Transcript CARDIOVASCULAR SYSTEM

General approach
 Inspection
 Palpation
 Percussion
 Auscultation
Heart murmurs
 Abnormal heart sounds produced as a result of
turbulent blood flow sufficient to produce audible
noise.
 Characteristics:
timing , shape, location, radiation , intensity, pitch and
quality.
Timing
 1 systolic murmurs
a- Mid-systolic ejection murmurs
b- late systolic murmurs
c- holosystolic murmurs
 2 Diastolic murmurs
a- early diastolic murmurs
b- mid-diastolic murmurs
c- late diastolic murmurs
 3 continuous murmurs
 4- interventions that change murmur sounds
 Location
5 places on the anterior sternum
 Radiation
Refers where the sound radiates
Regle of thumb : sound radiates in the direction of the blood flow
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Intensity
 Grade 1
Very faint,heard only after listener has
tuned in,may not be heard in all positions
 Grade 2
Quiet ,but heard immediately after placing
the stethoscope on the chest
 Grade 3
Moderately loud
 Grade 5
Very loud, with thrill .May he heard when
stethoscope is partly off the chest
 Grade 6
Very loud ,with thrill .May be heard with
stethoscope entirely off the chest
Pitch
is determined by whether it can be auscultated best
with the bell or diaphragm of a stethoscope.
Quality
 Blowing
 Harsh
 Rumbling and musical
Heart murmurs
 Aortic stenosis : crescendo-decrescendo systolic
murmur
 Aortic regurgitation : high-pitched blowing diastolic
murmur
 Mitral stenosis :rumbling late diastolic murmurs,
opening snap
 Mitral regurgitation : high –pitched holosystolic
murmur
 Mitral prolapse :systolic murmur with midsystolic
click, most frequent valvular lesion in young women
 VSD : holosystolic murmur
 PDA : continuous machine-like murmur
Respiration
 Right-sided murmurs typically increase with inspiration,
while left-sided murmurs generally are louder during
expiration. Valsalva maneuver Most murmurs decrease in
length and intensity during the Valsalva maneuver. Two
exceptions are the systolic murmur of hypertrophic
cardiomyopathy (HCM), which usually becomes much
louder, and the systolic murmur of mitral valve prolapse
(MVP), which becomes longer and often louder. Following
release of the Valsalva, right-sided murmurs tend to return
to baseline intensity earlier than left-sided murmurs
Exercise Murmurs caused by blood flow across normal
or obstructed valves (eg, mitral or pulmonic stenosis)
become louder with both isotonic and submaximal
isometric (handgrip) exercise. Murmurs of mitral
(MR) and aortic regurgitation (AR) and ventricular
septal defect (VSD) also increase with handgrip
exercise.
Positional changes
 Most murmurs diminish with standing due to reduced
preload. However, the murmur of HCM becomes
louder, and the murmur of MVP lengthens and often is
intensified. Similarly, most murmurs become louder
with prompt squatting (or usually passive leg raising),
while the murmurs of HCM and MVP typically soften
and may disappear
Sounds
 S1 mitral and tricuspid valve closure
 S2 aortic and pulmonary valve closure
 S3 end of rapid ventricular filling
 S4 high atrial pressure/stiff ventricle
Different types of dyspnea
 Tachypnea
 Orthopnea
 Trepopnea
 Platypnea
 Paroxysmal nocturnal dyspnea
Coronary artery disease
ANGINA
 Refer to substernal chest pain that originates
from myocardial ischemia( increased oxyxen
demand or decreased oxygen suppy).Pain
described as a substernal pressure,heaviness
radiating to the jaw,shoulder and arm.
3 types of Angina :stable , unstable and variant
(Prinzmetal’s ).
1) Stable angina
 Most common type
 Brought on by exertion or emotion
 Pain increases over several minutes
 Relieved by rest or medication
 Follows a pattern
Unstable Angina
• It is new
• It is accelerating
• Lasts longer
• Less responsive to medication
• Occurs at rest
Prinzmetal’s angina
• Due to coronary vasospasm
• Not linked to exertion
• Chronic, intermittent nature
• Occurs at a specific hour early in the morning
• Coronary vessels angiographically normal
Typical scenario
A 62 –year –old smoker presents complaining of three
episodes of severe heavy chest pain this morning .Each
episode lasted 3 or 5 minutes , but he has no pain now.
He has never had this type of pain
Scenario II
A 43 y/o woman presents with frequent episodes of dull
chest chest pain on and off for 8 months .He says the
pain wakes him from sleep.
Risk factors for CAD
Modifiables
 Smokings
 Hypercholesterol
 Hypertension
 Obesity
 Diabetes mellitus
 Physical inactivity
Nonmodifiables
 Age
 Male
 Family history
Differential
 Tension pneumothorax
 Aortic dissection
 Pulmonary embolism
 Unstable angina
 Costochondritis
 Intercostal neuritis
 Pericarditis
 pneumonia
Work-up
Resting ECG is normal in half of patient with angina
pectoris
ECG may show ST-segment depression or T-wave
flattening
Obtain cardiac enzymes every 8 hrs for 24 hrs to r/o MI
Exercise stress test can confirm suspected diagnosis of
CAD
Treatment
Stable angina
Nitrates :
• Cause systemic venodilation which relieves cardiac
workload.
