Cardiovascular PhysiologyPhysiological Anatomy of the Cardiac Muscle >Found in the heart >Usually single nucleus >prominent striations and branching >muscles are connected to each other via junctions called intercalated discs >pacemaker cells control their contraction which is involuntary >Contraction is slow Properties of Cardiac Muscles >Excitation of the heart is triggered by electrical impulse rather than neural transmitters. >Contraction of the heart is triggered by elevation of intracellular calcium influx > Myocytes depend heavily on oxygen & blood supply. > Not fatigued > Excitability Cycle Cardiac muscle as a syncytium Two parts: 1. Syncytium- two atrias 2. Ventricular Syncytium- two ventricles Role of a Long Refractory Period 1. Prevent ventricles from contracting at too high rates so that enough time is allowed for refill of the ventricles 2. Prevent retrograde excitation Autorhythm The heart can beat on its own without the need for exogenous commands.

The heart generates electricity. TERMINOLOGY >Excitation- definition: generation of action potentials; different from contraction >Contraction- definition: shortening of muscle cells; triggered by excitation Refractory Period of Cardiac Muscle Refractory period Interval of time during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscles. Normal refractory period of ventricle is 0.25 to 0.3 seconds, which is the duration of the action potential. Relative refractory period additional 0.05 second During which the muscle is more difficult than normal to excite but nevertheless can be excited. Refractory period of atrial muscle (0.15 second) shorter than the ventricles. And the relative refractory period is another 0.03 seconds. Excitation Contraction - Coupling Function of calcium ions and of the Ttubules >Diastole-Period of relaxation >Systole-Period of contraction Cardiac Cycle Shows the mechanical and electrical events of a single cardiac cycle. 7 phases Use ECG as an event marker Cardiac Cycle Ventricular systole -

isovolumic contraction ejection Ventricular diastole isovolumic relaxation filling - atrial contraction Cardiac Cycle Atrial Systole - preceded by the P-wave - Ventricular filling -

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Reduced Ventricular Ejection -slower ventricular ejection of blood.

- rapid

- atrial filling continues. Cardiac Cycle Isovolumetric Ventricular Relaxation - Repolarization of the Ventricles is now complete (T-wave). - aortic valve closes, followed by pulmonic valve Second Heart Sound (S2) - ventricular volume is constant because all the valves are closed. - dicrotic notch or incisura Cardiac Cycle Rapid Ventricular Filling - mitral valve is open and ventricular filling from the atrium begins. - rapid flow of blood from the atria into the ventricles causes the Third heart Sound (S3) - normal in children Ventricular filling Cardiac Cycle Reduced ventricular Filling - longest phase of the cardiac cycle. - slower ventricular filling rate. Hemodynamics Poiseuille Equation - relationship of flow, pressure and resistance Q = P1 P2 R Q flow P1 upstream pressure P2 downstream pressure

- Filling of the ventricle by atrial systole causes the Fourth Heart sound (S4) -A wave on the venous pulse curve Atrial contraction Cardiac Cycle Isovolumetric ventricular contraction - after the onset of the QRS wave, which represents electrical activation of ventricles. - AV valves closure First Heart Sounds (S1) - split sound - no blood leaves the ventricles during this phase because the Aortic Valve is closed. Isovolumic Ventricular Contraction Cardiac Cycle Rapid ventricular ejection - ventricular pressure reaches its maximum value during this phase. - most of the SV is ejected. - atrial filling begins. - the onset of T wave, which represents repolarization of the ventricles. Ventricular ejection Cardiac Cycle

R resistance of vessels between P1 and P2 Resistance vessel radius - the most important factor - inversely proportional to the fourth power of the radius - radius decreased by half, resistance increases 16-fold - radius doubles, resistance decreases to 1/16 of the original vessel length - the greater the length, the greater the resistance - if length doubles, resistance doubles - length decreases by half, resistance decreases by half Resistance blood viscosity - the greater the viscosity, the greater the resistance - prime determinant of blood viscosity is hematocrit - anemia = decreased viscosity; polycythemia = increased viscosity Reynolds number - predicts whether blood flow will be laminar or turbulent Reynolds number = (diameter) (velocity) (density) viscosity Cardiac Output >considered as circulating blood volume >the product of heart rate (HR) and stroke volume (SV) >at rest, HR is about 70 bpm, SV is 80 ml and CO is about 5.6 liters/min >stroke work = stroke volume X aortic pressure >cardiac O2 consumption is directly

proportional to the amount of tension developed and is increased by: increased afterload increased contractility increased size of heart increase HR

