Pathophysiology Flashcards

1
Q

Where is the heart located?

A

In the mediastinum between second rib and fifth intercostal space two-thirds to the left of the midsternal line

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2
Q

What is the function of the superficial fibrous pericardium?

A

Protects, anchors, and prevents overfilling

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3
Q

What are the layers of the serous pericardium?

A

Parietal layer lines the internal surface of the fibrous pericardium. Visceral layer (epicardium) on external surface of the heart. Separated by fluid-filled pericardial cavity

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4
Q

What is the function of the myocardium?

A

Anchors cardiac muscle fibers . Supports great vessels and valves. Limits spread of action potentials to specific paths

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5
Q

What is the coronary sulcus?

A

atrioventricular groove that encircles the junction of the atria and ventricles

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6
Q

What marks the position of the interventricular septum externally?

A

the anterior and posterior interventricular sulci

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7
Q

What vessels enter the right and left atriums?

A

R. atruim- superior vena cava, inferior vena cava, coronary sinus. L. atrium- right/left pulmonary veins

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8
Q

What lines the walls of the atria and ventricles?

A

pectinate muscles line atria and trabeculae carneae line ventricles.

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9
Q

What is the pathway of blood through the heart?

A

Right atrium–>tricuspid valve–>right ventricle–> pulmonary semilunar valve–>pulmonary trunk–> pulmonary arteries–> Lungs–>pulmonary veins  left atrium–>bicuspid valve–>left ventricle–>aortic valve–>aorta–>systemic circulation

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10
Q

Describe the characteristics of the coronary circulation

A

provides the functional blood supply to the heart muscle itself. Arterial supply varies considerably and contains many anastomoses. Has collateral routes

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11
Q

Name the arteries and veins of coronary circulation

A

arteries: Right and left coronary (in atrioventricular groove), marginal, circumflex, and LAD. veins: Small cardiac, anterior cardiac, and great cardiac veins

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12
Q

What is angina pectoris?

A

Thoracic pain caused by brief deficiency in blood delivery to the myocardium. Cells are weakened

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13
Q

What is a myocardial infarction?

A

Prolonged coronary blockage. Areas of cell death are repaired with noncontractile scar tissue

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14
Q

What anchors AV valve cusps to papillary muscles?

A

chordae tendineae

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15
Q

What is the intrinsic cardiac conduction system?

A

A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart

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16
Q

What is responsible for the pacemaking potential of autoarrhythmic cells?

A

opening of Na+ channels and closing of K+

channels that causes a slow depolarization of the membrane

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17
Q

When does depolarization occur?

A

when the pacemaker potential reaches threshold due to Ca+ influx

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18
Q

What is responsible for repolarization?

A

Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage

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19
Q

Describe the sinoatrial node as a pacemaker

A

Generates impulses about 75 times/minute (sinus rhythm). Depolarizes faster than any other part of the myocardium

20
Q

Describe the atrioventricular node as a pacemaker

A

Smaller diameter fibers; fewer gap junctions. Delays impulses approximately 0.1 second. Depolarizes 50 times per minute in absence of SAnode input

21
Q

What is the only electrical connection between the atria and ventricles?

A

Atrioventricular (AV) bundle (bundle of His)

22
Q

Describe the Purkinje system

A

Fibers lead from A-V node through A-V bundle into ventricles. Fast conduction; many gap junctions at intercalated disks

23
Q

Describe the AV bundle and Purkinje fibers as pacemakers

A

depolarize only 30times per minute in absence of AV node input

24
Q

What can happen as a result of a defective SA node?

A

Ectopic focus: abnormal pacemaker takes over. If AV node takes over, there will be a junctional rhythm (40–60 bpm)

25
Q

What can happen as a result of a defective AV node?

A

Partial or total heart block. Few or no impulses from SA node reach the ventricles

26
Q

How is heart rate modified by the ANS?

A

Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons. Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves

27
Q

Describe the first heart sound

A

lubb. occurs during ventricular systole and is the AV valves closing

28
Q

Describe the second heart sound

A

dupp. occurs during ventricular diastole and is the

pulmonary and aortic semilunar valves closing

29
Q

What occurs during the ventricular filling phase of the cardiac cycle?

A

takes place in mid-to-late diastole. AV valves are open and blood passively flows into ventricles. Atrial systole occurs, delivering the remaining blood.

30
Q

What is the end diastolic volume?

A

volume of blood in each ventricle at the end of ventricular diastole

31
Q

What occurs during the ventricular systole phase of the cardiac cycle?

A

Atria relax and ventricles begin to contract. Rising ventricular pressure closes AV valves. Isovolumetric contraction phase (all valves are closed). In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open

32
Q

What is the end systolic volume?

A

volume of blood remaining in each ventricle

33
Q

What occurs during the isovolumetric relaxation phase of the cardiac cycle?

A

takes place in early diastole. Ventricles relax. Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure)

34
Q

What is the difference between cardiac output and stroke volume?

A

CO is the volume of blood pumped by each ventricle in one minute whereas SV is the volume of blood pumped by a ventricle with each beat

35
Q

What is the cardiac reserve?

A

difference between resting and maximal CO

36
Q

What are the three main factors that affect SV?

A

preload, contractility, afterload

37
Q

What is preload?

A

degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart). Increased preload increases SV

38
Q

What is contractility?

A

contractile strength at a given muscle length, independent of muscle stretch and EDV. Increasing contractility shifts the isovolemic pressure-volume relationship leftward (decreasing ESV) increasing SV

39
Q

What are positive inotropic agents that increase contractility?

A

Increased Ca2+ influx due to sympathetic stimulation. Hormones (thyroxine, glucagon, and epinephrine)

40
Q

What are negative inotropic agents that decrease contractility?

A

acidosis, increased extracellular K+, calcium channel blockers

41
Q

What is afterload?

A

pressure that must be overcome for ventricles to eject blood. HTN increases afterload, resulting in increased ESV and reduced SV.

42
Q

What factors regulate heart rate?

A

Positive chronotropic factors increase heart rate. Negative chronotropic factors decrease heart rate

43
Q

Describe sympathetic effects on heart rate

A

Releases norepinephrine at sympathetic ending which causes increased sinus node discharge. increases pacemaker rate by decreasing K+ perm and increasing slow inward Ca++ and Na+

44
Q

How does the parasympathetic nervous system oppose sympathetic effects?

A

Parasympathetic (vagal) nerves release acetylcholine. Causes hyperpolarization because of increased K+ permeability in response to acetylcholine.

45
Q

What is the atrial (Bainbridge) reflex?

A

sympathetic reflex initiated by increased venous return. Stretch of the atrial walls stimulates the SAnode and atrial stretch receptors activating sympathetic reflexes

46
Q

How does tachycardia decrease CO?

A

there is not enough time for heart to fill during diastole resulting in a decreased end diastolic volume