3. Session Tips
– Differentiate types of cardiovascular testing
– Relate type of murmur (systolic or diastolic) with specific
valvular abnormalities.
– How echo, EC(K) used for CVD dx, Rx, prognosis
– About cardiac biomarkers
– When to order these testing
3
4. Human
Camel
Cat
4
Estimated average heart rate of the following mammals (beats/min)
70 Elephant
Whale
Lion
Mouse
28
200
376
40
9
30
Size of your heart?
5. Height? Width ?
Beats per day?
Beats 2.5 billion time in an average 70 yr. lifetime
Pumps about _____________ of blood each day:
Circulates blood completely 1000 times each day
Pumps blood through _________miles of vessels
Suffers 7.2 mil. CAD deaths worldwide each year
5
~100,000 times
12 x 9 cm4.8 inches tall 3.35 inches wide
2000 gallons 7600 liters
62,000
6. CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
– CO = 5250 ml/min (5.25 L/min)
6
7. Components
Heart
Blood
Vessels
– Arteries: Away from heart
– Veins: toward heart
– Capillaries
7
Link arterioles to veins
10. Heart :
– Provides the driving force for the cardiovascular system
– Organ at the center of the circulatory system.
– It pumps blood around the body
– Approximately the size of your fist
– Wt. = 250-300 grams
10
14. CVD afflicts an estimated 80 million people (i.e.~1 in 3 adults)
– Accounts for 35% of all deaths: US data
Total cost of CVD (HTN, CHD, HF, and stroke)~ $475.3 billion.
Atherosclerosis: cause of most CVD events.
– Typically present for decades before symptoms appear
14
17. Thorough history,
Comprehensive physical examination,
Appropriate testing,
17
• Sub-clinical CVD usually can be
identified,
• Symptomatic CVD can be assessed for
the risk of an adverse event and can
be managed appropriately.
18. The elements of a comprehensive history:
– Chief complaint,
– Current symptoms, …HPI
– Past medical history,
18
– Family history,
– Social history…..
– Review of systems
– Duration, quality, frequency, severity, progression, precipitating &
relieving factors, associated symptoms, & impact on daily activities
Diet, amount of regular physical activity, tobacco use,
alcohol intake, and illicit drug use
19. Chest pain is a frequent symptom
– Angina pectoris or infarction, non-cardiac conditions
(esophageal, pulmonary, or musculoskeletal disorders)
– Quality, its location and duration;
– Factors that provoke or relieve it are important in
ascertaining its etiology
Sensation of heaviness or pressure in the retrosternal area
– Radiate to the jaw, left shoulder, back, or left arm
– Typically lasts only a few minutes
19
20. Angina pain
– Precipitated by exertion, emotional stress, eating, smoking a
cigarette, or exposure to cold,
– Relieved with rest or a sublingual nitroglycerin
However, unstable angina pain is is increasing in severity, longer in
duration, or occurring at rest;
– Prompt the patient to seek medical attention expeditiously.
20
21. CHF and pulmonary vascular congestion
– Complain of shortness of breath (dyspnea) with exertion or
even at rest
– Orthopnea, PND, and nocturia
CHF & peripheral venous congestion
– Abdominal swelling (from hepatic congestion or ascites),
– Nausea, vomiting, lower extremity edema, fatigue, & dyspnea
21
23. With particular attention to the cardiovascular system
Assessment of
– Jugular venous pulse,
– Carotid and peripheral arterial pulses,
– Examination of the heart and lungs (i.e., palpation,
percussion, & auscultation),
– Inspection of the abdomen and extremities
23
24. JVP: indirect assessment of right atrial pressure
– Normal: 1 to 2 cm above the sternal angle
– Extent of elevation: to assess the severity congestion,
– Its diminution: to assess the response to therapy
Carotid arterial pulse
– Diminished pulsations: indicate reduced stroke volume,
atherosclerotic narrowing of the carotid artery, or obstruction
to LV outflow, as may occur with aortic valve stenosis or
hypertrophic obstructive cardiomyopathy.
24
25. – Very forceful, hyperdynamic, "bounding“ pulsations :
» Increased stroke volume,
» Chronic aortic valve regurgitation or
» High cardiac output [hyperthyroidism, marked anemia].
