*** A&p Ch. 20 Heart

Front 1

What is the cardiac cycle?

What is systole, diastole and MAP?

Back 1

The cardiac cycle: represents series of pressure and blood volume changes. Blood flow through heart during one complete heart beat; atrial systole & diastole followed by ventricular systole & diastole. Systole: period of heart contraction Diastole: period of heart relaxation MAP: mean arterial pressure; average pressure in patients arteries during 1 cardiac cycle.

Front 2

List in order and describe what is happening in each part of the cardiac cycle

Back 2

1. Atrial systole: VENTRICULAR FILLING: the atria contract, increasing atrial pressure & completing ventricular filling while the ventricles are relaxed. 2. Ventricular systole: ISOVOLUMETRIC CONTRACTION PHASE: the atria are relaxed, & blood flows into them from the veins. Ventricular contraction causes ventricular pressure to increase & causes the AV valves to close, which is the beginning of ventricular systole. The semilunar valves were closed in the previous diastole & remain closed during this period. 3. Ventricular systole: EJECTION PHASE: continued ventricular contraction causes a greater increase in ventricular pressure, which pushes blood out of the ventricles, causing the semilunar valves to open. 4. Ventricular diastole: ISOVOLUMETRIC RELAXATION: as the ventricles begin to relax at the beginning of ventricular diastole, blood flowing back from the aorta and pulmonary trunk toward the relaxing ventricles cause the semilunar valves to close. Note that the AV valves are closed also. 5. Ventricular diastole: PASSIVE VENTRICULAR FILLING: as ventricular relaxation continues, the AV valves open, & blood flows from the atria into the relaxing ventricles, accounting for most of the ventricular filling.

Front 3

Describe the 3 phases of the cardiac cycle.

Back 3

Phase 1: VENTRICULAR FILLING: mid to late diastole. Occurs by: rapid ventricular filling & atrial systole (atria contract). During diastole, ventricles expand (AV valves open & blood flows into ventricles). Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SV valves closed). Attial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle.

EDV: volume of blood in each ventricle at end of ventricular diastole. Depolarization spreads to ventricles (QRS wave). Atria finish contracting & return to diastole while ventricles begin systole.

Phase 2: VENTRICULAR SYSTOLE: atria relax; ventricles begin to contract, rising ventricular pressure causes closing of AV valves. Pressure in aorta is around 80 mmHg. ESV.

Two phases;

2a. ISOVOLUMETRIC CONTRACTION PHASE: all valves are closed, "isovolumetric" because even though ventricles contract, they do not eject blood. (Because pressure in the aorta (80mmHg) & in pulmonary trunk (10mmHg) is still greater than in the ventricles). Cardiocytes exert force, but w/ all 4 valves closed, the blood can't go anywhere. Atria repolarize & relax, ventricles depolarize, create the QRS complex & begin to contract. *** LUBB occurs at the beginning of the phase.

2b: EJECTION PHASE: ventricular pressure (ejection of blood) exceeds pressure in large arteries, forcing SL valves open. Blood spurts out of each ventricle rapidly at first. T wave occurs late in this phase. SV of about 70ml of blood is ejected of the 130ml in each ventricle. (EF of about 54%, as high as 90% in vigorous excercise). ESV= the 60ml of blood left behind.

Phase 3: ISOVOLUMETRIC RELAXATION: early diastole. "Isovolumetric" because SL valves are closed & AV valves have not yet opened. (Ventricles therefore taking no blood). Following ventricular repolarization (T wave), ventricles are relaxed; atria are relaxed & filling. Backflow of blood in aorta & pulm. trunk closes SL valves (causes dicrotic notch- brief rise in aortic pressure as blood rebounds off closes valve). Ventricles are totally closed chambers (isovolumetric). When atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again. Early ventricular diastole; when T wave ends & ventricles begin to expand. DUPP occurs as blood rebounds from the closed SL valves & the ventricle expands.

*all events in the cardiac cycle are completed in less than 1 second!

Front 4

Describe heart sounds and their causes

Back 4

- The first heart sound LUBB occurs with closure of AV valves (bicuspid & tricuspid).

- The second heart sound DUPP occurs with closure of SL valves (pulmonary & aortic).

- A faint third heart sound can be heard in some normal people (thin & young) caused by blood flowing in a turbulent fashion into the ventricles.

Heart murmurs: abnormal heart sounds heard when blood hits obstructions, usually indicate valve problems.

Incompetent valve: causes a swishing sound. Valve fails to close completely, allowing back flow of blood.