• Cause coronary arterial dilation
• Increase myocardial blood flow
• Used in sublingual form for relief of acute ischemia
• Side effects : hypotension, lightheadedness and
headache
2-Aspirin
 Limits platelet aggregation
3-Beta-adrenergic blocking agents
 Reduce myocardial workload by limiting adrenergic
increases in heart rate and contractility
 Side effects :fatigue, impotence, bradycardia and
worsening of heart failure
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Risk factors modification
Smoking cessation
Treatment of hyperlipidemia
Treatment of hypertension
Control diabetes
Weight loss
Reduction of physical and emotional stress
Improvement in physical improvement
Prinzmetal ‘s angina
Calcium channel blockers
 are coronary vasodilators
 Variable peripheral vasodilators
 Negative inotropic activity
 Negative chronotropic activity
Acute myocardial infarction
Epidemiology
• Common manifestation of CAD
• Each year 1 million suffer an AMI in USA
• Of these about 10% to 15% will die within within
several days and another 10 to 15 % will die within 1
year
Etiology /pathogenesis
• Most MI occur in the setting of underlying CAD.
• Rupture of an atherosclerotic with thrombus
formation is reponsible for most AMIs .
Other mechanisms can cause AMI:
 Coronary artery dissection
 Coronary vasospasm( cocaine)
 Vasculitis ( kawasaki’s disease)
Early death from AMI can be due to a number of
complications:
• Arrhythmia( ventricular fibrillation/tachycardia
• Cardiogenic shock
• Ventricular rupture (incidence 3 to 5 days
• Sudden arrhythmia
• Mitral papillary rupture
Clinical manifestations
• Retrosternal chest pain, prolonged and persistent
• Radiate to the shoulder, jaw and left arm
• Nitrates provide some reliefs but resolution of the pain
• Associated symptoms include:
i. Diaphoresis
ii. Anxiety
iii. Dyspnea
iv. Vomiting
v. nausea
Diagnostic Evaluation
ECG is important in the evaluation of possible AMI
 Serum Markers for MI
 Myoglobin : elevated within 1 hr but nonspecific
 CK –MB specific marker for myocardial tissue damage
 Troponin T or I : very specific and sensitive markers for
cardiac muscle injury.Elevated within 3 hrs and can
stay elevated for more > a week.
Treatment
 Relief of pain
 Reduction of myocardial oxygen demand
 Improvement /restoration of myocardial perfusion
 Recognition and treatment of complications
 Thrombolytic therapy with tissue plasminogen
activator if pain persists after the administration: O2,
aspirin, nitrates,opiates and beta-blockers
Absolute contraindications to thrombolytic therapy
• Uncontrolled hypertension on iv vasodilators(
systolic>180
• Recent stroke
• Recent major surgery
• Active GI bleeding
• Concurrent trauma
• Intracranial mass
Heart Failure
Heart Failure defined as the inability of the heart to
pump blood at a rate that meets metabolic demands.
Heart failure can be classified according to:
 The hemodynamic state of the cardiovascular system
(congestive versus high output)
 The predominance of the ventricle affected(left vs
right)
 The predominant form of myocardial dysfunction(
systolic or diastolic
 The time course (acute or chronic)
Major Risk Factiors
• Coronary artery disease
• Hypertension
• Valvular heart disease
• Pericardial disease
• cardiomyopathy
Left Heart failure
Right Heart failure
 Orthopnea
 Paroxysmal nocturnal
 RuQ pain due to hepatic
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dyspnea
Rales
Dyspnea on exertion
Cough
Nocturia
S3 gallop
Diaphoresis
tachycardia
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congestion
Hepatomegaly
Hepatojugular reflex
Ascites
Cyanosis
Peripheral edema
Diagnosis
 Chest film : enlargement of cardiac silhouette,
pulmonary vascular congestion with redistribution to
upper lobe.
 Echocardiogram :Assess left ventricular function (LVF)
 Basic natriuretic peptide(BNP):elevates in CHF
Treatment
1. ACE inhibitor ( decrease sx and mortality)
2. Diuretics
3. Beta blockers(decrease sx and improve survival
4. Digoxin ( for symtomatic relief only does not
improve survival)
5. Spironalactone ( decrease mortality by 34 %
Pericardial tamponade
Definition
Tamponade is the physiologic result of rapid
accumulation of fluid in the in-elastic pericardial sac
.Pericardial tamponade impairs cardiac filling and
reduces cardiac .
Etiology
 Pericarditis
 Trauma
 Aortic dissection
Signs and Symptoms
Beck’s Triad
 Hypotension
 Muffled heart sounds
 Jugular vein distention
Other symptoms/signs
Dyspnea
Tachycardia
Pulsus paradoxus :decrease by >10 sBP with inspiration
DIAGNOSIS
Auscultation may demonstrate distant heart sounds
ECG may show low voltage or electrical alternans
CXR may show enlarged cardial silhouette
Echocardiogram will show large pericardial effusion
Treatment
Immediate pericardiocentesis