25
26. Peripheral arterial pulses (Legs & arms)
– Diminished: in reduced stroke volume, peripheral arterial
disease (PAD)
– Percussion of the posterior chest: pleural effusion
– Auscultation of anterior and posterior lung fields:
» Pneumonia, airway obstruction, pleural effusion, or
pulmonary edema.
26
27. Typical "lub-dub" sound of the normal heart
S1:precedes ventricular contraction
– Due to closure of the mitral and tricuspid valves
S2: follows ventricular contraction
– Due to closure of the aortic and pulmonic valves
Other heart sounds [S3, S4, Murmur, gallop]: presence of underlying
heart disease
27
28. S3 sounds
– Aka ventricular gallop,
– Low-pitched sound heard at the cardiac apex
– Occur in early diastole (i.e. immediately after S2).
– Caused by vibrations that occur when blood rapidly rushes
from a "tense" atrium stiff, noncompliant ventricle.
– Associated with decompensated HF or intravascular volume
overload.
28
29. S4 sound
– Dull, low-pitched sound
– Caused by the vibrations that occur when atrial contraction
forces blood into a stiff, noncompliant ventricle.
– Audible at the cardiac apex just before ventricular contraction
(i.e., just before S1)
– Occur with aortic stenosis, systemic arterial hypertension,
hypertrophic cardiomyopathy, or CAD.
29
31. Murmurs
– Auditory vibrations resulting from turbulent blood flow within
the heart chambers or across the valves.
– Classified by timing & duration within the cardiac cycle
(systolic, diastolic, or continuous), intensity (grade 1 to 6, from
softest to loudest), pitch (high or low frequency),
– “Innocent" or "physiologic": in case of fever, anxiety, anemia,
hyperthyroidism, and pregnancy
31
34. Systolic murmurs
– Occur during ventricular contraction
– Begin with or after S1 and end at or before S2
– Can be mid-systolic or holosystolic (pansystolic).
Mid-systolic murmurs: pulmonic stenosis, aortic stenosis, and
hypertrophic obstructive cardiomyopathy
Holosystolic murmurs : when blood flows from a chamber of higher
pressure to one of lower pressure throughout systole
– In case of TR, MR, VSD
34
35. Diastolic murmurs
– Occur during ventricular filling
– Begin with or after S2
– High pitched: in AR & PR
– Low Pitched: in MS & TS stenosis
35
37. Troponin [I & T]
– Contractile proteins found only in cardiac myocytes
– Most sensitive, tissue-specific
– Detectable in the blood 2 to 4 hrs of onset of sxs
– Remains detectable for 5 to 10 days
37
39. Provides supplemental information to the physical examination
About the position & size of the heart & its chambers /adjacent structures
39
40. Graphic recording of the electrical potentials generated by the heart
Signals are detected by using electrodes attached to the extremities
and chest wall
Used to detect:
– Arrhythmias, conduction disturbances,
– MI, metabolic disturbances (e.g., hyperkalemia),
– Increased susceptibility to sudden cardiac death (e.g.,
prolonged QT interval
40
41. 41
Depolarization starts
Initiates atrial contraction.
Depolarization wave front spreads through the
ventricular muscle [from endocardium to epicardium]
triggering ventricular contraction
51. P-wave:
– Depolarization of the atria
– Duration: ~0.12 second
PR segment:
– Passage of impulse through AV node bundle of His its
branches
– Duration: 0.12 to 0.20 second.
51
52. QRS complex
– Electrical depolarization of the ventricles
– -ve deflection (Q wave) +ve deflection (R wave) -ve
deflection(S wave)
– Duration: <0.12 second
V1, V2: right ventricle: -ve
V5, v6: left ventricle: +ve
52
53. ST segment
– Plateau phase
– Duration: 0.005- 0.15 sec
T wave
– Repolarization of the ventricle
– Duration: 0.1 - 0.25 sec
QT interval
– From QRS complex to end of the T wave
– Time required for ventricular depolarization & repolarization
– Duration: <0.44 second.
– Prolonged: electrolyte disturbances (i.e., hypokalemia,
hypocalcemia, hypomagnesemia).
53
55. 55
STEMI in the inferior (leads III & aVF) & precordial (leads V1–V6) leads, indicating that
the inferior and anterior regions of the heart are affected