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06/26/13 10:30-12:30 Lecture#11

YL7 Module#2 Cardiology | Internal Medicine DIAGNOSIS OF CARDIOVASCULAR DISEASE


Dr. Jose Paolo Prado, MD, FPCP, FPCC

OUTLINE I. Outline IX. Heart Murmurs II. Introduction X. Local and Systemic III. Chest Pain Manifestations of Heart IV. BP Measurement Disease V. Arterial Pulse XI. Summary VI. Jugular Venous Pressure XII. Review Questions VII. Precordial Palpation XIII. Answers to Review VIII. Heart Sounds Questions

Acronyms: AI- Aortic insufficiency AR- Aortic regurgitation AS- Aortic stenosis JVP- Jugular venous pressure LA/V- Left atrium/ventricle MR-Mitral regurgitation MS- Mitral stenosis PAD- Peripheral Artery Disease PDA- Patent ductus arteriosus RA/V- Right atrium/ventricle I. Outline Focus: Approach to Physical Examination of a Cardiac Patient Arterial Pulse Blood Pressure Jugular Venous Pressure Precordial Pulsation Heart Sounds Heart Murmurs Local and Systemic Manifestations of Cardiac Disease II. Introduction Reasons Why A Cardiac Assessment is Sought Usually people go to the clinics for a CV consult because they want a confirmation and assessment if a suspected cardiac problem, lesion or disease Usually comes to the clinic with presence of abnormal cardiac findings on PE (e.g. heart murmur) and/or one of the laboratory tests (e.g. Abnormal ECG, CXR , Echo) from a previous doctor Usually present with cardiac symptoms (such as dyspnea, chest pain, syncope) Cardiac Symptoms and Their Appraisal Symptoms can be grouped to identify underlying pathology 1. Definite orthopnea and/or nocturnal dyspnea Symptoms usually indicate a problem in left atrium produced by high left atrial pressure. 2. Triad of dyspnea, chest pain, and exertional presyncope or syncope fixed cardiac output lesions - cardiac output fails to increase adequately during exercise (outflow tract obstruction e.g., aortic stenosis). - e.g. Patient was running then suddenly experienced syncope Heart cannot pump because of blockage in the exit of blood, usually in the aortic valve position (aortic stenosis). When the patient runs, the blood is blocked and cannot go to the brain causing syncope. 4G

3. Low-output symptoms Fatigue, lassitude and light-headedness - Severe inflow obstructive lesions, severe cardiomyopathy of ischemic or non-ischemic etiology, constrictive pericarditis, cardiac tamponade, or severe pulmonary hypertension - e.g. In aortic stenosis, blood cannot go to the brain. - E.g. If pump itself is failing in cardiomyopathy cases, whether ischemic or non-ischemic May be due to cocaine or methamphetamine abuse -> heart becomes weak -> pumping action is not enough to pump blood to brain -> you feel tired Sometimes, low output symptom may lead to cardiac tamponade because the heart is being crushed by the fluid inside the pericardial cavity. Syncope and presyncope - Significant bradyarrhythmia or tachyarrhythmia, hypotension of sudden onset brought on by postural change, vagal reaction, or be neurogenic origin - Also symptoms from low-output states but produced by bradyarrhythmia or tachyarrhythmia If hearts pumping action is too much or too slow, no pumping action, no blood goes to the brain syncope - In severe anxiety, pain or emotional outburst tachycardia dilated vasculature falls down Because of the effect of gravity, patient remains conscious since blood flows back to the brain. - Others experience situational syncope. They just suddenly fall down while peeing [trans thoughts: in reaction to a situation, not simply by peeing], etc. (abnormal vagal reaction). - Runners who do not cool down: After they finish their run, they just bend over, the IVC is compressed, no cardiac return, lose blood pressure to the brain, then you fall down. III. Chest Pain More common presenting symptom in the clinic 3 general types: 1. Typical angina (coronary) Central chest discomfort often described as (character) tightness, heaviness, squeezing or burning sensation, or sensation of oppression or weight on the chest with or without typical radiation to the arms, shoulders, back, neck, and/or jaw (radiation due to same dermatome level with the heart) with or without accompanying dyspnea related often to activity (precipitating factor) and relieved usually within a few minutes of rest or after nitroglycerin (relieving factor) 2. Atypical angina Same character but lacking in some features. - Not triggered by effort, not easily relieved by pain. the chest discomfort has some features characteristic of angina and yet other features not so typical; e.g., left anterior or central chest tightness related to physical exertion but requiring a long period of rest for relief such as having to lie down for extended period of time 3. Noncardiac chest pain Such as that related to musculoskeletal (in taking a deep breath; may be due to costrochondritis) , pleuritic, and esophageal,etc. Page 1 of 11

