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Advanced Patho UC > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Phases of cardiac cycle

A

…see study guide

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2
Q

QT interval

A

electrical systole of the ventricles

-varies inversely w/HR; approximates time of ventricular contraction

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3
Q

ST interval

A

ventricular myocardium depolarized

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4
Q

P wave

A

atrial depolarization

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5
Q

PR interval

A

time from onset of atrial activation to the onset of ventricular activation

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6
Q

QRS

A

sum all of ventricular depolarization

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7
Q

right ventricle preload =

A

CVP central venous pressure - estimate of R atrial pressure

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8
Q

left ventricle preload =

A

pulmonary artery occlusion or wedge pressure - measures L atrial pressure

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9
Q

decreased afterload causes the heart to contract at what pace?

A

more rapidly

*think about decreased afterload causing increase in the amount of blood ejected (increase in CO) bc there is less resistance - so decreased vascular resistance causes an increase in cardiac output

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10
Q

increased afterload causes the heart to

A

slows contractions and increases heart workload - increase in vascular resistance = decreased CO

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11
Q

right ventricle afterload =

A

PVR (pulmonary vascular resistance)

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12
Q

left ventricle afterload =

A

SVR - systemic vascular resistance

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13
Q

frank starling law

More stretch means what?

A

related to the volume of blood at the end of diastole/preload and stretch placed on the ventricle

myocardial stretch determines the force of myocardial contraction

More stretch = increased force of contraction. Greater stretch during diastole = greater force of contraction = greater amount of blood pumped out

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14
Q

Laplace law

A

smaller champers and thicker chamber walls equal increased contraction force

*in ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force

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15
Q

negative inotropes and examples

A

acetylcholine (vagus nerve)

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16
Q

hypoxia _____ contractility

A

DECREASED

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17
Q

EF is what? what is it normally?

A

amounts of blood ejected per heartbeat by the ventricles

Stroke volume/end-diastolic volume

normally is 55% or higher

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18
Q

Decreased cardiac input caused by?

A

anything that causes decreased contractility or decreased blood flow to the heart

*increased vascular resistance, MI, shock, bradycardia, decreased SV, negative inotropes, cardiac tamponade, hypovolemia, valvular heart disease, HIGH PEEP

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19
Q

Poiseuille’s law

A

greater resistance, the lower the blood flow

  • think when vessel wall injured it constricts to prevent excess flow
  • question: if pt receives a medication that causes vasoconstriction the student knows that according to Poiseuille’s law, what will happen to blood flow? Blood flow will decrease
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20
Q

the semilunar valves are?

A

pulmonic and aortic

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21
Q

excess K+ does what to heart contractility?

A

decreases contractility

  • hyperpolarization occurs - cannot initiate AP
  • with hyperkalemia, it’s easier to initiate AP initially, however, w/myocytes initial increase in K+ increases excitability, but further rise of K+ has the opposite effect
  • think lethal injection
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22
Q

excess Ca++ causes what in the heart?

A

spastic contraction

*opposite of hypercalcemia in skeletal muscle which causes decreased neuromuscular excitability + muscle weakness

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23
Q

low ca++ causes what in the heart?

A

cardiac dilation

*calcium abnormalities are not as big of a concern – blood levels are more regulated

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24
Q

electrical pathway of the heart

A

SA node – internodal pathway – AV node – AV bundles – left and right bundles of Purkinje fibers

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25
Q

SA node - causes what? HR?

A

pacemaker of the heart - spontaneously depolarizes and impulse spreads rapidly from SA node along individual atrial muscle cells to depolarize the right and left atria

causes atrial contraction

60-100bpm

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26
Q

AV node - what does it do? HR beginning from here rate?

A

delays cardiac impulse – allows atria to empty blood into the ventricles before ventricular contraction

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27
Q

AV bundles transmission time…

A

transmission time b/w AV bundles and last of the ventricular fibers is the QRS time (0.06 sec)

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28
Q

Purkinje fibers bpm and where are they

A

from AV node through AB bundle into ventricles

fast conduction – large fibers transmit AP quickly – gap junctions enhance velocity

20-40 bpm

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29
Q

Norepinephrine what does it do? what receptors does it interact with?

