Hemodynamic monitoring and Shock Dr. Mohammad Aljawadi PharmD, Msc, PhD PHCL 477 Clinical Pharmacy Department College of Pharmacy King Saud University April 2015

Inadequate tissue perfusion What is Shock? Inadequate tissue perfusion Cellular Injury Organ Dysfunction

To understand the hemodynamics of shock we need: To understand the basics of hemodynamics What is a pulmonary artery catheter and how it is used Let us start with the latter and go back to the former later

Pulmonary Artery Catheter Swan-Ganz Catheter 110 cm long Up to 5 ports Tip encloses a balloon  1.5 mL Ports at 19cm and 30cm for the infusion of drugs.

Pulmonary Artery Catheter Indications Myocardial infarction with shock/hypotension. Intraoperative cardiac or vascular surgery patients. Severe trauma. Relative Indications CHF Pulmonary hypertension Neurosurgical procedures Sepsis/septic shock Respiratory failure Uses Establish Diagnosis Guide therapies Monitor Treatment Assess O2 delivery

Central Venous Access Complications Line sepsis Thrombosis Pneumothorax Hemothorax Arrhythmias (Swan-Ganz) Air Embolus Infarction Catheter Knotting (Swan-Ganz)

How it is inserted? During diastole while mitral valve is open, left ventricle, left atrium and pulmonary capillary become one chamber.

The Basics of Hemodynamics Blood Pressure Cardiac Output Systemic vascular resistance Stroke Volume Heart rate Pre-load After-load Contractility

The Basics of Hemodynamics BLOOD PRESSURE CO SVR = X SV HR X

The Basics of Hemodynamics Cardiac Output (CO) Amount of blood that is pumped out of the heart in one minute. 5.6 L/min for a human male and 4.9 L/min for a female Stroke Volume The quantity of blood pumped out of the ventricles with every heart beat. ~ 70 mL in a healthy 70-kg man

Determinants of stroke volume PRELOAD AFTERLOAD CONTRACTILITY

DEFINITIONS Pre-Load Force on ventricles during relaxation phase (diastole) Measured at end-diastole (just before ejection) SV

DEFINITIONS Afterload Load on the ventricle during ejection (in systolic phase)

DEFINITIONS Contractility Force of ejection INOTROPE

MEASURES OF PRE-LOAD Right ventricular pre-load Central Venous Pressure (CVP) 0-4 mmHg Left ventricular pre-load Pulmonary Artery Occlusion Pressure (PAOP) (8-12 mmHg) Measured during diastole when the MV is open When mitral valve is open we assume PAEDP ~ PVEDP ~ LAEDP ~ LVEDP Pulmonary Artery End-diastolic Pressure

MEASURES OF PRE-LOAD Normally, PAOP approximates left atrial pressure, which in turn approximates left ventricular end-diastolic pressure (LVEDP). LVEDP reflects left ventricular end-diastolic volume (LVEDV). LVEDV is the actual target

MEASURES OF AFTERLOAD Afterload on Right Ventricle Pulmonary Vascular Resistance PVR =MPAP – PAWP x 80 (20-120 dyne x sec / cm-5) CO Afterload on Left Ventricle Systemic Vascular Resistance SVR = MAP – CVP x 80 (800-1200 dyne x sec / cm-5) MAP = SBP + 2(DBP) 3

CONTRACTILITY CO = SV x HR CARDIAC OUTPUT (4-7 L/min) Thermodilution: a thermistor near the end of the catheter injects cold saline into the bloodstream and the temperature change determines CO CARDIAC INDEX = CO/BSA (2.8-3.6 L/min/m2)

OXYGEN SUPPLY OXYGEN DEMAND

OXYGEN SUPPLY DO2 = CO X CaO2 (arterial O2 content) CO = SV x HR CaO2 determined by: HgB SaO2

OXYGEN DEMAND Determined by metabolic activity of tissues O2 extraction Usually about 25% for the entire body CvO2 determined by: HgB SvO2 (60-75%)  SvO2 = increased oxygen consumption Either decreased delivery, or increased demands Examples???

