic potentiation
- the beat after an extra systole has increased force of contraction because extra calcium entered the cells during the extra beat independent of ventricular filling
- due to increased availability of intracellular Ca††
FACTORS THAT DECREASE CONTRACTILITY
- Parasympathetic stimulation (Ach) via muscarinic receptors, decreases force of contraction by decreasing the inward calcium current during plateau phase of AP
- Calcium blocking agents
Ex. Verapamil - long acting
Nifedipine (Calcibloc) - short acting
- Impedes slow Ca++ channel – reducing the amount of Ca++ ions that enter the myocardial cells during plateau phase, thus diminishing strength of contraction
- Used in treatment of hypertension
- Hypercapnia
- Hypoxia
- Acidosis
- Drugs – barbiturates (quinidine, procainamide)
- Heart failure – Myocardial ischemia
Optimal concentrations of Na†, K† and Ca†† are necessary for cardiac muscle contraction (Sodium and Potassium)
- without Sodium - heart not excitable, will not beat
- reduction in extracellular Potassium
- has little effect on myocardial excitation and contraction
- increases in extracellular Potassium (hyperkalemia)
* loss of excitability of myocardial cells
* cardiac arrest in diastole called
- Potassium Inhibition – heart dilated and flaccid
Optimal concentrations of Na†, K† and Ca†† are necessary for cardiac muscle contraction (Calcium)
- removal of Ca++ from ECF results in
→decreased contractile force
→arrest in diastole
- increase in ECF Ca++ -enhances contractile force
- spastic contraction
- arrest in systole (Calcium Rigor)
The strength of cardiac contraction depends to a great strength on the cone, of Ca++ in the ECF
CONDITIONS AND AGENTS THAT CAN ALTER THE INOTROPIC STATE OF THE HEART
- Myocardial ischemia (lack of oxygen to heart) – results in inhibition of the calcium channels therefore (-) Inotropism
- Acidosis (increased plasma H+) – inhibits myocardial contractility
- Cardiac glycosides
- Have large amount of elastin in their walls.
- Highly distensible – this serves to dampen the pulsatile blood flow when blood is ejected from the ventricles and converted to a steady flow in the capillaries
- If arterial system not distensible, all blood during systole will flow to the peripheral vessels, no flow will occur during diastole
AORTA AND PULMONARY ARTERY
- thick walled with extensive development of elastic tissue, smooth muscle and connective tissue
- Transport blood under HIGH PRESSURE to the tissues.
- The volume of blood contained in the arteries called STRESSED VOLUME (blood volume under high pressure
Arteries
- The last small branches of the arterial system
- With extensive development of smooth muscle
- The medium-sized arterioles are the sites of highest resistance in the circulatory system called RESISTANCE VESSEL
- Act as CONTROL CONDUITS through blood is released to the capillaries.
Arterioles
(Arterioles)
Various factors that fall into two categories can influence the contractile activity, changing the resistance to blood flow in these vessels
- Local controls which are important in matching blood flow to the metabolic needs of specific tissues
- Extrinsic controls important in ABP regulation
- innervated by S fibers
- Alpha 1 adrenergic receptors arterioles and skin and splanchnic vascular (activation – vasoconstriction)
- Beta 2 adrenergic receptors in the arteriole of skeletal muscles (activation – vasodilation)
- Vasoconstrictor fibers exhibit tonic activity
- Ex. Sympathectomy – vasodilation
- Vasodilator fibers - no tonic activity
Arterioles
- exchange vessels
- thin – walled
- lined with single layer of endothelial cells, surrounded by a basal lamina
- lipid soluble substances (Carbon Dioxide and Oxygen) - cross capillary wall by dissolving in and diffusing across endothelial cells
Capillaries
- water soluble substance (ions) – cross capillary wall through water-filled clefts (spaces between endothelial cells) or through largest pores in capillary walls (FENESTRATED Capillaries)
- smallest diameter
- largest total surface area = 2500cm²
- slowest blood flow velocity
- selective perfusion of capillaries depending on metabolic needs of the body
- selective perfusion determined by degree of dilation or constriction of arterioles and pre capillary sphincters
Capillaries
- thin walled
- composed of endothelial cell layers, few elastic tissues, smooth muscles and connective tissues
- large capacity to hold blood because of few elastic tissues (CAPACITANCE Vessels)
- contain the largest % of blood in the CVS → 60% to 70%
- volume of blood in the veins called UNSTRESSED VOLUME (the blood volume under low pressure
- Contains one-way valves thus act as venous pumps or muscle pump.
- Venous Pressure in the lower extremities > VP in upper extremities.