Stenotic valve/aortic stenosis: causes high pitched sound or clicking. Narrowing of valve in the aorta. Valve fails to open completely, restricting blood flow through the valve.

Valve sounds:

AORTIC VALVE: sounds heard in 2nd intercostal space at right sternal margin.

PULMONARY VALVE: sounds heard in 2nd intercostal space at left sternal margin.

BICUSPID/MITRAL VALVE: sounds heard over heart apex (in 5th intercostal space)

TRICUSPID VALVE: sounds heard at right sternal margin of 5th intercostal space.

Front 5

Define cardiac output, stroke volume, heart rate and pulse

Back 5

Cardiac output (CO): is the volume of blood pumped by each ventricle in one minute.

Equation for CO= HR × SV

- Normal at rest= 5.25L/min

- Max. CO is 4-5x CO in non athletic people (20-25L/min).

- Max. CO may reach 35L/min is trained athletes

Stroke volume (SV): is the volume of blood pumped out by one ventricle with each beat (ml/beat), correlates with force of contraction.

Equation for SV= EDV - ESV

70ml/beat = EDV (120ml) - ESV (50ml)

- if SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR & contractility.

Heart rate (HR): number of beats per minute. (75 beats/min)

Pulse: the surge of pressure produced by each heart beat, which can be felt by palpating a superficial artery with the fingertips.

Front 6

What is cardiac reserve?

Back 6

Cardiac reserve: is the difference between resting and maximal CO

Front 7

What is EDV and ESV?

Back 7

EDV = end diastolic volume: volume of blood in each ventricle at end of ventricular diastole (~120ml/beat). Affected by length of ventricular diastole & venous pressure.

ESV = end systolic volume: volume of blood remaining in each ventricle after systole (~50ml/beat). Affected by arterial BP & force of ventricular contraction.

Front 8

What are the 3 main factors that affect SV?

Back 8

Preload, contractility and afterload.

Front 9

Define preload, afterload and venous return

Back 9

Preload: degree of stretch of cardiac muscle cells before they contract.

- at rest, cardiac muscle cells are shorter than optimal length = increased contractile force

Afterload: back pressure exerted by arterial blood (the BP in the aorta (80mmHg) & the pulm. trunk (10mmHg) immediately distal to the SL valves). Opposes the opening of these valves & limits SV.

* hypertension (high BP): increases afterload & opposes ventricular ejection. (Anything that impedes arterial circulation can also increase afterload. IE. Lung diseases that restrict pulmonary circulation)

Venous return: amount of blood returning to the heart. Slow heart rate & excercise increases venous return, then distends (stretches) ventricles & increases contractile force.

Front 10

Define contractility

Back 10

Contractility: contractile strength at given muscle length.

- independent of muscle stretch & EDV but decreased ESV.

INCREASED BY: sympathetic stim. to Ca2+ influx to more cross bridges & positive intropic agents (thyroxine, glucagon, epinephrine, digitalis, high extrac. Ca2+)

DECREASED BY: negative intropic agents (acidosis: excess of H+, increased extrac. K+, calcium channel blockers)

Front 11

What is the most important factor in stretching cardiac muscle?

Back 11

Venous return

Front 12

What is the Frank-Sterling Principle?

Back 12

The Frank-Sterling Principle/ Starling law of the heart describes the relationship between Preload & SV.

An increased preload causes the cardiac muscle cells to contract with a greater force & produce a greater SV.

increased venous return =

(high EDV) to (high SV) = high CO

Front 13

Compare and contrast the Intrinsic and Extrinsic controls of the heart, and describe ANS and hormonal control of heart rate

Back 13

Intrinsic & extrinsic regulatory mechanisms control cardiac output.

Intrinsic regulation: results from the hearts normal functional characteristics & does not depend on neural or hormonal regulation.

PRELOAD: extent to which ventricular walls are stretched.

AFTERLOAD: the pressure the contracting left ventricle must produce to overcome the pressure on the aorta & move blood into the aorta.

STARLING LAW OF THE HEART: the relationship between preload & the stroke volume of the heart. An increased preload causes the cardiac muscle cells to contract w/ a greater force & produce a greater SV.

Extrinsic regulation: (ANS-neural & hormonal control of the heart) neural regulation of the heart results from sympathetic & parasympathetic reflexes & the major hormonal regulation comes from epinephrine & NE. The heart is innervated by both sympathetic & parasympathetic nerve fibers which influence the pumping action of the heart by affecting both HR & SV.

* Parasympathetic control:

- Parasym. stim. is supplied by the Vagus nerve.