A word about O2 monitoring Oxygen Saturation (SpO2) normal > 90% Non-invasive Mixed venous oxygen saturation (SvO2) Normal 65%-75% invasive

RECAP PA catheter measurements RA or CVP (0-4 mmHg) PAP (25/10 mmHg) PAOP (8-12 mmHg) CO / CI (4-7 L/min, 2.8-3.6 L/min/m2) SVR (800-1200 dyne x sec / cm-5) SvO2 (65-75%) RIGHT HEART PRE-LOAD LEFT HEART PRE-LOAD BLOOD FLOW / PUMP PERFORMANCE LEFT HEART AFTERLOAD OXYGEN SUPPLY /DEMAND

Shock in the ICU

What is Shock? Inadequate tissue perfusion resulting in cellular injury. This causes the release of inflammatory mediators that further compromise tissue perfusion, resulting in organ failure and death unless quickly corrected Circulating volume must be identified and expanded quickly, and the underlying pathological process must be controlled.

Classification of Shock Hypovolemic Shock Cardiogenic Shock Distributive Shock Extra-cardiac Obstructive Shock

Organ dysfunction is the threat of shock

Hypovolemic Shock Loss of blood or fluid. Results from Loss of blood or fluid. Decreased circulating blood volume decrease in diastolic filling pressure and volume  inadequate CO, hypotension, and shock

Hypovolemic Shock Causes: dehydration, hemorrhage, gastrointestinal fluid losses, urinary losses, or decreased vascular permeability from sepsis hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

Hypovolemic Shock 10% Tachycardia, ↑ SVR , ↔ BP 20% to 25% Acute Loss in circulating Blood Volume Consequences 10% Tachycardia, ↑ SVR , ↔ BP 20% to 25% Mild hypotension, ↓CO, ↑lactate 40% Moderate-severe hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

Cardiogenic Shock Myocardial damage or cardiac mechanical abnormality Reduced cardiac function Decrease in cardiac output and blood pressure  Shock

Cardiogenic Shock Causes: Special signs: Q-wave myocardial infarctions. Special signs: Patients have signs of heart failure, an S3, elevated neck veins, and peripheral hypo-perfusion

Cardiogenic Shock (most frequent in-hospital cause) Q-wave MI ↑Ventricular volume ↑PAOP ↑ Preload ↑CVP ↓MAP ↓SV ↓CI an S3, elevated neck veins, and peripheral hypo-perfusion Signs of heart failure:

Distributive Shock Loss of peripheral resistance fluid leak to extracellular space Vasodilation  Decrease in preload  Hypotension  Normal or increased CO Myocardial depression frequently accompanies distributive shock. Decrease in SVR  inadequate blood pressure  shock and multi-organ dysfunction

Distributive Shock Causes: Sepsis Anaphylaxis, drug overdose, neurogenic causes, and Addisonian crisis

Extra-cardiac obstructive Obstruction to flow in the cardiovascular circuit. inadequate diastolic filling or decreased systolic function secondary to an increase in afterload and a drop in CO and blood pressure

Extra-cardiac obstructive Causes cardiac tamponade, constrictive pericarditis, pneumothorax, mediastinal tumors and pulmonary embolus

Tip of the mountain

Causes:

Pathophysiology

Auto-regulation

Body auto-regulation during shock

Manifestations of shock CNS: Alerted level of consciousness from confusion to coma Ischemia

Manifestations of shock CVS: Hypotension Decreased coronary artery perfusion pressure Ischemia in patients with coronary artery disease Tachycardia. (which type of shock is not associated with it?)  Contractility will increase in most types Cardiogenic

Manifestations of shock Respiratory: Increase in minute ventilation  Hypocapnia  Severe hypo-perfusion  Respiratory muscle weakness  Respiratory alkalosis Respiratory Failure

