Anatomy Of The Heart Review PDF

REVIEWER (WEEK 1 - 5) WEEK 1 ANATOMY OF THE HEART Heart muscle, RV (lesser extent) ○ Circumflex coronary artery cone-shaped hollow muscular organ...

REVIEWER (WEEK 1 - 5) WEEK 1 ANATOMY OF THE HEART Heart muscle, RV (lesser extent) ○ Circumflex coronary artery cone-shaped hollow muscular organ – LA, lateral & posterior located in the mediastinum surfaces of LV, portion of between the lungs interventricular septum, SA Pumps about 60ml/beat or 5L/min node, AV node Pericardium – protective covering Right Coronary Artery of the heart ○ RA, RV, inferior portion of 3 layers of cardiac muscle tissue: LV Epicardium – outermost layer Myocardium – middle layer Endocardium – innermost layer 4 Chambers Right atrium (0-5 mmHg) ○ SVC, IVC, Coronary sinus Right Ventricle (25 mmHg) Left atrium Left ventricle Valves - AV valves Note: Branching pattern of the coronary - Semilunar valves arteries varies considerably among individuals Electrophysiologic Properties of the Heart Automaticity - initiate an impulse spontaneously & repetitively Excitability (depolarization) - respond to a stimulus Conductivity Coronary arteries - Transmit electrical impulses Left Coronary Artery Contractility ○ Left anterior descending – - Contract LV, Ventricular septum, Refractoriness chordae tendineae, papillary  - Inability to respond until – Carries cellular waste to the repolarization excretory organs – Allows lymphatic flow to drain tissue fluid back into the Conduction System of the Heart circulation – SA node (60-100 times/min) – Returns blood to the heart – AV node (40-60 beats/min) for recirculation – Bundle of His – R & L bundle branches CARDIOVASCULAR DRUGS ACE INHIBITORS - Reduce blood – Purkinje fibers (20-40 pressure and heart strain. (eg. beats/min) Captopril) PRIL BETA-BLOCKERS - slow heart Sequence of events during cardiac cycle rate, reduce blood pressure (eg. Atenolol) OLOL DIURETICS -removes excess fluid Systole (contraction) – emptying (eg. Furosemide) ANTICOAGULANT - prevent Diastole (relaxation) – filling clotting (eg. Warfarin) Mechanical Properties of the Heart DIAGNOSTIC TESTS Cardiac Output ELECTROCARDIOGRAPHY (ECG) HR - Graphically measures & records - ANS, ⭡ endogenous catecholamines the electrical current traveling - Parasympathetic NS (vagus nerve), through the conduction system beta blockers, Ca++-channel generated by the heart - Measured by electrodes placed on blockers the skin & connected to an SV amplifier & strip chart recorder Preload – volume of blood distending the In a standard 12-lead ECG: ventricles at the end of diastole just five electrodes attached to the before contraction arms, legs, & chest measures electrical current from Afterload – resistance that the 12 different views or leads ventricles must overcome to eject blood Bipolar limb leads Contractility ○ Lead I ○ Lead II Cardiac Output = HR x SV ○ Lead III Unipolar augmented leads Vascular System: FUNCTIONS ○ aVR – Provide conduits for blood to ○ aVL travel from the heart to ○ aVF nourish the various tissues of the body Unipolar precordial leads ○ V1 (4th ICS, right sternal  border) ○ V2 (4th ICS, left sternal border) ○ V3 (midway between V2 and V4) ○ V4 (5th ICS, anterior axillary line) ○ V5 (5th ICS, midaxillary line) Electrocardiographic Paper electrocardiogram (ECG) strip: each small block measures 1 mm in height P wave – represents atrial depolarization & width PR segment – represents the time required for the impulse to travel standard speed:25mm/sec through the AV node, where it is delayed, – 1 small block = 0.04 sec 1 large and through the Bundle of His, Bundle branches, & Purkinje fiber network, just block = 5 small blocks before ventricular depolarization – 1 large block = 0.20 sec 5 large PR interval – represents the time required for atrial depolarization as well blocks = 1 sec as impulse travel through the conduction – 15 large blocks = 3 sec 30 system and Purkinje fiber network, large blocks = 6 sec inclusive of the P wave and PR segment. It is measured from the beginning of the P wave to the end of the PR segment Echocardiography (0.12-0.20 sec) QRS complex – represents