Sinus Bradycardia

In sinus bradycardia the heart rate is less than 60 bpm. Bradycardia means “slow heart.” Sinus bradycardia has a normal P-QRS-T pattern, and the rhythm is regular (Figure 6-2). Athletes often normally demonstrate this finding because of increased cardiac stroke volume and other poorly understood mechanisms. Common pathologic causes of sinus bradycardia include a weakened or damaged sinoatrial (SA) node, severe or chronic hypoxemia, increased intracranial pressure, obstructive sleep apnea, and certain drugs (most notably the beta-blockers). Sinus bradycardia may lead to decreased cardiac output and blood pressure. In severe cases, sinus bradycardia may lead to a decreased vascular perfusion state and tissue hypoxia. The patient may demonstrate a weak or absent pulse, poor capillary refill, cold and clammy skin, and a depressed sensorium.

Sinus Tachycardia

In sinus tachycardia the heart rate is greater than 100 bpm. Tachycardia means “fast heart.” Sinus tachycardia has a normal P-QRS-T pattern, and the rhythm is regular (Figure 6-3). Sinus tachycardia is the normal physiologic response to stress and exercise. Common causes of sinus tachycardia include hypoxemia, severe anemia, hyperthermia, massive hemorrhage, pain, fear, anxiety, hyperthyroidism, and sympathomimetic or parasympatholytic drug administration.

Sinus Arrhythmia

In sinus arrhythmia the heart rate varies by more than 10% from beat to beat. The P-QRS-T pattern is normal (Figure 6-4), but the interval between groups of complexes (i.e., the R-R interval) varies. Sinus arrhythmia is a normal rhythm in children and young adults. The patient’s pulse will often increase during inspiration and decrease during expiration. No treatment is required unless significant alteration occurs in the patient’s arterial blood pressure.

Atrial Flutter

In atrial flutter the normal P wave is absent and replaced by two or more regular sawtooth waves. The QRS complex is normal and the ventricular rate may be regular or irregular, depending on the relationship of the atrial to the ventricular beats. Figure 6-5 shows an atrial flutter with a regular rhythm with a 4 : 1 conduction ratio (i.e., four atrial beats for every ventricular beat). The atrial rate is usually constant, between 250 and 350 bpm, whereas the ventricular rate is in the normal range. Causes of atrial flutter include hypoxemia, a damaged SA node, and congestive heart failure.

Atrial Fibrillation

In atrial fibrillation the atrial contractions are disorganized and ineffective, and the normal P wave is absent (Figure 6-6). The atrial rate ranges from 350 to 700 bpm. The QRS complex is normal, and the ventricular rate ranges from 100 to 200 bpm. Causes of atrial fibrillation include hypoxemia and a damaged SA node. Atrial fibrillation may reduce the cardiac output by 20% because of a loss of atrial filling (the so-called “atrial kick”).

Premature Ventricular Contractions

The premature ventricular contraction (PVC) is not preceded by a P wave. The QRS complex is wide, bizarre, and unlike the normal QRS complex (Figure 6-7). The regular heart rate is altered by the PVC. The heart rhythm may be quite irregular when there are many PVCs. PVCs can occur at any rate. They often occur in pairs, after every normal heartbeat (bigeminal PVCs), and after every two normal heartbeats (trigeminal PVCs). Common causes of PVCs include intrinsic myocardial disease, hypoxemia, acidemia, hypokalemia, and congestive heart failure. PVCs also may be a sign of theophylline or alpha- or beta-agonist toxicity.

Ventricular Tachycardia

In ventricular tachycardia the P wave is generally indiscernible, and the QRS complex is wide and bizarre in appearance (Figure 6-8). The T wave may not be separated from the QRS complex. The ventricular rate ranges from 150 to 250 bpm, and the rate is regular or slightly irregular. The patient’s blood pressure is often decreased during ventricular tachycardia.

Ventricular Flutter

In ventricular flutter the QRS complex has the appearance of a wide sine wave (regular, smooth, rounded ventricular wave; Figure 6-9). The rhythm is regular or slightly irregular. The rate is 250 to 350 bpm. There is usually no discernible peripheral pulse associated with ventricular flutter.