Fick Principle >used to calculate blood flow through an organ Flow = Uptake AV >pulmonary venous oxygen = systemic arterial >pulmonary arterial oxygen = systemic venous >lowest pO2 = pulmonary artery Flow Laminar Flow - flow in layers - occurs throughout the entire cardiovascular system except heart - highest velocity = center of the tube Turbulent Flow - nonlayered flow - creates murmurs (bruits); produces more resistance - increased turbulence (increased Reynolds number) : increased tube diameter, increasing velocity, decreased blood viscosity, vessel branching and narrow orifice Wall Tension Laplace Law T Pr T = wall tension P = pressure r = radius

aorta = the artery with the greatest wall tension (greatest pressure and radius) Vessel Compliance C=V P how easily a vessel is stretched (distensibility) if easily stretched, a vessel is said to be a very compliant vessel stiff vessel noncompliant vessel

Mean Arterial Pressure average arterial pressure (more closer to diastolic than systolic) mean pressure = diastolic + 1/3 pulse pressure = 2/3 diastolic + 1/3 systolic MAP = CO X TPR Fast Response AP Phase 0 increased membrane conductance to Na; fast Na channels open; Na influx (depolarization) Phase 1 slight repolarization (voltage gated K channels); closure of fast Na channels Phase 2 most important phase; slow Ca channels open; Ca influx; K efflux through ungated channels; voltage gated K channels are closed Phase 3 slow Ca channels closed; voltagegated K channels open; large K efflux; repolarization Slow Response AP to have a pacemaker potential or prepotential all cells have an unstable phase 4 (slow gradual depolarization towards threshold) Phase 0 increase in Ca conductance; Ca influx; slow Ca spike Phase 3 repolarization; increased K conductance; rapid K efflux Phase 4 slow gradual depolarization; increased Na conductance; Na influx; automaticity Excitability

Arterial Pressure Systolic Pressure - peak pressure during systole - increase in SV, decrease in HR and vessel compliance all causes an increased systolic pressure Diastolic Pressure - lowest pressure at the end of diastole - decrease in TPR, HR, SV and vessel compliance all causes a decreased diastolic pressure Pulse Pressure >difference between systolic and diastolic pressure >most important determinant of pulse pressure is stroke volume >Factors that increase (widen) pulse pressure: increased stroke volume (systolic increases more than diastolic) decreased vessel compliance ( systolic increases, diastolic decreases)

the ability of the heart to initiate an AP reflects the recovery of the channels that carry the inward currents for the upstroke of the AP absolute refractory period

>compliant artery = small pulse pressure >stiff artery = wide pulse pressure

- begins with upstroke and ends after the plateau - no AP can be elicited relative refractory period - the period after the absolute refractory period when repolarization is almost complete - an AP can be elicited, but not at full magnitude Ventricular Volumes End-diastolic volume (EDV) : volume of blood in the ventricle at the end of diastole End-systolic volume (ESV) : volume of blood in the ventricle at the end of systole Stroke volume (SV) : volume of blood ejected by the ventricle per beat SV = EDV - ESV Frank-Starlings Law systolic performance is determined by the overall force generated by ventricular muscle during systole (number of cross-bridge cycling) greater number of cross-bridge cycling = greater force of contraction Factors that affect the number of crossbridge cycling: >amount of preload on the muscle >level of contractility Preload in skeletal muscle, the load on the muscle in a relaxed state the load or prestretch on ventricular muscle at the end of diastole best index of preload = LVEDV contractility = a change in the force of contraction at any given sarcomere length (inotropism) common clinical index of contractilty = EF