ventricular - uses ultrasound waves to assess depolarization and is measured from the cardiac structure & mobility, beginning of the Q (or R) wave to the end particularly at the valves of the S wave (0.04 - 0.10 sec) - ST segment – represents early Hemodynamic Monitoring ventricular repolarization T wave – represents ventricular - Use to assess the volume & repolarization pressure of blood in the heart & U wave – represents late ventricular vascular system by means of a repolarization surgically inserted catheter QT interval – represents the total time Stress Test required for ventricular depolarization - Assesses heart function under and repolarization and is measured from physical stress the beginning of the QRS complex to the end of the T wave ELECTROCARDIOGRAPHY (ECG)  PERICARDITIS Inflammation of the pericardium often causes sharp chest pain. Associated w/ the following: – Malignant neoplasms – Idiopathic cause – Infective organisms (bacteria, viruses, fungi) – Post-MI syndrome (Dressler’s syndrome) pericarditis, fever, pericardial & pleural effusion 1-12 weeks after MI) – Postpericardiotomy syndrome – Systemic connective tissue disease – Renal failure PATHOPHYSIO - Chronic pericardial inflammation causes fibrous thickening of the VARIOUS FORMS OF ECG pericardium Resting ECG “Chronic Constrictive Pericarditis” Ambulatory ECG | (Holter monitoring) – 24 hrs. rigid pericardium Exercise ECG (Stress test) | Disturbances in O2 Transport inadequate ventricular filling Mechanism | Infectious Disorders Heart Failure ○ Pericarditis, Myocarditis, Endocarditis, RHD Assessment: Coronary Artery Disease – PAIN radiating to the neck, ○ Atherosclerosis shoulder & back ○ Angina pectoris aggravated by ○ Myocardial infarction inspiration, coughing Congestive Heart Failure & swallowing Pulmonary edema worst in supine Arrhythmias  position (relieved by or more on expiration sitting up & leaning than on inspiration) forward) – ⭣ cardiac output - Pericardial friction rub (scratchy – Muffled heart high pitch sound) sounds - If w/ chronic constrictive – Circulatory collapse pericarditis: Signs of RSHF - Echocardiography, CT scan – Emergency care: reveals thickening of pericardium PERICARDIOCENTESIS - ⭡WBC count - It is a procedure to remove excess - Atrial fibrillation is also common fluid from the pericardium (sac around the heart). Interventions: HEART FAILURE - “Pump failure”, inadequacy of the – NSAIDs for PAIN heart to pump blood throughout – Corticosteroids the body – Antibiotics CONGESTIVE HEART FAILURE – Pericardial drainage – accumulation of blood & fluid – Radiation or chemotherapy if in organs & tissues due to caused by malignancy impaired circulation – Hemodialysis (uremic Types: pericarditis) – Left-sided heart failure – Assist to assume position of – Right-sided heart failure comfort Causes: – Pericardiectomy (chronic – Damage to muscular wall constrictive pericarditis) (M.I.), Cardiomyopathy, – Monitor for complications: Hypertension, CAD, Valvular pericardial effusion defects, Infections | CARDIAC TAMPONADE - Build-up of blood or other fluid in the pericardial sac that puts pressure on the heart, which may prevent it from pumping effectively. Findings: – Jugular distention – Paradoxical pulse (systolic BP 10mmHg  Assessment: Major/ Classic symptoms Polyarthritis – Swelling of several joints (knees, ankle, hips, shoulders) that is warm, red and painful Chorea (Sydenham’s chorea, St. Vitu’s dance) – Involuntary grimacing & inability to use skeletal INFECTIVE ENDOCARDITIS muscles in a coordinated - Infection of the inner surface of manner the heart valves or endocardium – Involvement of CNS usually due to bacteria. Subcutaneous nodules PATHOPHYSIO: – Sometimes marble-sized Antibodies are formed to destroy the nodules appear around the group A ß-hemolytic strep joints microorganism | Erythema marginatum Antibodies “mistakenly” cross-react – Red, spotty rashes on the against the proteins in the trunk that disappears rapidly connective tissue of the heart, leaving irregular circles on the joints, skin & nervous system skin | MURMUR GRADING PanCARDITIS (all layers) due to - Murmurs