Ventricular Fibrillation

Ventricular fibrillation is characterized by chaotic electrical activity and cardiac activity. The ventricles literally quiver out of control with no perfusion beat-producing rhythm (Figure 6-10). During ventricular fibrillation, there is no cardiac output or blood pressure, and the patient will die in minutes without treatment.

Asystole (Cardiac Standstill)

Asystole (cardiac standstill) is the complete absence of electrical and mechanical activity. As a result the cardiac output stops and the blood pressure falls to zero. The ECG tracing appears as a flat line and indicates severe damage to the heart’s electrical conduction system (see Figure 6-10). Occasionally, periods of disorganized electrical and mechanical activity may be generated during long periods of asystole; this is referred to as an agonal rhythm or a dying heart.

Increased Heart Rate (Pulse), Cardiac Output, and Blood Pressure

Increased heart rate, pulse, and blood pressure develop frequently during the acute stages of pulmonary disease. This can result from the indirect response of the heart to hypoxic stimulation of the peripheral chemoreceptors, primarily the carotid bodies. When the carotid bodies are stimulated, reflex signals are sent to the respiratory muscles, which in turn activate the so-called pulmonary reflex, which triggers tachycardia and an increased cardiac output and blood pressure. The increased cardiac output is a compensatory mechanism that at least partially counteracts the hypoxemia produced by the pulmonary shunting in respiratory disorders.

This process is perhaps best understood by assuming that the body’s oxygen use remains relatively constant over time. When the cardiac output increases during a period of steady metabolic requirements, oxygen transport increases, and the amount of oxygen extracted from each 100 mL of blood decreases. This results in an increase in the oxygen saturation of the returning venous blood, which in turn reduces the hypoxemia produced by the shunted blood. In other words, venous blood that perfuses underventilated alveoli will have less of a shunt effect if the oxygen content of the systemic venous blood is 13 vol% compared with, say, 10 vol%.

Other causes of increased heart rate, pulse, and blood pressure include severe anemia, high fever, anxiety, massive hemorrhage, certain cardiac arrhythmias, and hyperthyroidism. When the heart rate increases beyond 150 to 175 bpm, cardiac output and blood pressure begin to decline (the Starling relationship).

Decreased Perfusion State

The perfusion state can be evaluated by examining the patient’s color, capillary refill, skin, and sensorium. Under normal conditions the patient’s nail beds and oral mucosa are pink. If these areas appear cyanotic or mottled, poor perfusion and tissue hypoxia are likely present. When the nail beds are compressed to expel blood, they should normally refill quickly and turn pink when the pressure is released. If the nail beds remain white, perfusion is inadequate. Under normal conditions a patient’s skin should be dry and warm. When the skin is diaphoretic (wet), cool, or clammy, local perfusion is inadequate. Finally, when the patient is disoriented as to person, place, and time, a decreased perfusion state and cerebral hypoxia may be present.

Pulmonary Artery Catheter

The pulmonary artery catheter (Swan-Ganz catheter) is a balloon-tipped, flow-directed catheter that is inserted at the patient’s bedside; the respiratory care professional monitors the pressure waveform as the catheter, with the balloon inflated, is guided by blood flow through the right atrium and right ventricle into the pulmonary artery (Figure 6-11). The pulmonary artery catheter is used directly to measure the right atrial pressure (via the proximal port), pulmonary artery pressure (via the distal port), left atrial pressure (indirectly via the pulmonary capillary wedge pressure), and cardiac output (via the thermodilution technique).

Arterial Catheter

The arterial catheter (line) is the most commonly used mode of invasive hemodynamic monitoring. It is generally inserted in the radial artery for patient comfort and convenient access reasons. The indwelling arterial catheter allows (1) continuous and precise measurements of systolic, diastolic, and mean blood pressure; (2) accurate information regarding fluctuations in blood pressure; and (3) guidance in the decision to up-regulate or down-regulate therapy for hypotension or hypertension. The arterial catheter also is useful in patients who require frequent or repeated arterial blood gas samples (e.g., the patient being mechanically ventilated). The blood samples are readily available, and the patient is not subjected to the pain of repeated arterial punctures.

