Hemodynamics 2023 PDF

HEMODYNAMICS Pumps, Pipes, Fluids, and the Electrical System Original Work, Developed and Researched By Steve Casarez, RN, MICN, Paramedic Updated 2023  Disclaimers  All work and research is original based off clinical...

HEMODYNAMICS Pumps, Pipes, Fluids, and the Electrical System Original Work, Developed and Researched By Steve Casarez, RN, MICN, Paramedic Updated 2023  Disclaimers  All work and research is original based off clinical practice, current resuscitation guidelines, physician interviews and critical care education symposiums and lectures.  Please follow local jurisdictions and hospital protocols and guidelines  Hemodynamics Fundamentally, the most important concept to understand as a Paramedic All your drugs affect Hemodynamics HR, RR, skin signs, EKG, SpO2, EtCO2 IV, Fluids, Drug TX Pt Positioning  Figure 04.F01: The cardiovascular system. AAOS. (2004). Paramedic: Anatomy & Physiology. Sudbury, MA: Jones & Bartlett Learning.  Hemodynamics “It’s all about the” PUMP, PIPES, FLUID, and the ELECTICAL SYSTEM  Hemodynamics Terms: Cardiac Output Cardiac Index Heart Rate Preload Afterload Contractility Electrical System of the Heart (ECG)  Hemodynamic Overview MAP Stroke Volume Elevated Afterload Decreased Afterload 1. NTG 1. Dopamine Right Ventricle Lungs Left Ventricle 2. Nitroprusside (Nipride) 2. Dobutamine Pulmonary Systemic 3. Nicardipine 3. Epinephrine 4. Hydralazine 4. Levophed CO/CI = HR x PVR PAP SVR SAC 5. Labetalol 5. Phenylephrine 4-8/2.5-4 60-100 20-120 15-25 800-1200 6. A,B,C,D’s CVP PCWP DPF Elevated Preload Decreased Preload 0-8 8-15 8-12 1. NTG 1. Fluids 2. Diuretics 2. Blood 3. “Some above” 3. cardiac drugs Contractility Ejection Fraction 60-70% 4. Dialysis 4. pacemaker 5. A,B,C,D’s Organ Perfusion Chronotropic Inotropic Dromotropic ( Electrical Impulse) - HR +HR - Contractility +Contractility Electrical Activity 1. ABCD’S 1. Atropine 1. ABCD’s 1. Dopamine SAC = Depolarization = Active phase = PQRS 2. Epinephrine 2. Dobutamine DPF = Repolarization = Resting phase = T 3. Epinephrine Hemodynamic Formula CO = HR x SV Stroke Volume is: (Preload, Afterload, Contractility)  “Easy way to remember” C H A M P Stroke Volume C =H x (A M P) Cardiac Output Heart Rate Afterload Mechanical Contraction Preload And Contractility  Heart Rate “Feeling the pulse rate.” Palpation This gives simple information regarding the strength of the circulation system via the systolic resistance (Systemic Vascular Resistance)SVR and heart rate “Visualizing the heart rhythm.” EKG and 12L The quality of conduction Rate of conduction Is it too fast? Is it too slow? Do I need to shock it back into place?  Assessing Pulse Pressure Rating Palpable Pulses 0 = No Pulse +1 = Weak Pulses = (not good) +2 = Normal Pulses = (good) +3 = Bounding Pulses = (not good) Example of use: “Pt has +3 pulses at the Left Radial site!”  Heart Rate Heart Rate Influenced by Chronotropic Determined by the rate of spontaneous depolarization at the SA node, which is (your P wave) Can be modified by the Autonomic Nervous System Sympathetic and Parasympathetic tones The rate is also influenced by: Street Drugs ETOH RX medications Figure 04.F07: Electrical conduction through the heart Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Mean Arterial Pressure Normal (MAP) is 70-110 mmHg Minimal (MAP) to perfuse Kidney is 55-65 mmHg Is a measurement of End Organ Perfusion Pressures Helps determine the actual pressure of blood against the arterial walls MAP is part of the formula for calculating Cerebral Perfusion Pressures (CPP = MAP – ICP) Calculated by: (Diastolic x 2) + Systolic 3  MAP Clinical Significance 1. The rate at which the heart pumps blood into the large arteries 2. The rate of blood flow out of the large arteries to enter smaller arteries and arterioles 3. Arterial wall compliance. Suppose the ventricles spent an eh of time in systole and diastole. In that case, the mean arterial pressure could simply be the mathematical average of systolic and diastolic pressure values. In reality, however, the ventricles spend approximately one-third (1/3) of their time in systole and two-thirds (2/3) in diastole 4. MAP allows the Paramedic to have a better clinical evaluation of blood pressure as MAP is physiological to arterial wall compensation or disease  MAP = CO x Stroke Volume MAP Stroke Volume High Afterload Low Afterload 1. NTG 1. Dopamine RV Lungs LV 2. Nitroprusside (Nipride) 2. Dobutamine Pulmonary Systemic 3. Nicardipine 3. Epinephrine 4. Hydralazine 4. Levophed CO/CI = HR x PVR PAP SVR SAC 5. Labetalol 5. Phenylephrine 4-8/2.5-4 60-100 20-120 15-25 800-1200 CVP