are created by turbulent inflammation, WBC migrate to flow of blood. endocardium causing accumulation of - Grades I - VI: From very faint inflammatory debris “vegetations” (GRADE I) to very loud palpable around the valve leaflets thrill (GRADE VI). GRADING SCALE GRADE I - very faint, may not be hard in all areas, not pathological GRADE II - faint but clear, usually harmless but easily audible GRADE III - moderately loud GRADE IV - easily audible, associated with thrill GRADE V - easily audible, associated with | a thrill, still heard with the stethoscope Fatty streak development only lightly on the chest (intimal layer) GRADE VI - audible without a | stethoscope, severe pathology Plaque (partial or complete FRICTION RUB occlusion of blood flow) - A harsh, grating sound that can be | heard in both systole and diastole Complications is called a friction rub. Calcifications Ulceration WEEK 2 Thrombosis Coronary Artery Disease ASSESSMENT: –Atherosclerosis BP (hypertension) –Angina pectoris Elevated cholesterol & –Myocardial infarction /MI triglycerides CORONARY ARTERY DISEASE Presence of abdominal obesity - Narrowing or blockage of coronary Elevated FBS arteries, usually due to Elevated homocysteine atherosclerosis – blocks the production of nitric ATHEROSCLEROSIS oxide on the endothelium making cell wall less elastic & – Is a specific type of permitting plaque to build up arteriosclerosis caused by – test results are interpreted formation of PLAQUE (chiefly as: optimal: less than 12 composed of cholesterol) w/c mol/L), borderline: 12 to 15 can restrict blood flow mol/L), and high risk: greater – Leading contributor to than 15 mol/L) coronary artery and ❖ B-complex vitamin rich diet cerebrovascular disease (folic acid) = ⭣homocysteine Arteriosclerosis The American Heart Association (AHA) - Thickening or hardening of the now suggest the term ACUTE arterial wall CORONARY SYNDROME to describe any Pathophysiology group of clinical symptoms compatible Etiology: unknown with acute myocardial ischemia Vascular damage (cause – Atherosclerosis 🡪 ischemia inflammation)  – Ischemia – insufficient blood Impaired glucose tolerance supply = ⭣ O2 Obesity Physical inactivity – insufficient blood supply = Stress ANGINA PECTORIS AND PATHOPHYSIO MYOCARDIAL INFARCTION ✔ Sudden coronary obstruction caused ANGINA PECTORIS by thrombus formation over a - “Chest pain” of cardiac origin ruptured or ulcerated plaque, the acute coronary syndrome results. - most common clinical manifestation of myocardial ✔ Thus, MI occurs as a result of ischemia sustained ischemia, causing irreversible cellular damage - the cause is insufficient coronary blood flow, resulting in a Unstable angina is associated with decreased oxygen supply when short-term occlusion, whereas MI results there is increased myocardial from significant or complete occlusion demand for oxygen in response to that lasts more than 1 hour. physical exertion or emotional stress - ‘the need for oxygen exceeds the supply’ MYOCARDIAL INFARCTION Etiology & Genetic Risk: PRIMARY FACTOR: Atherosclerosis Nonmodifiable risk factors and Modifiable risk factors Elevated serum cholesterol levels CIGARETTE SMOKING!!! Hypertension  Calcium Channel Blockers Thrombolytics/ Fibrinolytics WEEK 3 ANATOMY OF RESPIRATORY Transmural MI: involves the entire thickness of the myocardium Subendocardial MI: damage has not penetrated through the entire thickness DIAGNOSIS ECG- Changes occur first in the ST segment then the T wave and finally the Q wave. As the myocardium heals the ST and T waves return to normal but the Q wave changes persist. Interventions: Pain management: MONA Morphine 2- to 10-mg IV q 5-15 minutes AE: respiratory depression, hypotension, bradycardia, severe vomiting Antidote: Naloxone (Narcan) 0.2 – 0.8 mg IV Oxygen: 2-4L/min by nasal cannula Accumulation of secretions is the Nitroglycerin most common cause of airway Aspirin obstruction Positioning – semi Fowler’s Normal: 100 ml of mucous Provide a quiet & calm environment We clean our airway with secretions through coughing Medications: If you have patient that is Nitrates comatose, ○ -Nitroglycerine, Isosorbide