Veins
DISTENSIBILITY vs COMPLIANCE
- All blood vessels are distensible
- Veins – most distensible
- Arteries – 8x less distensible than veins
- Arterial wall stronger than veins
- A vessel that is highly distensible and has a slight volume may have less compliance than a less distensible vessel that has a large volume
WHY?
- Compliance = Distensibility x Volume
- Thus the compliance of a systemic vein is 24x than that of artery
WHY?
- Because vein is 8x as distensible and has a volume of 3x as great
Compliance → 8 x 3 = 24
- Study of physical properties that govern blood flow through the blood vessels and the heart
- Blood Flow – the quantity of blood that passes a given point in the circulation in a given period of time
- Expressed in ml/min or L/min (cm3/min)
Hemodynamics
Factors that promote blood flow through the Circulatory System
- Forward motion imparted by the pumping of the heart
- Diastolic recoil of the arterial walls
- The skeletal muscle pump
- The negative intra thoracic pressure during inspiration
- the measure of the tendency for turbulence to occur
Re = (v · d · p) / η v = velocity of blood flow (cm/sec) d = diameter of vessel (cm) p = density of blood η = viscosity of blood (in poise)
Reynold’s Number (Re)
Reynold’s Number (Re)
- Reynold’s number above 200 to 400 – turbulent flow
- Turbulent flow – blood flowing in all directions in the vessels, moving in a disorderly pattern forming whorls of blood called eddy currents, often accompanied by audible vibrations (murmur)
- Turbulent flow favored by low blood viscosity, Stenotic valve, Thrombus (which narrow the diameter of the vessel)
- Volume of blood which passes through blood vessels per unit time (ml/min)
- Depends on
Pressure Gradient (P = P1 –P2)
P1 → Arterial Blood pressure – directly related to blood flow
P2 → Venous Pressure – inversely related to blood flow - The force that pushes the blood through the vessel (the driving force for blood flow
BLOOD FLOW
Depends on:
a. dimension of vessel (length and radius)
b. physical properties of blood (blood viscosity)
- depends mainly on hematocrit (percentage of volume of blood occupied by the rbc)
- amount of protein in blood (Hyperimmunoglobulin D, E and M)
- resistance of the cell to deformities (hereditary spherocytosis)
BLOOD FLOW
- Magnitude of blood flow (Q) directly proportional to size of pressure gradient (P)
Blood Flow (Q) inversely proportional to Resistance
R = P/Q - This relationship can be used to measure the resistance of the entire systemic vasculature (or the TPR); can be used to measure resistance in a single organ or single blood vessel
TPR – Total Peripheral Resistance
SVR – Systemic Vascular Resistance - When radius of blood vessel decreases, its resistance increases to the 4th power
Ex. Radius decreased by ½, Resistance increases by 16 fold
POISEUILLE FORMULA
- Illustrated by the arrangement of blood vessels within a given organ.
- Within the organ, blood flows from the major artery to smaller arteries then to arterioles, capillaries, venules, veins
- The total resistance of the system arranged in series is equal to the sum of individual resistances expressed as:
R total = R artery + R arterioles + R Capillaries + R venules
Series Resistance
__ is the greatest. Therefore the total resistance of a vascular bed is determined in large part by this.
Arteriolar resistance
- Illustrated by the distribution of blood flow among the various major arteries branching off the aorta
- Recall: CO flows through aorta and distributed on a % basis among the different organs
-When blood flow is distributed through a set of parallel resistances, - the flow through each organ is a fraction of the total blood - Adding a resistance to the circuit causes total resistance to decrease, not to increase
Ex. Total Resistance = 2.5
Parallel Resistance
__ in a blood vessel. Lateral Pressure decreases as flow velocity of the blood increases.
- Applies to single tube or many tubes arranged in parallel
- When a vessel is narrowed,
» Velocity of blood flow in a narrowed portion increases
» The lateral or distending pressure decreases in order to Maintain volume flow of 200 cc / sec and Keep the total energy of the system constant
BERNOUILLI’S PRINCIPLE
T = Pr P = Distending Pressure T = Wall Tension R = Radius
- Explains how the narrow lumen and thin wall of capillaries can withstand high pressures without bursting.
- Wall tension opposes the distending force that tends to pull apart a theoretical longitudinal slit in the vessel
- Wall tension acts to prevent rupture of the vessel wall.
LAW OF LAPLACE
- force exerted by the blood per unit area of the vessel wall (pressure is exerted equally in all directions).
Blood Pressure
- average pressure in any segment of the cardiovascular system during cardiac cycle.