Central Venous Pressure Catheter

The central venous pressure (CVP) catheter readily measures the CVP and the right ventricular filling pressure. It serves as an excellent monitor of right ventricular function. An increased CVP reading is commonly seen in patients who (1) have left ventricular heart failure (e.g., pulmonary edema), (2) are receiving excessively high positive pressure mechanical breaths, (3) have cor pulmonale, or (4) have a severe flail chest, pneumothorax, or pleural effusion.

Table 6-1 summarizes the hemodynamic parameters that can be measured directly. Table 6-2 lists the hemodynamic parameters that can be calculated from results obtained from the direct measurements.

Table 6-1

Hemodynamic Values Measured Directly

Hemodynamic Value	Abbreviation	Normal Range
Central venous pressure	CVP	0-8 mm Hg
Right atrial pressure	RAP	0-8 mm Hg
Mean pulmonary artery pressure		10-20 mm Hg
Pulmonary capillary wedge pressure (also called pulmonary artery wedge; pulmonary artery occlusion)	PCWP	4-12 mm Hg
	PAW
	PAO
Cardiac output	CO	4-6 L/min

Hemodynamic Monitoring in Respiratory Diseases

Because respiratory disorders can have a profound effect on the structure and function of the pulmonary vascular bed, right side of the heart, left side of the heart, or a combination of all three, the data generated by the previously described invasive hemodynamic monitors are commonly used in the assessment and treatment of these patients. For example, respiratory diseases associated with severe or chronic hypoxemia, acidemia, or pulmonary vascular obstruction can increase the pulmonary vascular resistance (PVR) significantly. An increased PVR, in turn, can lead to a variety of secondary hemodynamic changes such as increased CVP, RAP, , RVSWI, and decreased CO, SV, SVI, CI, and LVSWI (see Tables 6-1 and 6-2 for abbreviation definitions). Table 6-3 lists common hemodynamic changes seen in pulmonary diseases known to alter the patient’s hemodynamic status.

Table 6-3

Hemodynamic Changes Commonly Seen in Respiratory Diseases

Disorder	Hemodynamic Indices
	CVP	RAP		PCWP	CO	SV	SVI	CI	RVSWI	LVSWI	PVR	SVR
COPD	↑	↑	↑↑	∼*	∼	∼	∼	∼	↑	∼	↑	∼
Chronic bronchitis
Emphysema
Cystic fibrosis
Bronchiectasis
Pulmonary edema (cardiogenic)	∼	↑	↑	↑↑	↓	↓	↓	↓	↑	↓	↑	↓
Pulmonary embolism	↑	↑	↑↑	↓	↓	↓	↓	↓	↑	↓	↑	∼
Adult respiratory distress syndrome (ARDS)—severe	∼↑	∼↑	∼↑	∼	∼	∼	∼	∼	∼↑	∼	∼↑	∼
Lung collapse	↑	↑	↑	↓	↓	↓	↓	↓	↑	↓	↑	↓
Flail chest
Pneumothorax
Pleural disease (e.g., hemothorax)
Kyphoscoliosis	↑	↑	↑	∼	∼	∼	∼	∼	↑	∼	↑	∼
Pneumoconiosis	↑	↑	↑↑	∼	∼	∼	∼	∼	↑	∼	↑	∼
Chronic interstitial lung diseases	↑	↑	↑↑	∼	∼	∼	∼	∼	↑	∼	↑	∼
Cancer of the lung (tumor mass)	↑	↑	↑	↓	↓	↓	↓	↓	↑	∼	↑	∼
Hypovolemia	↓↓	↓	↓	↓	↓	↓	↓	↓	↓	↓	∼	↑
Hypervolemia (burns)	↑↑	↑	↑	↑	↑	↑	↑	↑	↑	↑	∼	∼
Right heart failure (cor pulmonale)	↑↑	↑↑	↓	↓	∼	∼	∼	∼	∼	∼	∼	∼

^*∼, Unchanged.