Flash Cards

WVC Cardiac 2011 lesson 1 year 1

Question Answer
The Heart anterior to and between the lungs in the mediastinum, apex is above the diaphragm tilted slightly left of midline
Pericardial Membranes Three layers of pericardial membranes: 1. Fibrous pericardium – outer layer 2. Parietal pericardium – serous lining the fibrous pericardium 3. Visceral pericardium – also called epicardium on the surface of the heart muscle
Heart Chambers Walls of the heart is made of cardiac muscle called myocardium Chambers of the heart are lined with smooth endocardium Four heart chambers
Right Atrium and Ventricle Superior vena cava brings blood from the upper body Inferior vena cava brings blood from lower body Both empty into the right atrium
Left Atrium and Ventricle Blood returns from the lungs through the pulmonary veins and into the left atrium Through the mitral valve into the left ventricle Through the aortic valve into the aorta and out to the body
Coronary Vessels Supply oxygen to the myocardium itself Right and left branches come off the ascending aorta Blockage of coronary artery causes ischemia or infarction
Cardiac Cycle Sequence in one heartbeat contraction of the atria, followed a fraction of a second later by the simultaneous contraction of the ventricles. Blood flows passively into the atria but all blood to the arteries is actively pumped by the ventricles
Heart Sounds The first, loudest sound is the ventricular systole closing the tricuspid and mitral valves The second sound is the closing of the aortic and pulmonary semilunar valves Valves not closing properly cause heart murmurs
Conduction Mechanical Function of heart is regulated by electrical activity The natural pacemaker is the sinoatrial (SA) node located in the wall of the right atrium Impulses travel to the atrioventricular node Down the Bundle of His into the Purkinje fibers
Cardiac Cycle Beginning of one hbeat to the beginning of the next At beginning of systole,ventricles contract forcing AV valves to close (S1) & semilunar valves to open At end of systole/beginning of diastole, the semilunar valves close (S2) and AV valves open
Cardiac Output Volume of blood ejected by the heart in each minute – 4 to 7 liters Stroke volume- the amount of blood ejected by the left ventricle during each systole This is influenced by heart rate, contractility, preload and afterload
Contractility The inherent ability of the myocardium to stretch and contract normally The more stretch during diastole, the greater the systolic contraction – Starling’s law The more volume in the ventricles, the greater the stretch
Preload The degree of myocardial muscle fiber stretch at the end of diastole. Preload is determined by the left ventricular end-diastolic volume Excessive filling of the ventricles results in excessive LVED and a decreased cardiac output
Afterload The pressure the left ventricle must overcome to get blood out of the heart The higher the pressure in the aorta, the more force the ventricles must use to eject the blood Resistance is the pressure the heart must work against to get the blood out
Assessment Outside – Pulses, Blood Pressure, Edema, Pain, EKG Inside- Heart Sounds, Breath Sounds
Pulses and Blood Pressure Part of vital signs Be able to listen for apical-radial pulse simultaneously Check peripheral pulses Check blood pressure in both arms Check for edema, particularly in the lower extremities
Postural Vital Signs change in circulating volume-dehydration or vasodilation. Check BP and pulse while lying supine, for 3+ min. prior to measurement check bp & pulse 1-2 min. sit &stand. decrease of 20+ mmHg sys. BP, 10+ mmHG in dia., as well as increase of hr by 10-20%.
History Health history Risk factors Hereditary factors Medications
Inspection Jugular vein distention PMI – point of maximum impulse. Found midclavicular, 5th intercostal space (the mitral area at the apex) Edema- lower extremities. Classified as mild, moderate or severe (1+ to 4+) or as pitting or non-pitting Respiratory rate
Pain and Palpation Where is it? Does it radiate? When did it start? Have you ever had similar pain? What have you done for it? Did it help?
Murmur The valve either does not close or resists opening Causes turbulence This shows mitral regurgitation top) Aortic stenosis is on the bottom
Rub Occurs with heart beat Sign of infection, inflammation or infiltration Pericarditis, cardiac tamponade
Diagnostics 12-Lead EKG Serum Markers, other blood tests Stress Tests CXR EEG Angiography Cardiac Catheterization
Electrical Conduction myocardium responds to electro impulses of special cells Electrodes pick up the electrical impulses on the ecg Sinoatrial node (SA) is the primary pacemaker of the heart Atrioventricular node (AV) Bundle of His, right and left Purkinje fibers
SA Node Located near opening of the vena cava in the right atrium Initiates atrial depolarization Rate 60 – 100 bpm
AV Node Located floor of the right atrium Delays conduction 0.05 seconds to allow ventricular filling Takes over as primary pacemaker if SA node fails Rate 40-60 bpm