Mean Blood Pressure
- The force exerted by the blood against the walls of the arteries by ventricular ejection
- A routine measurement that reflects the status of the CVS
ARTERIAL BLOOD PRESSURE
The energy transferred to the arterial system by ventricular ejection generates 2 Pressure Pulses:
- Systolic Pressure
2. Diastolic Pressure
Arterial Blood Pressure
- Systolic pressure (100 – 120 mmHg)
maximal arterial pressure within cardiac cycle - Diastolic pressure (70 – 80 mmHg)
minimal arterial pressure within cardiac cycle
- Maximum pressure attained in the arterial system during ventricular systole / during cardiac ejection
- Reflects the elasticity of the arterial system as it receives blood from the ventricle
- Less elastic aorta — increase SP
- Governed by the ability of ventricle to contract
- Weak ventricle — lower SP
- Influenced by the amount of blood in the ventricle
Hemorrhage – less blood volume — decrease S
SYSTOLIC PRESSURE
- Minimum pressure attained in the arterial system during ventricular diastole
- Produced by the recoil of aorta during diastole
- Reflects elasticity of vascular wall
- Is dependent on the duration of diastole
Slow HR — longer diastole
More time for DP to go down — lower DP
DIASTOLIC PRESSURE
- Also dependent on the PERIPHERAL RUN-OFF which in turn is dependent on the caliber of the arteriole
Constricted arterioles — poor run-off — higher DP
Dilated arterioles — better run-off — lower DP
DIASTOLIC PRESSURE
- The average pressure that push blood through the circulatory system
- The average pressure in the aorta, driving blood into the tissues throughout the cardiac cycle
MEAN ARTERIAL PRESSURE
Arithmetic Mean Pressure vs Functional Mean Pressure
ARITHMETIC MEAN PRESSURE:
= (Systolic Pressure + Diastolic Pressure) / 2
FUNCTIONAL MEAN PRESSURE:
= Diastolic Pressure + 1/3 Pulse Pressure
PULSE PRESSURE = SP minus DP
*More accepted because value is closer to DP in actuality
Pulse Pressure
Pulse Pressure = Stroke Volume / Arterial Compliance
2 Major factors that affect Pulse Pressure
- Stroke Volume
- Compliance – total distensibility of the arterial tree
*The greater the SV - the greater the amount of blood that must be accommodated in the arterial tree with each heartbeat therefore the greater the pressure rise during systole and fall during diastole – greater PP
*Less compliant arterial system – greater the rise in pressure
Ex. Arteriosclerosis (arteries less elastic – non compliant – increase PP 2x as normal
Factors that maintain normal ABP
- Total Peripheral Resistance – the resistance offered by the
- Arterioles which have great capacity to change radius
- Blood Viscosity – imparted firstly by RBC and secondly by plasma proteins - Cardiac Output
- Stroke Volume
- Heart Rate
Determinants of Arterial Blood Pressure
- Physical Factors or Fluid Mechanical Characteristics
- fluid volume (blood volume)
- static elastic characteristics (compliance of arterial system) - Physiological Factors
- cardiac output (stroke volume X heart rate)
- total peripheral resistance
Basis for ABP measurement: turbulent flow of blood KOROTKOFF’S SOUNDS:
- Thud or tapping sound
- Tapping sound + bruit (murmuring quality)
- Loud snapping sound
- Muffled, dull, softer sound
- Complete disappearance of sound
Methods of Measuring Blood Pressure
A. Direct Method
B. Indirect Method
1. Auscultatory Method
2. Palpatory Method
increased pressure ———– HYPERTENSION
decreased pressure ———– HYPOTENSION
thin-walled lined with a single layer of endothelial cells, which are surrounded by a basal lamina
Capillaries
Capillaries
- Lipid soluble substances (O2 and CO2) cross the capillary wall by dissolving in & diffusing across the endothelial cells
- H2O soluble substances (ions) cross the capillary either
a. Through water-filled clefts (spaces) between the endothelial cells or
b. Through large pores in the wall of some capillaries (ex. Fenestrated caps)
Not all capillaries are perfused with blood at all times. Instead, there is __ of capillary beds – depending on the metabolic needs of the tissues.
o This selective perfusion is determined by the degree of dilation or constriction of the arterioles and pre-capillary sphincters (smooth muscle bands that lie before the capillary)
o The degree of dilation or constriction is in turn, controlled by the: sympathetic innervation of the vessel smooth muscle and by Vasoactive metabolites produced in the tissues
selective perfusion
Structure of capillary wall
- lined by single layer of endothelial cells
- surrounded by very thin basement membrane
- total thickness = 0.5 micrometer
- diameter = 4 to 9 micrometers
- endothelial cells, basement membrane
- (-) smooth muscle and (-) elastic tissue
- tight junctions, fenestrations (pores), intercellular cleft and and pericytes
- Total area exceeds 6300 m2 and 1 µm thick
Types of Capillaries
- Continuous capillaries
- Fenestrated capillaries
- Sinusoidal capillaries
- the rate of filtration at any point along the capillary depends upon the balance of forces called Starling’s Forces across the capillary wall.
