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CARDIO RESPIRATORY ROTATION CVS Hx and Ex Important Pointers to know for practice and EXAMS Symptoms to elicit 1) Dyspnoea

a a. LV Failure >> Increase in LA pressure and thus increase in pulmonary interstitial and alveolar pressure. b. This makes the lungs stiff and less compliant which increases the effort of breathing. c. Tachypnoea d. Variants: Orthopnoea and Paroxysmal Nocturnal Dyspnoea. 2) Chest Pain a. Cardiac or Non Cardiac Origin. Need to decide. b. Usually Chest pain of cardiac origin is due to IHD. c. Angina Pectoris d. Variants : Stable, Unstable (worry) e. AMI pain. f. Other causes of chest pain : Pericarditis (affected by movt), dissecting aortic aneurysm, anxiety, pleurisy, Reflux disease and many more. 3) Palpitations a. Awareness of the normal heart beat. b. Fast heart beat c. Slow heart beat. d. Missed heart beat >> Premature beats followed by sudden, strong beat. e. Irregular rhythm of beating. 4) Syncope: 3 main categories for cardiac causes : Arrythmias, Obstruction and Situational. a. Arrythmias i. Ventricular Tachy ii. SVT iii. Sinus Arrest iv. AV Block b. Obstruction i. Aortic Stenosis ii. HOCM iii. Pulmonary hypertension/embolism c. Situational i. Vasovagal >> Vasodilation ii. Postural Hypotension >> Many causes

5) Oedema a. Na and Water retention in CCF. b. Worse during the day and better at night as venous return improves. 6) Others : Fatigue, Intermittent claudication, Weight loss and anorexia (Cardiac cachexia) On Examination (need to understand the pathophysiology for clinical reasoning) 1) General Inspection a. Obesity b. Jaundice c. Cachexia d. Respiratory Distress e. Cyanosed 2) Hands a. Clubbing i. Cyanotic Heart Diseases ii. Infective Endocarditis b. c. d. e. f. g. Splinter hemorrhages Oslers nodes Janeway lesions Capillary return Peripheral Cyanosis Palmar creases

CENTRAL CYANOSIS is seen on the tongue and lips. Due to de-saturation of central arterial blood. Seen In cardiac and resp disorders. Peripheral Cyanosis occurs with central cyanosis or due to peripheral vasoconstriction, stasis of blood which leads to extraction of more oxygen and results in the presence of de-oxyhaemoglobin. Conditions such as CCF, Shock, cold and peripheral circulation anomalies can give rise to this. 3) Pulse a. b. c. d. Rate Rhythm Character R-R delay and R-F delay

4) Blood Pressure 5) JVP

a. b. c. d. e.

Double palsations Not palpable Decreases on Inspiration. Hepatojugular Reflex Causes of Elevated JVP i. Heart Failure ii. Constrictive pericarditis iii. Renal disease with salt and water retention iv. Fluid overload v. SVC obstruction, seen without pulsation.

With pericarditis or Cardiac tamponade, JVP increases with inspiration >> Kussmauls sign JVP Waveform 1) 2) 3) 4) a wave : atrial systole c wave : transmission of the RV pressure v wave : filling of the atrium y wave : tricuspid valve opens and the pressure drops just to increase again when atrium contracts at a wave again.

Anomalies 1) Large a waves a. Increased resistance to RV filling >> in RV hypertrophy. b. Tricuspid stenosis. Rare, as patients with this are on AF and do not have a waves 2) Cannon a waves a. Very large a wave b. Against a closed tricuspid valve c. In complete heart block 3) Large v waves a. Tricuspid regurgitation. EXAMINATION OF THE PREORDIUM Inspection a) Deformities b) Scars c) Apex beat