AVELLANA. CRISTOBAL. DE CASTRO. ESTANISLAO. LIRIO. NG. SANGALANG. TUGBANG. VIOLAGO.

DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


Note: For Table 1. Categories of Congenital Heart Defects and Table 2. Categories of Acquired Heart Defects, please refer to Appendix 1 and 1 respectively.

Contour abnormalities Hear bruits from AV fistulas Pulsus alternans (an alternating strong and weak pulse) Peripheral signs e.g. aortic regurgitation Pulsus Paradoxus More common abnormality we usually look for. More than 10 mmHg fall in systolic pressure with inspiration - Normally, when we inhale, BP decreases a bit Since there is more negative pressure in the chest, you suck in more blood into the right atrium When it falls to more than 10, it is called pulsus paradoxus, which is considered pathologic and a sign of cardiac or pulmonary disease Can also mean cardiac tamponade - E.g. initial BP is 100/60; if you ask the patient to inhale and BP falls to 80/60 positive pulsus paradoxus

IV. Blood Pressure Measurement Patient seated comfortably, back supported, bared upper arm, legs uncrossed If legs are crossed or hanging, BP increases. Arm should be at heart level If patient is at left lateral position, BP increases. Cuff length/width should be 80%/40% of arm circumference Small cuff gives falsely high BP; big cuff gives falsely low BP Cuff should be deflated at <3 mmHg per second Column or dial should be read to nearest 2mmHg First audible Korotokoff sound is systolic pressure; last sound, diastolic pressure No talking between subject and observer Abnormalities differential of more than 10 mm Hg between the left and the right can be associated with subclavian artery disease (subclavian stenosis causing low BP reading) (atherosclerotic or inflammatory), or an output problem (supravalvular aortic stenosis, aortic coarctation, or dissection). Legs generally should have the same blood pressure as the arms . Systolic leg pressures may exceed arm pressures by as much as 20 mm Hg; greater leg-arm pressure differences are seen in patients with severe AR (Hill sign) and patients with extensive and calcified lower extremity peripheral arterial disease (PAD). Orthostatic Hypotension fall in blood pressure of more than 20 mm Hg systolic and/or more than 10 mm Hg diastolic in response to moving from a supine to a standing position within 3 minutes More common in patients with hypovolemia, dehydration or medication effect. e.g. alpha blockers in the morning vasodilation patient stands up sudden drop in BP patient falls down - Advised to take prostate medicines at night when patient is supine and does not suffer from orthostasis/orthostatic hypotension. If orthostatic hypotension is due to dehydration or volume depletion, there is a compensatory tachycardia. But may be accompanied by a lack of compensatory tachycardia in autonomic insufficiency, as can be seen in patients with diabetes or Parkinsons disease. V. Arterial Pulse Assessment Rates, rhythm, and pulse deficit Symmetry and radio-femoral delay - All pulses in all extremities should be graded (+1/+2, absent/present) - All pulse points should have a pulse; if there is a deficit it could mean of peripheral arterial disease Vessel wall characteristics - Old age makunat pulse points or stiffened by calcifications Amplitude Upstroke 4G

Fig 1. A. Pulsus paradoxus accentuated by inspiration; B. Cardiac tamponade

Pulsus Alternans Beat-to-beat variability of the pulse amplitude

Fig 2.Pulsus alterans

Upstroke: peak systolic pressure Dichotic notch: peak diastolic pressure Indicated by graphically alternating high-low peaks Taken invasively (catheter hooked into machines) Pulse alternates from weak to strong Page 2 of 11

AVELLANA. CRISTOBAL. DE CASTRO. ESTANISLAO. LIRIO. NG. SANGALANG. TUGBANG. VIOLAGO.

DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


Severe heart failure and is exaggerated in severe AR, hypertension, and hypovolemic states c wave just a manifestation of an arterial event, a carotid pulsation (which is beside the JVP). When RA is filled, tricuspid valve closes, pushing it into RA (v wave). Relaxation (y descent) - In diseased states, there are changes in the a-c-x-v-y wave.

Fig 3. Difference in amplitude of pulses. - Depending on where you palpate pulse, there is a difference in

amplitude (aortic can be different from femoral).

Fig 5. Normal jugular venous pulse. THE JVP COMPONENTS FURTHER EXPLAINED:

Fig 4. Abnormal pulses.

- There may be obvious abnormalities when pulse is palpated: dichotic pulse 2 peaks pulsus tardus - no sharp pulsus alternans bigeminy two Pulsus paradoxus - pulse decreases upon inspiration; usually in pericardial problem VI. Jugular Venous Pressure What is JVP? Normally, when you inhale, RA and RV fill up with blood; when you exhale, nothing much happens. - This is why respiratory maneuvers are important. Deep breathing heart (RA and RV) is filled up with blood get pressure wave forms from RA translate to JV wave form: - Composed of a-c-x-v-y waves, representing events in RA - Contract relax fill empty When RA contracts, pressure increases (a wave). When RA relaxes, pressure decreases (x descent). 4G

A wave is due to right atrial systole; it coincides with the first heart sound and precedes the carotid pulsation C wave is due to transmission of rapidly increasing right ventricular pressure before the tricuspid valve closes; it is small and rarely visible X descent is due to relaxation of the right atrium V wave is due to the venous return filling the right atrium as the tricuspid valve remains closed during ventricular systole: o it occurs simultaneously with the carotid pulsation o its height provides an indication of the right heart filling pressure o in cardiac failure, it is greater than 2 cm o an early V wave followed by a steep Y descent is a sign of tricuspid regurgitation

Y descent is due to opening of the tricuspid valve and rapid ventricular filling; a steep Y descent is seen in pericardial disease and tricuspid regurgitation Thus, A, C, and V are positive deflections; X and Y are negative ones. From the start of the C wave to the Y descent, the ventricles are in systole.

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


How to Measure JVP Heart at a 45 angle; shine a light Theres a column of blood that fills up the column from the RA to the midclavicle, about 5-6mmHg; but if you add up to JVP it will be up to 8 mmHg. Anything >8mmHg signifies elevated right atrial pressure or JVP.

Table 3. JVP abnormalities and probable causes.

Fig 6. Measuring the JVP

Distinguishing Jugular Venous Pulse from Carotid Pulse


Fig 7. JVP in Different Cardiac Abnormalities

JVP has 2 pulsations and has respiratory variation vs. carotid which has 1 pulsation and not affected by respiration If you press on your neck, JVP will be obliterated but carotid will not be compressed Abnormal JVPs

e.g. Complete AV block - Ventricles are contracting independently of the atria AV nodes function is to conduct impulse from the SA node to the ventricles But in AV block, ventricles work on its own: Ventricles beat at a slower rate of 40 Atrial is faster at >60 - Therefore, no a-c waves; just a cannon a-wave (reflecting RA) - Also cannot see RV due to AV block In atrial fibrillation, no sinus node and chaotic atriathey are just nanginginig,, fibrillating. - If the atria is fibrillating, you should not see any "a" waves because there are no organized contractions. So you see loss of "a" waves in atrial fibrillation. Conversely, you see cannon "a" waves in complete AV block. In constrictive pericarditis, the pathology is the sac that contains the heart constricts the heart. The problem here is that the heart can't relax. So diastole is affected. You would expect a problem in relaxation, a shallow "x" descent or loss of "x" descent. In tricuspid stenosis, the blood from the RA does not empty/has difficulty emptying to the RV. There is not much "x" descent, or you have a loss of the "x" descent. Page 4 of 11