- Parasym. stim. decreases HR.

- Postganglionic neurons secrete ACh, which increases membrane permeability to K+, producing hyperpolarization of the membrane.

* Sympathetic control:

- Symp. stim. is supplied by the cardiac nerves. (Sympathetic nerve fibers originate in the thoracic region of the spinal cord as preganglionic neurons. These neurons synapse with postganglionic neurons of the inferior cervical & upper thoracic sympathetic chain ganglia, which project to the heart as cardiac nerves)

- Symp. stim. increases HR & force of contraction (SV).

- The postganglionic sympathetic nerve fibers innervate the SA & AV nodes, the coronary blood vessels, & the atrial & ventricular myocardia.

- Postganglionic neurons secrete NE, which increases membrane permeability to NA+ and Ca2+ and produces depolarization of the membrane.

- Baroreceptor & chemoreceptor reflexes: sensory neurons carry APs from sensory receptors to the medulla oblongata. Symp. & parasym. neurons exit the spinal cord or medulla oblongata & extend to the heart to regulate its function. Epinephrine & NE from the adrenal gland also help to regulate the hearts action (SA=sinoatrial).

Hormonal control: epinephrine & NE are released into the blood from the adrenal medulla as a result of the symp. stim. The effects of epinephrine & NE on the heart are long lasting, compared w/ those of neural stimulation. Epinephrine & NE increase the rate & force of heart contraction.

Front 14

Explain in more detail the extrinsic regulation, sympathetic & parasympathetic control of the heart and heart rate

Back 14

1. Sensory neurons carry APs from baroreceptos & carotid body chemoreceptors to the cardioregulatory center. Chemoreceptors in the medulla oblongata also influence the cardioregulatory center.

2. The cardioregulatory center controls the frequency of APs in the parasympathetic neurons extending to the heart through the Vagus nerves. The parasympathetic neurons decrease the HR.

3. The cardioregulatory center controls the frequency of APs in the sympathetic neurons. The sympathetic neurons extend through the cardiac nerves & increase the HR & SV.

4. The cardioregulatory center influences the frequency of APs in the sympathetic neurons extending to the adrenal medulla. The sympathetic neurons increase the secretion of epinephrine & some NE into the systemic circulation. Epinephrine & NE increase HR & SV.

Front 15

What are baroreceptors and chemoreceptors?

Back 15

Baroreceptors: are receptors sensitive to changes in pressure. Baroreceptor reflexes detect changes in BP, and lead to changes in HR & force of contraction. The cardioregulatory center has 2 parts: the cardioacceleratory center increases HR and the cardioinhibitory center decreases HR.

Chemoreceptors: a sensory cell or organ responsive to chemical stimuli. They monitor blood PH, carbon dioxide & oxygen levels. Chemoreceptor reflexes increase or decrease symp. stim. and increase or decrease parasym. stim. of the heart.

Front 16

Describe the mechanisms that function to control heart rate

Back 16

Blood pressure:

pressure:

Baroreceptor reflexes detect changes in BP, and lead to changes in HR & force of contraction.

The cardioregulatory center has 2 parts: the cardioacceleratory center increases HR and the cardioinhibitory center decreases HR.

Effects of PH, carbon dioxide & oxygen:- Chemoreceptors monitor blood PH, carbon dioxide & oxygen levels. Chemoreceptor reflexes increase or decrease symp. stim. and increase or decrease parasym. stim. of the heart.

Effect of extracellular ion concentration: an increase or decrease in extrac. K+ decreases HR. Increased extrac. Ca2+ increases force of contraction of the heart & decreases HR. Decreased Ca2+ levels produce the opposite effect (decreases force of contraction & increases HR).

Effects of body temperature: HR increases when body temp. increases & it decreases when body temp. decreases.

Front 17

What is endocarditis? What is pericarditis?

Back 17

Endocarditis: inflammation of the heart valve- an infection of the hearts inner lining, usually involving the hearts valves.

- usually occurs when germs from elsewhere in the body travel through the blood & attach to damaged areas of the heart. People with damaged or artificial valves are most at risk.

Pericarditis: a swelling & irritation of the pericardium. May be caused by a viral infection or heart attack, in many cases the cause is unknown.

Front 18

What are calcium channel blockers?

Back 18

Calcium channel blockers: aka calcium antagonists, relax blood vessels, increase supply of blood & O2 to the heart. Slow development of the pacemaker potential, thus reducing HR.