you must have suction apparatus at dinitrate (Isordil), the bedside Isosorbide mononitrate We can also be obstructed by a (Imdur) foreign Beta Blockers body or (allergy) broncho laryngospasm Pleura – covering of the lung DISEASE (COPD) Parietal pleura – outermost layer - A group of chronic (obstructive) lung diseases cold that includes: Visceral pleura – inner layer EMPHYSEMA Pleural space/cavity – space between BRONCHITIS parietal and visceral pleura BRONCHIAL ASTHMA Intrapleural pressure – pressure in the BRONCHIECTASIS pleural cavity MOST IMPORTANT RISK FACTOR FOR 760 mmHg – atmospheric pressure at sea COPD: SMOKING level Effects of Tobacco Smoke: 755 mmHg – intrapleural pressure in the pleural cavity o Tobacco smoke triggers the Intrapulmonic/Intrapulmonary pressure – release of EXCESSIVE pressure inside the lung amounts of elastase protease Right lung – 3 lobes that breaks down elastin which is a major component of Left lung – 2 lobes alveoli Negative – below 760 mmHg o Impairs & inhibits the action Positive – above 760 mmHg Ventilation – of cilia movement of air in during inhalation and out during exhalation Diffusion – movement of gas from higher to lower ACTIVE smokers – 100% pressure PASSIVE smokers – 80% Mechanism of Inhalation/Inspiration - When the respiratory muscles Clinical Manifestations contract together with intercostal muscles, the diaphragm will go General appearance down, thorax will increase in size, RR of 40-50 breaths/min intrapleural pressure will Presence of “Barrel chest” decrease, lung will increase in size, Cyanosis, Clubbing of fingers and intrapulmonic pressure will Manifestations of RSHF(right decrease. sided heart failure) (dependent Mechanism of Exhalation/Expiration edema) Psychosocial assessment - The Diaphragm Will Group,thorax will decrease in size, intrapleural - Socialization may be reduced pressure will increase (755 to 757 when friends avoid the client with mmHg), lung will decrease in size, and intrapulmonic pressure will COPD because of annoying rise (760 to 763 mmHg). coughs, excessive sputum, or dyspnea Laboratory assessment CHRONIC OBSTRUCTIVE PULMONARY  - Abnormal ABG results (hypoxemia, hypercarbia), Sputum C/S, Hgb./Hct., serum electrolyte levels are examined because 🡣phosphate, K+, Ca & Mg++ ++ reduces muscle strength - CXR to rule out other chest diseases & to check the progress of clients with respiratory infections or chronic disease - Pulmonary Function Test (Vital capacity, Residual volume, Total lung capacity) Interventions: Mainstays of COPD management: Airway maintenance Monitoring Airway maintenance: Drug Therapy Controlled coughing O2 therapy - advise client to cough on Airway maintenance: arising on the morning, o Keep the client’s head, neck and before mealtimes, before chest in alignment bedtimes To cough effectively, the client o Assist the client to liquefy sits in a chair or on the side of a secretions and clear the airway of bed with feet placed firmly on the secretions floor. Instruct the client to turn the shoulders inward and to bend o Breathing Techniques the head slightly downward hugging a pillow against the stomach. The client then takes a few deep breaths. After the 3rd to 5th deep breath ( pursed-lip breathing), instruct the client to bend forward slowly while coughing two or three times from the same  breath o Respiratory Infections – due Chest physiotherapy & postural to 🡩 mucus & poor oxygenation drainage (most common: S. pneumoniae, Monitoring: H. influenzae, Moraxella catarrhalis) o Assess COPD client at least q2° ⮚ due to infection, COPD manifestations worsens O2 Therapy: due to increasing o The need for O2 therapy & its inflammation & mucus effectiveness can be production determined by ABG values & o Cardiac Dysrhythmias – O2 saturation by pulse results from 🡣O2 supply to oximetry the , other cardiac disease, o usually, 2-4 L/min or even 1-2 drug effects, or acidosis L/min via nasal cannula or up o Cor Pulmonale – RSHF caused to 40% via venturi mask by pulmonary disease o Low-flow O2 because low BRONCHITIS arterial oxygen level is the 🠶 Acute Bronchitis COPD client’s primary drive o