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Updated 2024/2025 (Graded A+)
Cardiac Output (CO) - ✔✔Heart rate x Stroke Volume Things that can increase HR - ✔✔Stimulation of SNS Hypotension Medications w/ positive chronotropic effects Things that can decrease HR - ✔✔Stimulation of PNS Vagal nerve stimulation (Vagal down) Cardiac conduction abnormalities Medication w/ negative chronotropic effects Pulse Pressure (PP) - ✔✔systolic pressure - diastolic pressure Low/Narrowing Pulse pressure - ✔✔Results from decreased left ventricular stroke volume, blood loss, shock, or cardiac tamponade High/widening pulse pressure - ✔✔May be transient and normal result from exercise. May also be caused by chronic conditions (Atherosclerosis or aortic regurgitation) or acute conditions (Aortic dissection, aneurysms, patent ductus arteriosus, endocarditis, ect.) Chronotropes - ✔✔affect heart rate Inotropes - ✔✔Affect contractility or force of contraction Dromotropes - ✔✔Medications that affect automaticity or rate of electrical impulse within the heart
Stroke Volume (SV) - ✔✔The amount of blood pumped out of the heart with each contraction. Positively influenced by contractility and preload. Contractility - ✔✔Strength of myocardial contraction. Affected by preload, afterload, electrolytes, myocardial oxygenation, functional myocardium, and inotropic medications. Preload - ✔✔Volume of blood resulting in pressure or stretch of ventricles during diastole. Affected by the amount of venous return to the heart. Increased by peripheral venous constriction, shock, admin of excess IV fluids, blood products, or renal failure. decreased preload - ✔✔Decreased intervascular volume Hemorrhage Vomiting Diaphoresis Third spacing Diarrhea Redistribution of blood flow Vasodilators Increased preload - ✔✔Alpha-adrenergic Epinephrine Norepinephrine Med-High dose dopamine Afterload - ✔✔Resistance to ventricular emptying during systole Afterload increasing factors - ✔✔Vasoconstrictions or mechanical obstruction of ventricular outflow. Aortic or pulmonic stenosis HTN Hypothermia
Normal cardiac output for infants/neonates - ✔✔0.8-1.3 L/min Normal stroke volume for Infants/Neonates - ✔✔ 5 - 13 mL/beat Normal BP for infants 0- 1 month - ✔✔above 60mm Hg Normal BP for infants 1-12 months - ✔✔above 70mm Hg Normal central venous pressure for infants - ✔✔ 0 - 8 mmHg Alpha- 1 - ✔✔Stimulation causes peripheral vascular constriction Beta- 2 - ✔✔Stimulation causes bronchial smooth muscle dilation ACE inhibitors - ✔✔Block conversion of angiotensin I to angiotensin II *prils (Lisinopril) ARB - ✔✔Angiotensin II Receptor Blocker (sartan) Calcium channel blockers - ✔✔Negative Ino, Chrono, Dromo (weak, slow, blocks conduction) *-zems, - dipines, - isotopin Beta Blockers - ✔✔Negative Ino, Chrono, and Dromo effects. Cardio and Non-cardio selective *olol ACE inhibitors - ✔✔Reduce afterload associated w/HF Pregnancy class D
Angiotensin Receptor Blockers (ARBs) - ✔✔Vasodilation and decreased aldosterone levels Increased excretion of Na+. K+ sparing Oral medication usually cardioselective beta blockers - ✔✔Works on Beta-1 receptors Decrease HR, BP, and contractility Works on kidneys by inhibiting the release of renin, reducing BP through the renin-angiotensin- aldosterone system. Non-cardioselective beta blockers - ✔✔Works on Beta-1 and 2 receptors Affects the lungs Dilation of airway Bronchial smooth muscle relaxation Don't give to asthmatics Nicardipine (Cardene) - ✔✔Calcium channel blocker Coronary, peripheral dilator Labetalol - ✔✔Beta Blocker, nonselective; Alpha-1 blocker Slows HR, decreases PVR, CO, and BP Moderately decreases preload and afterload Gradually lowers BP to avoid infarct/ischemia Nesiritide (Natrecor) - ✔✔Agent used in acutely decompensated CHF resembling B-type natriuretic peptide Venous/Arterial vasodilator Nitroglycerin (Nitrostat) - ✔✔Coronary artery dilator
Norepinephrine - ✔✔Increases CO, HR, and SVR Increases BP, coronary blood flow Tissue necrosis w/ infiltration Phenylephrine (Neo-Synephrine) - ✔✔Decreases HR Increases SVR and Systolic BP Tissue necrosis w/ infiltration Adenosine - ✔✔Given for Paroxysmal SVT, Wolf-Parkinson White Slows SA node and AV node conduction and HR. RAPID PUSH May cause transient heart block or asystole Amiodarone (Cordarone) - ✔✔Given for unstable VT/VF and SVT Decreases AV conduction Prolongs action potential and refractory period Digoxin (Lanoxin) - ✔✔Given for AFIB/Flutter, Paroxysmal SVT Increases force of myocardial contraction Decreases SA,AV node conduction Monitor serum drug level ditalezam - ✔✔Given for angina, HTN, uncontrolled AFIB/flutter Slows AV conduction Calcium channel blocker Solution stable for 24hr only Esmolol (Brevibloc) - ✔✔Given for sinus tach, SVT, and HTN
