Lecture 14 Flashcards
Cardiac Function
Muscular pump; propels blood through the lungs to the tissues and transports nutrients, oxygen, carbon dioxide, hormones, and blood cells (immunity, hemostasis)
Location of heart
Within mediastinum; extends obliquely about 5 inches from second rib to fifth intercostal space; rests on the diaphragm; anterior to vertebral column and posterior to sternum
Pericardium
Double-walled fibrous sac, outer layer of tough connective tissue (mesothelial cells)
Epicardium (mesothelial)
Visceral layer of pericardium covering myocardium
Epicardium
Outer layer of connective tissue, coronary arteries
Myocardium
Middle layer, muscular, thickest layer, workhorse of the heart
Endocardium
Thin endothelial layer- Innermost layer, smooth membrane, covers heart valves - part of endocardium
Function of the layers of the heart wall
Form fibrous framework tissue which provide support and divides atria/ventricles so they can function independently
T/F: There is direct communication between right and left halves of the heart
False, no direct communication (divided by septum)
Atria function
Receive blood returning to the heart
Ventricle function
Pump blood away to lungs/aorta
Right half
Right atrium (RA) and right ventricle (RV), Pulmonary pump, circulates blood into the pulmonary artery, and lungs
Left half
Left atrium (LA) and left ventricle (LV), Systemic pump, circulates blood into the aorta, organs, and tissues
Systole
During contraction of Ventricles, no tension, blood flow forces closure
Diastole
During relaxation as ventricle refill, causes tension on valves through chordae, causing them to open
Atrioventricular (AV) valves (Lub)
Flap-like valves between atria and ventricles; prevent back flow of blood into atria when ventricles contract (4 valves keeping blood flow in one direction) attached and supported by chordae
Tricuspid valve (AV)
Three flexible flaps; directs blood flow from RA to RV, prevents backflow to RA when RV contracts
Bicuspid valve or mitral valve
Directs blood flow from LA to LV; prevents backflow to LA when LV contracts
Semilunar valves – dub (Aortic/Pulmonary)
Prevent backflow of blood into ventricles during diastole; Cup shaped – 3 cusps on both
Ventricular contraction
Coordinates valve functions – Closure of AV valves and opening of semilunar valves
Pulmonary valve
From RV to pulmonary trunk
Aortic valve
From LV to aorta
Coronary arteries
Main blood supply of the heart, Shortest circulation in the body
Aorta branches (aortic sinus)
Carry arterial blood to the heart when relaxed
Right coronary artery (RCA)
Supplies posterior wall and posterior part of interventricular septum with blood
Left coronary artery (LCA) and branches
Supplies anterior wall, anterior part of interventricular septum
Anastomoses
Connections that terminal branches of coronary arteries communicate through (compensatory mechanism if there is blockage of an artery)
Do heart muscles/cells proliferate?
No, they do not proliferate to replace damaged muscle fibers. Areas of cell death are repaired with noncontractile scar tissue
Heart conduction system
Electrical impulses through depolarization in the sinoatrial (SA) node in RA near the opening of the superior vena cava; intrinsic; does not depend on the nervous system
Sinoatrial (SA) node
Controls normal cardiac rhythm - “cardiac pacemaker” Initiates atrial contraction
Where does conduction system terminate
Perkinje fibers that activate heart muscle contraction
How does the autonomic NS influence the depolarization rate?
Sympathetic – increase, Parasympathetic - decrease
Cardiac cycle
Atrial systole → atrial diastole → ventricular systole → ventricular diastole
Cardiac output
Typically 5L/min pumped out by each ventricle
How many veins does blood enter each atrium from?