Capillary Fluid Shift
Starling’s Forces
- Total Filtration Pressure
- Capillary Hydrostatic Pressure
- Tissue Colloid Osmotic Pressure - Total Absorption Pressure
- `Plasma Colloid Osmotic Pressure
- Tissue Hydrostatic Pressure
The __ in the capillaries tends to force fluid and its dissolved substances through the capillary pores into the interstitial spaces.
hydrostatic pressure
osmotic pressure caused by the plasma proteins (called __) tends to cause fluid movement by osmosis from the interstitial spaces into the blood. This osmotic pressure exerted by the plasma proteins normally prevents significant loss of fluid volume from the blood into the interstitial spaces.
colloid osmotic pressure
Starling’s Forces
- The CAPILLARY PRESSURE (PC), which tends to force fluid outward through the capillary membrane.
- The INTERSTITIAL FLUID PRESSURE (Pif), which tends to force fluid inward through the capillary membrane when Pif is positive but outward when Pif is negative.
- The CAPILLARY PLASMA COLLOID OSMOTIC PRESSURE (Πp), which tends to cause osmosis of fluid inward through the capillary membrane.
- The INTERSTITIAL FLUID COLLOID OSMOTIC PRESSURE (Πif), which tends to cause osmosis of fluid outward through the capillary membrane.
If the sum of these forces-the net filtration pressure-is positive, there will be a __ across the capillaries.
net fluid filtration
If the sum of the Starling forces is negative, there will be a __ from the interstitial spaces into the capillaries.
net fluid absorption
Pores
- Intercellular cleft – a thin-slit channel between adjacent endothelial cells called “slit-pores”
- Plasmalemmal vesicles – which coalesce to form vesicular channels all the way through the endothelial cells
- most __ permit only molecules with radius less than 3 – 6 mm to pass through vessel wall
- allowed to pass through small pores
- water, inorganic ions, glucose, amino-acids, water-soluble solutes
- not allowed to pass through
- serum albumin, globular proteins, blood cell components
- lipid soluble molecules (O2 and CO2) pass through lipid components of endothelial cell membrane
Pores
Porosity of capillaries NOT the same in all organs (Brain and Spinal Cord)
Have continuous tight junctions between endothelial cells. Thus only the smallest water-soluble molecules pass through (H2O, O2 and CO2)
Porosity of capillaries NOT the same in all organs (Capillaries in cardiac and skeletal muscles)
- have low porosity to water and small water-soluble substances
Porosity of capillaries NOT the same in all organs (Liver and GIT)
Liver – the clefts between endothelial cells wide open. So, almost all dissolved substances of plasma (plasma proteins) can pass from blood to liver tissues
GIT – midway between liver and muscles
Porosity of capillaries NOT the same in all organs (Glomerular tuft of kidneys and Spleen and Bone Marrow Capillaries)
Glomerular tuft of kidneys – numerous small oval windows (fenestrae) penetrate all the way through endothelial cells. Only plasma protein cannot pass.
Spleen and Bone Marrow Capillaries – large pores
- main determinant of transcapillary exchange
- force exerted by the blood against the walls of capillaries
- pushing pressure – pushes fluid from capillary to interstitium
Capillary Hydrostatic Pressure (CHP)
Capillary Hydrostatic Pressure (CHP): Normal Values
arteriolar end - 35 mm Hg
venular end - 15 mm Hg
average CHP - 25 mm Hg
- normal THP: -7 to 1 mm Hg
- pushing pressure – pushes fluid from interstitium back to the capillaries and veins through the lymphatic system
Tissue (Interstitial) Hydrostatic Pressure (THP)
- normal PCOP: 25 mmHg
- also known as Osmotic Pressure of Plasma Proteins (OPPP) and Oncotic pressure
- exerted by the plasma proteins (particularly albumin)
- pulling pressure – pulls fluid from interstitium to capillaries
Plasma Colloid Osmotic Pressure (PCOP)
- normal TCOP: 7 – 8 mm Hg
- exerted by plasma proteins that leaked through the capillary wall and go into the interstitium
- pulling pressure – pulls fluid from capillaries to interstitium
Tissue (Insterstitial) Colloid Osmotic Pressure (TCOP)
Circulatory Adjustments are effected by:
- Altering the output of the heart – CO
- Changing the diameter of the resistance vessels – TPR
- Altering the amount of blood pooled in the capacitance vessels
Caliber of Arterioles adjusted or effected by:
- autoregulation
- locally produced Vasodilator Metabolites
- subs secreted by Endothelium
- systematically produced by circulating vasoactive subs (Hormones)
- the nerves that innervate the arterioles (Neural)
Caliber of veins adjusted by:
- the circulating Vasoactive subs
2. Vasomotor Nerves
- Capacity of tissues to regulate their own blood flow
- Due to the intrinsic contractile response of smooth muscle to stretch (Myogenic Theory of Autoregulation)
- Due to vasodilator metabolites that accumulate in active tissues (Metabolic Theory of Autoregulation)
- Well developed in the Kidneys
AUTOREGULATION
VASOCONSTRICTORS (local)
- Serotonin
- drop in temperature – localized vasoconstriction
- increased calcium conc.
