**6. Cardiac tamponade**

Cardiac tamponade is characterized by the accumulation of pericardial fluid causing significant impairment in cardiac function due to the pressure effect of external pericardial content causing compression of all cardiac chambers. Increase in intrapericardial pressure reduces the myocardial transmural pressure with a reduced ventricular wall diastolic compliance and a decrease in cardiac output and blood pressure. In cardiac tamponade, unlike constrictive pericarditis, most of the inspiratory decline in the intrathoracic pressure is transmitted through

the pericardium to the right ventricle and results in increased venous return and right ventricular distention. The higher intrapericardial pressure limits the right ventricular free wall expansion, resulting in bulging of the right ventricular septum to the left ventricle. This bulge diminishes the compliance of the left ventricle, which results in decreased filling and cardiac output [4, 77]. A similar mechanism contributes to pulsus paradoxus, an abnormal decline in systolic blood pressure (>10 mmHg) with inspiration. Cardiac tamponade is a treatable cause of cardiogenic shock that can be rapidly fatal.

Usually, cardiac tamponade is seen after pericarditis, tuberculosis, iatrogenic (secondary to cardiac interventions), trauma, neoplasm, with other uncommon causes including, collagen vascular disorder, radiation therapy, post-myocardial infarction, uremia, aortic dissection, and a bacterial infection.

#### **6.1 Etiology**

Cardiac tamponade could be acute, subacute, low-pressure type, or regional. Acute cardiac tamponade is sudden in onset and acutely life-threatening if not treated. Subacute cardiac tamponade is less dramatic compared to acute, but once the intrapericardial pressure reaches the threshold, patients experience classical tamponade symptoms related to decreased cardiac function. Low-pressure tamponade is a condition that appears in hypovolemic patients (such as traumatic hemorrhage, over diuresis, etc.). Correction of volume status reveals a typical tamponade pattern. Regional tamponade occurs from loculated effusion or a localized hematoma causing compression of only selected chambers. It is usually seen after myocardial infarction or pericardiotomy [77].

#### **6.2 Clinical presentation**

Depending on the severity of the tamponade, a variety of clinical findings are seen. Sinus tachycardia as a physiologic response to maintain the cardiac output is common. Elevated jugular venous pressure, muffled heart sounds, and systemic hypotension together referred to as Beck's triad is a pathognomonic sign for tamponade.

#### **6.3 Diagnosis**

The diagnostic approach and the evaluation of cardiac tamponade are similar to that for patients with suspected pericardial effusion. The ECG findings include sinus tachycardia, low voltage of QRS complex, and frequently electrical alternans, which is beat-to-beat changes in the position of the heart with relation to cardiac tamponade. The presence of total electrical alternans, including P wave, QRS complex, and ST segment alternans, is highly specific for cardiac tamponade, but sensitivity is very low with findings present in only 5–10% of cases. The presence of lone QRS alternans is more common but is not very specific for tamponade. The presence of QRS vector alternans (axis shift) is more specific than QRS amplitude alternans for the cardiac tamponade [77, 78].

TTE is the standard first-line imaging technique recommended for the evaluation of cardiac tamponade with excellent safety and efficacy. The size of the pericardial effusion does not indicate significance. Since respiration has an impact on intracardiac pressures, mainly on the right side of the heart, this respirophasic flow pattern becomes more evident in tamponade, which can be measured by Doppler echocardiographic variations in blood flow across the mitral (>25% variation) (**Figure 3**) and tricuspid valves (>40% variation) as well as pulmonary and

**23**

**Figure 4.**

*arrow).*

**Figure 3.**

*Doppler echocardiographic variations in blood flow across the mitral valve.*

*Diastolic collapse of the right ventricular wall (top arrow) and diastolic period of cardiac cycle (bottom* 

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

systemic outflow. Right atrial collapse and RV collapse on diastole (**Figure 4**) are usual signs of cardiac tamponade, but in the setting of severe pulmonary hypertension, right-sided chamber collapse may be delayed and preceded by left atrial collapse. In most cases, the thickness of the left ventricular wall and lower compliance prevents LV collapse. As the tamponade worsens, there are progressive impairments in hemodynamics and intracardiac flows. Elevated pressures in the right atrium can

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

*Inflammatory Heart Diseases*

**6.1 Etiology**

genic shock that can be rapidly fatal.

myocardial infarction or pericardiotomy [77].

alternans for the cardiac tamponade [77, 78].

