Clinical Examination of the Cardiovascular System

The classical signs of cardiac tamponade

Dr Sanam shakya9th February 2020

Cardiac tamponade is the medical emergency in which fluids accumulate in the pericardium and results in the confining of heart. It may be agile(acute) or steady(subacute). It is also known as pericardial tamponade. Signs of cardiac tamponade must be understood as soon as possible because it is one of the medical emergency.

Cardiac tamponade is m by a large or unconstrained pericardial effusion, the buildup of fluid inside, the pericardium. It generally occurs because of chest trauma, also produced by myocardial rupture, cancer, uremia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissections, and because of anticoagulant therapy. In this post, you will be able to apprentice the details about the signs of cardiac tamponade.

Signs of cardiac tamponade

The three classicistic signs of cardiac tamponade, which doctors refer to as Becks triad, are:

• Low blood pressure
• Muffled heart sound
• Swollen or bulging neck veins called distended neck veins

Some other signs of cardiac tamponade are:

• Signs of shock-like cold, calmy skin, dizziness, weakness and fainting
• Decreasing the level of consciousness
• Tachycardia
• Dyspnoea

Low blood pressure in cardiac tamponade

Low blood pressure is one of the initial signs of cardiac tamponade. Cardiac tamponade is a complication of pericardial effusion and occurs when pericardial pressure is high enough to interfere with ventricular filling. The volume of fluid demanded to cause cardiac compression varies considerably. If it has collected slowly, 1-2 liters may be present.

However, with rapid collections of fluid within the pericardium, very much smaller volumes may lead to cardiac tamponade,’ which is characterized by a reduction in the diastolic filling of the ventricles, decreased stroke volume, and lowered arterial blood pressure.

This increased intra-pericardial pressure is exerted equally on all the chambers of the heart, to result in the equilibration of intra-pericardial, right atrial, right ventricular diastolic, left atrial and left ventricular diastolic pressures. The stroke volume of both ventricles is reduced because of the reduced diastolic volume in each ventricle. Decreased stroke volume usually results in sympathetic nervous system activation (tachycardia, vasoconstriction) in the attempt to maintain cardiac output; this is supported as long as the central venous pressure is above right ventricular end-diastolic pressure.

There were initially no abnormal clinical signs of cardiac tamponade inpatient apart from the profound hypotension after induction. There was, in particular, no compensatory tachycardia in this previously fit young man. This absence of tachycardia may be the result of a decrease in diastolic volume, which mimics that of profound hypovolaemia. Hypovolaemia can also be regarded as one of the vital signs of cardiac tamponade.

Sensory receptors in the left ventricle are activated during an acute reduction in blood volume. This signal from the heart appears to obtund the compensatory baroreflex mechanism via endogenous opiate receptors (governed by delta receptors) located in the ventricles of the brain.

Patients who are hypotensive from acute blood loss may develop relative bradycardia, and transfusion not only restores arterial blood pressure but also causes an increase in the heart rate. Tachycardia is also regarded as the signs of cardiac tamponade.

This suggests that once blood volume (and thus left ventricular end-diastolic volume) is restored. To a critical level, the cardiovascular responses are switched on again.

Bradycardia is observed during acute tamponade, and severe hemorrhage in dogs anesthetized with pentobarbitone, despite bilateral cervical vagotomy, sympathectomy, and intravenous atropine. It was suggested that sinoatrial node ischemia was the cause of the shift of the pacemaker and resultant bradycardia in both cardiac tamponade and severe hypovolemia.

Indeed bradycardia may be protective because it prevents myocardial damage by allowing improved ventricular filling when preload decreases. General anesthesia and controlled ventilation can lead to profound hypotension as a result of decreased venous return, peripheral vasodilatation, and direct myocardial depression, especially in association with unrecognized hypovolaemia.

However, this patient appeared clinically to be adequately resuscitated before induction. Other possible causes of hypotension, such as sudden concealed hemorrhage, pneumothorax, and allergy, were considered but not confirmed by clinical signs. Tachycardia and pulsus paradoxus ( > 10 mmHg), are well recognized early signs of cardiac tamponade, neither of which was evident at any stage in this patient.

The central venous line was used for vascular access alone, and no measurements of venous pressure were made pre-operatively. This might have suggested the diagnosis. Acute cardiac tamponade may follow both blunt and sharp chest trauma and may result in unexpected clinical effects.'” Compression wedge fracture of the body of L, suggested significant trauma, in the case described, and in retrospect, another occult injury should have been suspected, in particular, blunt chest trauma.

Some sternal tenderness was noted before the operation, but this was not considered to be significant, and the sternal fracture was not checked for on lateral X-ray views. SAG-M blood was administered into a central venous ‘cannula.’ This was inserted via a low right supraclavicular approach, which may have produced traumatic entry into the mediastinum, although the source of the intra-pericardial blood was not confirmed at operation.

Perhaps the most critical factor in early diagnosis of cardiac tamponade during anesthesia is a high index of suspicion since there are no specific physical signs. Indeed, any or all of the standard features (elevated jugular venous pulse, tachycardia, Pulsus paradoxus, pulse pressure < 30 mmHg, systolic arterial blood pressure < 100 mmHg, friction rub, Kussmaul’s sign, decreased heart sounds) may be absent.

Muffled heart sound in cardiac tamponade

This is the second sign of cardiac tamponade, which helps in the diagnosis. The physiology behind the muffled heart sound is due to the muffling effects of fluid surrounding the heart.

Distended neck vein

The distended neck vein is due to raised central venous pressure in a non-supine position. It is caused by the reduced diastolic filling of the right ventricle, due to tension from the adjacent expanding pericardial sac. This results in a substitute of fluid into the veins draining into the heart, most notably, the jugular veins or neck veins. In severe hypovolemia, the neck veins may not be distended. So neck vein distended is also one of the significant components of becks triad and signs of cardiac tamponade.

Summary

The frequency of cardiac tamponade is unclear. It is estimated to occur in 2% of those with stab or gunshot wounds to the chest. People with a non-cancerous cause of cardiac tamponade have a mortality rate of less than five percent. Prompt diagnosis by going with signs of cardiac tamponade and early treatment significantly improves the outlook for people with cardiac tamponade.