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


- The heart contracts and relaxes. The tricuspid valve opens at "x" and fills. The RV contracts and forms a bump (the "v" wave). Kussmauls Sign Normal JVP decreases with inspiration and increases with expiration - Normally when you lie down, you suck in more blood into the heart, your JVP will disappear. In the Kussmaul's sign, it's the other way around. When you inhale, it fills up more. Veins that fill at inspiration (Kussmaul sign), however, are a clue to constrictive pericarditis, pulmonary embolism, or RV infarction - Usually happens with constrictive pericarditis, the heart is constricted (nakasakal). When you inhale, the blood is not able to enter the heart due to constrictive pericarditis physiology and the neck veins are filled up. You have a paradoxical increase in the neck veins during inspiration. Hepatojugular Reflux When compression is applied to the liver or the abdomen during normal respirations, the jugular venous pressure will be seen to increase transiently in normal subjects. - in a patient with heart failure, the venous pressure will increase and stay increased until the pressure is released ( POSITIVE HEPATOJUGULAR REFLEX) If the patient has a persistently elevated JVP during the compression of more than 30 seconds, that's called a positive hepatojugular reflex. Usually it happens in patients with poor ejection fractions or left ventricular heart dysfunction or heart failure. - patient should not hold the breath or perform a Valsalva maneuver during the compression - compression should be applied for at least 30 s. VII. Precordial Palpation Precordial palpation Supine position at 30 degrees - If not palpable in this position: left lateral decubitus position with the left arm above the head in the seated position, leaning forward - The ideal position in chest palpation: supine at 30 degrees, left lateral decubitus position You bring the heart closer to the chest wall. You have an opportunity to feel the maximum impulse of the heart which is usually at the 5th intercostal space midclavicular line. Point of maximal impulse is normally over the left ventricular apex in the midclavicular line at the fifth intercostal space. - The normal size should be smaller than 2 cm in diameter or 2 finger breadths, and moves quickly away from the fingers If bigger than 2, the heart is considered big. It should only be the apex that you can feel (tumutusok) against the chest wall. If the heart is bigger, you have a more diffuse apical impulse beat. - The impulse is best felt at end-expiration because the lungs are empty and the heart is closer to the chest. Heave a persistent upliftment of the chest Thrill like vibrations that you can feel from your fingertips 4G Assessment of the Apical Impulse Lateral most point of systolic outward motion that can be felt on the chest wall - Location is usually 10 cm from midline - Area (2.53.0 cm in diameter) More than 3 is left ventricular hypertrophy or dilated left ventricles. - Ventricle causing the impulse If it's subxiphoid, it's most likely the RV. - Character - Palpable sounds and murmurs in the area of the apical impulse. Remember that some patients have dextrocardia! VIII. Heart Sounds There are 2 normal heart sounds: S1 and S2. But S1 can be divided into M1 and T1, and S2 into A2 and P2. S1 and S2 can be divided because the heart has 2 sides and they beat synchronously. - "Lub", the first heart sound, is lower pitched and longer in duration - "Dub", second heart sound, is sharper, shorter and higher frequency. When the beating of the right and left are not synchronized (naghihiwalay), you will have extra heart sounds. So you can have splits or S3s and S4s. Anything beyond "lub dub" is an extra heart sound. Formation S1 = M1 + T1 (simultaneous mitral and tricuspid closure) - Heard loudest at the apex - Low pitched and longer in duration - The reason they sound like that is, some experts say the closure of the values is silent, has no sound. The sound is produced by the sudden deceleration of the blood when they hit the valves when they're closed. It's like swishing a bottle. - At the onset of a carotid pulse or the apical impulse - Lubbb S2 = A2 + P2 (simultaneous aortic valve and pulmonic valve closure) - Sharper, shorter, higher frequency dub Timing

Fig 8. Wiggers diagram.