PCWP DPF High Preload 1. NTG Low Preload 1. Fluids 0-8 8-15 8-12 2. Diuretics 2. Blood 3. “Some above” 3. cardiac drugs 4. Dialysis 4. pacemaker Contractility Ejection Fraction 60-70% Organ Perfusion Chronotropic Inotropic Dromotropic ( Electrical Impulse) - HR +HR - Contractility +Contractility Electrical Activity 1. ABCD’S 1.Atropiine 1. ABCD’s 1. Dopamine SAC = Depolarization = Active phase = PQRS 2.Epinephrine 2. Dobutamine DPF = Repolarization = Resting phase = T 3. Epinephrine  Cardiac Output Cardiac Output The product of Heart Rate and Stroke Volume Normal range is 5-6 Liters/min Factors Affecting Cardiac Output Body Metabolism Pregnancy Body Temperature Sympathetic Activity Shock Organ diseases example: Renal, Liver, Lung, Heart, Gastrointestinal Paramedics can assess it: GCS Skin signs Blood Pressure Urine Output  Stroke Volume Stroke Volume Determined by Afterload, Preload, Contractility Is the amount of blood pushed out of the left ventricle  Stroke Volume Is Afterload / Preload / Contractility SAC DPF Systolic – Afterload – on Contraction Diastolic – Preload – Filling time of LV  Afterload Afterload Is Left Ventricle Systolic pressure against the high-pressure “It’s Resistance” Resistance of ventricular ejection with every contraction Measured by systemic vascular resistance SVR Resistance determined by lumen diameter and pre-capillary sphincters Controlled by sympathetic tone (beta receptors and chemo receptors) Controlled by Renin-Angiotensin Aldosterone System (RAAS) Systolic = Afterload = Contractions Diastolic  Treatment for Low Afterload Treatment for Low Systolic pressures Dopamine Catecholamine Inotropic agent (contractility) Levophed (norepinephrine) Alpha/Beta adrenergic agonist Epinephrine Alpha/Beta adrenergic agonist Neo-synephrine Pure alpha  Treatment for High Afterload Tx for high Systolic pressures Nitroglycerin Nitrate vasodilator Relaxes smooth muscle Nipride Vasodilator Relaxes vascular smooth muscle Amrinone Inotropic agent Pulmonary vasodilator  Right Radial Artery Without Pressors On Levophed for 10 min at 20mcg/min “Normal pipe diameter” “I’m pinching the pipe” Ultrasound  Preload Preload It is the Left Ventricle Diastole pressures “Filling time.” Starlings law affects preload Ventricle volume at the end of diastole Dependent on venous return Always treat low blood pressure with preload before you treat afterload!  Treatment to Increase Preload “Fill the tank” Treatment for Low Diastolic pressures Fluids, Fluids, Fluids, Fluids, Fluids, Fluids, Fluids….!!!!!!!!!!!! Blood replacement for hemorrhagic shock Cardiac dysrhythmias drugs to control HR so we can have better Cardiac Output Pacemaker is a potential tx for rate control AFIB Sick Sinus Syndrome Systolic = Afterload = Contraction Diastolic = Preload = Filling Time  Fluid Challenges A Fluid Challenge is using a bolus of isotonic fluid (250ml, 500ml) Under pressure….!!!!!!!!!!!!!! To Increase Preload Once the fluid challenge is complete, obtain a B/P SBP goes up > 20mmhg = Rapid Responder SBP goes up within 2-5min = Transient Responder SBP does not change = Reassess and Find the Source Consider more Fluids Consider Blood Consider Pressors  Treatment to Decrease Preload “Empty the Tank” Treatment Examples for High Diastolic pressures High blood pressure and high pulmonary pressures Diuretics Lasix, Bumex, Hydrochlorothiazide (HCTZ) Dialysis  Contractility Contractility “The Power of the Cardiac Muscle.” Influenced by Inotropic effects The ability of the myocardium to contract It needs a functioning Electrical System (EKG)  Three Factors Influencing Contractility DIC Dromotropic – Inotropic –Chronotropic Cardiac Electrical Impulse Cardiac Contractility Heart Rate Chronotropic Drugs Affects the rate and rhythm produced by the SA node Dromotropic Drugs Affects the conduction speed in the AV node Inotropic Drugs Alters the force of energy of muscular contraction Figure 04.F07: Electrical conduction through the heart Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Central Venous Pressure (CVP)  Is a measurement of preload.  CVP measures pressures in the vena cava blood RETURNING to the right atrium and ventricle.  Abdominal and Thoracic pressure variations will affect CVP.  CVP is dependent on BLOOD VOLUME.  When the CVP is high > 8-12 mmHg there is too much volume  Example is fluid volume overload  When the CVP is low < 0 mmHg there is no volume  Example is hypovolemia Paramedic CVP Exam  Systemic Vascular Resistance (SVR)  It’s a measurement of Afterload  SVR is influenced by the diameter of the vessels.  SVR Is resistance within the circulatory system that creates BLOOD PRESSURE.  