Focused Preanesthetic Assessment of Cardiovascular System

Focused Preanesthetic Assessment of Cardiovascular System

Cardiovascular assessment is an extension of general preanesthetic assessment. History of the patient, physical examination and laboratory studies should be reviewed from the patient chart. Consultation to different medical specialty or physician is vital importance for understanding patient status. Module eight of session one, two and three explain the specific preanesthetic assessment of cardiovascular problems which the students are adviced to refer. Routine laboratory investigation hematocrit/hemoglobin, platelet count and bleeding time, liver and renal function are part of patient assessment.

The History Is of Prime Importance in Patients With Heart Disease

Questions should encompass symptoms (include chest pains, dyspnea, poor exercise tolerance, syncope, or near syncope), current and past treatment (potential interactions of medications used in the treatment of CVS disease with drugs used to produce anesthesia must also be considered), and the results of cardiologist/internist/physician evaluations. Coexisting diseases include hypertension, peripheral vascular disease, chronic obstructive pulmonary disease from cigarette smoking, renal dysfunction associated with chronic hypertension, and diabetes mellitus should be assessed. This information alone is usually enough to provide some estimate of disease severity and ventricular function. The relationship between symptoms and activity level should be established. Activity should be described in terms of everyday tasks such as walking or climbing stairs.

Physical Examination

The maximum percentage that the cardiac output can increase above normal is called the cardiac reserve. Thus, in the healthy young adult, the cardiac reserve is 300 to 400 per cent. Any factor that prevents the heart from pumping blood satisfactorily will decrease the cardiac reserve. This can result from ischemic heart disease, primary myocardial disease, vitamin deficiency that affects cardiac muscle, physical damage to the myocardium, valvular heart disease, and many other factors. As long as persons with low cardiac reserve remain in a state of rest, they usually will not know that they have heart disease. However, a diagnosis of low cardiac reserve usually can be easily made by requiring the person to exercise either on a treadmill or by walking up and down steps, either of which requires greatly increased cardiac output. The acute effects are as follows:

• Immediate and sometimes extreme shortness of breath (dyspnea) resulting from failure of the heart to pump sufficient blood to the tissues, thereby causing tissue ischemia and creating a sensation of air hunger.
• Extreme muscle fatigue resulting from muscle ischemia, thus limiting the person's ability to continue with the exercise.
• Excessive increase in heart rate because the nervous reflexes to the heart overreact in an attempt to overcome the inadequate cardiac output.

The preoperative ECG should be examined for evidence of myocardial ischemia, prior myocardial infarction, cardiac hypertrophy, abnormal cardiac rhythm or conduction disturbances, and electrolyte abnormalities. The exercise ECG simulates sympathetic nervous system stimulation as may accompany perioperative events such as direct laryngoscopy, tracheal intubation, and surgical incision. The resting ECG in the absence of angina pectoris may be normal despite extensive coronary artery disease. Nevertheless, an ECG demonstrating ST-segment depression more than 1 mm, particularly during angina pectoris, confirms the presence of myocardial ischemia. Any ECG abnormality requires physician involvement.

Other Common Cardiovascular Examination Includes

The rate (the number of heart beats per unit time in adult it ranges from 60 to 100 beats per minute), rhythm (regular intervals between each beat), pulse character, and the nature of the vessel wall can usually be assessed from the radial pulse. Although the pulse pattern may suggest a diagnosis for the underlying rhythm an ECG is always necessary for confirmation. An easily palpable radial vessel wall is usually an indication of abnormal thickening and possibly calcification, and suggests more generalized vascular disease.

Blood pressure is the force exerted by the blood against any unit area of the vessel wall. When one says that the pressure in a vessel is 50 mm Hg, one means that the force exerted is sufficient to push a column of mercury against gravity up to a level 50 mm high. If the pressure is 100 mm Hg, it will push the column of mercury up to 100 millimeters.