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


S3 - Near S2 - Early phase of the ventricular filling characterized by sudden vigorous expansion associated with rapid inflow of the blood - The peak of this filling period may be accompanied by a sound, which is termed the third heart sound, or S3. - Physiological S3 occurs in children and in pregnant women and in other conditions associated with rapid circulation such as anemia and thyrotoxicosis - Pathological S3 Volume overload Ventricular dysfunction Pericardial knock S4 - A pre-S1 sound - Strong atrial contraction during this phase augments the ventricular filling, which could be decelerated abruptly if the ventricular compliance is reduced for any reason, producing an S4. Splitting If you remember Wiggers diagram (refer to Fig 8), this is timed at the closure of the valves. - The phonograph displays the heart sounds "lub dub". The sounds coincide with pressure events in the heart. The blue curve (ventricular pressure) is a pressure tracing inside the heart. Systolic is at 120. Diastolic is after aortic valve closure. Aortic valve closure is S2. Mitral and tricuspid closure is S1. - S1 marks the start of the systolic period. S2 is diastolic. - S3 is the sound produced by the vigorous sudden expansion of the left ventricle during diastole. That's why the S3 occurs after S2. "Lub dub S3. Lub dubub. Lub dubub." Usually occurs during volume overload, left ventricular dysfunction, or sometimes it can be heard as a pericardial knock. - S4 is because of the atrial contraction against ventricular filling. The timing is pre-systolicso it is near S1. "Bulub dub. Bulub dub." appreciate the physiologic splitting of the S2 when you inhale because you augmented right ventricular output. Normal breathing: "Lub dub. Lub dub." During inhalation, higher pitched: "Lub durub. Lub durub." If there is fixed splitting, it's because there is a problem most probably an atrial septal defect. There is a hole in the septum. The splitting is delayed but occurs in both inspiration and expiration. The difference of the right bundle branch block split from the physiologic split: it is fixed but the split is wider during inspiration. Exhalation: "Lub durub. Lub durub. Lub durub." Inhalation, higher pitched: "Lub duruuuub. Lub duruuuub. Lub duruuuub." Reverse split of left bundle branch block: Delayed polarization of the left compared to the right. The right contracts before the left. Now your split is opposite (baliktad naman). Exhalation: "Lub durub. Lub durub. Lub durub." Inhalation, faster and higher pitched: "Lub durub. Lub durub. Lub durub." Your respiratory maneuvers affect where the split occurs.

Fig 10. Splitting in relation to respiratory maneuvers.

Summary: - Normal heart sound: "Lub dub. Lub dub." - S3: "Lub durub. Lub durub." - S4 is near S1: "Bulub dub. Bulub dub." - Splits: "Lub durub. Lub durub." - Quadruple rhythym, everything is there, like a horse:: "Bulub durub. Bulub durub." You can download the heart sounds podcast. Includes all physiologic and pathologic sounds (murmurs, congenital heart diseases): Texas Heart Institute Heart Sounds Series.

Fig 9. Physiologic splitting of S2

- Splitting: Remember that hearts are [divided into] left and right. The closure is timed simultaneously, that's why there's one sound. But if they split, it's because there's a delay in one side. For example: You have a right bundle branch block. The electrical impulses that stimulate the right side of the heart is delayed. You'll have contraction that is asynchronousleftright, left-right, left-right. So you'll have splitting of the second heart sound. "Lub durub. Lub durub." Physiologically, there should be some degree of splitting. Because when you inhale, you put in more blood into the right. You delay the closure of the pulmonic valve. You will 4G AVELLANA. CRISTOBAL. DE CASTRO. ESTANISLAO. LIRIO. NG. SANGALANG. TUGBANG. VIOLAGO. Page 6 of 11

DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________

Fig 11. Algorithm for Splitting.

Extra sounds

Listen to the heart : in the right 2nd interspace close to the sternum, along the left sternal border in each interspace from the 2nd through the 5th, and at the apex. Stethoscope: a. The diaphragm high pitched sounds of S1 and S2, the murmurs of aortic and mitral regurgitation, and pericardial friction rubs. b. The bell- low-pitched sounds of S3 and S4, and the murmur of mitral stenosis IX. Heart Murmurs Formation Laminar vs. turbulent flow Grading

Fig 12. Extra Heart Sounds

Auscultation Areas Mnemonic: Always Pray To Mary (During Doc's time: Ako Po'y Tau Mu.) - Aortic, Pulmonic, Tricuspid and Mitral Auscultatory areas do not necessarily indicate where valves are. Rather, the areas reflect where the blood flows through the valves. - The mitral valve is in the AV groove. But its auscultatory area is near the apex, 5th ICS midclavicular line. - Tricuspid valve is auscultated near the parasternal border of the 5th ICS. - Pulmonic is near the left 2nd ICS parasternal border. Opposite that is the aortic. - REMEMBER: You do not listen to the valve itself but to the blood flow from the valve.

