Health Assessment Quiz 3 (Cardiac)

• Pain in arms or legs
• Intermittent claudication – pain in legs when walking
• Cold, numb extremities, pallor in legs, hair loss
• Swelling in calves, legs or feet
• Color changes in fingertips, toes in cold weather
• Swelling with redness or tenderness
• Smoking Hx

their distance from the heart

the artery lies close to body surface

temporal and carotid arteries

• Brachial: at bend of elbow just medial to biceps tendon
• Radial: lateral flexor surface at wrist 
• Ulnar: medial flexor surface (overlying tissues may obscure)

• Femoral: below inguinal ligament
• Popliteal: passes medially behind the femur; palpable behind knee
• Dorsalis pedis: dorsum of foot; lateral to extensor tendon of big toe
• Posterior tibial: behind medial malleolus of ankle

• 3+  Bounding
• 2+  Brisk, expected (normal)
• 1+  Diminished, weaker than expected
• 0  Absent, unable to palpate

 thin-walled and highly distensible

~90% venous return from lower extremities and are well-supported by surrounding tissues

• Subcutaneous with poor tissue support
•  - Include great saphenous and small saphenous veins
•  - Anastomotic veins connect two saphenous veins
•  - Perforating veins connect superficial (saphenous) system with deep system

Propel blood toward heart, preventing pooling, venous stasis, and backward flow

• Inspection – size, shape, note color, edema, ulcerations, venous pattern
• Palpate for temperature, edema-  is it pitting, texture, grade pulses
• Assess is there Arterial vs Venous Insufficiency
• Special tests 
• ¤Allen Test
• ¤Homan’s Sign
• ¤Doppler

Raynauds

lymphadenopathy

vericose veins

Ejection

Regurgitant

Systolic

distolic

• Rheumatic fever
• Heart murmur
• Risk factors for coronary artery disease (CAD)
• Family history of CAD
• -Hypertension
• -Diabetes
• -Tobacco use
• -Dyslipidemia
• Functional, Psychologic, Social and Economic Status
• Clinical manifestations of heart disease

• Chest pain
• Dyspnea
• Palpitations
• Fatigue and decreased exercise tolerance
• Syncope
• Edema
• Cyanosis

• *Supply‐demand mismatch
• ¨Angina Pectoris
• ¨Atypical Angina
• ¨Angina Equivalents
• ¨Unstable angina
• ¨Non‐ischemic chest pain

• ¨Quality
• ¤Oppressive feeling, pressure, tightness,  burning in precordium
• ¨Duration
• ¤5‐15 minutes
• ¨Provocation
• ¤Triggered by exercise or excitement
• ¤Relieved with rest or nitroglycerin (NTG)

¨Atypical angina‐2/3 classic components

• ¤Pleuritic
• ¤Fleeting¤Localized (1 finger localization)

• ¤New onset
• ¤Crescendo pattern
• ¤Resting angina

• ¨On exertion (DOE)
• ¨Orthopnea (worse lying flat)
• ¨Paroxysmal nocturnal dyspnea (PND)
• ¨Angina Equivalent (symptoms of CV disease is SOB)
• ¨Differentiate from noncardiac dyspnea
• ¤Pulmonary disease
• ¤Anemia
• ¤Deconditioning

• ¨Awareness of heart beat
• ¨Associated symptoms
• ¤Lightheadedness
• ¤Angina
• ¤Dyspnea
• ¤Neurologic symptoms (syncope)
• ¨Provocation (coffee brings it on..etc)

• ¨Symmetrical?
• ¨Neck vein distention?(JVD)
• ¨Pulmonary congestion?
• ¨Evidence for other volume overload states?
• ¤Renal disease
• ¤Hepatic disease
• ¤Low oncotic
• pressure

• ¨Routine activities
• ¨Exercise program
• ¨Nature and requirements of job
• ¨“How far can you walk on level ground?”
• ¨“How many flights of stairs can you climb?”