Manifestations of shock Renal: Because of auto-regulation glomerular filtration is maintained by efferent arteriole constriction Late in shock: Cortical and medullary ischemia  tubular necrosis ↓ urine output followed by ↑ BUN and SCr

Manifestations of shock GI: Very sensitive to sympathetic vasoconstriction: Ileus Gastritis Pancreatitis Acalculous cholecystitis (not due to stone gallbladder inflammation) Colonic submucosal hemorrhage Ischemia of the gut can lead to translocation of bacteria from the gut to the circulation

Manifestations of shock Liver: LFTs elevations Hematological: Disseminated intravascular coagulation Dilutional thrombocytopenia due resuscitation Metabolic: Hyperglycemia due ↓ insulin production Protein catabolism negative nitrogen balance

Manifestations of shock Cardiogenic shock: jugular venous distension, an S3 and S4, and regurgitation murmurs. Pulmonary embolus: patients present with hypoxia, dyspnea, and elevated right heart pressures. Septic shock patients may have fevers, chills, and usually a nidus of infection ( a source of infection)

Labs: Low or high WBC count with a left shift and bands High or normal hemoglobin levels High to low platelets Low serum bicarbonate High anion gap High or normal creatinine High lactate (unless hemorrhagic shock) Why?

Hemodynamic monitoring: Arterial pressure and CVP  monitor vasopressors effect Mixed venous oxygen saturation (Svo2) Normal 65%-75% Inversely proportional to perfusion level Pulmonary artery catheter  no evidence of decreased mortality

Shock Hemodynamics CO SVR PAOP CVP pre-resusc Hypovolemic Cardiogenic Distributive pre-resusc post-resusc Extra-cardiac obstructive Shock (pulmonary embolism) or normal

Goals of therapy: Prevent target organ damage Achieve adequate CO and MAP Treat underlying cause

Therapy Adequate oxygenation (mechanical ventilation) Goal: Oxygen saturation 90% or greater Volume resuscitation Mainly crystalloids (NaCl 0.9%) Colloids (Albumin) Good in severe sepsis Hetastarch Limited use in renal failure Other colloids include: dextrane , hetastarch and pentastarch Other crystalloids include: dextrose, ringer’s lactate

Therapy Once volume resuscitation is optimized  vasopressors and inotropes What happened if you start with a vasopressor before fluid resuscitation?

Vasopressors: Norepinephrine: Dopamine: Reliable increase in blood pressure and inotrope Dopamine: Low dose: mild inotropic effect as well as some renal effects. high dose: vasoconstriction Higher incidence of mesenteric ischemia than norepinephrine

Vasopressors: Epinephrine: Phenylephrine: 1st choice in anaphylactic shock Watch for: Tachycardia and arrhythmia Mesenteric ischemia Phenylephrine: Pure α-agonist Good for patients with underlying tachycardia

Vasopressors: Vasopressin: In refractory cases not responding to previous vasopressors ↓ heart rate and cardiac output ↑ blood pressure and pulmonary artery pressure May lead to myocardial ischemia due a decrease in coronary artery blood flow

Inotropes: Dobutamine: Milrinone: β1 and β2 agonists CO SVR Milrinone: phosphodiesterase inhibitor It is a potent vasodilator Decreases both pulmonary vascular resistance and SVR.

Therapy Hypovolemic Shock: Cardiogenic: Rapid reversal with blood, colloid, or crystalloid Cardiogenic: Left ventricular MI: Intra-aortic balloon pump, cardiac angiography, and revascularization Right ventricular MI: Fluids and inotrops

Therapy Extra-cardiac obstructive shock: Cardiac tamponade: Pericardiocentesis or surgical drainage Pulmonary embolism: Thrombolytics, Heparin and embolectomy

Therapy Distributive shock: Septic: Anaphylactic: Antibiotics + fluid resuscitation+ vasopressors or inotropes Anaphylactic: Steroids, diphenhydramine, H1 and H2 blockers, and epinephrine

Questions