Impact of Sleep On Cardiovascular Function 1

"    The shift of central nervous system state from wakefulness to non-REM sleep is normally accompanied by progressive reductions in metabolic rate, sympathetic nervous system activity, heart rate, stroke volume, cardiac output, and systemic blood pressure, and by a progressive increase in vagal tone. An important consequence of these physiologic changes is a reduction in myocardial workload. Compared to wakefulness, non-REM sleep is a time of relative autonomic and circulatory stability. This stability is disrupted from time to time by brief microarousals from sleep that provoke sudden transient increases in sympathetic nervous activity, heart rate, and blood pressure.

    The effects of REM sleep on cardiovascular activity are more complex than those of non-REM sleep. In animals, renal sympathetic nerve activity decreases during REM sleep, but in humans sympathetic outflow to skeletal muscle vasculature increases and blood pressure rises to the levels comparable to those of wakefulness. Whether these differences are species related or are caused by nonuniform activation of various branches of the sympathic nervous system remains to be determined. Despite these changes, because adults spend 80% to 85% of their total sleep time in non-REM sleep, the overall effect of sleep is to rest the cardiovascular system. Disruptions of sleep, as occur in such disorders as sleep apnea, interfere with this state of cardiovascular quiescence and, in so doing, stress the heart and circulation."


"An electrocardiogram (ECG or EKG, abbreviated from the German Elektrokardiogramm) is a graphic produced by an electrocardiograph, which records the electrical activity of the heart over time. Its name is made of different parts: electro, because it is related to electronics, cardio, Greek for heart, gram, a Greek root meaning "to write".

The heart muscles create electrical waves when they pump. These waves pass through the body and can be measured at electrodes (electrical contacts) attached to the skin. Electrodes on different sides of the heart measure the activity of different muscles. An ECG displays the voltage between pairs of these electrodes, and the muscle activity that they measure from different directions. This display indicates the overall rhythm of the heart, and weaknesses in different muscles. It is the best way to measure and diagnose abnormal rhythms of the heart, particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by levels of salts, such as calcium, that are too high or low. In myocardial infarction (MI), the ECG can identify damaged heart muscle. But it can only identify damage to muscle in certain areas, so it can't rule out damage in other areas. The EKG cannot reliably measure the pumping ability of the heart; ultrasound is used for that."

Adult ECG Lead Placements


Normal adult 12-lead ECG The diagnosis of the normal electrocardiogram is made by excluding any recognized abnormality. It's description is therefore quite lengthy.

Cardiac: EKG: Causes of ST Depression

Subendocardial infarct
Reciprocal ST elevation
Ventricular Hypertrophy
Bundle branch block

ST segment depression

ST segment depression can be caused by ischemia, digitalis, rapid heart rate, and temperature or electrolyte abnormality. It can also be a “reflected” or reciprocal ST elevation (showing an inverted view of what’s happening at another place in the heart). The shape of the ST segment, and whether the abnormality is localized to leads looking at one area of the heart, often allows the cause of ST depression to be diagnosed.

ST segment depression is considered significant if the ST segment is at least one box below baseline, as measured two boxes after the end of the QRS. As with infarction, the location of the ischemia is reflected in the leads in which the ST depression occurs.

Measure: 2 mm beyond QRS
Significant: 1 mm


When ST segment depression is transient, it’s almost always due to acute myocardial ischemia. The ECG signs of ischemia may come and go fairly quickly — over a matter of minutes.

ST segment depression is MOST specific for ischemia if the ST segment slopes down from the J point. Horizontal or flat STs are also quite suspicous for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.

“J point” depression at the beginning of the QRS complex is not significant if the location of measurement (two boxes past the QRS) finds the ST segment has risen back to the baseline.


ST depression can also be seen in infarction, typically in non Q-wave infarction, often called subendocardial infarction. This type of infarct does not extend through the ventricular wall (non-transmural). Subendocardial infarctions involve small areas of injured tissue, with larger areas of overlying ischemia. These infarctions may show ST segment depression (rather than elevation) because of the larger areas of ischemia.

ST depression can also be seen as a “mirror” of what’s happening on the other side of the heart. For example, the inferior leads may show ST depression as a reflection of what’s happening in the upper lateral side of the heart.

Ventricular hypertrophy:

Left ventricular hypertrophy or strain commonly causes ST segment depression, often with T wave inversions. These changes are seen in the “lateral” leads — those that record activity over the left ventricle. In LVH, ST and T wave abnormalities are commonly seen in leads I, L, and V4-V6.

Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.

Ventricular conduction block:

Left bundle branch block produces ST depression and inverted T waves in leads I, L, and V5-V6. In general, the ST will slope away from the direction of the QRS: a large wide R wave will have a down-sloping ST ending in an inverted T, while a deep wide S wave will have an upsloping ST segment ending in an upright T.

Other causes of ST segment abnormality:

Patients on digitalis often show mild ST depression. This depression is usually less than 1 mm, and produces a “scooped” appearance — the “Salvador Dali mustache” ST. These ST abnormalities are seen in multiple leads.

