Pre-Clinical Lecture Series - Lecture 3
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THE CARDIAC CRITICAL CARE PATIENT: PHYSIOLOGY AT ITS EXTREMES Alice Clarke - 10/11/21 AIMS FOR TODAY’S LECTURE Example Case The Basics Pathophysiology Monitoring Pharmacological Mechanical Support Support 60 YEAR OLD MALE • Presents to ED with central, crushing, chest pain 60 YEAR OLD MALE • Presents to ED with central, crushing, chest pain •myocardial infarction (specifically a STEMI)agnosis of 60 YEAR OLD MALE • In ED he is given generic medical management: • Morphine • Oxygen(IF REQUIRED) • Nitrates (sublingual GTN) • Aspirin 60 YEAR OLD MALE • For patients who've had a STEMI (i.e. one of the coronary arteries has become occluded) the priority of blocked vessel.o reopen (or re-vascularise) the 60 YEAR OLD MALE • For patients who've had a STEMI (i.e. one of the coronary arteries has become occluded) the priority of management is to reopen (or re-vascularise) the blocked vessel. • -> he is transferred to Papworth for PCI PCI • since the early 2000's thrombolysis has been superseded by percutaneous coronary intervention (PCI) • In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future • This is done via a catheter inserted into either the radial or femoral artery 60 YEAR OLD MALE • Procedure is successful • Transferred to CCU (cardiac critical care) following the procedure for monitoring 60 YEAR OLD MALE Nurses bleep you to say he seems a bit confused and maybe a little bit short of breath. 60 YEAR OLD MALE • Cold extremities • AMS/Confusion • Pale Mottled skin • Does not know where he is • Peripheral pulses are faint • SOB • Regular pulse • Respiratory rate 20 • HR 120BPM • You think that you can • BP 100/70 hear “crackles” on auscultation of his lungs • 40ml of urinary output over last hour (catheterized) 60 YEAR OLD MALE CLINICAL SIGNS OF HYPOPERFUSION CLINICAL SIGNS OF PULMONARY OEDEMAWHAT COMPLICATION HAS THIS MAN DEVELOPED?(CARDIOGENIC) SHOCK CARDIOGENIC SHOCK • Cardiogenic shock = a low-cardiac-output state • Occurs secondary to extensive left ventricular (LV) infarction • It is characterized by systolic and diastolic dysfunction • -> leading to end organ hypoperfusion • Autopsy studies have shown that cardiogenic shock is generally associated with the loss of more than 40% of the LV myocardial muscle MYOCARDIAL PATHOLOGY • interruption of blood flow in an epicardial coronary artery • -> the zone of myocardium supplied by that vessel loses the ability to shorten and perform contractile work • If a sufficient area of myocardium undergoes ischemic injury… • -> LV pump function become depressed • -> systemic hypotension develops IMPORTANT PHYSIOLOGY CO = HR X stroke volume MAP = CO X SVR MYOCARDIAL PATHOLOGY • Patients who develop cardiogenic shock from acute MI (like this patient) have been shown consistently to have evidence of progressive myocardial necrosis with infarct extension • There is a vicious cycle that leads to cardiogenic shock and potentially death… 1. Decreased coronary perfusion pressure 2. Decreased cardiac output 3. Increased myocardial oxygen demand 60 YEAR OLD MALE You rule out alternatives and diagnose cardiogenic shock. 1 2 3 4 Maintain BP Maintain Respiratory Reversal of Cardiac Support underlying Output cause 1 2 Maintain BP Maintain Cardiac OutputCO = HR X SV MAP = CO X SVRJUST GIVE FLUID?PHARMACOLOGIC INTERVENTIONS PHARMACOLOGIC INTERVENTIONS 1. Inotropes 2. vasopressors INOTROPES Inotropes increase cardiac contractility -> increasing cardiac output -> increase BP Positive inotropes are the specific group that increase the force of cardiac contractility (as opposed to negative inotropes such as Ca-channel blockers used in hypertension, which decrease it) Ca Dependent Examples of positive inotropes include: Digoxin; Dobutamine; milrinone; dopamine VASOPRESSORS Vasopressors induce vasoconstriction -> increase systemic resistance-> increase BP They work by targeting arterioles, where the smooth muscle contains several receptors. This leads to stimulation of smooth muscle contraction (increasing arteriolar tone) -> Decreasing vessel diameter -> Increasing systemic vascular resistance. Examples of vasopressors used in ITU include: norepinephrine (noradrenaline); vasopressin (ADH); adrenaline; dopamineCO = HR X SV MAP = CO X SVR +/- DIURETICS Once systolic BP is > 90 mm Hg, start diuretic therapy! Loop diuretics are the common choice, e.g. furosemide! Diuretics should be administered intravenously (if possible) Assess the effect of the diuretics (e.g. urine output, symptoms) every 6 hoursMECHANICAL SUPPORT MECHANICAL SUPPORT 1. IABP (intra-aortic balloon pump) 2. Ventricular assist devicesINTRA-AORTIC BALLOON PUMP INTRA-AORTIC BALLOON PUMP The balloon sits in the aorta, ~2cm from subclavian artery The balloon inflates and deflates via counter pulsation, meaning it actively deflates in systole and inflates in diastole. Systolic deflation decreases afterload through a vacuum effect and thus indirectly increases forward flow from the heart. Diastolic inflation increases blood flow to the coronary arteries via retrograde flow. THESE ACTIONS COMBINE TO… Decrease myocardial O2 demand increase myocardial perfusion & O2 supply indirectly increases cardiac output through afterload reductionCOMPLICATIONS...1 2 3 Respiratory SupportRESPIRATORY SUPPORT RESPIRATORY SUPPORT 1. POSITIONING – ensure the patient is positioned upright 2. SUPPLEMENTAL O2 - for patients with an SpO2 < 90% or PaO2 < 60 mm Hg 3. HFNC (High-flow nasal cannula): Consider in patients with an SpO2 < 90% non-responsive to basic oxygen delivery system 4. NIPPV: for patients with respiratory distress despite supplemental oxygen 5. INVASIVE MECHANICAL VENTILATION • Indications include: Hypoxemic respiratory failure; unresponsive to NIPPV; Refractory hypoxemia (PaO2 < 60 mm Hg); Hypercapnia (PaCO2 > 50 mm Hg); Acidosis (pH < 7.35)1 2 3 4 Reverse the causeHOW DOES OCCLUSION OCCUR? • 1. GRADUALLY • 2. SUDDENLYTHE FINAL OPTION?PLEASE FILL IN THE FEEDBACK FORM! Alice Clarke - 10/11/21