Slows sinus HR, decreases CO, and reduces BP Administer through large bore infusion NO PUSH Ibutilide - ✔✔Given for rapid conversion of recent onset AFIB/flutter Slows SA node rate and AV conduction Dose related prolongation of QT interval Can cause Torsades within 4-8 hr of admin Lidocaine - ✔✔Given for PVCs, VTACH/FIB Decreases depolarization, automacity, excitability of ventricles during diastole Monitor for central nervous system toxicity w/ repeated doses Procainamide - ✔✔Given for AFIB, SVT, PVCs, VTACH Increases threshold of ventricles Decreases myocardial excitability, conduction velocity Depresses myocardial contractility Monitor for paradoxical response w/ extremely rapid ventricular rate during treatment of AFIB Reduce infusion if QRS widened by 50% or w/ rapid BP drop. May lead to complete heart block w/ lower degree AV blocks Propranolol (Inderal) - ✔✔Given for SVT Slows sinus HR Decreases cardiac output, BP, and myocardial ischemia severity. Maximum undiluted IV push in 1mg/min Dilute in 10mL D5W, administer 1mg over 10-15min Verapmil - ✔✔Given for paroxysmal SVT and AFIB/Flutter
Complete obstruction of one or more coronary arteries w/ thrombosis Chest pain assessment - ✔✔Onset Provokes Quality Radiates Severity and Symptoms Timing transvenous pacemaker - ✔✔Catheter electrode is threaded into the right atrium or ventricle via the subclavian internal jugular, brachial, or femoral vein transcutaneous pacing - ✔✔Pacing pads or paddles are placed on the patient's chest and back. It is quick and easy w/ decreased risk of infection Fixed pacing - ✔✔Constant pace rate is set. More common mode Demand pacing - ✔✔Allows for variable pacing based on the patient's cardiac output needs. Pacemaker will add beats as needed. Transcutaneous pacing assessment - ✔✔Assess for and provide sedation and pain management. Apply pads as indicated. Press pacing button and choose fixed or demand. If fixed, set the rate. Typically 60-70. Adjust mA to desired initial energy level. Start low and gradually increase until a pacer spike precedes each QRS complex, indicating electrical capture. AHA guidelines recommend increasing the energy level by an additional 5-10mA for a margin of safety. Check for pulse that matches electrical activity, indicating mechanical capture of the heart. Electrical Cardioversion - ✔✔Hemodynamically unstable pt. Decompensating ventricular tachycardia w/ pulse
SVT
New onset/rapid ventricular of atrial fibrillation or flutter refractory to pharmacological intervention Cardioversion assessment - ✔✔Assess and provide sedation and pain management Activate sync mode Verify marker is present for each R wave before delivering synchronized energy Defibrillation candidates - ✔✔Someone w/o spontaneous circulation VFIB Pulseless VTACH biphasic defibrillator - ✔✔delivers current from two directions requires lower amounts of energy Interior wall findings - ✔✔Consider right-sided 12 lead to identify right ventricular infarction Cautious use of NTG to avoid profound hypotension Lead I - ✔✔High lateral lead Lead aVR - ✔✔not used for diagnostic purposes Lead V1 - ✔✔Septal; Left anterior descending artery Lead V4 - ✔✔Anterior; Right coronary artery Lead II - ✔✔Inferior (RCA) Lead aVL - ✔✔Lateral
Injury to myocardium - ✔✔Reversible w/ appropriate intervention Elevated ST segments in at least two contiguous leads Myocardial infarction - ✔✔Elevated ST segments Inverted T waves Abnormal Q waves may indicate old infarction An Acute MI may not have ST segment changes EKG changes w/ inferior MI - ✔✔ST segment elevation in II,III, aVF ST segment depression in I and aVL Troponin - ✔✔Elevates within 3-12 after infarct Peaks 10-24 hours CK-MB - ✔✔Elevates 4- 12 Peaks 10- 24 Morphine - ✔✔Decreases associated pain and reduce anxiety. Generally reserved for patients w/ persistent cardiac pain, unrelieved by NTG Oxygen - ✔✔May be used in patients w/ pulse ox readings below 94% or those w/ severe respiratory symptoms or signs of shock Nitroglycerin (NTG) - ✔✔Reduces myocardial oxygen demand, causes coronary vessel dilation, and improves collateral blood flow to ischemic myocardial tissue. Dilates peripheral vasculature and reduces preload; may reduce afterload Aneurysms - ✔✔Bulge in the wall of an artery