Bundle of His Right and Left branches to right and left ventricles Intrinsic rate 40-60 bpm Can take over if SA node fails
Purkinje Fibers Web of fibers going deep into the myocardium Cause ventricular depolarization Can beat at 20-40 bpm if all else fails
P Wave Represents atrial depolarization Smooth, rounded and upright in leads I, II and 1 0.5-2.5 mV amplitude PR interval is atrial depolarization and repolarization 0.12 to 0.20 mm is normal
QRS complex Ventricular depolarization Impulse down the Bundle of His to the Purkinje system Coincides with mitral and tricuspid closing (S1)
T Wave Ventricular repolarization Follows the same deflection as the P wave Absolute refractory period is the time for lethal arrhythmias
Abnormal T Wave Peaked in hyperkalemia, with a prolonged QRS and PR interval Low and rounded in hypokalemia with ST depression and U wave
ST Segment Early ventricular repolarization From the J point to the beginning of the T wave Length changes with heart rate Normal not elevated more than 0.5 mm
QT Interval Ventricular depolarization and repolarization Beginning of the QRS complex to the end of the T wave Varies with age, sex and heart rate
QT Interval cont. Can be lengthened with certain medications, electrolyte imbalances and subarachnoid hemorrhage A prolonged QT can predispose the person to Torsades de Pointes ventricular tachycardia (hypomagnesemia)
Normal Cardiac Cycle All the components that make up one heartbeat When working correctly, the heart rhythm is regular and beats 60-100 times per minute
Approach to EKG Interpretation Is it regular or irregular? Is it fast or slow? Are there P-waves? Is there a P-wave for every QRS? Measure the PR interval Measure the QRS Measure the QT interval
Examples of Dysrhythmias… Atrial Fibrillation Bradycardia
Atrial Fibrillation/Flutter Rapid firing of SA node in flut Disorganized firing of many atrial foci in fib Flutter is more difficult to convert Fibrillation has more hemodynamic consequences Treatment for both is aimed at controlling rate and re-establishing sinus rhythm
Symptoms of Atrial Fibrillation Usually dependent on ventricular rate Can hear and feel irregular pulse Take an apical-radial pulse for a full minute to determine rate Monitor shows an irregular-irregularity No discernible P-waves QRS complexes are narrow
Atrial fibrillation Disorganized impulses from multiple atrial foci No atrial contractions, atrial kick is lost Irregular ventricular response Favors formation of multiple thrombi
Drugs for A-fib Heparin or Enoxaprin, Dofetilide, Ca Channel blockers, Digoxin, Quinidine Cardioversion, Ablation
Co-morbidities with AF AMI Mitral stenosis Atrial-septal defect CHF Cardiomyopathy Post-surgery CABG Hyperthyroidism Pulmonary emboli WPW syndrome Congenital heart disease Chronic obstructive pericarditis
Bradycardia A pulse rate of less than 60 bpm How is the patient tolerating the rhythm? Are there medications causing the rhythm? Is there an underlying medical condition causing the rhythm?
Causes of Bradycardia Athlete’s normal rate Excessive vagal stimulation Hypoxia Inferior MI Beta-adrenergic blockers Calcium channel blockers Digitalis
Hemodynamics of Bradycardia Myocardial oxygen demand is reduced Coronary perfusion time is adequate because of prolonged diastole If the rate is too slow, cardiac output and blood pressure may drop and this will decrease coronary perfusion causing symptoms
Symptoms of bradycardis Dizziness, syncope Weakness Confusion Hypotension Dyspnea Ventricular ectopy Angina
Interventions for bradycardia Treat only if symptomatic Atropine 0.5 mg – 1.0 mg IV push, end point is 0.04mg/kg Treat hypotension with fluid replacement or vasopressors Withhold medications that cause bradycardia Pacemaker
Cardiac Risk Factors Age Heredity Gender Smoking Obesity Sedentary Stress Dietary habits Diabetes Hypertension Hyperlipidemia
Changes Associated With Aging… Decreased vessel elasticity Increased calcification of vessels Impaired valve function Decreased muscle tone (including the heart Decreased baroceptor response to blood pressure changes Decreased conduction ability of the heart
Smoking The major risk factor in CAD and PVD Tar, nicotine and carbon monoxide 4 cigarettes/day = 2X the risk 20 cigarettes/day = 4X the risk
Dietary Habits Too much of a good thing High fat High sodium Big portions Low fiber
Obesity Linked to a sedentary life style and poor diet Contributes to diabetes, hyperlipidemia and hypertension
Serum Lipids Elevated serum lipids indicate risk for coronary artery disease Total lipids: 400-1000 mg/dL Cholesterol: 122-200 mg/dL Triglycerides: 35-160 mg/dL HDL: 45-60, good for you LDL: 60-180, bad for you
Physical Inactivity Regular exercise promotes cardiovascular fitness 30 minutes/day is recommended
Poor Disease Control Diabetes – Prolonged hyperglycemia damages vascular system Hypertension- Poorly controlled hypertension causes increased strain on the heart and blood vessels Hyperlipidemia- Promotes the formation of plaque on the vessels and leads to atherosclerosis

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