Typically begins as an URTI for breathing (viruses, bacteria) ⮚ H. influenzae, S. Drug Therapy: pneumoniae, M. - involves the same inhaled and pneumoniae o Chemical irritants (noxious systemic drugs for asthma - fumes, gasses, air mucolytics [acetylcysteine contaminants) (Mucomyst), Guaifenesin] 🠶 Assessment Findings: o Fever, chills, malaise, PNEUMONIA - one of the most common headache, dry irritating complications of COPD nonproductive cough (initial) 🡪 mucopurulent sputum * Teach clients to avoid large crowds and 🠶 Medical Management: stress the importance of receiving a o Usually self-limiting pneumonia vaccination and a yearly o Bedrest, antipyretics, influenza vaccine “flu shot” expectorants, antitussives, ⭡fluids, humidifiers, COMPLICATIONS (COPD) antibiotics o Hypoxemia & acidosis – due Nursing Management to impaired exchange of Monitor breath sounds and gasses monitor VS q 4 hrs, especially with  fever. Forced Vital Capacity (FVC) – volume of Encourage coughing and deep air exhaled from full inhalation to full breathing q 2 hrs while awake. exhalation Provide humidification to loosen bronchial secretions. Peak Expiratory Rate Flow (PERF) – Change bedding and clothes if fastest airflow rate reached at any time damp. during exhalation Offer fluids frequently. Methacholine is inhaled (induces Prevent infection by washing hands bronchospasm) & then FVC, FEV1 & PERF frequently. is measured then bronchodilators will be Teach to cover the mouth when given 🡪 an ⭡ 12% of values: asthma sneezing & coughing. Discard soiled tissues in a plastic Chronic Bronchitis BRONCHOSCOPY - reveals increased size of bronchioles, atelectasis & changes Prolonged bronchial inflammation in the pulmonary tissues (insertion of a and cough. camera into the airways) Caused by cigarette smoking, bronchial asthma, RTI, and air Grading of chronic asthma pollution. Assessment findings: thick white 1. Intermittent Asthma mucus, yellow, purulent, copious, Symptoms: Less than twice a week. blood streaked sputum. Night-time awakenings: Less than Other symptoms include twice a month. bronchospasm, acute respiratory Use of short-acting beta-agonists infections, cyanosis, dyspnea on (e.g., albuterol): Less than twice a exertion, and RSHF. week. Medical Management Interference with normal activity: None. Smoking cessation: Lung function: Normal FEV1 (≥80% Bronchodilators, fluid intake, of predicted), normal FEV1/FVC balanced diet, postural drainage, ratio between episodes. steroid, antibiotic therapy. Nursing management: educating 2. Mild Persistent Asthma clients, monitoring air quality, avoiding cold air, wind exposure, Symptoms: More than twice a infection prevention, week, but not daily. immunizations, sputum monitoring, Night-time awakenings: 3-4 times proper use of MDIs. per month. Use of short-acting beta-agonists: FORCED EXPIRATORY VOLUME 1 - More than twice a week, but not volume of air blown out as hard and fast daily. as possible during the first second of the Interference with normal activity: most forceful exhalation after the Minor limitation. greatest full inhalation Lung function: FEV1 ≥80% of predicted, normal FEV1/FVC ratio. 3. Moderate Persistent Asthma (Atrovent) Symptoms: Daily. 🠶 Anti-inflammatory Agents: Night-time awakenings: More than once a week, but not nightly. Corticosteroids Use of short-acting beta-agonists: - oral – Prednisolone, Prednisone Daily use. Interference with normal activity: - inhaler – Budesonide, Fluticasone, Some limitations. Beclomethasone, Triamcinolone, Lung function: FEV1 60-80% of Flunisolide predicted, FEV1/FVC ratio reduced by 5%. 🠶 Mast cell stabilizer - Cromolyn sodium (Intal); helps 4. Severe Persistent Asthma prevent atopic asthma attacks (prevent mast cell membranes Symptoms: Throughout the day. from opening when an allergen Night-time awakenings: Often, binds to IgE) but are not useful typically every night. during an acute episode Use of short-acting beta-agonists: Several times per day. 🠶 Monoclonal antibodies Interference with normal activity: - Omalizumab (Xolair), approved in Extremely limited. 2003 only – binds to IgE receptor Lung function: FEV1