(SV/EDV) loss of contractility is due to loss of functioning sarcomere Afterload in skeletal muscle, the load on the muscle during contraction acceptable indices of afterload : mean aortic pressure and peak left ventricular pressure an acute increase in afterload reduces the volume of blood ejected blood not ejected remains in the LV and increases preload in the next cycle increased preload and increased force of contraction restores SV Heart Sounds S1 closure of AV valves (mitral, tricuspid) S2 closure of semilunar valves (aortic, pulmonic) S3 early diastole in children, well-conditioned athlete ( due to rapid ventricular filling) and heart failure S4 occurs in late diastole when the atrium contracts; as blood is propelled into hypertrophied low-compliance ventricle * valves on the right side of heart opens first, but closes last Ventricular Pressure Volume Loop These are constructed by combining systolic and diastolic pressure curves The diastolic pressure curve is the relationship between diastolic pressure and diastolic volume in the ventricles. The systolic pressure curve is corresponding relationship between systolic and systolic volume in the ventricles. Steps in the cycle BC Isovolumetric Contraction)

CD Ventricular Ejection DA Isovolumetric Relaxation AB Ventricular Filling Pressure-Volume Loop Cardiac and Vascular function Curve The Cardiac Output, or Cardiac Function Curve The Venous Return, Vascular Function, curve Venous Return Mean systemic pressure Slope of the Venous Return Curve Combining cardiac Output and Venous Return INOTROPIC AGENTS CHANGE THE CARDIAC OUTPUT CURVE Positive Inotropics 1. Beta -1 Stimulation 2. Increase extracellular calcium concentration 3. Decrease extracellular Na concentration 4. Digitalis 5. Increase in HR Negative Inotropics 1. Heart failure 2. Decrease pH 3. Decrease 02 4. Increase C02 Stroke Work >The work the heart performs on each beat Equals to FORCE x DISTANCE FORCE = Ao pressure x Stroke volume Cardiac 02 consumption increased by: afterload - increased - increased size

of the heart increase contractility CONTROL OF HEART RATE

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intrinsic heart rate = 110/beats per minute resting heart rate is lower than intrinsic HR Neural Influences parasympathetic : right vagus predominates in SA node; left vagus in AV node sympathetic : stimulation causes tachycardia Bainbridge Reflex - stretch receptors in the right atrium (increase stretch = increase HR) - afferent : vagus efferent : vagus

Chromotropic Effects - on the heart rate - positive chromotropic effects = increases HR by increasing the firing rate of SA node - negative chromotropic effects = decreases HR by decreasing the firing rate of SA node Dromotropic - on conduction velocity in the AV node - positive dromotropic effects = increased conduction velocity at the AV node - negative dromotropic effects = decreases conduction velocity at the AV node Autonomic Effects Regulation of Arterial Pressure Baroreceptor Reflex CONTROL OF BLOOD PRESSURE Baroreceptor Reflex (short-term) Cerebral Ischemia - when brain is ischemic, CO2 and H concentration in brain increases

- chemoreceptors respond by increasing both sympathetic (increased contractility and TPR) and parasympathetic (increased HR) outflow = Cushings reaction - blood flow to other organs are reduced to preserve blood flow to the brain Chemoreceptors - located in bifurcation of common carotid arteries and aortic arch - very sensitive to hypoxia (decreased MAP) Vasopressin - located in atria - receptors in atria respond to a decrease in volume or pressure, cause the release of vasopressin from posterior pituitary - increases TPR (V1) and increases H2O reabsorption in distal tubule of kidney and collecting ducts (V2) Atrial Natriuretic Peptide (ANP) - increased atrial pressure = released of ANP in atria - causes vasodilation and decreased TPR - increases salt and water excretion (decreased blood volume) - inhibits renin release Inspiration >intrapleural pressure becomes more negative >increased systemic venous return >increased right ventricular output causing delay in closing of pulmonic valve (splitting of heart sounds) >volume of blood in pulmonary circuit increases >decreased left ventricular output Expiration >intrapleural pressure becomes more positive (increased)

>decreased systemic venous return >decreased right ventricular output >volume of blood in pulmonary circuit decreases >right atrium is compressed so blood pressure increases causing a reflex decrease in heart rate >increased left ventricular output >Valsalva maneuver increase intrapleural pressure and CVP; also decreases venous return Microcirculation >flow and pressure within the system is controlled by varying the radius (resistance) of the arterioles vasodilation = increased flow and pressure vasoconstriction = decreased flow and pressure >capillaries are permeable to all dissolved substances via simple diffusion except plasma proteins >the lymphatic system removes proteins in the interstitial space >filtration and reabsorption are the main processes by which fluid moves between plasma and interstitium due to pressure differences (bulk flow) FILTRATION Capillary Hydrostatic Pressure -increased by arterial dilation and venous constriction -decreased by arteriolar constriction (eg HPN) Interstitial Oncotic Pressure -increased by chronic lymphatic blockage -increased capillary permeability (eg. burns)