Two pressures are recorded when measuring blood pressure, systolic pressure is the peak arterial BP attained during ventricular systole, and diastolic pressure is the minimum arterial BP between heartbeats at which the heart get its own blood supply. The mean arterial pressure is the average of the arterial pressures. Tissue perfusion and organ perfusion depend on mean arterial pressure (MAP). MAP should exceed 70 to 80 mm Hg for cells to receive the oxygen and nutrients needed to metabolize energy in amounts sufficient to sustain life. It is not equal to the average of systolic and diastolic pressure because the arterial pressure remains nearer to diastolic pressure than to systolic pressure during the greater part of the cardiac cycle.

Several systems contribute to the regulation of arterial blood pressure. Blood pressure is determined mainly by cardiac output, blood volume, and peripheral resistance.

The Jugular Venous Pulse or Pressure (JVP) is indirectly observed pressure over the venous system via the visualization of internal jugular vein. The JVP is examined with the patient semi-recumbent at an angle of about 45° with the patient's head partially rotated to one side. The normal JVP is about 5-10 mmHg and if it is raised it indicates some cardiac problem and this is serious and you should consider consultation. Causes of elevated JVP are right heart failure, right ventricular infarction, pulmonary hypertension, hypervolemia, superior vena cava compression, reduced right ventricular compliance and pericardial constriction/tamponade.

The cardiac examination always involves thorough palpation all over the front of the chest. This will pick up abnormal movement of the chest wall related to the contraction of the underlying heart,. and thrills (Vibration felt by the examiner on palpation) which are palpable murmurs (a pathological heart sounds that are produced as a result of turbulent blood flow that is sufficient to produce audible noise). Abnormalities may be brought out by sitting the patient forward and feeling the chest in expiration, and also rolling the patient onto their left side. Thrills are palpable murmurs and the associated murmur is nearly always loud. They are usually best felt in the areas where the murmur is best heard.

Heart sounds and murmurs are often not difficult to time in the cardiac cycle but if there is doubt, palpation of the carotid pulse is extremely useful.

Systolic events tend to occur at the same time as the carotid pulse since as there is only a short distance between the aortic valve and the carotid artery, the systolic pulse wave in the carotid artery occurs only a matter of milliseconds after the ejection phase of LV systole. Diastolic events occur between the palpable pulses.

• Normal heart sounds: First heart sound (S 1) and second heart sound (S 2) are usually the only heart sounds heard on auscultation of a normal heart. S 1 results from closure of the mitral and tricuspid valves and has two components in close proximity. S 2 results from closure of the aortic and pulmonary valves. Heart sounds other than S 1 and S 2 are usually abnormal but S 3 and an ejection sound can occur in normal subjects the S 3 coincides with rapid filling of the left ventricle (LV) and in fit young subjects and the athlete (usually young people), often with a slow heart rate and compliant ventricle, LV filling is fast enough to produce a dull thudding third sound. In disease, S 3 is heard either when the LV is abnormal and usually dilated with reduced compliance or when there is rapid filling of the LV. An ejection sound occurs as the aortic or pulmonary valve opens and is close to S 1.
• Abnormal heart sounds: Murmurs are audible vibrations produced by turbulent flow through the heart
• Innocent murmurs: Not all murmurs are pathological and innocent murmurs are common, occurring in situations where the circulation is hyperdynamic, e.g. normal children, but also in pregnancy, fever, anemia, and hyperthyroidism.
• Systolic murmurs: The flow of blood through or across a pathological structure generates the murmur and this flow is determined by the pressure difference on opposite sides of the responsible pathology (abnormal valve, septal defect, etc.). The sound generated is louder when the pressure difference across the pathological structure is greater and higher velocity of flow and greater turbulence is generated. The murmur does not start until ejection begins and peaks when blood flow is greatest, the murmur stops before S2 since ejection is finished.
• Diastolic murmurs from the AV valves can be extremely difficult to hear. They are often very low pitched and rumbling and the inexperienced auscultator simply thinks they are ambient noise. Typically they are produced by mitral stenosis (and, in rare cases, tricuspid stenosis)