A

vasoconstrictive by interacting with blood vessel alpha 1 receptors

Does not act on beta 2 receptors

30
Q

Epinephrine what does it do? what receptors does it work on?

A

vasoconstrictor (alphas 1) and vasodilator (beta 2)

beta 2 - vasodilation of bronchioles and skeletal muscle tissue

31
Q

Adrenergic (adrenaline - SNS) receptor function

A

Beta 1, beta 2, alpha 1

32
Q

beta 1 and b2 both do what? chronotrophy is what? inotropy?

A

increase HR (chronotrophy) and force of contraction (inotropy)

33
Q

beta 1 - activation leads to, which hormones act on these receptors?

A

normal heart

  • activation leads to increase in contractile force and HR
  • norepinephrine and epinephrine
  • renin release - aldosterone - vasoconstriction - increase in BP
34
Q

beta 2 - located where, and does what? which hormones act on?

A

vascular and non-vascular smooth muscle

-located on: smooth muscle, GI tract, bladder, skeletal muscle, arteries, bronchial tree, some coronary arteries (increased coronary blood flow)

  • epinephrine only
  • and activation leads to vascular and non-vascular smooth muscle relaxation

-vasodilation of bronchioles and skeletal muscle tissue

35
Q

alpha 1 - direct response. Does what and what hormones act on?

A

activity or muscle tone is increased

located on all vascular smooth muscle, GI and urinary sphincters, dilator muscle of the iris, arrestor pilli muscles in hair follicles (goosebumps)

norepinephrine and epi bind

norepinephrine binds with alpha 1 receptors causing smooth muscle contraction and vasoconstriction of the coronary arteries

36
Q

acetylcholine receptors

A

PSNS - muscarinic (slows HR, decreases contractility, bronchial constriction)

nicotinic (only involved in muscle contraction, neuromuscular junction)

37
Q

left circumflex artery

A

supplies left atrium and left ventricle

38
Q

left anterior descending artery

A

supplies the right ventricle, left ventricle, and interventricular septum

39
Q

left marginal artery

A

supplies the left ventricle

40
Q

right marginal artery

A

supplies the right ventricle and the apex

41
Q

right coronary artery

A

supplies the right atrium and the right ventricle

42
Q

troponin is the most specific marker and elevates in what amount of time?

A

2-4 hours

43
Q

zone of infection/necrosis ECG

A

wide QRS

44
Q

zone of injury ECG

A

ST elevation

45
Q

zone of ischemia ECG

A

inverted T wave

46
Q

Dresseler syndrome

A

post infarction syndrome - delayed form of acute pericarditis; r/t antigen/antibody complexes in response to necrotic myocardium

47
Q

Causes of pericarditis

A

viruses (coxsackie B, echovirus), bacteria, non-infectious: autoimmune, drugs, malignancy, radiation; post MI: Dressler syndrome

48
Q

s/s of pericarditis

A

pleuritic CP, better when the pt leans forward and worse with inspiration and lying down; fever, pericardial rub with auscultation

49
Q

Constrictive pericarditis (pericardium rigid and impairs filling of heart chambers) similar s/s to, and remember what sign?

A

heart failure

Kussmaul’s sign: increased JVP during inspiration - heart can’t stretch like it normally does during inspiration

50
Q

pericardial effusion can cause what + s/s of this? what is it?

A

accumulation of fluid in pericardial sac

  • can cause tamponade: severe restriction of cardiac motion
  • fatal if not resolved
  • s/s of tamponade are hypotension, increased JVP, distant heart sounds
51
Q

most common valvular abnormality

A

aortic stenosis

52
Q

aortic stenosis murmur?

A

systolic ejection murmur heard b/w s1 and s2 - crescendo-decrescendo murmur (softer s2)

53
Q

s/s of aortic stenosis

A

angina, syncope, faint pulses, heart failure, carotid upstroke (less force - weakened and delayed)

54
Q

causes of aortic stenosis

A

congenital bicuspid aortic valve, degeneration with aging, inflammatory damage caused by rheumatic heart disease; same risk factors as CAD

55
Q

mitral stenosis causes what to happen to the atrium? most common cause?