- Sl. decrease H† conc.
SUBSTANCES SECRETED BY ENDOTHELIUM
a. PROSTACYCLIN – inhibits platelet aggregation and promotes vasodilation
b. THROMBOXANE A2 - produced by platelets; promotes platelet aggregation and vasoconstriction
c. EDRF (Endothelium Derived Relaxing Factors) now called NITRIC OXIDE (NO) - Vasodilator
d. ENDOTHELIN 1 – potent vasoconstrictor
Vasoconstrictor Hormones:
- Norepinephrine (NE) – powerful vasoconstrictor
- Epinephrine – less powerful than NE; may cause vasodilation in coronary arteries during increased heart activity
- Angiotensin II
- Vasopressin – more powerful than Angiotensin II as a Vasoconstrictor
- KININS - bradykinin
- VIP
Antagonizes the action of vasoconstrictor agents and lowers BP
Atrial Natriuretic Peptide
NEURAL FACTOR (Rapid Control of ABP)
• All blood vessels except capillaries and venules contain smooth muscle and receive innervation from sympathetic nervous system
- The fibers to the arterioles regulate tissue blood flow and arterial pressure
- The fibers to the capacitance vessels vary the volume of blood stored in the veins
Ex. Venoconstriction
♣ decreased venous capacity
♣ increased venous return
NORADRENERGIC FIBERS TO BLOOD VESSEL
• vasoconstriction
• contain NEUROPEPTIDE Y – which is a vasoconstrictor
• vasoconstrictor fiber exhibit tonic activity
(S tone to blood vessel)
Cut S to b.v. → b.v. dilates
• S vasoconstrictor effects esp. powerful in the kidneys, spleen, skin; less in brain and skeletal muscles
SYMPA CHOLINERGIC TO BLOOD VESSEL SKELETAL MUSCLES
• Vasodilator – called Sympathetic Vasodilator System
• Contain VIP which produced Vasodilation
*NO tonic activity
ARTERIAL PRESSURE CONTROL
- begins with life saving measures of the nervous control mechanism
- continues with the sustaining characteristics of the intermediate mechanisms
- finally, is stabilized at the long term mechanism by the renal – body fluid mechanism
Arterial pressure is regulated by several inter-related systems each of which performs a specific function
CONTROL MECHANISM
(CONTROL MECHANISM)
- begins to act within seconds or minutes but cannot maintain ABP because they adapt to prolonged change in pressure
- attempts to restore BP rapidly toward normal
- Involves participation baroreceptors and chemoreceptors located in the peripheral circulation
- begin to act within seconds or minutes
- Powerful control mechanism
- most nervous control of BP is achieved by reflexes that originate in the baroreceptors and chemoreceptors located in the peripheral circulation outside the brain
Rapidly Acting Pressure Control Mechanism
(Rapidly Acting Pressure Control Mechanism)
- Activated instantly by any BP change
- Attempts to restore BP rapidly toward normal
- Cannot maintain BP because they adapt to prolonged change in pressure. Thus, Short – term Regulator of ABP
- Involves participation of baroreceptors in arch of aorta and carotid sinus
Baroreceptor Feedback Mechanism
Rapidly Acting Pressure Control Mechanism
A. Baroreceptor Feedback Mechanism
B. CNS ISCHEMIC MECHANISM - Ex. Cushing Reaction
C. ATRIAL STRETCH REFLEXES
- BAINBRIDGE REFLEX (Atrial Reflex control of HR)
- VASOPRESSIN / ADH
D. CHEMORECEPTOR MECHANISM
- Chemoreceptors in the Carotid and Aortic bodies
Intermediate Time Period Control Mechanism
A. RAAS
B. Capillary Fluid Shift Mechanism
C. Stress – Relaxation of the Vasculature
- It takes a few hours to show significant response
- This mechanism can eventually return the arterial pressure all the way back to normal pressure that will provide normal output of salt and water by the kidneys
- Has multiple interactions with the RAAS and the Nervous System
The Renal Body Fluid Pressure Control Mechanism or Renal-Blood Volume Pressure Control Mechanism
- Reflex Arc Components
- Vasomotor Area or VMC (groups of neurons in the Medulla Oblongata responsible for the main control of ABP)
- Afferent fibers end in the Nucleus of Tractus Solitarius (NTS)
- After the baroreceptor signals have entered the NTS of Medulla, secondary signals inhibit the VMC (Gaba) and excite the CIC (Glutamate)
- VMC transmits sympathetic impulses to blood vessels
- Lateral portion of VMC transmit excitatory impulses through S to heart
- Medial portion of VMC transmits PS signals to dorsal motor nucleus of CN X to heart
Baroreceptor Reflex/ Sino-aortic Reflex/ Marey’s Law of the Heart
Practical application of baroreceptor reflex
- Changes in body posture
- Direct pressure on the carotid sinus – ↓ HR
- This maneuver is used to treat paroxysmal tachycardia
Increases baroreceptors discharge decreases ABP. How?