• ¨General appearance
• ¨Vital signs
• ¨Maybe clues to presence of cardiac disease
• ¨Abnormal heart rate or rhythm
• ¨Abnormal BP
• ¤Abnormal pulses
• ¤Respiratory difficulty
• ¤Skin findings

• ¨VS in each arm
• ¨Supine and erect
• ¨Timing and amplitude of arterial pulses
• ¤Parvus and tardus
•    --On palpation, pulse is weak/small (parvus)
• & late (tardus)
• ¤Compare upper & lower extremity
• Pulse pressure
• “Paradoxical pulse”

• 1 inch
• 40%
• halfway (10" in adults)

¨With the patient lying on the abdomen, an 8‐inch wide cuff should be applied with the compression bag over the posterior aspect of the mid‐thigh and should be rolled diagonally around the thigh to keep the edges snug against the skin

¨Auscultation should be carried out in the popliteal fossa

left ventricular enlargement

constrictive pericarditis

midclavicular line

• ¨Use the fingertips or the area just proximal to them
• ¨Timed with the simultaneously palpated carotid pulse or auscultated heart sounds
• ¨Chest completely exposed and elevated to 30 degrees
• ¨Both supine and in the partial left lateral decubitus positions

left ventricle

right ventricle

PMI

• medial and superior to the intersection of the
• left midclavicular line and the fifth intercostal space
• and is palpable as a single, brief outward motion

TRUE

FALSE. More than 3cm is a sign of LV enlargement

• Concentric hypertrophy
• ¤left ventricular dilatation without volume overload

Sustained outward movement of area larger than 2 to 3 cm in diameter

• ¨Palpable anterior systolic movement (replacing
• systolic retraction) in the left parasternal region
• ¤felt by the proximal palm or fingertips
• ¤patient supine

• ¨Right ventricular enlargement
• ¨Pulmonary HTN &  increased pulmonary blood flow frequently produce a prominent systolic pulsation of the pulmonary trunk in the second intercostal space just to the left of the sternum

¨The flat of the hand or the fingertips usually best appreciate thrills, which are vibratory sensations that are palpable manifestations of loud, harsh murmurs having low‐ to medium‐frequency components

• ¤Cardiac apex
• ¤Left and right sternal borders interspace by interspace
• ¤Base (outflow tract)
• ¤Subxiphoid

increased anteroposterior chest dimensions (emphysema)

• ¨The initial component is most prominent at the
• cardiac apex when the apex is occupied by the left ventricle

• ¨The second component, if present, is normally
• confined to the lower left sternal edge, is less
• commonly heard at the apex, and is seldom heard at the base

The first major component is associated with closure of the mitral valve and coincides with abrupt arrest of leaflet motion when the cusps, especially the larger and more mobile anterior mitral cusp, reach their fully closed positions

The origin of the second component of S1 has been debated but is generally assigned to closure of the tricuspid valve based on an analogous line of reasoning

• Short PR interval (<160 msec)
• Tachycardia or hyperkinetic states
• "Stiff" left ventricle
• Mitral stenosis
• Left atrial myxoma
• Holosystolic mitral  valve prolapse

• Long PR interval (>200 msec)
• Depressed left ventricular contractility
• Premature closure of mitral valve ( e.g., acute aortic regurgiation)
• Left bundle branch block
• Extracardiac factors (e.g., obesity, muscular chest, chronic obstructive pulmonary disease, large breasts)
• Flail mitral leaflet

S3

S4

during the rapid filling phase of the ventricle

Frequent in normal children and in patients with high cardiac output

• In older patients an S3 is abnormal
• ¤Impairment of ventricular function
• ¤AV valve regurgitation

• Other conditions that increase the rate or
• volume of ventricular filling

• Left sided S3
• ¤Bell piece of the stethoscope
• ¤Left ventricular apex during expiration
• ¤Left lateral position

• Right‐sided S3 
• ¤Left sternal border or just beneath the xiphoid
• ¤Louder with inspiration

• Second filling phase‐diastasis
• ¤Variable in duration
• ¤Usually < 5 % of ventricular filling

• Third phase of diastolic filling
• ¤In response to atrial contraction
• ¤15 % of normal ventricular filling

S4 is generated during the atrial filling phase

• Low‐pitched, presystolic sound
• ¤Associated with an effective atrial contraction
• ¤Best heard with the bell piece of the stethoscope
• ¤Loudest at apex
• ¤Left lateral decubitus position

• Diminished ventricular compliance
• Frequently accompanied by visible and palpable presystolic distention of the left ventricle

• Systemic hypertension
• Aortic stenosis
• Hypertrophic cardiomyopathy
• Ischemic heart disease
• Acute mitral regurgitation
• Most patients with an acute myocardial infarction and sinus rhythm have an audible S4