Table 5. Grading of Murmurs

Grade 4 to 6 is related to a thrill. Grade 6 is the loudest that you can hear the murmur with the stethoscope off the chest. Grade 1 is the loudest. Timing Page 7 of 11

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


- E.g. Pulmonary stenosis nd Location: Left 2 ICS

Fig 16. Murmur of PS.

Fig 13. Timing of murmurs

Systolic murmur murmur after S1 (Lub-Tuk) Diastolic murmur murmur after S2 (Lub-Tukishhhhhh-Lub) Systolic ejection murmurs - Systolic ejection murmurs are associated to a loud P2 when a patient has Pulmonary Hypertension - Aortic Stenosis, Mitral Valve Prolapse and Pulmonary Stenosis are similar in murmurs. The difference between the two is the location. - E.g. Aortic Stenosis with a constrictive aortic valve Because the constriction causes a turbulent flow, there will be disturbance. Occurs during left ventricular contraction Expect a Lubbsssssshhhh-Tuk Location: Right 2nd ICS

Diastolic ejection murmurs - E.g. Aortic Regurgitation You expect a laminar sound after systole During diastole, the blood will go back to the left ventricle. Expect a Lub-dub-ahhhhh Continuous murmurs - E.g. Patent Ductus Arteriousus - Machinery-like - Expect a Shhhahhhhshhhhahhhh Auscultatory location X. Local and Systemic Manifestations of Cardiac Disease SKIN MANIFESTATIONS Central cyanosis - Significant RL shunting at the level of the heart or lungs depending on the pathology - Allows deoxygenated blood to reach the systemic circulation Blue lips and oral mucosa due to low oxygen in the blood - Usually occurs in congenital abnormalities E.g. congenital heart diseases such as TOF - Normally blood from the right ventricle go to the lungs to get oxygen then come back to the left atrium oxygenated. - In TOF, the blood is shifted from the right to the left, bypassing the lungs. This will result to having deoxygenated blood entering the system through an ASD. - There is still communication but there is also the presence of Pulmonic Stenosis. Peripheral cyanosis - Reduced blood flow because of small vessel constriction seen in severe heart failure, shock, or peripheral vascular disease - Relate this to central cyanosis. The patient must be pink with oxygenated blood and therefore it is not due to a congenital abnormality. - The arteries are constricted of the patient is in shock that the blood does not reach the distal vasculature. - Central cyanosis is absent. Differential cyanosis - Affecting the lower but not the upper extremities Toes are blue but hands are pink. - Occurs with a PDA and pulmonary artery hypertension with RL shunting at the great vessel level The blood circulation from the arms comes from the great vessels of the heart which is given off proximal to the PDA

Fig 14. Murmur of AS

- E.g. Mitral Valve Regurgitation When the left ventricle contracts, AV and PV are open. MV and TV should be closed. If there is MVR, blood from LV will flow to the aorta and LA Expect a Lubbsssssshhhh-Tuk Location: Apex

Fig 15. Murmur of MS.

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


and reaches the distant arteries resulting to pink fingernail beds. Because of PDA is the connection of the with the pulmonary artery, some deoxygenated blood mixes with the circulating system and reaches the legs resulting to bluish nail beds in the toes. Cerebral symptoms: almost fainted blood was not reaching the brain Differential Diagnosis Heart failure something to do with the pumping Obstructive cardiac lesion like aortic stenosis R-sided problems like preloading problem or pulmonic stenosis Cardiac examination findings: Patient slightly tachypneic, 57, weighing 185 lbs; BP 125/80, HR 95/min, RR 25/min Arterial pulse: normal volume or amplitude pulse with normal upstroke in the carotids. All pulses palpable and symmetrical. - You can assume that there is no arterial problem. JVP: 8 cm above sternal angle at 45 degrees. The contour showed X=y; the venous pressure tended to rise on inspiration. - The patient has Kussmel Sign. Something is wrong with filling in the right. Maybe cardiac Tamponade, MI involving right ventricle, a clot, or Pulmonary Embolism. Precordial pulsations: apical impulse normal with medial retraction; RV impulse palpable on deep inspiration by subxiphoid palpation - RV heave nd Auscultation: S2 palpable at the 2 L ICS, S2 splitting appeared to be somewhat wide but appeared to vary normally on inspiration. S3 and S4 were both heard at the lower L sternal area and over the xiphoid area and appeared to increase slightly on inspiration. No significant murmurs. Chest was clear. - Compatible with pulmonary hypertension Diagnostics ECG X-ray 2D Echo to look for problems in the right side of the heart CT angiography to look for the blood vessels of the heart Synthesis 1. So far the predominant R-sided signs all point to the presence of significant pulmonary hypertension with RV diastolic dysfxn. Because the patient is described as previously well and the history is rather sudden and recent onset, acute cause of pulmonary hypertension, such as acute pulmonary embolism, must be considered to be present unless proven otherwise. 2. Such a conclusion is also suggested by the presence of mild tachycardia and mild tachypnea 3. Such an analysis should lead to immediate application of measures of management, including treatment and diagnostic investigations. XI. SUMMARY
Fig 18. Schramoths sign in clubbing.

