Cardiac Cycle Pressure Changes

• Pressure changes occur in each cardiac chamber during the cardiac cycle.

Review of Cardiac Physiology

• The cardiac cycle consists of systole (ventricular contraction) and diastole (ventricular relaxation).
• At the start of systole, ventricular pressure rises above atrial pressure, resulting in the passive closing of the mitral and tricuspid valves.
• The closure of the mitral and tricuspid valves creates the S1 heart sound.
• As myocytes contract, intraventricular pressures increase until they surpass the pressure in the aorta and pulmonary artery, causing the aortic and pulmonic valves to open and ventricular ejection of blood to occur.
• When intracellular calcium levels decrease, ventricular relaxation begins.
• When arterial pressures exceed intraventricular pressures, the aortic and pulmonic valves close creating the S2 heart sound which occurs slightly earlier on the left than the right.
• When intraventricular pressures fall below atrial pressures, the mitral and tricuspid valves open, initiating the rapid and passive ventricular phase of diastole.
• At the end of diastole, atrial contraction supports ventricular filling.

Pressure Tracings

• Right atrial pressure can be directly measured using a catheter (Swan-Ganz catheter, pulmonary artery catheterization, or right-sided heart catheterization).
• Right atrial pressure can be assessed using the estimated Central Venous Pressure, seen via Jugular venous distension.
• Left atrial pressure can only be measured indirectly and is done by occluding a small pulmonary artery branch to measure the pressure distally (Pulmonary capillary wedge pressure).
• Normal Values for Common Hemodynamic Parameters are:
• Heart Rate: 60-100 Beats/Minute
• Central venous/Right atrial Pressures: ≤9 mm Hg
• Right ventricular Systolic Pressure: 15-30 mm Hg
• Right ventricular End-diastolic Pressure: ≤9 mm Hg
• Pulmonary arterial Systolic Pressure: 15-30 mm Hg
• Pulmonary arterial Diastolic Pressure: 3-12 mm Hg
• Pulmonary capillary wedge/Left atrial Pressure: ≤12 mm Hg
• Left ventricular Systolic Pressure: 100-140 mm Hg
• Left ventricular End-diastolic Pressure: 3-12 mm Hg
• Aortic Systolic Pressure: 100-140 mm Hg
• Aortic Diastolic Pressure: 60-90 mm Hg.

Challenge Questions

• In cardiogenic shock, both right atrial pressure and left atrial pressure (pulmonary capillary wedge pressure) are elevated, while they are low in hypovolemic shock.
• Cardiogenic shock involves volume overload, not allowing pressure to pump correctly, causing back up into the left atria and lungs.
• Hypovolemic shock involves low blood volume so there is no pressure because it is not the right amount for pressure to occur.
• Pulmonary artery hypertension (PAH) causes elevated right atrial pressure but normal pulmonary capillary wedge pressure/ left atrial pressure.

Indications for Invasive Hemodynamic Cardiac Monitoring

• Assists in making a differential diagnosis.
• Guides the management of patients with heart/lung disease/shock of all types.
• Monitors hemodynamic pressures during fluid resuscitation.
• Monitors inotropic/vasoconstrictor/vasodilator drug infusion therapy.
• Assesses complications of myocardial infarction and heart failure.
• Monitors hemodynamics with complicated surgical procedures.

Cardiac Performance

• Factors that affect cardiac performance are:
• Preload (left ventricular diastolic volume).
• Afterload (impedance against which the left ventricle must eject blood).
• Contractility (cardiac performance independent of preload or afterload).
• Heart rate.

Blood Pressure

• Blood pressure (BP) is the force that blood exerts against the walls of arteries as it passes through them.
• BP = Cardiac output (CO) x Peripheral vascular resistance (PVR), think as a representation of afterload.
• Less afterload means lower blood pressure and vice versa.
• Pulse Pressure (PP) = Systolic BP - Diastolic BP.
• Normal pulse pressure is around 40 (30-50).
• Systolic BP is the force exerted against the wall of the arteries when ventricles contract and is largely a result of CO, blood volume, and compliance of the arterial tree.
• As you get older and arteries stiffen, PVR increases, systolic increases and pulse pressure gets wider.
• Diastolic BP is the force exerted against the wall of the artery when the heart is filling and is primarily a function of peripheral vascular resistance (PVR).