Palpation a) Apex Beat a. Most inferior and most lateral point of cardiac pulsation. b. At the mid clavicular line at the left, 4th/5th intercostal space c. Several abnormalities i. Tapping ii. Thrusting : Hyperdynamic, characteristic of volume overload iii. Heaving : Sustained and vigorous, pressure overloaded b) Thrills : Palpable murmurs Auscultation a) b) c) d) mitral area, tricuspid area, pulmonary area and aortic area. S1 : Closing of the AV valves S2: Closing of the pulmonary and aortic valves. S2 is physiologically split during inspiration due to increased venous return and thus longer time to expel. e) Reversed splitting. Pulmonary before Aorta. Why? Aortic Stenosis, LBBB and LVF. f) Wide splitting : RBBB or Pulmonary stenosis g) S3: immediately after S2, during the early passive filling phase. Normal in children. > 40y.o, pathological and can indicate regurgitation. h) S4: Just before S1. ALWAYS PATHOLOGICAL. DUE TO STIFFNESS of the ventricles and reduced compliance. i) Other sounds : Systolic Clicks, Opening Snaps, MURMURS Murmurs are caused by TURBULENT BLOOD FLOW. What causes TURBULENT BLOOD FLOW? High blood flow thru a normal valve Normal blood flow thru an abnormal valve. Regurgitation of blood thru a leaky valve.


MURMURS with NORMAL HEART Soft, short, early systole. When? High cardiac output states: Thyrotoxicosis, Anemia and Pregnancy. Its a FLOW MURMUR. With skeletal anomalies : Kyphoscoliosis Small VSD, in early systole.

PATHOLOGICAL MURMUR Systolic Diastolic Continous.

SYSTOLIC MURMURS a) Ejection Mid Systolic Crescendo- Decrescendo Rises then falls. Causes o Aortic Stenosis : Heard best at Aortic Area and RADIATES TO THE CAROTIDS ( as opposed to Aortic Sclerosis) o Pulmonary Stenosis : Heard best on left sternal edge on INSPIRATION. o Left and Right outflow obstruction. Like HOCM.

b) Pansystolic Murmur First to Second Heart sound. Constant in Intensity. Causes i. MR: Blowing, Apex to Axilla. ii. Tricuspid Regurgitation : Left edge iii. VSD : Loud and Rough. c) Late Systolic Murmur Coarctation of the aorta Mitral Valve prolapse DIASTOLIC MURMUR ALWAYS ASSOCIATED WITH CARDIAC DISEASE

a) Mid Diastolic Usually from the mitral and tricuspid valve ; others : Aortic Regurgitation, blood flows back into the LV and may partially obstruct the mitral valve producing a mitral mid diastolic murmur (Austin Flint Murmur) Causes o Mitral Stenosis o Tricuspid Stenosis o Austin Flint Murmus

b) Early Diastolic Murmur Usually from Aortic Regurgitaion. Pulm Regurgitaion.

CONTINOUS MURMUR Usually due to patent ductus arteriosus.

Extra Cardiac Sounds Bruits Pericardial friction rub

SUMMARY OF ECGs from the book ECGs made Easy

IT IS ONLY A TOOL TO AID IN Dx. It does not make the Dx. It just shows anomalies in the cardiac rhythm. Conduction System of the Heart Contraction of muscles associated with electrical changes known as depolarization. These changes detected at the surface of the body. Patient must be fully relaxed as other contractions can stray the ECG recording. SA Node >> Atrial Muscle Fibers >> AV node (delay) >> Bundle of His >> Left and Right bundle branch >> Purkinje Fibers. Normal Rhythm (aka Sinus rhythm) is controlled by SA node.