- inhibits the tonic discharge of the vasoconstrictor nerves→vasodilation→ decreases PR
- excites the vagal innervation of the heart→decreases HR and CO
- Venodilation - decreases ABP due to pooling of blood
- Not stimulated by pressure between 0mmHg and 50 to 60 mmHg
- Responds rapidly above this level and reach a maximum of 180 mmHg
Carotid Sinus Baroreceptors
Factors that affect the Vasomotor Area or VMC: Excitatory inputs from
- Excitatory inputs from the higher centers like hypothalamus and cortex
Ex. Emotions like anger and sexual excitement
→ Increased HR and vasoconstriction
→ Increased ABP - Excitatory inputs pain pathways and muscles
Ex. Acute pain → increased BP via afferent impulses in the reticular formation converging on the VMA
Exception: Prolonged severe pain→ Vasodilation → decreased BP → fainting
Factors that affect the Vasomotor Area or VMC: Inhibitory Inputs from
- Cortex via hypothalamus
Ex. Fear and grief → bradycardia and vasodilation → decreased BP→ Syncope - Lungs
Inflation of lungs → inhibit vasomotor discharge through CN X→ Vasodilation and decreased BP
- ABP also controlled by the VMC in the brain in response to diminished blood flow to the brain
Cerebral Ischemia → increased ABP → decreased HR
CNS ISCHEMIC MECHANISM
- is an example of the response to cerebral ischemia
- is a special type of the CNS ischemic response that results from an increased pressure in the cranial vault
- happens when CSF pressure rises to equal ABP
*compresses arteries in the brain
*cuts off blood supply to brain
*cerebral ischemia
*increases ABP to a level higher than CSF pressure
*blood flows once again to brain vessels
8relieve the cerebral ischemia - SIG: helps protect the vital centers of the brain from loss of nutrition when the CSF pressure rises at a level high enough to compress the Cerebral arteries
CUSHING REACTION
- operates primarily as an emergency arterial control system that acts rapidly and powerfully to prevent further decrease in ABP when blood flow to brain decreases. Called the “LAST DITCH STAND” pressure control mechanism
- is one of the most powerful of all the activators of the Sympathetic vasoconstrictor system because can elevate MAP to as high as 250 mmHg, to a point that some peripheral vessels become almost totally occluded.