**6.2 Clinical presentation**

tamponade.

**6.3 Diagnosis**

the pericardium to the right ventricle and results in increased venous return and right ventricular distention. The higher intrapericardial pressure limits the right ventricular free wall expansion, resulting in bulging of the right ventricular septum to the left ventricle. This bulge diminishes the compliance of the left ventricle, which results in decreased filling and cardiac output [4, 77]. A similar mechanism contributes to pulsus paradoxus, an abnormal decline in systolic blood pressure (>10 mmHg) with inspiration. Cardiac tamponade is a treatable cause of cardio-

Usually, cardiac tamponade is seen after pericarditis, tuberculosis, iatrogenic (secondary to cardiac interventions), trauma, neoplasm, with other uncommon causes including, collagen vascular disorder, radiation therapy, post-myocardial

Cardiac tamponade could be acute, subacute, low-pressure type, or regional. Acute cardiac tamponade is sudden in onset and acutely life-threatening if not treated. Subacute cardiac tamponade is less dramatic compared to acute, but once the intrapericardial pressure reaches the threshold, patients experience classical tamponade symptoms related to decreased cardiac function. Low-pressure tamponade is a condition that appears in hypovolemic patients (such as traumatic hemorrhage, over diuresis, etc.). Correction of volume status reveals a typical tamponade pattern. Regional tamponade occurs from loculated effusion or a localized hematoma causing compression of only selected chambers. It is usually seen after

Depending on the severity of the tamponade, a variety of clinical findings are seen. Sinus tachycardia as a physiologic response to maintain the cardiac output is common. Elevated jugular venous pressure, muffled heart sounds, and systemic hypotension together referred to as Beck's triad is a pathognomonic sign for

The diagnostic approach and the evaluation of cardiac tamponade are similar to that for patients with suspected pericardial effusion. The ECG findings include sinus tachycardia, low voltage of QRS complex, and frequently electrical alternans, which is beat-to-beat changes in the position of the heart with relation to cardiac tamponade. The presence of total electrical alternans, including P wave, QRS complex, and ST segment alternans, is highly specific for cardiac tamponade, but sensitivity is very low with findings present in only 5–10% of cases. The presence of lone QRS alternans is more common but is not very specific for tamponade. The presence of QRS vector alternans (axis shift) is more specific than QRS amplitude

TTE is the standard first-line imaging technique recommended for the evaluation of cardiac tamponade with excellent safety and efficacy. The size of the pericardial effusion does not indicate significance. Since respiration has an impact on intracardiac pressures, mainly on the right side of the heart, this respirophasic flow pattern becomes more evident in tamponade, which can be measured by Doppler echocardiographic variations in blood flow across the mitral (>25% variation) (**Figure 3**) and tricuspid valves (>40% variation) as well as pulmonary and

infarction, uremia, aortic dissection, and a bacterial infection.

**22**

systemic outflow. Right atrial collapse and RV collapse on diastole (**Figure 4**) are usual signs of cardiac tamponade, but in the setting of severe pulmonary hypertension, right-sided chamber collapse may be delayed and preceded by left atrial collapse. In most cases, the thickness of the left ventricular wall and lower compliance prevents LV collapse. As the tamponade worsens, there are progressive impairments in hemodynamics and intracardiac flows. Elevated pressures in the right atrium can

**Figure 3.** *Doppler echocardiographic variations in blood flow across the mitral valve.*

#### **Figure 4.**

*Diastolic collapse of the right ventricular wall (top arrow) and diastolic period of cardiac cycle (bottom arrow).*

be assessed from a plethora of the inferior vena cava (IVC) which is a lack of change in IVC caliber in response to respiratory flow pattern (<50% reduction in IVC diameter during inspiration). The swinging movement of the heart within the pericardial sac is another echocardiographic sign. These TTE findings in cardiac structural and functional change with a decline in cardiac function often occur well before the onset of pulsus paradoxus and significant clinical deterioration, and thus, they are an important indicator in cardiac tamponade [11, 79]. Cardiac CT and CMRI may provide valuable information about the functional and structural change of the heart and pericardium, but they are only required in special conditions such as localized tamponade, loculated pericardial effusion, or hematoma [61, 79].