Is used to maintain organ perfusion and cardiac output.  When SVR is high, there is increased resistance.  Example: Hypertension would have an >1200 mmHg SVR.  When SVR is low, there is no resistance  Example: Hypotension would have a decreased < 800 mmHg SVR.  What Other Key Elements That Affect Hemodynamics?  Pressures with manual and mechanical ventilation  Medications  Hormones and Receptors  Electrolytes (sodium, potassium, calcium)  Kidneys  Heart diseases  Peripheral Vascular Disease (PVD)  Pulmonary diseases  CVP & BVM  Positive Pressures Ventilations from a BVM may decrease venous return to the right heart.  It is important only to provide the correct amount of volume and pressure as needed. Anything > 15 cmH20 will start impeding CVP.  BVM inspiratory pressures compared to CVP  5 cmH20 is = to 4 mmHg  10 cmH20 is = to 7 mmHg  15 cmH20 is = to 11 mmHg  20 cmH20 is = to 15 mmHg Manometers  Hemodynamics Medications that influence hemodynamics The Blockers (ABCDs) A = Angiotensin II Receptor Blocker (ARBs) A = Angiotensin-Converting Enzyme Inhibitors(ACE) B = Beta Blockers C = Calcium Channel Blockers D = Digoxin, Digitalis, Diuretics  Hemodynamic Compensation Kidney’s It filters waste products keeping acid-base homeostasis Manages preload via urine It starts the Renin-Angiotensin System if this is disturbed RAS affects preload, afterload, cardiac output Carotid Bodies Chemoreceptors Detects changes in PaCO2 Afterload, and cardiac output, are affected High-pressure Arteries and low-pressure Cardiopulmonary Beroreceptors Detects acute changes in blood pressures Afterload, preload, cardiac output, and heart rate is affected  Hemodynamic Compensation Adrenergic receptors (alpha & beta) a1- Receptors, a-2 Receptors & β1-Receptors β2- Receptors β3-Receptors It acts on stress responses Sympathetic Nervous System “fight or flight” It picks up on the release of Epinephrine (catecholamine) Both alpha and beta affect Hemodynamics  a1- Receptors Works with CA++ channels at the cellular level Involved with smooth muscle contractions Helps with NA+ absorption in the Kidney’s Drugs Given by EMS Phenylephrine (neo-synephrine) Causes Vasoconstriction to Blood Vessels Kidney’s Brain  a2- Receptors At the Presynaptic receptors It slows down NA+ uptake at the cell levels Inhibits the release of catecholamines Smooth muscle relaxation 3 subtypes: a2A = slows insulin release in the pancreas when BS lowers a2B = pumps out glucagon in the pancreas when BS lowers a2C= contraction of GI sphincters EMS treatment for Hypoglycemic Treatment for food bolus  β1-Receptors Located in Kidney’s and Heart (primary in cardiac) Increase Renin secretion (RAAS) Affects all DIC Affects cardiac output Affects end-organ perfusion Patients who need to block all beta receptors take Beta Blockers!  β2-Receptors Located in the Lungs Smooth muscle relaxant for bronchi and GI Stimulates insulin secretion Thickens secretions of salivary glands Inhibit histamine and prostaglandin release Releases Renin EMS treatment that utilizes this effect: Albuterol  β3-Receptors Less clinically relevant Located in your adipose tissues Used for Bladder incontinence Good weight loss drug with minimal side effects. However, FDA does not allow its use  Hemodynamic Overview MAP Stroke Volume Elevated Afterload Decreased Afterload 1. NTG 1. Dopamine Right Ventricle Lungs Left Ventricle 2. Nitroprusside (Nipride) 2. Dobutamine Pulmonary Systemic 3. Nicardipine 3. Epinephrine 4. Hydralazine 4. Levophed CO/CI = HR x PVR PAP SVR SAC 5. Labetalol 5. Phenylephrine 4-8/2.5-4 60-100 20-120 15-25 800-1200 6. A,B,C,D’s CVP PCWP DPF Elevated Preload Decreased Preload 0-8 8-15 8-12 1. NTG 1. Fluids 2. Diuretics 2. Blood 3. “Some above” 3. cardiac drugs Contractility Ejection Fraction 60-70% 4. Dialysis 4. pacemaker 5. A,B,C,D’s Organ Perfusion Chronotropic Inotropic Dromotropic ( Electrical Impulse) - HR +HR - Contractility +Contractility Electrical Activity 1. ABCD’S 1. Atropine 1. ABCD’s 1. Dopamine SAC = Depolarization = Active phase = PQRS 2. Epinephrine 2. Dobutamine DPF = Repolarization = Resting phase = T 3. Epinephrine  Ventricle Breakdown a-MHC and b-MHC is Alpha or Beta-Myosin Heavy Chain, which is a cardiac muscle-specific protein involved with active force generation  Paramedic Take Home Concepts Cardiac Output You will assess GCS and Skin Signs You will assess MAP and Urine Output Central Venous Pressure This is a diastolic pressure Prevent an increase in Intrathoracic pressures You will always treat preload FIRST Systemic Vascular Resistance This is a systolic pressure Resistance to the Left Ventricle