Turbulent blood flow

graded l‐Vl

• ¤Location and radiation
• ¤Timing in cardiac cycle
• ¤Configuation
• ¤Pitch

• ¨Heart rate and rhythm
• ¨Chamber enlargement
• ¨Prior infarction
• ¨Ischemia
• ¨Metabolic abnormalities
• ¨Drug effects
• ¨Risk for lethal arrhythmias (prolonged QT)

• ¨Cardiac size
• ¨Great vessels
• ¨Pumonary vasculature
• ¨Interstitial or alveolar edema
• ¨Non cardiac causes of dyspnea

• ¨Chamber dimensions
• ¨L & R ventricular function
• ¨Valve structure
• ¨Abnormal flow
• ¤Valvular regurgitation or stenosis
• ¤Intracardiac shunts
• ¨Congenital lesions
• ¨Pericardial disease

• ¨Exercise tolerance
• ¨Coronary blood flow reserve
• ¤Ischemic ECG changes
• ¤Wall motion abnormality by echocardiography
• ¤Perfusion defect with nuclear imaging

• ¨Presence and degree of coronary artery disease
• ¨Left ventricular systolic and diastolic function
• ¨Presence and hemodynamic consequences of valvular disease

• ¤Can assess functional capacity
• ¤Safe and widely available
• ¤Long history of data in varying populations
• ¤No radiation exposure

• ¤Sensitivity lower than with imaging (70%)
• ¤Specificity poor if abnormal baseline ECG
• Doesn’t localize or quantify ischemia

• ¤Good sensitivity and specificity (85%)
• ¤Well validated studies to detect CAD and assess prognosis
• ¤Can determine the extent and location of ischemia

• ¤Intermediate radiation exposure
• ¤Time consuming
• ¤$$$
• ¤Inaccurate in the presence of left bundle branch block

• ¤Good sensitivity and specificity
• ¤Quick, readily available
• ¤No radiation
• ¤Less expensive than nuclear imaging
• ¤Localization of ischemia
• ¤“other” data

• ¤Obese or very thin may not image well
• ¤Less accurate in setting of baseline abnormalities
• ¤Interpretation is subjective and nonstandardized

• ¤Readily available and inexpensive
• ¤Not limited by conduction system abnormalities
• ¤No need to exercise
• ¤Non‐invasive

• ¤No functional information
• ¤Very low specificity, esp. in pts >60yo
• ¤Radiation exposure
• ¤No good reproducible data on outcomes
• ¤Inappropriate utilization

• ¤Non‐invasive
• ¤Very good at identifying native coronary disease

• ¤High radiation dose
• ¤Inability to intervene
• ¤No functional information, only anatomic

• ¤Direct visualization of the coronary lumen
• ¤Good prospective therapeutic data based on
• coronary angiographic results
• ¤Ability to intervene

• ¤Does not assess functional significance of lesion
• ¤Radiation exposure
• ¤Invasive

Inability to identify plaques that are vulnerable to rupture and thus development of acute coronary syndrome.

• ¨EKG
• ¨Hypotension
• ¨Hypertension

the inferior wall

lateral wall

anteroseptal

anterolateral

• ¤Most common complication: skin & tissue  compression which can lead to skin irritation and bruising
• ¤Prolonged use and frequent blood pressure determinations → venous pooling and congestion
• ¤Excessive venous pressures →tissue ischemia and nerve damage.

¤Highly irregular or rapid cardiac rhythms because of great beat to beat variability (most NIBP devices employ oscillometric technology that is dependent on fairly regular cardiac rhythms to determine blood pressure)

¤Excessive patient movement such as shivering, restlessness, or external movement such as that from a helicopter, ambulance transport, or a rapid-cycling ventilator can interfere with detection of cardiac oscillations by the NIBP monitor→ erroneous blood pressure measurements

¤Surgical team leaning on cuff!!*

• D Developmental (valvular heart disease)
• D Drugs (Anesthetics & other drugs)
• D Degenerative (Neurologic)
• V Vascular (CV instability)
• I Infectious/Iatrogenic (Adverse reactions, surgical)
• T Toxic/Traumatic (Hemorrhage, sepsis)
• A Autoimmune/Anoxic (Anoxic brain injury)
• M Metabolic/Medical (Medical causes)
• I Endocrine (Pregnancy)
• N Neoplastic (Cancers)
• S Special (Postoperative, deliberate)

• Hypovolemia…NPO!
• Antihypertensive agents (ACEI and ARBs)
• IV contrast agents
• Methylmethacrylate…cement!!!
• Allergens
• Opioids
• Antibiotics
• Inhalational agents
• Hypnotics
• Regional anesthetics
• --Epidural anesthesia
• --Spinal anesthesia

¨

Technique in general anesthesia in which a short-acting hypotensive agent is administered  to reduce blood pressure and thus bleeding during surgery. The procedure facilitates  surgery by making vessels and tissues more visible and reducing blood loss.