REABSORPTION Capillary Oncotic Pressure

-increased by dehydration due to excessive sweating -decreased by liver and renal disease -decreased by saline infusion Interstitial Hydrostatic Pressure -clinically significant changes are seen in the pulmonary circuit -subatmospheric pressures will increase pressure (eg. respiratory distress syndrome)

Active Hyperemia - blood flow is proportional to its metabolic activity Reactive Hyperemia - an increase in blood flow occurs after a period of occlusion of flow - the greater the period of occlusion, the greater the increase in blood flow above preocclusion levels Tissues least affected by nervous reflexes: cerebral, coronary, renal, pulmonary and skeletal muscle during exercise SPECIAL CIRCULATIONS Coronary Circulation - controlled almost entirely by local metabolic factors (hypoxia and adenosine) = flow equals metabolism - exhibits autoregulation; active and reactive hyperemia - during systole, mechanical compression of the coronary vessels reduces blood flow causing reactive hyperemia Cutaneous Circulation - has extensive sympathetic innervation - temperature regulation is the principal sympathetic innervation Skeletal Muscle Circulation -at rest, sympathetic control of blood flow predominates -during exercise, local metabolic control overrides sympathetic control (sym has no effect on flow) -stimulation of receptors = vasoconstriction -stimulation of receptors = vasodilatation Cerebral Circulation -the most important local vasodilator is arterial

REGULATION OF BLOOD FLOW AT ORGAN LEVEL Autoregulation (Intrinsic) - blood flow is regulated, not resistance - no nerves or circulating substances involved - blood flow should be independent of blood pressure 2 hypothesis: >metabolic hypothesis tissue produces a vasodilatory metabolite that regulates flow (eg CO2, H, K, lactate, adenosine) >myogenic hypothesis increased perfusion pressure stretched the smooth muscle (arterial wall) wherein the arteriole radius decreases with no significant increase in flow (eg GIT) Extrinsic Regulation - tissues that are controlled by nervous and humoral factors originating outside the organ - cutaneous circulation and resting skeletal muscles - circulating epinephrine acts on 2 receptors causing vasodilatation - parasympathetic system does not affect arterioles and has little or no effect on TPR except the penis LOCAL CONTROL OF BLOOD FLOW

PCO2 (or pH) regulating blood flow -if arterial PCO2 is increased (hypoventilation; pH decreased) = vasodilatation -if arterial PCO2 is decreased (hyperventilation; pH increased) = vasoconstriction Renal and Splanchnic Circulation - a small in blood pressure will invoke autoregulatory mechanism to maintain renal blood flow - increased sympathetic activity (hypotension) causes intially vsodilatation then vasoconstriction, and a decreased blood flow - venous PO2 is high in renal circulation

include: -total peripheral resistance increases -heart rate increases Basic Alterations During Exercise -assuming that the person is in steady state, performing moderate exercise at sea level Pulmonary Circuit >blood flow (cardiac output) - large increase >pulmonary arterial pressure - slight increase >pulmonary vascular resistance - large decrease >pulmonary blood volume - increase

EFFECTS OF GRAVITY -below heart level, there are equal increases in systemic arterial and venous pressures (assuming no muscular action) -above heart level, systemic arterial pressures progressively decrease -surface veins above the heart cannot maintain a significant pressure below atmospheric; except deep veins in the cranium which maintain a pressure that is significantly below atmospheric -a severed or punctured vein above heart level has potential for introducing air into the system due to negative intrathoracic pressure Effects of supine to upright position: -pressure in dependent vein increases -blood volume in dependent veins increases -circulating blood volume (cardiac output) decreases -stroke volume decreases -arterial blood pressure decreases slightly (due to reduction in CO) Compensation via carotid sinus reflex will

>number of perfused capillaries - increase >capillary surface area - increase (for gas exchange) BASIC ALTERATIONS DURING EXERCISE Arterial System PO2 - no significant change PCO2 - no significant change pH - no change or decrease (lactic acid) MAP - slight increase Blood flow - large increase TPR - large decrease (dilation of skeletal muscle beds) BP - minimal change (slight increase) CO - slight increase