A

results in dilation of the atrium since blood has trouble getting into the ventricle - back of blood into the lungs. Untreated will cause pulmonary HTN, Right HF

most common cause is rheumatic fever

56
Q

mitral stenosis murmur

A

opening snap heard b/w s2 and s1 - increased atrial pressure on narrowed valve

57
Q

aortic regurgitation

A

inability of the aortic valve to close properly during diastole

58
Q

aortic regurgitation murmur & s/s

A

diastolic murmur b/w s2 and s1

s/s: widened pulse pressure as a result of increased stroke volume and diastolic back flow

59
Q

If a murmur is diastolic it will be heart b/w

A

s2 and s1

60
Q

mitral regurgitation - what is it and what does it cause?

A

permits backflow from the left ventricle into the left atrium - results in left ventricular hypertrophy because of increased volume in the left atrium entering the ventricle

61
Q

mitral regurgitation murmur

A

systolic murmur - presence of s3 (splashing sound)

62
Q

most common cause of mitral regurgitation

A

mitral valve prolapse and rheumatic heart disease

63
Q

mitral valve prolapse - what is it? what can it cause? affected valves at increased r/f? s/s?

A

anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole

can cause mitral valve regurgitation

affected valves at increased r/f infective endocarditis

s/s: asymptomatic

64
Q

rheumatic fever causes what kind of deposits? what is rheumatic fever

A

fibrinoid necrotic deposits: Aschoff bodies

RF is abnormal immune response to the M protein that cross react w/normal tissues

65
Q

s/s of rheumatic fever - causes what?

A

carditis - murmur; polyarthritis (large joints); chorea - sudden aimless irregular involuntary movements; erythema marginatum - truncal rash

can cause STENOSIS, and is the most common cause of this (especially mitral)

66
Q

Systolic heart failure results in a LVEF of what? what happens to ventricle?

A

LVEF <40% and ventricular remodeling/hypertrophy HFrEF

-also under left heart failure in the notes

67
Q

s/s and PE findings with LHF

A

dyspnea, orthopnea, cough w/froth, fatigue, decreased urine output, edema, paroxysmal nocturnal dyspnea

PE: pulmonary edema (cyanosis, inspiratory crackles, pleural effusion), HYPOTENSION OR HYPERTENSION, s3 gallop d/t fluid overload (slapping), evidence of underlying CAD or HTN

68
Q

Diastolic heart failure LVEF?

A

LVEF > 40% HFpEF

filling problem
also listed under left heart failure

  • pulmonary congestion despite normal stroke volume and cardiac output or ejection fraction
  • decreased compliance of left ventricle and abnormal diastolic relaxation which leads to increase in end diastolic pressure – transmitted to pulmonary circulation – causes pulmonary congestion
69
Q

Right heart failure seen with? normally due to?

A

seen with pulmonary disease = cor pulmonale

normally due to left-sided heart failure

70
Q

s/s of RHF?

A

pedal edema, ascites, hepatosplenomegaly, elevated JVP-JVD, sacral edema, nocturia, jaundice, coagulopathy

71
Q

classes of heart failure

A
  • Class I - no limitation of physical activity (PA)
  • Class II - slight and leads to fatigue, palpitation, dyspnea, or anginal pain but person is comfortable at rest
  • Class III - marked limitation of PA in which less-than-ordinary activity results in same s/s as II. Pt ok at rest.
  • Class IV - inability to carry out any PA w/o symptoms of HF or the anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken
72
Q

staging of HF

A

A - high risk for HF but without structural heart disease or symptoms of HF

B- structural heart disease but w/o s/s of HF (LVH, LV dysfunction)

C- structural heart disease w/current or past symptoms of heart failure

D- refractory heart failure requiring specialized interventions (pacemaker, LVAD, tranplant)

Advanced Patho UC (14 decks)

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