• Sodium nitroprusside commonly used
• ¤Afterload reducer w/ rapid onset &  short half-life
• ¤Easy to titrate
• ¤Disadvantages:

• Can also use NTG & esmolol or Inhalational agents!!
• In normal patients, perfusion preserved at MAP > 50mm Hg

• ¨Essential HTN
• ¨Endocrine
• ¨Renal
• ¨Neurogenic
• ¨Systolic HTN with wide pulse pressure (older people)
• ¨Miscellaneous causes

• Preexisting HTN
• Early acute MI
• Aortic dissection
• IICP
• Autonomic hyperreflexia

• ¤Prolonged tourniquet time
• ¤Aortic cross-clamping
• ¤Postmyocardial revascularization

• ¤Pain/catecholamine release
• ¤Inadequate depth of anesthesia
• ¤Hypoxia
• ¤Hypervolemia
• ¤Hypercarbia
• ¤MH
• ¤Shivering
• ¤Improperly sized BP cuff (too small)
• ¤Transducer artifact-increased resonance
• (improperly low position of transducer)

• ¤Rebound HTN (if clonidine, BB, or
• methyldopa d/c’d)
• ¤Systemic absorption of vasoconstrictors
• ¤IV indigo carmine dye

• ¨Others
• ¤Bladder distention
• ¤Hypothermia & vasoconstriction
• ¤Hypoglycemia

• Frequent, readily treatable causes:
• ¤Pain, hypothermia with shivering, bladder
• distention, essential HTN

• Other causes to consider:
• ¤Hypoxemia, hypercarbia, fever & its etiologies, anemia, hypoglycemia, tachydysrhythmias, withdrawal, myocardia ischemia, meds, PMH, surgical procedures, intraop events

• Rare causes:
• ¤Hyperthyroidism, pheochromocytoma, MH

• Spurious or incorrect readings
• ¤Zero art line, size of BP cuff

• Decreased SVR
• ¤Regional anesthesia sympathectomy

• Hypovolemia
• ¤Unreplaced fluid deficit, unrecognized EBL, 3rd
• spacing, ongoing fluid loss

• Ventricular dysfunction
• ¤Ischemia, impaired contractility, fluid overload, mobilization of fluid following regional anesthesia

• Mechanical problems
• ¤Tension pneumothorax or tamponade

• Arrhythmias
• ¤Preexisting heart disease, ischemia, decreased CO, meds

• ¨Must be treated swiftly & aggressively
• ¨Volume expansion!!!!
• ¨Then if necessary, vasopressors or inotropes

• ¨Determine preexisting cardiac disease
• ¨Disease severity, stability, prior treatment
• ¨Functional capacity
• ¨Co-morbid conditions
• ¨Type of surgery planned

• ¨Unstable Coronary Syndrome
• ¨Decompensated Heart Failure
• ¨Significant Arrhythmias
• ¨Severe Valvular disease

• ¨Known CAD
• ¨Advanced age
• ¨HTN
• ¨Diabetes
• ¨Hypercholesteremia
• ¨Smoker
• ¨Family History of premature CAD

• ¨How much of myocardium is at risk?
• ¨How much stress can myocardium handle before it becomes ischemic?
• ¨What is patient’s LV function?
• ¨Is the patient medically optimized?

• ¨Definition SBP >140 or DBP >90mmHg
• ¨Stage 3 HTN
• ¤SBP>180 mmHg
• ¤DBP>110 mmHg

• ¤Reduces perioperative hemodynamic instability.
• ¤Reduces instances of myocardial ischemia & CVA

• ¤Symptomatic = delay or cancel
• ¤Severe AS = Need study less than 12 months old
• ¤What if patient is not a candidate or refuses AVR?---Don’t give a spinal!!!