Venous System PO2 - decrease PCO2 increase

BASIC ALTERATIONS DURING EXERCISE

Exercising Skeletal Muscle blood flow increases (increased SV & pulse pressure) vascular resistance decreases capillary pressure increases capillary filtration increases lymph flow increases venous PO2 decreases (to extremely low levels) increased extraction of O2 (increased AV O2 diff) decreased cutaneous blood flow, then increases to dissipate heat increased coronary blood flow no change in cerebral blood flow decreased renal and splanchnic blood flow light to moderate exercise, no increase in preload; increased preload in heavy exercise

decreased PO2 (hypoxia) activates chemoreceptors while decreased PCO2 activates central chemoreceptors increasing sympathetic outflow increased released of epi/NE by adrenal medulla further increasing sympathetic outflow increased released of RAA and ADH arteriolar vasoconstriction decreases capillary pressure favoring capillary reabsorption thus increasing blood volume ELECTROCARDIOGRAM History In 1790, using dissimilar metals like copper and zinc, the resulting electrical current can stimulate the frogs legs to jump In 1855, Kollicker and Mueller found that when a motor nerve of a frogs leg was placed over its isolated beating heart, the leg would kick on every heartbeat John Sanderson obtain a record of his patients heartbeat through the skin using a Lippman capillary electrometer coming from the idea of Alexander Muirhead History Augustus Waller is the first to systematically approach it in an electrical viewpoint still using the same machine In 1903, Willem Einthoven first used the string galvanometer which is a large magnet suspended in a silvered wire drilled 2 holes in both poles of the magnet Emmanuel Goldberger adds the augmented limb leads to Einthoven six chest leads Electrocardiogram (12 Lead) ECG or EKG -Records the electrical activity of the heart as well as valuable function about the hearts function and structure -In resting situation, the muscle cells of the

Hemorrhage -a decrease in blood volume decreases mean systemic pressure resulting in decreased CO and arterial pressure -carotid sinus baroreceptors are activated, increasing sympathetic and decreasing parasympathetic outflow -increased heart rate -increased contractility -increased TPR -decreased unstressed volume and increased stressed volume -vasoconstriction occurs in skeletal, splanchnic or cutaneous (except coronary or cerebral) Hemorrhage

heart are polarized (negatively charge), and when they are depolarized, they contract Consists of 6 limb leads and 6 precordial leads ECG Tracing Paper Principles Action potentials on cardiac muscles create extracellular voltages The thorax acts as a volume conductor so that voltages generated by the cells are conducted to the body surface Deflections in the ECG corresponds to electrical activity or events on the heart Can be recorded using an active or exploring electrodes connected to an electrode either via bipolar or unipolar leads Bipolar Leads Used before unipolar leads are developed It uses two active electrodes The limb leads forms the points of what is known as the Einthovens triangle Current flows only in the body fluids, the records obtained are those that would be obtained if the electrodes were at the points of attachment of the limbs, no matter where on the limbs the electrodes are placed Einthoven Triangle Lead I - is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode Lead II - is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode Lead III - is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode Unipolar Leads

Consists of the augmented limb leads (aVF, aVR, aVL) and the 6 precordial leads (V1-V6) The augmented limb leads are derived from leads I, II and III in which the recording on one limb is augmented by 50% The augmented limb leads plus leads I, II, and III forms the hexaxial reference system (frontal plane) Precordial leads views the horizontal plane of the heart (Z axis) Unipolar Leads Lead augmented vector right (aVR) has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm. Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm. Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg. Hexaxial Reference System Normal axis: -30o to +90o Left axis deviation: -30o to -90o Right axis deviation: +90o to +180o Extreme axis deviation: -90o to -180o Normal ECG P wave - atrial depolarization (SA node to AV node)

PR interval - initial depolarization of the ventricle QRS complex - ventricular depolarization and atrial repolarization QT interval - entire period of depolarization and repolarization of the ventricle ST segment - entire ventricle is depolarized (isoelectric); the plateau or initial phase of repolarization T wave - ventricular repolarization Precordial Leads V1 - In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone). V2 - In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum. V3 - Between leads V2 and V4. V4 - In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the imaginary line that extends down from the midpoint of the clavicle (collarbone). V5 - Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.) V6 - Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient's armpit.) Normal 12 Lead ECG INTERPRETATION OF ECG Rate

