CARDIOVASCULAR SYSTEM

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CARDIOVASCULAR SYSTEM
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• General approach
• Inspection
• Palpation
• Percussion
• Auscultation

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• 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.

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• Timing
• 1 systolic murmurs
• a- Mid-systolic ejection murmurs
• b- late systolic murmurs
• c- holosystolic murmurs

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• 2 Diastolic murmurs
• a- early diastolic murmurs
• b- mid-diastolic murmurs
• c- late diastolic murmurs
• 3 continuous murmurs
• 4- interventions that change murmur sounds

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• 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

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• 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

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• Pitch
• is determined by whether it can be auscultated
  best with the bell or diaphragm of a
  stethoscope.
• Quality
• Blowing
• Harsh
• Rumbling and musical

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• 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

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• Mitral prolapse systolic murmur with midsystolic
  click, most frequent valvular lesion in young
  women
• VSD holosystolic murmur
• PDA continuous machine-like murmur

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• 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

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• 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.

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• 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

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• 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

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• Different types of dyspnea
• Tachypnea
• Orthopnea
• Trepopnea
• Platypnea
• Paroxysmal nocturnal dyspnea

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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.

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• 3 types of Angina stable , unstable and variant
  (Prinzmetals ).
• Stable angina
• Most common type
• Brought on by exertion or emotion
• Pain increases over several minutes
• Relieved by rest or medication
• Follows a pattern

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• Unstable Angina
• It is new
• It is accelerating
• Lasts longer
• Less responsive to medication
• Occurs at rest

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• Prinzmetals 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

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• 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

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• 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.

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Risk factors for CAD

• Modifiables
• Smokings
• Hypercholesterol
• Hypertension
• Obesity
• Diabetes mellitus
• Physical inactivity

• Nonmodifiables
• Age
• Male
• Family history

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• Differential
• Tension pneumothorax
• Aortic dissection
• Pulmonary embolism
• Unstable angina
• Costochondritis
• Intercostal neuritis
• Pericarditis
• pneumonia

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• 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

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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

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• 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

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• Prinzmetal s angina
• Calcium channel blockers
• are coronary vasodilators
• Variable peripheral vasodilators
• Negative inotropic activity
• Negative chronotropic activity

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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

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• 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 ( kawasakis disease)

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• 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

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• 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
• Diaphoresis
• Anxiety
• Dyspnea
• Vomiting
• nausea

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• Diagnostic Evaluation
• ECG is important in the evaluation of possible AMI

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• 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 gt a
  week.

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• 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

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• Absolute contraindications to thrombolytic
  therapy
• Uncontrolled hypertension on iv vasodilators(
  systolicgt180
• Recent stroke
• Recent major surgery
• Active GI bleeding
• Concurrent trauma
• Intracranial mass

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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)

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• Major Risk Factiors
• Coronary artery disease
• Hypertension
• Valvular heart disease
• Pericardial disease
• cardiomyopathy

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• Left Heart failure

• Right Heart failure

• Orthopnea
• Paroxysmal nocturnal dyspnea
• Rales
• Dyspnea on exertion
• Cough
• Nocturia
• S3 gallop
• Diaphoresis
• tachycardia

• RuQ pain due to hepatic congestion
• Hepatomegaly
• Hepatojugular reflex
• Ascites
• Cyanosis
• Peripheral edema

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• 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

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• Treatment
• ACE inhibitor ( decrease sx and mortality)
• Diuretics
• Beta blockers(decrease sx and improve survival
• Digoxin ( for symtomatic relief only does not
  improve survival)
• Spironalactone ( decrease mortality by 34

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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

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• Signs and Symptoms
• Becks Triad
• Hypotension
• Muffled heart sounds
• Jugular vein distention
• Other symptoms/signs
• Dyspnea
• Tachycardia
• Pulsus paradoxus decrease by gt10 sBP with
  inspiration

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• 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

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• Treatment
• Immediate pericardiocentesis