Hypothermia and severe hypokalemia routinely cause ST segment depression in multiple leads. Hypothermia will tend to lengthen all ECG intervals, including the PR and QT, while hypokalemia will often lengthen the PR while shortening the ST segment slightly.
ST segment depression is called “nonspecific ST abnormality” rather than “ST segment depression” if the ST segments are less than 1 mm depressed and are accompanied by a normally-oriented T wave.

ST segment elevation

ST segment elevation is usually attributed to impending infarction, but can also be due to pericarditis or vasospastic (variant) angina. In some healthy young adults, a form of ST elevation can be normal.

The height of the ST segment is measured at a point 2 boxes after the end of the QRS complex. ST segment elevation is considered significant if it exceeds 1 mm in a limb lead or 2 mm in a precordial lead.

Causes of ST Elevation
Vasospastic angina
Early repolarization

Measure: 2 mm beyond QRS
Significant: 1 mm limb lead
                     2 mm chest lead


In transmural infarction, ST segment elevation will be among the first manifestations. The ST segment elevation will be seen in those leads involved in impending infarction.

ST segment elevation decreases as T wave inversion begins. ST segments may remain elevated when ventricular aneurysm develops.

ST segment elevation that persists beyond three months following myocardial infarction suggests ventricular aneurysm. ST elevation will be present in about 1/3 of ventricular aneurysms. When the patient with ventricular aneurism presents with acute chest pain, a baseline ECG may help avoid misdiagnosis of impending infarction (and use of non-needed thrombolytic drugs).

Vasospastic angina:

ST segment elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetal’s angina. While exercise angina involves the subendocardium, vasospastic angina causes severe transmural loss of blood flow. ST elevation simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetal’s angina). At this point, the injury is reversible.


Pericarditis, an inflammation of the space between the pericardial sack and outer surface of the heart, causes widespread ST segment elevation. Physical damage and irritation of the heart’s surface produces a “current of injury” in virtually all ECG leads.
Generalized ST segment elevation, unrelated to the distribution of any coronary artery, implies pericarditis. One must be very cautious in diagnosing pericarditis from the ECG. For example, an inferolateral transmural infarction with pre-existing junctional ST elevation in the anterior leads, could produce widespread ST elevation that could be confused with pericarditis.

Later in the course of pericarditis, ST segment elevation resolves, without development of Q waves. After days to months, ST elevation is replaced by widespread T wave inversions.

Early repolarization:

“Early repolarization” is a cause of ST elevation. This innocent condition typically occurs in young healthy males. The T wave begins early, adding elevation to the ST segment.

Usually, early repolarization shows elevation of the J point (the junction between the end of the QRS and the ST segment) and a concave upward curve towards the T wave. (“Concave upward” means the hollow portion of the curve is on top.)

Early repolarization is usually seen in the anterior precordial leads of the ECG, but can be seen in limb leads to a lesser degree.
Early repolarization cannot always be differentiated from myocardial infarction. In the chest pain patient, it’s safest to assume ST elevation to be infarction until proven otherwise by reviewing a previous ECG or by obtaining serial ECGs. 

T Wave Abnormalities

T wave abnormalities can provide added evidence to support clinical diagnosis. Except for hyperkalemia, T wave abnormality alone is not diagnostic of any particular condition. The T wave must be considered along with QRS and ST segment abnormalities. T waves will usually be abnormal in ventricular hypertrophy, left bundle branch block, chronic pericarditis, and in electrolyte abnormality.

Tall, peaked T waves occur due to hyperkalemia. If the tall T waves are seen throughout the ECG, general hyperkalemia is present. P waves will be small, PR interval short.

When typical tall, peaked T waves are seen only within a specific set of cardiac leads, it suggests impending infarction. The tall Ts are due to potassium leak through damaged membranes in the area of the infarct.

T Wave Categories
Tall, peaked = hyperkalemia if generalized
                       infarction if localized
Inverted = evolving infarction
                 chronic pericarditis
                 conduction block
                 ventricular hypertrophy
                 acute cerebral disease
                 other cardiac disease
Flattened = nonspecific

In chronic pericarditis, T waves show wide-spread inversion, not corresponding to any coronary artery distribution. General inversion of T waves can also be due to an evolving global subendocardial infarct.

Inverted T waves are seen during the evolution of myocardial infarction. The T inversion appears in the leads “looking at” the infarcted area. Several hours after an infarct, T waves begin to invert. T wave inversion may persist for months.

Left ventricular hypertrophy or strain commonly causes T wave inversion. In “strain” pattern, the ST segment slopes down to an inverted T in the leads “looking at” the affected ventricle.

Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2. The T wave will be inverted over right heart leads showing evidence of hypertrophy and strain.

Left bundle branch block can cause ST depression and inverted T waves in leads I, L, and V5-V6. The ST depression is usually not great. The T wave tends to be oriented opposite the QRS in LBBB.

Flat T waves can be seen in many conditions, including ischemia, cardiac scar, evolving infarction, and electrolyte abnormality (such as hypokalemia).

In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T waves may be seen. These Ts are often biphasic or deeply and sharply inverted. The QT interval is often dramatically lengthened (0.5 to 0.7 seconds). 


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2- "Textbook of Respiratory Medicine - Mason, Broaddus, Murray, Nadel: Volume 2"

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