Coronary venous system

Coronary venous system

The heart receives its oxygenated blood supply via the coronary system. Deoxygenated blood returns to the right atrium via the coronary venous system. The opening through which the coronary veins drain into right atrium is known as the coronary sinus. This opening is located in the lower posterior portion of the right atrium.

Atrial systole

Sino- Atrial Node Impulse (P wave)

Atrial Contraction (25-30% Vent fill)

Atrial pressure > Ventricular pressure - Opening of AV valves, atrial blood volume moves across AV valves, rise in ventricular pressure.

Ventricular systole

Isovolumetric Phase

AV node impulse causes ventricular contraction (QRS), abrupt rise in ventricular pressure forces AV valves closed. Ventricular Preload (ventricular wall tension) > Ventricular afterload (arterial circulation pressure, SVR), semi-lunar valves open, blood flows to systemic arterial and pulmonic circulations (ejection)

Ventricular diastole

Ventricular pressure <>

Stroke volume components

Preload

Reflects diastolic filling and is monitored in the clinical setting by the left and right atrial pressures, the pulmonary artery wedge pressure, pulmonary artery diastolic

pressure and by systolic blood pressure. Pharmacological agents, increasing fluid volume, temperature alterations and haemoglobin, may alter these.

Afterload

Afterload is the amount of wall tension that the ventricles must generate to expel their blood volume. Afterload is influenced by aortic distensibility and by systemic and pulmonary vascular resistance. Systolic and mean arterial pressures provide information about the patient’s afterload status. Medications, mechanical assist devices (IABP, ventricular assist) may be used to reduce afterload.

Contractility

Contractility cannot be directly measured in the clinical setting. Noting the preoperative ejection fraction provides information about the patient’s myocardial contractility. Left ventricular and right ventricular stroke volume provides additional information. Poor contractility may be increased with optimising preload and afterload and by using inotropic agents and pacing.

Heart rate

The heart rate is a determinant of cardiac output (HR x SV = Cardiac output). Increased and decreased heart rate affects cardiac output and tissue oxygen levels. Optimal heart rate is 60-100bpm. There are many clinical indications, which affect HR (pain, anxiety, hypoxia, hypercapnia, hypovoelaemia and so on). Treatment of heart rate is aimed at treating the underlying cause. Bradycardia may be treated with pacing and medications. Tachycardia may be treated with medications, cardioversion and override pacing

Cardiac output

Adequate cardiac output is essential for meeting the patient’s metabolic needs. Improvement in cardiac output can be achieved by manipulating preload, afterload, contractility, heart rate and improving tissue oxygen levels. Determining the appropriate measures needed for optimising the cardiac output can be a challenge for the nurse caring for patients after cardiothoracic surgery. Knowledge of fluids, vasoactive medications and mechanical assist devices is essential in choosing effective therapeutic interventions. Maximising a patient’s cardiac output depends on a stable heart rate and stroke volume.

Management of invasive lines

Strict asepsis and adherence to protocol is necessary for optimal patient outcomes. Invasive lines are a potential source of introgenic infection, therefore a good principal is that all lines are to be removed at the earliest opportunity. This is as true for intravenous lines as it is for the more invasive lines such as Pulmonary artery catheters (PAC). Pulmonary artery catheters are only required for unstable patients requiring vasoactive drug +/- intra -aortic counterpulsation. All entry sites are to be observed at least once a shift and invasive lines removed with the tip cultured, if inflammation or exudate is evident.