Hemodynamics Made Easy
Principles of Hemodynamics Gurmeet Kaur Gurdav Singh RN,CCRN,BSc,MSc
Objectives Brief review • Normal Cardiac Anatomy • The physiology of blood flow
Discuss ‘cardiac cycle’ Discuss ‘cardiac output’ Review myocardial oxygen balance
Hemodynamics The study of “the movement of blood”
Anatomy
Anatomy
Blood Flow • Atria receives blood • Ventricle ejects blood • Unidirectional blood flow • Blood flows from high to low pressure
Cardiac Cycle
SYSTOLE Contracting & Emptying
Systole 3 Phases Isovolumetric contraction (IVC) Rapid ventricular ejection Reduced ventricular ejection
Systole (3 Phases)
Systole – Phase 1
Diastole
Ventricular Filling
Isovolumetric Contraction
Systole – Phase 3
Systole – Phase 2
Rapid Ejection
Reduced Ejection
Diastole 3 Phases Isovolumetric relaxation (IVR) Rapid (but PASSIVE) ventricular filling Atrial contraction
Systole – Phase 3
Diastole (3 Phases) Diastole – Phase 2
Diastole – Phase 1
Isovolumetric Relaxation
Reduced Ejection
Diastole – Phase 3
Atrial Contraction
Rapid (PASSIVE) Filling
Systole – Phase 1
Isovolumetric Contraction
Cardiac Output The volume of blood ejected in 1 minute
CO = HR
(Heart Rate)
x SV
(Stroke Volume)
CO assessed by measuring blood pressure and evaluating perfusion
Blood Pressure • Pulse Pressure Difference between the systolic and diastolic pressures Normal range = 15 - 40 mm Hg or < 25% of SBP
• Mean Arterial Pressure (MAP) Systolic + (2 x Diastolic) ÷ 3
e.g.
120/80 (93) mmhg
Cardiac Output Determinants Heart Rate Stroke Volume
Heart Rate Affected by: Tachycardia Bradycardia Irregularity / Arrhythmia
Stroke Volume The volume of blood ejected per heart beat
Affected by: Preload Afterload Contractility
Preload The volume of blood present in the ventricles at the end of diastole Venous return RVEDP / LVEDP
Increased Ventricular Preload
Increased Ventricular Pressure
=
Venous Changes
CONSTRICT
DILATE
↑ Preload
↓ Preload
Preload Preload affected by: • Diuretics
↓ preload
• Nitrates (e.g. GTN) ↓ preload • Fluid bolus
↑ preload
Afterload The resistance the ventricles must overcome to eject blood Resistance - the opposition to blood flow in a vascular bed • Blood density - Hct • Systemic vascular bed - AEDP • Pulmonary vascular bed - PAEDP
Increased Ventricular Afterload
Increased Ventricular Pressure
=
Arterial Changes
CONSTRICT
DILATE
↑ Afterload
↓ Afterload
Afterload Afterload affected by: • Nitrates (e.g. SNP)
↓ afterload
• Antihypertensive
↓ afterload
• Noradrenaline
↑ afterload
Afterload As afterload increases, stroke volume may decrease if myocardium cannot contract forcefully enough The greater the afterload, the greater the myocardial oxygen consumption
Contractility The intrinsic ability of the myocardial cells to contract
â&#x20AC;˘ Stroke Volume â&#x20AC;˘ Ejection Fraction 60 - 80 %
Ejection Fraction : 60-80 %
Contractility Contractility affected by: • Positive inotropic factor
↑ contractility
• Negative inotropic factors
↓ contractility
NB: Frank Starling Law of the Heart
Myocardial Oxygen Balance Supply Coronary artery anatomy Coronary artery perfusion • Diastolic pressure • Diastolic time
O2 extraction • Hb
Demand Heart rate LV wall tension • Preload • Afterload
Contractility
Myocardial Oxygen Supply • 90 % of the O2 supply occurs during diastole • Diastolic BP is the driving force for coronary perfusion pressure • Tachycardia decreases diastolic time and therefore coronary filling time
Myocardial Oxygen Extraction • 60 - 70 % of O2 delivered is extracted by the myocardium • 90 % of the O2 used is during the IVC phase of systole
References Marino, P.,L., (2007). The ICU Book, 3rd Edition, Lippincot Williams&Wilkins, USA: Philadelphia Howard, P., K., Steinmann, R.,A., editors (2010). Sheehy’s Emergency Nursing: Principles and Practice, 6th Edition, Mosby Elsevier, USA: St Louis Manoach, S., Weingart, S.,D., Charchaflieh, J., (2012). The evolution and current use of invasive hemodynamic monitoring for predicting volume responsiveness during resuscitation, perioperative, and critical care. Journal of Clinical Anesthesia 24, pp 242–250.
Thank You