- Ex. Kidneys almost entirely stop production of urine because of arteriolar constriction
- Powerful so that ABP rise high enough to correct brain ischemia before it causes nutritional depression and death of neuronal cells
CNS INSCHEMIC RESPONSE
- elicits reflexes parallel to baroreceptor reflex
- BAINBRIDGE REFLEX
- this reflex help prevent damming of blood in veins, in atria, and in pulmonary circulation
ATRIAL STRETCH REFLEXES
- Rise in CVP as in increased blood volume
→ distend right atrium
→ (+) atrial stretch receptors
→ afferent signals to medulla through CN X
→ efferent signals to heart through S
→ increased HR and contractility
BAINBRIDGE REFLEX
ATRIAL STRETCH REFLEXES
- under conditions of HYPERVOLEMIA, Bainbridge reflex predominates over sino – aortic reflex
- under conditions of HYPOVOLEMIA, sino – atrial reflex predominates over Bainbridge reflex
- involved in the regulation of BP in response to hemorrhage, but not in minute to minute regulation of normal BP
- synthesized mainly by the supra-optic nuclei of hypothalamus and to a lesser extent by the paraventricular nuclei
- stored and released by posterior pituitary gland
VASOPRESSION (ADH)
adequate stimulus for ADH release:
decreased blood volume ADH is released when atrial receptors detect a decrease in blood volume
ADH secretion is inhibited by:
A stretch in atrial wall caused by increased Venous Return due to increased blood volume
Target organs of VASOPRESSION (ADH)
- Smooth muscles of arterioles
- Kidneys (Distal Convoluted Tubule and Collecting Duct)
Effects of VASOPRESSION (ADH)
- Vasoconstriction — increased TPR
- Increased permeability of DCT and CD to water
- ↑ Water reabsorption
- ↑ Plasma volume
- ↑ CO
CHEMORECEPTORS in the CAROTID and AORTIC BODIES
- Located along aortic arch and near the bifurcation of common carotid arteries
- Important at BP below 80 mmHg
- Have very high rates of oxygen consumption
- Sensitive to oxygen lack, carbon dioxide and hydrogen excess
- an enzyme that catalyzes the conversion of Angiotensinogen (liver) to Angiotensin I
- secretion increased when ABP falls or ECF volume reduced
RENIN
- catalyzes conversion of Angiotensin I to II primarily in the lungs
ACE (Angiotensin Converting Enzyme)
- block conversion of Angiotensin I to II, thus lowers ABP
- act on β2 receptors to produce the cough that is an annoying side effect in 20% of patients treated with ACE inhibitors
ACE INHIBITORS (Ex. Captopril)
- vasoconstrictor, increase SP or DP
- 4 to 8 times as active as NE
- its pressor activity is decreased in SODIUM depleted individual and in patients with Cirrhosis
- acts directly on adrenal cortex (ZONA Glomerulosa) to increase secretion of aldosterone
- acts on the brain to decrease the sensitivity of he baroreceptor reflex
- acts on the brain to increase water intake and increase secretion of vasopressin and ACTH
ANGIOTENSIN II (Hypertensin or Angiotonin)
- has about 40% of the pressor activity of Angiotensin II, but 100% of the aldosterone stimulating activity
- is the natural aldosterone – stimulating peptide while Angiotensin II is the natural BP – regulating Peptide
ANGIOTENSIN III
- increases SODIUM reabsorption by the Renal distal convoluted tubule
- increases water reabsorption
- Thus, increasing ECF volume (plasma volume)
- Increase total blood volume
- Increase cardiac output
- Without the RAAS, the effect of excessive salt intake on arterial pressure is 10 times as great
ALDOSTERONE
- Recording electrical activity of the heart using electrodes placed on skin surface
- Physiologic basis Human ECF is NaCl-based, making it a good conductor of electricity
- Provides indirect information about cardiovascular function
Electrocardiography
- Deflection produced by atrial depolarization
- Does not include atrial repolarization, which is “buried” in the QRS complex
P Wave
- Interval from the start of the P wave to the beginning of the QRS complex
- Represents the time required for SA node impulse to travel through the conduction system
- Normal value of 0.12 - 0.20 sec
PR Interval
Changes in PR Interval
- Varies with conduction velocity through the atrioventricular (AV) node
–if AV nodal conduction decreases (as in heart block), the PR interval increases - Decreased (i.e., increased conduction velocity through AV node) by stimulation of the sympathetic nervous system
- Increased (i.e., decreased conduction velocity through AV node) by stimulation of the parasympathetic nervous system
Represents the time from the end of atrial depolarization to the start of ventricular depolarization
PR Segment
- Represents ventricular depolarization
- Atrial repolarization is buried in the QRS complex
QRS Complex
QRS Complex
Q – first negative wave
R – first positive wave
S – first negative wave after an R wave
- Interval from the beginning of the Q wave to the end of the T wave
- Represents the entire period of ventricular depolarization and repolarization
- Normal value of 0.44 second
QT Interval
- Segment from the end of the S wave to the beginning of the T wave
- represents time from end of ventricular depolarization to the start of ventricular repolarization
- Considered an isoelectric segment
ST Segment
- Deflection produced by ventricular repolarization
- Most variable waveform
T Wave
Waveform: What It Represents
P WAVE - Atrial depolarization
QRS COMPLEX - Ventricular depolarization
T WAVE - Ventricular repolarization
Leads
- The ECG examines the electrical activity of the heart at various perspectives using 12 different leads.
- Lead – an electrical picture of the heart that makes use of 2 electrodes.