- Treat a variety of conditions such as high BP, migraines, and raynauds disease. Also used to treat various cardiac disorders, including tachycardia & certain arrhythmias.

Front 19

Define PVCs and VT, describe the clinical significance of them

Back 19

PVCs: (premature contraction of ventricle) extra heart beats that begin in one of your ventricles. Sometimes causing you to feel fluttering or skipped beat in your chest.

- caused by:

ectopic foci in ventricles, lack of sleep, too much caffeine, irritability, occasionally occurs with coronary thrombosis.

VT: (ventricular tachycardia) Ventricles beat very quickly, problem with hearts electrical impulses.

- caused by: often associated with damage to AV node or ventricular muscle.

Front 20

What is ectopic focus?

Back 20

Ectopic focus: an abnormal pacemaker (group of cells) that takes over pacing.

Front 21

What can occur if coronary flow is interrupted?

Back 21

1. Myocardial infarction

2. Angina pectoris

3. Coronary ischemia/myocardial ischemia

4. Necrosis

Front 22

Define myocardial infarction

Back 22

Myocardial infarction: sudden death of a patch of myocardium resulting from long term obstruction of coronary circulation

Front 23

Define angina pectoris myocardial infarction

Back 23

Angina pectoris myocardial infarction: Thoracic pain caused by felting deficiency in blood delivery to myocardium. Heavy pressure or squeezing pain in chest radiating into the left arm.

Front 24

Define coronary ischemia/myocardial ischemia

Back 24

Coronary ischemia/myocardial ischemia: an inadequate blood supply to an organ or part of the body, especially the heart muscles.

Front 25

Define necrosis

Back 25

Necrosis: the death of most or all the cells in an organ or tissue due to disease or failure of the blood supply.

Front 26

Describe congestive heart failure (CHF)

Back 26

Congestive heart failure (CHF): progressive condition due to a heart that is weakened.

- Results from the failure of either ventricle to eject blood effectively.

Ultimately weakens other side leading to decompensated, seriously weakened heart.

- Fluid accumulates in tissue.

Treatment: removal of fluid, drugs to reduce afterload & increase contractility.

Unbalanced ventricular output:

*** LEFT SIDED FAILURE RESULTS IN:

Fluid accumulation in pulmonary tissue.

Pulmonary congestion: blood backs up into the lungs causing pulmonary edema. (Shortness of breath or sense of suffocation)

*** RIGHT SIDED FAILURE RESULTS IN:

Fluid accumulation in systemic tissue.

Peripheral congestion: blood backs up in the vena cava causing systemic or generalized edema. (Enlargement of liver, ascites, distention of jugular veins, swelling of fingers, ankles and feet)

Front 27

Define tachycardia and bradycardia

Back 27

Tachycardia: abnormally fast heart rate. (>100 beats/min)

- loss of blood or damage to myocardium.

- caused by stress, anxiety, drugs, fever, heart disease.

- may lead to fibrillation.

Bradycardia: slow heart rate.

(<60 beats/min)

- caused/affected by sleep, low body temp., & endurance trained athletes.

Front 28

Define arrhythmias, fibrillation and defibrillation

Back 28

Defects in intrinsic conduction system may cause:

Arrhythmias: irregular heart rhythms, uncoordinated atrial & ventricular contractions.

Fibrillation: rapid, irregular contractions. Heart becomes useless for pumping blood, causing circulation to cease, may result in brain death.

Treatment: defibrillation:

Controlled electric shock to allow restoration of the normal rhythm. Interrupts chaotic twitching, giving heart a "clean slate" to start regular, normal depolarizations "reset to system".

Front 29

What is an angiogram?

Back 29

Angiogram: uses X-rays to take pictures of your blood vessels. Dye is used to make them visible on the X-ray.

Angio = blood vessels

Front 30

What is a heart block?

Back 30

Heart block: a disorder in the heart's rhythm due to a fault in the natural pacemaker. An abnormal heart rhythm where the heart beats too slowly (bradycardia ). In this condition, the electrical signals that tell the heart to contract are partially or totally blocked between the upper chambers (atria) and the lower chambers (ventricles).

SA node block: A sinoatrial block is a disorder in the normal rhythm of the heart, that is initiated in the sinoatrial node.

- caused by: ischemia, tissue damage due to infarction.

AV node block: 1st, 2nd, 3rd degree.

Atrioventricular block is a type of heart block in which the conduction between the atria and ventricles of the heart is impaired.

- causes by: Inflammation of AV bundle, excessive vagal stim., ischemia of AV nodal fibers or compression of AV bundle.