Aortic dissection - ✔✔Tear in intimal layer of aorta Exposes medial layer to forces of blood pressure Dissection of the two layers of arterial wall Risk factors for aneurysm and dissection - ✔✔HTN Atherosclerosis Age > Previous cardiovascular sx Connective tissue disease Cocaine use Trauma Type 1 dissection - ✔✔Ascending aorta, aortic arch, descending thoracic aorta Type 2 - ✔✔Ascending aorta Type 3a - ✔✔Descending thoracic, aorta distal to left subclavian artery,. proximal to celiac artery Type 3b - ✔✔Thoracic and abdominal aorta distal to left subclavian artery Symptoms of dissection - ✔✔Chest pain, flank pain, shoulder pain, ripping/tearing pain. No relief w/ pain meds. Significant differences in BP in upper extremities Symptoms of ascending dissection - ✔✔Altered LOC Indications of stroke, acute MI, cardiac tamponade, and aortic valvular insufficiency Symptoms of descending dissection - ✔✔Renal failure
Aesthetic complications Uterine atony Cardiac disease HTN/Pre/eclampsia Other's H and Ts Placentae abruptio/previa Sepsis Targeted temperature management - ✔✔Improves neurological recovery after return of spontaneous w/ persisting neurological deficits Target temps 32-36c for 12-24 hours Control shivering Obtain baseline electrolytes and Q1hr glucoses Dysrhythmias - ✔✔Abnormal cardiac electrical activity May be asymptomatic or result in symptoms relating to altered cardiac output Bradycardia - ✔✔Occurs to an impaired or delayed electrical impulse Impairment or SA node or activation of heart by CNS Less than 60bpm in adults Tachycardia - ✔✔Over 100bpm Wolff-Parkinson-White Syndrome - ✔✔Fast rate from extra or abnormal pathway between atria and ventricles Impulses travel through normal route and extra pathways Delta waves on QRS complexes Rate between 100- 250
Torsades De Pointes Treatment - ✔✔IV magnesium endocarditis - ✔✔Inflammation of the endocardium including the cardiac valves Endocarditis symptoms - ✔✔Fever Anorexia Weight loss Night Sweats Myalgia Fatigue Pleuritic chest pain Abdominal/back pain Hemoptysis Conjunctival petechiae Heart failure - ✔✔Inadequate cardiac output and delivery of oxygen to tissues Left ventricle ejection fraction is typically less than 40% Left-Sided heart failure - ✔✔1. SOB
- Crackles
- Oliguria
- Frothy Sputum
- Displaced Apical Pulse (Hypertrophy)
- S3 present Right-sided heart failure - ✔✔1. Jugular Vein Distention
- Ascending Dependent Edema
Caused by; Viral/ Bacterial infection, Acute MI, Aortic dissection, cancer, renal failure, mediastinal injury, connective tissue ST segment elevation in most or all leads Tall, peaked T waves (except AVR and V2) PR segment depression in lead II periphreal vascular disease (PVD) - ✔✔Slow and progressive circulatory disorder Affects arteries, veins, lymphatic system Primary cause is atherosclerosis Peripheral Arterial Occlusion - ✔✔Pain is constant, worsens with movement and exercise improves with rest Burning discomfort Area of occlusion distally Excruciating pain Cold extremity, decreased pulses that may progress to paralysis Peripheral venous occlusion - ✔✔Pain is more common with standing and diminishes with rest/elevation deep and aching/throbbing in nature swelling in extremity with darkened color and possible fever elevate affected extremity Localized to area of occlusion Pain that evolves Atherosclerosis - ✔✔Hardening of arteries Buildup of plaque on arterial wall Narrowing and stiffness
Arteries cannot dilate and meet greater blood flow demand Leg muscles work harder to get oxygenated blood as they are furthest extremities away from the heart Peripheral artery disease - ✔✔Narrowing or hardening of arteries outside the heart Diminished blood flow due to compromised vessels Organs supplied by these arteries are damaged due to deceased blood flow, oxygen, and nutrients May be asymptomatic Weakness/numbness Sores w/ delayed healing Decreased or absent pedal pulses hair loss Cramping Chronic venous insufficiency - ✔✔Form of peripheral venous disease One or more veins do not adequately return blood flow from lower extremities back to heart due to damaged venous valves Dilatated veins Edema Leg pain Skin fibrosis venous ulcers cramping w/ ambulation cellulitis ulcer delayed wound healing Deep vein thrombosis - ✔✔Clot develops in a deep vein w/ potential to dislodge or travel throughout body