Blood enters RA via three veins, Superior vena cava (from body regions above diaphragm), Inferior vena cava (from body areas below diaphragm), Coronary sinus (collects blood that drains from myocardium), Blood enters LA via four pulmonary veins (Blood that is low in oxygen returns to the heart)
Pulmonary circulation
Oxygen-poor blood enters RA → RV through tricuspid valve → pulmonary artery → lungs
Systemic circulation
Freshly oxygenated blood leaves lungs through pulmonary veins → LA → LV through mitral valve → aorta → rest of the body
Blood Pressure
Blood flow in the arteries results from the force of ventricular contraction, Pressure is decreased due to elasticity of blood vessels
Systolic pressure
Pressure is highest when ventricles contract
Diastolic pressure
Pressure is lowest when ventricles relax
Atherosclerosis
Loss of elasticity of blood vessels which leads to increased BP
ECG
Measures electrical activity of heart; diagnostic tool
P wave
Atrial depolarization, atrial systole
QRS complex
Ventricular depolarization, ventricular systole
T wave
Ventricular diastole
PR interval
Time for depolarization to pass from atria to ventricles via AV bundle
Echocardiogram
Ultrasound imaging of heart and helps to Identify valve/chamber/blood flow abnormalities
Congenital Heart Disease cause
German measles (viral infections), Down syndrome, drugs, genetic factors, undetermined causes (Fetal bypass channels fail to close normally)
Ductus arteriosus (pulmonary artery-aorta)
Redirects blood from lungs
Foramen ovale
Maintains blood flow between RA to LA(one way valve) while heart is developing
Abnormalities/diseases obstructing blood flow in heart
Pulmonary stenosis, aortic stenosis, coarctation of the aorta
Abnormal formation of aorta and pulmonary artery or abnormal connection of vessels
Tetralogy of Fallot, transposition of great vessels
Patent ductus arteriosus
shunts blood from aorta into pulmonary artery
Atrial and ventricular septal defects
Usually cause by non-closure of foramen ovale
Pulmonary or aortic valve stenosis
Obstructed/narrowed valve
Tetralogy of Fallot
Ventricular septal defect
Myocarditis (what is it, its cause, and treatment)
Inflammation; injury and necrosis of individual muscle fibers
Cause: Viruses, parasites (Trichinella), fungi (Histoplasma), or hypersensitivity (acute rheumatic fever); abrupt onset; may lead to acute heart failure
Treatment: underlying cause, most time subsides without permanent damage
Cardiomyopathy
No evidence of inflammation, 2 types (Dilated cardiomyopathy and hypertrophic cardiomyopathy)
Dilated cardiomyopathy (what is it, cause, and treatment)
Enlargement of heart and dilatation of chambers; impaired ventricular action leads to chronic heart failure; cause uncertain
Treatment: None
Hypertrophic cardiomyopathy (what is it an treatment)
Hereditary, transmitted as a dominant trait, muscle fibers in disarray with marked hypertrophy of heart muscle; reduces the size of ventricles
Treatment: Genetic screening, use beta blockers to slow the heart, calcium channel blockers to reduce contractions, or surgical resection of blocking septum
Rheumatic Fever
Commonly encountered in children, A response to a bacterial infection; an immunologic reaction that develops weeks after the initial streptococcal infection (group A beta-hemolytic streptococcal)
Rheumatic heart disease
Scarring of heart valves following rheumatic inflammation; Causes inflammation in connective tissues throughout the body especially the mitral and aortic valves and joint tissues; eventually leads to heart failure
Rheumatic heart disease prevention
Treat beta strep infection promptly and Prophylactic penicillin throughout childhood and young adulthood to prevent strep infections and reduce the risk of recurrent rheumatic fever and further heart valve damage (Surgical removal and replacement of valve if severely damaged)
Aortic Stenosis (what is it, outcomes, prevention, and treatment)
Strain on heart valve which can lead to heart failure, Occur due to aging, coronary atherosclerosis
Prevention: Control risk factors (high cholesterol, diabetes, hypertension)
Treatment: Surgical repair/replacement
Valvular Heart Disease (What is it, diagnosis, and treatment)
Common, but only a few patients develop problems; One or both leaflets enlarge, stretch, and prolapse into LA during ventricular systole, clicking sound on systole followed by a faint systolic murmur, can cause chordae rupture
Diagnosis: echocardiogram
Treatment: surgical repair/replacement
Infective Endocarditis
Inflammation and causes severe symptoms of infection and valve destruction; affects normal heat valves; is Caused by organisms of low virulence (bacterial - Staphylococci) and is a complication of any valvular heart disease. Platelets and fibrin may deposit on abnormal or damaged valves then serve as sites for bacteria to implant or for thrombi to form
Who are at risk of infective endocarditis and how does it affect them?