Rate

Rhythm Axis Hypertrophy Infarction

The SA node generates a Sinus Rhythm at a range of 60 to 100 beats per minute Tachycardia = > 100 beats per minute Bradycardia = < 60 beats per minute Rate can be determine either by observation alone or when bradycardic, via computation Automaticity Foci (Ectopic Foci) These are other potential pacemakers which has inherent ability to pace if normal SA node pacemaking fails Rhythm On ECG, there is a consistent equal distance (duration) between similar waves during a normal regular cardiac rhythm The automacity of the SA node precisely maintains a constant cycle duration between the pacing impulses it generates And because the sequence of depolarization is the same in each repeating cycle, there is a predictable pattern of regularity in the waves Rhythm Sinus Arrythmia A normal physiological mechanism that is related to phases of respiration Not a true arrythmia >Inspiration = stimulates sympathetic action on the SA node causing a slight increase in HR >Expiration = stimulates parasympathetic action on the SA node causing a slight decrease in HR

Sinus Arrythmia Arrythmias -Irregular Rhythms -Escape -Premature Beats -Tach-arrythmias -Heart blocks -Wandering Pacemaker -A irregular rhythm produce by the pacemaker activity of the atrial foci -Normal rate range (>100, its called Multifocal Atrial Tachycardia) -MATs are usually seen in COPD and toxicity with digitalis meds -Wandering Pacemaker Atrial Fibrillation An irregular ventricular rhythm An erratic atrial spikes from multiple atrial foci ( no P waves seen) Escape The hearts response to a pause in pacing Caused by an unhealthy SA node when it fails to emit a pacing stimulus Sick Sinus Syndrome A wastebasket of arrhythmias caused by SA node dysfunction with unresponsive or dysfunctional supraventricular automaticity foci that cant employ their normal escape mechanism Most often seen in elderly patients with heart disease Young healthy individuals (athletes) often have excessive parasympathetic hyperactivity at rest, have some signs of SSS (pseudo Sick Sinus Syndrome)

Premature Beats Originates in an irritable automaticity focus that fires spontaneously producing a beat Irritability is a result of increase sympathetic stimulation, presence of stimulants like caffeine, ampethamines or coccaine, excess digitalis, hyperthyroidism or low O2 Premature Beats Tachy-arrythmias Rapid rhythms originating in very irritable automaticity foci Easily recognized by rate alone Paroxysmal Tachycardia Flutter Fibrillation Heart Blocks An unhealthy SA node misses one or more cycles, and usually resumes pacing but the pause may evoke and escape response from an ectopic focus Blocks electrical conduction that prevent (or delay) the passage of depolarizing stimuli Could either be a sinus block, AV block, bundle branch block or hemiblock (block of anterior or posterior fascicle of LBB 1. Partial (First-Degree) Block - slowed conduction to AV node - prolonged PR interval (>220msec) 2. Second Degree Block - some impulses not transmitted thru AV node - 2 types: Mobitz I and Mobitz II Heart Block Mobitz I (Wenckebach) - PR interval progressively lengthens

Mobitz II - no lengthening of PR interval 3. Complete (Third-Degree) Block - No impulses conducted through atria to ventricle (beats independently) - No correlation of P waves to QRS complexes Axis Refers to the direction of the movement of depolarization, which spreads throughout the hart to stimulate the myocardium to contract In patients with ventricular hypertrophy, the mean QRS vector points towards the area of hypertrophy For example, in patients with myocardial infarction, there is dead or necrotic area of the heart and does not depolarize. So the mean QRS vector moves away from the infarct Hypertrophy Hypertrophy or increase in muscle mass of the heart can be diagnosed using an ECG Right Atria = diphasic wave, initial larger Left Atria = diphasic wave, terminal larger Right Ventricle = large R wave, V1 Left Ventricle = large S, V1 and large R, V5 (sum should be > 35mm) Infarction Refers to the complete occlusion of a coronary artery wherein it becomes non-viable and neither depolarizes nor contracts Ischemia = inverted T waves; ST segment depression Injury = elevated ST segment Subendocardial infarct = ST segment derpression Infarction = presence of Q wave (>.04 sec); ST segment elevation