Fig 17. Differential cyanosis.

Telangiectasia - Hereditary telangiectases on the lips, tongue, and mucous membranes (Osler-Weber-Rendu syndrome) resemble spider nevi and, when in the lungs, can cause right-to-left shunting and central cyanosis. Scleroderma can also cause telangiectasias - Usually connotes systemic connective tissue problems. - Appear as spider veins Xanthoma - Various lipid disorders can manifest with xanthomas, subcutaneously, along tendon sheaths, or over the extensor surfaces of the extremities - Deposit of cholesterol on the skin especially on the eyelids. - Usually the patient has high lipid levels, specifically LDL and triglycerides Digital Clubbing - Schamroths sign/window = clubbing + cyanosis - No Schamroths window = clubbing and cyanosis - Due to digital osteoarthropathy usually seen in congential heart disease Chronic unoxygenated kids with shunting have bones that do not grow. - Expect clubbing in PDA

Case 35 year old male, chronic smoker, previously well, presents with history of 2 recent episodes of lightheadedness (presyncopal feeling) while climbing 2 flights of stairs Pertinent Findings Light headedness after climbing should have tachycardia to deliver more blood 4G

CARDIAC SYMPTOMS AND ITS APPRAISAL Definite Orthopnea high left atrial pressure Dyspnea, Chest and Syncope fixed cardiac output lesion Triad severe inflow obstructive lesion severe pulmonary hypertension Fatigue, Lasitude & Lightsevere cardiomyopathy headedness constrictive pericarditis cardiac tamponade Syncope & Pre-syncope bradyarrythmia Page 9 of 11

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DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


tachyarrythmia sudden hypotension CHEST PAIN central chest pain discomfort with or without radiation with or without dsypnea relieved within a few minutes of rest or after nitroglycerin with some features of angina yet not so typical requires long period of rest for relief usually related to movement Central cyanosis - Significant RL shunting at the level of the heart or lungs b. Peripheral cyanosis reduced blood flow due to small vessel constrictions c. Differential cyanosis occurs with PDA and PA hypertension d. Telangiectasia resemble spider nevi e. Xanthoma associated with lipid disorders DIGITAL CLUBBING a. XII. REVIEW QUESTIONS

Typical Angina

Atypical Angina

Non-Cardiac Chest Pain BLOOD PRESSURE Should be at the heart level Should be deflated at <3mmHg/sec First audible sound is Systolic; last sound is Diastolic ORTHOSTATIC HYPOTENSION fall in blood pressure of >20 mmHg systolic AND/OR >10mmHg diastolic in response to moving from supine to standing position ARTERIAL PRESSURE Beat-to-beat variability of the pulse amplitude Pulsus Alternans Seen in severe heart failure and hypovolemic states > 10 mmHg fall in systolic pressure with inspiration Pulsus Paradoxus Sign of pericardial or pulmonary disease KUSSMAUL SIGN Normally, JVP decreases with inspiration and increases with expiration In Kussmail Sign, veins are filled at inspiration and JVP increases HEPATO-JUGULAR REFLEX Venous pressure will increase and stay increased until the pressure from compression of the abdomen is released. Compression should be applied at least 30 secs. HEART SOUNDS 1. Formation: S1= M1 + T1: low pitched, longer duration lubb S2 = A2 + P2: Sharper, shorter, higher frequency dub S3 = Early phase of the ventricular filling characterized by sudden vigorous expansion associated with rapid inflow of the blood o Physiological o Pathologic S4 Splitting Extra sounds 2. Splitting 3. Auscultation areas HEART MURMURS 1. Formation: Laminar and turbulent flow 2. Grading 3. Timing LOCAL AND SYSTEMIC MANIFESTATIONS OF HEART DISEASE 1. Skin manifestations 4G