• <1cm is severe
• <0.6cm is critical
• 1.5-1cm is moderate AS

¤At increased risk for heart failure

¤Only surgically repair valve prior to non-cardiac surgery if there is a need that is not related to proposed surgery

• ¤Superficial procedures?
• --Normalize INR then restart post-op

• ¤Otherwise?
• --Heparin bridge to surgery

• Class I
•   Benefit>>>Risk

• Class IIa
•   Benefit>>Risk

• Class IIb
•   Benefit> or = to Risk

• Class 3
•   Risk> or = to Benefit

¨Provide a framework to consider cardiac risk for non-cardiac surgery

¨Use this knowledge to individualize care

¨Class IIa: Patients with dyspnea of unknown origin,

¨Class IIa: Patients with current or prior heart failure. (if not been evaluated in past 12 months)

¨Class IIb: Reassessment of LV function in previously documented cardiomyopathy in  clinically stable patient is not well established.

¨Class III Routine perioperative evaluation of LV function is not recommended.

•Class I: Patients with at least 1 clinical risk factor undergoing vascular procedures.  (diabetes, CHF, etc) *not for bunuectomy

•Class I: Patients with known CAD, PVD, cerebrovascular disease undergoing intermediate risk surgical procedure  (thyroidectomy).

•Class IIa: No risk factors but having vascular procedure (healthy person getting carotid surgery,  get EKG)

• •Class IIb: Patients with at least 1 risk factor
• having intermediate risk operation.
• (HTN & thyroidectomy-get EKG?)

• •Class III Pre-op and post-op resting 12
• lead ECG is not indicated for asymptomatic patients having low risk surgery.

•Class I: Active cardiac conditions in which non-cardiac surgery is planned should be evaluated and treated before surgery.

•Class IIa: Patient’s with 3 or more clinical risk  factors and poor functional capacity who require vascular surgery.

•Class IIb: May consider for patients with 1-2 clinical risk factors and poor functional capacity who require intermediate risk surgery.

•Class IIb: May consider for patients with 1-2 clinical risk factors and good functional capacity having vascular surgery.

•Class III: No clinical risk factors having intermediate risk or low risk surgery.

Class I: Patients with stable angina who have significant LM disease.

Class I: Patients with stable angina who have 3 vessel disease.

Class I: Patients with stable angina who have 2 vessel disease with significant proximal LAD  stenosis and EF less than 50% or demonstrable ischemia on non-invasive stress testing

Class I: Patients with high risk unstable angina or non ST segment elevated MI.

Class I: Patients with acute ST-elevation MI.

Class IIa: PCI to mitigate cardiac symptoms in patients who need elective surgery in next 12M.

Class IIa: Patients who have received drug- eluting stents needing urgent surgery that mandate discontinuing thienopyridine therapy.

• Class IIb: Not well established for patients with
• high risk ischemia or low risk ischemia. (dobutamine echo with 5 segements of wall motion abnormalities or 1 to 4 segements)

Class III: Routine prophylactic revascularization is not recommended in patients with stable CAD.

Class III: Elective surgery is not recommended for 4-6 weeks after bare metal stents, 12 months for drug eluting if dual antiplaelet therapy needs to be discontinued  perioperatively.

Class III: Surgery is not recommended for 4 weeks after PTCA.

¨Class I: Continue beta blockers for those taking beta blockers for angina, symptomatic arrhythmia’s, HTN.

¨Class I: Give to patients undergoing vascular surgery who are at high cardiac risk according to preoperative testing.

Class IIa: Recommended for patients who pre-op assessment testing identifies CAD.

• Class IIa: Probably recommended for patients
• having vascular surgery with 1 clinical risk  factor. (HTN, taking diuretic for control)

• Class IIa: Probably recommended for patients
• identified as having CAD or high cardiac risk by the presence of 1 more than 1 clinical risk  factors.

Class III: Avoid use in those with absolute contraindications for beta blocker therapy.

¨Class I: If on a statin, continue.

• ¨Class IIa: Reasonable use for those with or
• without clinical risk factors having vascular surgery.

• ¨Class IIb: Consider for those with at least 1
• clinical risk factor having intermediate risk procedure.

• ¨Class IIb: May consider for pre-op control of HTN
• in those with CAD or at least 1 clinical risk factor.

¨Class III: Avoid in those patients with absolute contraindication for these medications.

• Class IIb:
• ICU monitoring with Swan Ganz catheter in order to optimize hemodynamic status should be used only in highly select patients who are unstable and have multiple comorbid conditions

Class IIb: Can be beneficial to maintain anesthesia in hemodynamically stable patients at risk for ischemia

Class IIb: Unclear if intraop use for patients at high risk for myocardial ischemia is warrented

Class IIb: Reasonable to use in emergent case to determne cause of acute persistent hemodynamic abnormality.