Intravenous drug users; affect the tricuspid valve instead of mitral or aortic valves, Unsterile materials or contaminants (surgery) enter the right side of the heart, form large bacteria-laden growths on valves, can dislodge into pulmonary circulation and cause pulmonary infarct
Cardiac Arrhythmias
Disturbances in heart rate or rhythm (Artial and ventricular fibrillation)
Atrial fibrillation (AF)
Atria contract in irregular pattern: 400bpm- “quiver” versus normal contraction; Can also affect ventricular rate and Ventricles beat irregularly and fast (140-160), shortening diastole (pulse deficit due to inadequate ventricular filling), lack of P wave and variable QRS complex
Ventricular fibrillation (VF) + treatment
Ventricles unable to contract normally, incompatible with life- no blood circulation, Heart block which is usually caused by arteriosclerosis
Treatment: Pacemaker to stimulate ventricular contraction at a determined rate
Acute Coronary Syndrome
Sudden blockage of a coronary artery from a thrombus or atheromatous debris, hemorrhage, or arterial spasm - can trigger a heart attack (caused by sudden greatly increased myocardial oxygen requirements and arteriosclerosis of coronary arteries)
Cardiac arrest may result from:
Arrhythmia (abnormal heart rhythm) from myocardial ischemia which disrupts ventricular contraction and asystole is the ending of cardiac contractions
Stable angina
Temporary chest pain relieved by vasodilator (nitroglycerine) or rest
Unstable angina
Needs anticoagulation and antithrombotic drugs
Myocardial Ischemia
Heart attack, Caused by the inadequate blood supply to the heart muscle -precipitated by atherosclerosis, thrombosis
Myocardial Infarction: Location
Left ventricle and septum (Thicker walls require rich blood supply; work harder to pump blood into systemic circulation; rarely involves atria or right ventricle)
Clinical manifestations of Myocardial ischemia
Asymptomatic (free of symptoms), Angina pectoris (pain of the chest) bouts of oppressive chest pain that may radiate into neck or arms; caused by myocardial ischemia, Myocardial infarction: Actual necrosis of heart muscle, Cardiac arrest: Cessation of normal cardiac contractions
NSTEMI
Complete occlusion of minor coronary artery or partial occlusion of major; Results in partial thickness damage to cardiac muscle
STEMI
Complete occlusion of major coronary artery; Results in full thickness damage
Cocaine-Induced Arrhythmias and Infarcts
Prolongs and intensifies effects of sympathetic nervous system (increased HR, muscle irritability, peripheral vasoconstriction and coronary artery spasm (High BP)
Myocardial Infarction: Diagnosis
Medical history, Laboratory data
ECG, Cardiac imaging, Enzyme tests; enzymes leak out from necrotic cells after an infarct
- The larger the infarct, the longer for elevated levels to return to normal
What Enzymes are present after an MI
Troponin T and Troponin I (Appears in 3h, peaks in 24 hours, remains high for 10 to 14 days)
Myocardial Infarction: Treatment
Drug treatment (beta-blockers and nitro), Thrombolytic therapy (should not be used in stroke patients, hypertension, recent operation, or bleeding disorder), angioplasty (preferred method), bed rest, pacemaker, cardioverter-defibrillator, aspirin, control risk factors
Myocardial Infarction: Complications
Arrhythmia, heart failure, intracardiac thrombi, and pericarditis
Intracardiac thrombi
Mural thrombus forms on ventricular wall; bits of clot embolize into systemic circulation causing infarct in brain, kidneys, spleen
Pericarditis
Infarct extends to epicardial surface, leads to inflammation and fluid accumulation in pericardial sac; may cause chest pain
What does Aspirin do?
Interferes with platelet function by permanently inactivating thromboxane A2 that causes platelets to aggregate and start the clotting process, Reduces risk of cardiovascular disease and stroke, Increases risk of bleeding in the brain if person has stroke
Cardiac rupture
Blood leaks into pericardial sac from perforation in necrotic muscle, prevents ventricular filling, and rupture may occur in ventricular septum or papillary muscle
Papillary muscle dysfunction
Infarcted papillary muscle unable to control mitral valve leaflet, resulting in mitral valve prolapse and mitral insufficiency
Ventricular aneurysm
Late complication; outward bulging of healing infarct during ventricular systole; reduces left ventricular function and cardiac output; rather than being ejected, blood fills aneurysm sac
What are factors that affected survival of a MI?
Size of infarct, Age of patient, Complications, and Other diseases
Heart Failure
No longer able to pump adequate amount of blood, can develop slowly (chronic) or rapidly (acute)
Forward failure (Left)
Reduced blood flow to tissues → reduced renal blood flow → salt and water retention to increase blood volume and venous pressure → edema
Backward failure (Right)
Blood backups in veins drain to the heart → increased venous pressure, congestion, edema
Heart failure treatment
Diet/ lifestyle modification, Diuretic drugs (promotes excretion of excess salt), Cardiac/ Arrythmia Drugs, Angiotensin-converting enzyme (ACE) inhibitors, and pacemakers