1. What is false about murmur of aortic regurgitation? a) best heard in 4th ics on right sternal edge b) may be mistaken for breath sounds c) may be associated with Austin Flint murmur d) murmur is high pitched and decrescendo in quality 2. Which of the following is most likely to be related to unequal blood pressures in the upper extremities? a) Abdominal aortic dissection b) Thoracic aortic aneurysm c) Transecting trauma of the thoracic aorta d) Abdominal aortic aneurysm 3. During auscultation, one can tell the end of systole when you hear? a) S1 b) S2 c) Before S1 d) In-between S1 and S2 4. S1 is often accentuated in all the following conditions EXCEPT: a) Anemia b) Fever c) Pregnancy d) Heart failure 5. A drop in systolic blood pressure of more than 10 mmHg with inspiration refers to: a) Pulsus alternans b) Pulse deficit c) Electrical alternans d) Pulsus paradoxus 6. What is the skin manifestation of cardiac disease that involves PDA and PA hypertension with RL shunting at the great vessel level? a. Xanthoma b. Differential cyanosis c. Telangiectasia d. Central cyanosis 7. Test for digital clubbing a. Schamroths window b. Kussmauls sign c. JVP d. None of the above 8. Murmurs described to be loud with palpable thrill a. Grade 1 b. Grade 2 c. Grade 3 d. Grade 4 9. During diastole, the blood will go back to the left ventricle a. Pulmonary stenosis b. Aortic regurgitation c. Mitral valve regurgitation d. Aortic stenosis AVELLANA. CRISTOBAL. DE CASTRO. ESTANISLAO. LIRIO. NG. SANGALANG. TUGBANG. VIOLAGO. Page 10 of 11

DIAGNOSIS OF CARDIOVASCULAR DISEASE INTERNAL MEDICINE __________________________________________________________________________________________________________________________________________


T/F. (nos. 10-13) 10. S3 is characterized by sudden vigorous expansion associated with rapid inflow of the blood during early phase of ventricular ejection 11. Central cyanosis reduced blood flow because of small vessel constriction 12. Various lipid disorders can manifest with xanthomas, subcutaneously, along tendon sheaths. 13. VSD is a continuous murmur 14. What is false about murmur of aortic regurgitation? th a) best heard in 4 ics on right sternal edge b) may be mistaken for breath sounds c) may be associated with Austin Flint murmur d) murmur is high pitched and decrescendo in quality 15. Which of the following is most likely to be related to unequal blood pressures in the upper extremities? a) Abdominal aortic dissection b) Thoracic aortic aneurysm c) Transecting trauma of the thoracic aorta d) Abdominal aortic aneurysm 16. During auscultation, one can tell the end of systole when you hear? a) S1 b) S2 c) Before S1 d) In-between S1 and S2 17. S1 is often accentuated in all the following conditions EXCEPT: a) Anemia b) Fever c) Pregnancy d) Heart failure 18. A drop in systolic blood pressure of more than 10 mmHg with inspiration refers to: a) Pulsus alternans b) Pulse deficit c) Electrical alternans d) Pulsus paradoxus XIII. ANSWERS TO QUESTIONS 1. A 2. B 3. B 4. D 5.D 6. B = Central cyanosis - Significant RL shunting at the level of the heart or lungs Peripheral cyanosis reduced blood flow due to small vessel constrictions Differential cyanosis occurs with PDA and PA hypertension Telangiectasia resemble spider nevi Xanthoma associated with lipid disorders 7. A 8. D (see table on Gradation of murmurs) 9. B 10. False. S3 happens during early phase of ventricular filling 11. False. Peripheral cyanosis 12. True 4G AVELLANA. CRISTOBAL. DE CASTRO. ESTANISLAO. LIRIO. NG. SANGALANG. TUGBANG. VIOLAGO. 13. False. PDA 14. A 15. B 16. B 17. D 18. D *APPENDIX

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