Determinants of Arterial Pressure

• Arterial pressure is influenced by stroke volume, heart rate, vascular structure, and vascular function.

Cardiac Output

• Cardiac output = Stroke volume x Heart rate.

Hypotension

• Cardiac and vascular origins of arterial hypotension are:
• Cardiac: Arrhythmias (bradycardia and tachycardia), Structural Disease, and Obstructive.
• Arrhythmias such as bradycardia caused by 3rd degree heart attack, tachycardia caused by SVT, and fibrillation.
• Structural Diseases such as a valve disease, ischemic heart disease, pericardial disease, cardiac tamponade, congenital disease, obstructive cardiomyopathy, dilated cardiomyopathy, and primary pulmonary hypertension.
• Vascular: Hypovolemia (hemorrhage, diarrhea, dehydration, orthostatic volume shifts, drugs (diuretics)) and Vasodilation (sepsis causes vasodilation, anaphylaxis that needs epinephrine, neurogenic, autonomic dysfunction, drugs).
• Obstructive: pulmonary embolism is likely the cause of pulmonary shock only if it is massive, resulting in poor PVR and low BP.

Cardiac Index

• Cardiac Index = CO / BSA (2.8-4.3 L/min/square meter).
• CO = SV x HR

Ejection Fraction

• Ejection Fraction (EF) = (SV/EDV) x 100.
• SV = EDV - ESV.
• EF is most widely used and is a parameter for quantifying overall ventricular function particularly useful in management & evaluation of cardiac failure.
• N = ≥60%.
• An echo test will give you the EF, as well as a mugascan.

Preload

• Preload = LVDV (Left ventricular diastolic volume) and it represents the amount of volume in the left ventricle @ the end of diastole.
• Unlike Heart Failure. a normal heart can increase stroke vollume at the end of diastole.
• Increases in preload augment stroke volume in normal hearts (Frank Starling Law).
• Conditions that decrease volume will reduce preload & reduce stroke volume such as hemorrhage, diarrhea, and dehydration.
• Atrial contraction contributes to preload (important when there is reduced ventricular compliance).

Decreasing Preload

• Temporary: Valsalva maneuver (vasovagal), standing up fast, and an altered intrathoracic pressure
• Longer: Diuretics (will alter blood volume), and nitrates (vasodilation).

Increasing Preload

• Have the patient lay down (supine) and lift their legs or squat, which squeezes the veins and causes venoconstriction.
• Longer Term: Give IV Fluids or a vasoconstrictor (ex: norepinephrine or phenylephrine).

Afterload

• Afterload is the impedance against which the left ventricle must eject blood, think as the BP, a result of increasing the afterload decreases SV.
• Afterload is approximated by arterial BP.
• Afterload is a key determinant in stroke volume (quantity of blood ejected by the left ventricle).

Decreasing Afterload

• Temporary: Use of amyl nitrate and amyl nitrate drugs.
• Longer: Use artery vasodilators (CCBs such as hydralazine, nitropresside), ARBs,and ACE-I.
• ACE-Is decrease preload and afterload!

Increasing Afterload

• Temporary: Doing a hand grip exercise.
• Longer term: Vasoconstrictors of the arterial side (Norepinephrine, vasopressin).

Contractility/Inotropy

• Contractility (inotropy) refers to intrinsic strength of muscle fibers.
• With increased contractility (inotropy), stroke volume (SV) is increased at any level of preload.
• Digoxin (medication examples).

Myocardial Contractility

• Drugs that can increase inotropy/myocardial contractility are Digoxin, Dobutamine, and Milrinone.
• Pathologic conditions that decrease inotropy/myocardial contractility are due to heart failure.

Stroke Volume

• Stroke Volume (SV) is the amount of blood ejected with each ventricular contraction.
• End Diastolic Volume (EDV) - End Systolic Volume (ESV).
• SV = EDV - ESV.
• Influenced by:
• Preload (+++)
• Afterload (----)
• Myocardial Contractility/Inotropy (+++).