Chapter 19 - Heart Flashcards by Kristen Beatty

Layers of Heart

Fibrous Pericardium, Parietal Serous Pericardium, Pericardial Cavity, Visceral Serous Pericardium (Epicardium), Myocardium, Endocardium, Heart Chamber

How well did you know this?

Not at all

Perfectly

Pericarditis

Inflammation of the pericardium

How well did you know this?

Not at all

Perfectly

Myocardium

Thick muscle layer around heart surrounded by Epicardium and Endocardium

How well did you know this?

Not at all

Perfectly

Atria

receiving chambers, small thin walls, contribute little to propulsion of blood

How well did you know this?

Not at all

Perfectly

Ventricles

most of volume of heart, thicker walls, actual pumps, especially the left

How well did you know this?

Not at all

Perfectly

Functions of heart valves

unidirectional blood flow, open and close in response to pressure, 2 Atrioventricular Valves (Mitral -L and Tricuspid -R)and 2 Semilunar valves (aortic - L and Pulmonary - R)

How well did you know this?

Not at all

Perfectly

Valve Open vs Closed

Open = Slack, relaxed; Closed = Taut, Contracted

How well did you know this?

Not at all

Perfectly

Pulmonary Circuit

Right side = receives O2 poor blood from tissues and pumps to lungs to exchange CO2 for O2

How well did you know this?

Not at all

Perfectly

Systemic Circuit

Left Side = Receives O2 rich blood from lungs and pumps to body tissues

How well did you know this?

Not at all

Perfectly

Valve Problems

Incompetent Valve = Heart re-pumps same blood over and over; Valvular Stenosis = Stiff Flaps

How well did you know this?

Not at all

Perfectly

Route of blood

Blood enters right atrium via tricuspid AV valve Right ventricle contracts forcing the opening of pulmonary semilunar valve and into pulmonary trunk, sent to lungs. Gets rid of Co2 and pick up 02. Back from lungs and into left atrium via pulmonary veins. Fills Atrium, mitral valve opens and blood fills left ventricle, mitral valve closes into left ventricle. Then through the aortic semilunar valve and into the aorta, aorta delivers 02 rich blood to tissues of body.

How well did you know this?

Not at all

Perfectly

Circuit Differences

Pulmonary = low pressure, short and slow; Systemic = High pressure, long and strong

How well did you know this?

Not at all

Perfectly

Ventricle Differences

Left side is 3x stronger than right

How well did you know this?

Not at all

Perfectly

Angina Pectoris

Thoracic pain caused by fleeting deficiency in blood delivery to myocardium, cells weakened

How well did you know this?

Not at all

Perfectly

Myocardial Infarction

Heart Attack, coronary blockages, areas of cell death repaired with scar tissue

How well did you know this?

Not at all

Perfectly

Describe Cardiac Muscle

Striated, short branched, interconnected by intercalated discs containing desmosomes and gap junctions, 1 nuclei, many mitochondria,

How well did you know this?

Not at all

Perfectly

2 intercellular junctions

Desmosomes - prevent cells from separating; Gap Junctions - allow pass through of ions and allow coordinated movement of single unit

How well did you know this?

Not at all

Perfectly

Cardiac Veins

Collect blood from Capillary veins and ensure myocytes get oxygen as well

How well did you know this?

Not at all

Perfectly

Cardiac Muscle Contraction

Don’t need nervous system stimulation, automatically, all cardiomyocytes contract as one unit, intercalated discs connected by desmosomes, many mitochondria for aerobic respiration

How well did you know this?

Not at all

Perfectly

Autorhythmic Cells

Have unstable resting membrane potentials, pacemaker potentials, due to slow opening of Na+ channels ( Continuously depolarized)

How well did you know this?

Not at all

Perfectly

Events of Cardiac Conduction

Sinoatrial (SA) node (pacemaker) generates impulse. 2. The impulse pauses (.1sec) at the atrioventricular (AV) node 3. The AV Node connects to the AV bundle connects the atria to ventricle 4. The bundle branches conduct the impulses through the interventricular septum 5. The Subendocardial conducting network depolarized the contractile cells of both ventricles.

How well did you know this?

Not at all

Perfectly

Arrhythmias

Irregular heart rhythms, uncoordinated atrial and ventricular contractions (defective nodes)

How well did you know this?

Not at all

Perfectly

Fibrillation

rapid, irregular contractions; useless for pumping blood, brain death, defibrillation to treat

Defective SA Node

Ectopic focus: abnormal pacemaker; AV node may take over

Defective AV node

Few or no impulses reach ventricles, so heart beats too slow for life - need artificial pacemaker

P Wave

Atrial depolarization initiated by SA Node

With Atrial depolarization complete, short delay

Ventricular depolarization begins at Apex, causing the QRS complex

Atrial repolarization

Stall after ventricular depolarization is complete

Repolarization of ventricle begin at Apex creates T wave

P-R Interval

Beginning of atrial excitation to beginning of ventricular excitation

S-T Segment

Entire ventricular myocardium depolarization

Q-T Interval

Beginning of ventricular depolarization to ventricular repolarization

Lub Dub Sound

Valve closures; First: Bicuspid & Tricuspid, Second: Semilunar Valves, Pause: The filling of blood

Heart Murmurs

Inefficiencies in the valves

Systole

Contraction during cardiac cycle

Diastole

Relaxation during cardiac cycle

Cardiac Cycle

Ventricular Filling: AV valves are open, pressure low; 80% of blood passively flows into ventricles, atrial systole delivers remaining 20%. Ventricular Systole: Ventricles contract, rising ventricular pressure, closing AV Valves, Ejection phase - vent pressure exceeds pressure in large arteries so SL Valve opens. Isovolumetric Relaxation: Ventricules relax, atria relax and filled, backflow of blood in aorta and pulmonary trunk closes SL valves.

Calculation of Cardiac Output

CO = Heart Rate (BPM) x Stroke Volume ( volume of blood pumped out by 1 ventricle with each beat)

Calculation of Stroke Volume

SV = End Diastolic Volume x End Systolic Volume

3 factors to effect Stroke Volume

Preload, Contractibility, Afterload

Preload

Frank-Starling Law of Heart - degree of stretch of cardiac muscle cells before they contract, length-tension relationships. Most important factor in stretch is venous return

Contractibility

Contractile strength of given muscle length, independent of muscle stretch and EDV; increased by sympathetic and Ca2+ influx

Afterload

Pressure ventricles must overcome to eject blood, hypertension increases afterload, resulting in increased ESV and reduced SV

Atrial (Bainbridge) Reflex

Sympathetic reflex initiated by increased venous return and increased atrial filling, stretch receptors stimulates SA Node

Tachycardia

Abnormally fast heart rate, may lead to fibrillation - \> 100 beat/min

Bradycardia

Heart rate slower than 60 beats/min; inadequate blood circulation but can also be due to endurance training

Congestive heart failure

progressive condition; CO2 low, circulation inadequate, weakened myocardium caused by atherosclerosis, high BP, myocardial infarction

Fetal Heart Structures

Foramen Ovale connects 2 atria, Arteriosus connects pulmonary trunk to aorta

Age related Changes to Heart

Sclerosis - thickening of flaps; Decline in cardiac reserve; Fibrosis of cardiac muscle; Atherosclerosis

End Diastolic Volume

Volume of blood in ventricles at end of ventricular diastole

End Systolic Volume

Blood in ventricles after systole

Dicrotic Notch

Brief rise in aortic pressure as blood rebounds off close valve.

Cardiac Output (image)