Class I: Recommended for most procedures  other than in ones where hypothermia is intended to provide organ protection

• Class IIa: Reasonable to control glucose in DM
• patients and those at risk for myocardial ischemia having vascular and high risk surgery with planned ICU admission.

Class IIb: Strict glucose control appears uncertain in DM patients or acute hyperglycemia patietns having surgery without planned ICU admission.

• Class IIb: May be reasonable in patients at risk
• for hemodynamic disturbances easily detected by PA catheter.

Class III: Routine use is not recommended

• Class IIa: Intra and post-op monitoring can be
• useful in monitoring those with known CAD and those having vascular surgery.

• Class IIb: May consider use in those with 1 or
• multiple risk factors for CAD.

Class I: Measure troponin on patients with ECG changes or with chest pain typical for acute  coronary syndromes.

¨Class IIb: Not well established for stable patients having had vascular or intermediate risk surgery.

¨Class III: Not recommended for asymptomatic patients having had low risk surgery

• ¨Class IIb: Uncertain for patients with only 1
• clinical risk factor having intermediate risk procedure or vascular procedure.

• ¨Class IIb: Uncertain for those having vascular
• surgery and not currently on beta blocker.

• Evaluate pacemaker 3-6 months prior to surgery
• Evaluate pacemaker after surgery
• Set to asynchronous if pacer dependant or use magnet
• ICD set tachyarrhythmia settings to off

Duration of ventricular systole

SIX

SIX

• •Lead I
• •Lead AVL

• •Lead II
• •Lead III
• •Lead AVF

•V1

•V2

•V3

•V4

•V1

•V2

•V5

•V6

•V3

•V4

• •1. Rate
• •2. Rhythm
• •3. Axis
• •4. Hypertrophy
• •5. Infarction

• •Abnormal accessory pathway, bundle of Kent
• •Short circuits usual delay through AV node
• •Delta wave on EKG, has illusion of shortened PR interval and lengthened QRS.

• •Sinus block
• •Sick sinus syndrome
• •Tachy-Brady syndrome
• •1st degree AV block
• •2nd degree AV block
•    Wenckeback (formerly type 1)
•    Mobitz (formerly type 2)
• •3rd degree block
•    Junctional focus
•    Ventricular focus

• •QRS is 0.12 seconds or greater
• •Check V1 and V2 for RBBB
•      R,R’ pattern
• •Check V5 and V6 for LBBB
•      R,R’ pattern

• •Measure the Vector of electrical stimulus
• •Follows the general direction of the  depolarization of the heart (uppper R to lower L)
• •Mean RS vector
• •Normal vector is downward and to the patient’s left
• ----Between 0 degrees and +90 degrees is normal
•       * 0 degrees is due left
•       * +90 degrees is due south

• hypertrophy

• Infarct

YES! (two thumbs up rule)

right axis deviation

left axis deviation

• •Then extreme right axis deviation
• (# is extremely +)

• •QRS normally begins more negative in V1 and becomes more positive in V6
• •V3 and V4 are generally isoelectric
• •QRS is about equal above and below
• •Rightward rotation occurs when V1 or V2 are isoelectric
• •Leftward rotation occurs when V5 or V6 are isoelectric

• •Check Lead V1
• •Usually see a diphasic P wave
•    -If initial component is larger then Right atrial enlargement
•    -If terminal component is larger then Left atrial enlargement

• •Lead V1
•   - Large R wave, small S wave
•   - R wave gets progressively smaller from V2-V6
• •Also See
•    - Right Axis Deviation
•    -More vectors directed towards the  hypertrophied Right ventricle
•   - Rightward rotation in horizontal plane

• Check V1
• •Usually deep S wave but with LVH even deeper
• •Also Left axis deviation and left rotation of vector
• •V5 see Tall R wave
• •So, measure depth of S wave in V1 and Height of R wave in V5
•   (If total is greater than 35mm the LVH)

• •Ischemia
• •Injury
• •Necrosis
• •Dead Tissue

• •Q wave is diagnostic for infarction
• •Significant Q waves are absent in normal EKG’s
• •Tiny q waves are insignificant
• •Q wave >.04 seconds or 1/3 of QRS
• amplitude is significant

• •V1
• •V2
• •V3
• •V4

• •Lead II
• •Lead III
• •Lead AVF

• •Lead I
• •Lead AVL

• •Lead V1
• •Lead V2
• •But….QRS is upside down relative to Anterior MI

True!