Shape of a normal ECG

P wave : Atrial Contraction QRS : Ventricles depolarized T: Ventricular repolarisation. In QRS, if the first deflection is downward, it is the Q wave. An upward deflection is called an R wave whether its preceded by a Q wave or not. Below the baseline following an R wave is the S wave. 1 small square : 0.04s I big square : 0.2s For fast calculation of HR, remember this pattern for the R-R interval in terms of large squares o o o o o o 1 : 300 2 : 150 3 : 100 4 : 75 5 : 60 6 : 50

PR Interval : Beginning of P wave to the beginning of the QRS complex. This is time taken for the excitation to travel from the SA NODE THRU THE ATRIAL MUSCLE AND THE AV NODE, DOWN THE BUNDLE OF HIS AND INTO THE VENTRICULAR MUSCLE. Normal PR interval: 0.12 to 0.2s, 3 to 5 small squares.

Duration of the QRS complex: time taken for the current to pass thru the ventricles. Usually 0.12 s ( 3 small squares) Any anomalies of conduction will cause widened QRS complexes.

LEADS 12 Lead ECG 6 standard leads, attached to the limbs ; looks at the heart in a vertical plane. Leads I, II and VL look at left lateral surface of the heart. Leads III and VF at the inferior surface Lead VR looks at the right atrium. Chest Leads: V (1) to V(5) look at the horizontal plane. V1 and V2 look at the Right Ventricle. V3 and V4 look at septum between the ventricles and ant wall of the ventricles. V5 and V6 looks at the ant and lat. Walls of the left ventricle. Each chest lead shows a different ECG pattern, due to their position with relative to the heart.

SHAPE OF THE ECG Depolarisation towards the lead, deflection upwards. Depolarisation away from the lead, deflection downwards. QRS predominantly positive (that is R wave greater than S wave), the depolarization is moving towards the lead. If depolarization is moving at right angles, Q and S wave are of the same size. VR and Lead II are looking from opposite directions. So VR will be negative and II will be positive.


Average direction of spread. Need to know whether this is in normal direction or not. Can be easily determined from Leads I, II and III If normal, the depolarizing wave in lead I, II and III will be positive. RV hypertrophy, one would think of Right Axis Deviation. What happens to the ECG? o Lead I becomes negative o Lead III becomes more positive.

LV Hypertrophy, Left axis deviation. What to see in ECG? o Lead III becomes negative. o If Lead II is also negative, start worrying. There might be a conduction defect.

QRS IN V LEADS: IMPORTANT!! Septum depolarized first Then the current moves from the LBB to RBB. More muscles on the left than right, so left exerts more influence. V1 and V2: RV; V3 and V4: Septum; V5 and V6: Left Ventricle.

What to report back? Name and Date of the ECG Rhythm Rate PR interval QRS Duration T wave ST Segment Cardiac Axis Normal or Abnormal? If abnormal, the possible pathology.

CONDUCTION PROBLEMS Normal: SA node to AV node to Bundle of His to LBBB and RBBB 1) Problems with AV node and Bundle If PR interval is prolonged, 1st degree heart block. o Causes : CAD, Acute Rheumatic Carditis, Digoxin toxicity 2nd degree heart block: excitation completely fails to pass thru the AV node. Occurs intermittently, known as 2nd degree heart block. 3 variations, o Mostly normal. o At times, P waves occur without a following QRS complex.(1) o 2:1 heart block. Alternating. 3rd degree heart block: Complete block. No atrial depolarization is conducted to the ventricles. Need to see for relationship between P wave and QRS complexes. Are there any differences in rate? Abnormal shaped QRS?

BUNDLE BRANCH BLOCKS Two types: Left Bundle Branch Blocks and Right Bundle Branch Blocks. Need to know if these exist immediately as the presence make the ECG interpretation null and void at times. RBBB LBBB Septum is depolarized from Right to Left. V1 and V6 pattern are interchanged. RV depolarized before LV R wave in V1 and S wave in V6. Further depolarization, S wave in V1 and R wave in V6. They appear notched. Good to look at V6. No conduction down the RBB. The beginning in V1 and V6 are normal. Left heart depolarized before Right heart as conduction needs to travel from the left heart to the right heart now due to the block. Characteristic RSR pattern in V1. Might be a normal variant in some ppl.