Types of ECG Leads
- 3 Bipolar Limb Leads
- 3 Augmented Unipolar Leads
- 6 Precordial or Chest Leads
- Bipolar means that the ECG is recorded from two electrodes on the body
Bipolar Limb Leads
Lead I
Negative Terminal: Right Arm
Positive Terminal: Left Arm
Lead II
Negative Terminal: Right Arm
Positive Terminal: Left Leg
Lead III
Negative Terminal: Left Arm
Postitive Terminal: Left Leg
- States that: The electrical potential of any limb equals the sum of the other two
- Positive and negative signs of leads must be observed
EXAMPLE:
–If lead I = 1.0 mV, Lead III = 0.5 mV, then Lead II = 1.0 + 0.5 = 1.5 mV
Einthoven’s Law
- Designated as V1 to V6
- Very sensitive to electrical potential changes underneath the electrode
Chest or Precordial Leads
Placement of Precordial Leads
V1- 4th Intercostal Space (ICS) Right parasternal border
V2 - 4th ICS Left parasternal border
V3 - between V2 and V4
V4 - 5th ICS Left Mid Clavicular Line
V5 - 5th ICS Left Anterior Axillary Line
V6 - 5th ICS left Mid Axillary Line
aVR
Negative Terminal: Left Arm; Left Leg
Postitive Terminal: Right Arm
aVL
Negative Terminal: Right Arm; Left Leg
Positive Terminal: Left Arm
aVF
Negative Terminal: Left Arm; Right Arm
Positive Terminal: Left Leg
Anatomical Perspective of ECG Leads: V1, V2
Septal wall
Anatomical Perspective of ECG Leads: V3, V4
Anterior wall
Anatomical Perspective of ECG Leads: II, III, aVF
Inferior wall
Anatomical Perspective of ECG Leads: I, aVL, V5, V6
Lateral wall
__ does NOT face the epicardial wall of the heart,
so it is NOT useful for assessing ischemia
aVR
- along sternal borders
- supplied by left anterior descending artery
Septal Wall
- left anterior chest
* supplied by left anterior descending artery
Anterior Wall
- inferior view from leg
- supplied by:
•right coronary artery (90%)
•left circumflex artery (10%)
Inferior Wall
- view from left arm
- supplied by left circumflex artery
Lateral Wall
ECG Paper
5 Large boxes = 1.0 second
1 Large Box = 0.2 seconds
Small Box = 0.04 seconds
Standardization of Normal Values
Heart Rate 60 – 100 beats/min
–Bradycardia 100 beats/min
PR interval 0.16 sec (NR: 0.12 – 0.20)
QRS duration
Determination of Heart Rate
- Rule of 300
- Mathematical Formulae
- Six Second Strip Method
Rule of 300
- Always remember! 300-150-100-75-60-50
- Count the number of big boxes between two R waves
1 large square = 300/min
2 large squares = 150/min
3 large squares = 100/min
4 large squares = 75/min
5 large squares = 60/min
Mathematical Formulae: using large boxes between R-R
Heart rate = 300/number of large boxes between R-R
Mathematical Formulae: using small boxes between R-R
Heart rate = 1500/number of large boxes between R-R
- If there are no P waves, count the number of R waves in a 6-second strip and multiply this number by 10 to get the heart rate
Six Second Strip Method
Determination of Rhythm
Are normal P waves present?
–NORMAL: Yes, P waves are present.
Are QRS complexes narrow (0.12s)?
–NORMAL: The QRS complexes are narrow.
What is the relationship between the P waves and the QRS complexes?
–NORMAL: There is one P wave for every QRS complex.
Is the rhythm regular or irregular?
–NORMAL: The rhythm is regular
Types of Rhythms
SINUS RHYTHM
–Originates from the sinoatrial node
–Intrinsic rate of 60-100 beats/minute
NODAL RHYTHM
–Originates from the AV node
–Intrinsic rate of 40-60 beats/minute
VENTRICULAR RHYTHM
–Originates from the Purkinje fibers
–Intrinsic rate of 20-40 beats/minute
Determination of Axis
- Vectorial Analysis
- Thumbs Method
- Isoelectric Lead Method
- Mathematical Formula
(Thumbs Method)
Lead I: Up
avF: Up
Normal Axis
(Thumbs Method)
Lead I: Up
avF: Down
Left axis deviation
(Thumbs Method)
Lead I: Down
avF: Up
Right axis deviation
(Thumbs Method)
Lead I: Down
avF: Down
Extreme right axis deviation
- Isoelectric lead refers to lead with equal forces in the positive and negative direction
- Often this is the lead with the smallest QRS
- The QRS axis is perpendicular to the orientation of the isoelectric lead
Isoelectric Lead Method
