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Patho key terms 1-3 > Cardiac day 2 > Flashcards

Cardiac day 2 Flashcards

1
Q

What is cardiomyopathy

A

remodeling disease of the heart muscle

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2
Q

describe hypertrophic cardiomyopathy

A

Thickening of the muscle or tissue around the heart

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3
Q

Describe restrictive cardiomyopathy

A

stiffening in the left ventricle

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4
Q

describe dilated cardiomyopathy

A

muscle is thin in the left ventricle

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5
Q

Diagnosing cardiomyopathys

A

Echocardiogram

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6
Q

Cardiomyopathy (CM)

A

SOB, HEART VALVE ISSUES, chest pain, abnormal rhythms, and can lead to death and

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7
Q

what is acute pericarditis?

A
  • iNFLAMMATION of the pericardium.
    -with local vasodilation with increased capillary permeability.
    This causes leaking of plasma proteins and accumulation of WBCs in the pericardial space

eti- viruses, bacterial infection, MI, trauma, neoplasm most commonly VIRAL

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8
Q

acute pericarditis CM

A

chest pain (worse with deep breathing or coughing
-pericardial friction rub
-sinus positional change
-ECG Changes

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9
Q

Cardiac tamponade

A

Accumulation of fluid in the pericardial space
ETI- PERICARDIATIS
-FLUID OVERLOAD
-HF
-hypoproteinemia.
Complication: compression of the heart caused by the accumulation of fluid

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10
Q

what is beck triad and what cardiac effect is it in?

A

low blood pressure, distension of the jugular veins and decreased or muffled heart sounds upon cardiac auscultation. EMERGENCY

Found in cardiac tamponade.

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11
Q

stenosis

A

-narrowing of the valveopening so it wont open
-harder for blood to get through
-Leads to hypertrophy of muscle and increases cardiac workload, and decrease cardiac output

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12
Q

regurgitation

A

-permits backward flow of blood when the valve should be closed
-inability of leaflets to close

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13
Q

stenosis and regurgitation can cause

A

sob fatigue dizziness

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14
Q

aortic valve stenosis

A

blood backs up in left ventricle

Valve related outflow obstruction fo left ventricle.
-leads to an increase in left ventricular pressure and hypertrophy

-overtime cardiac output decreases

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15
Q

aortic valve regurgitation

A

BLOOD BACK UP: LEFT VENTRICLE

back flow resulting in volume overload in the left ventricle increase in end diastole.

-Allows heart to compensate and maintain SV/CO but eventually leads to HF

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16
Q

mitral valve stenosis

A

impaired flow from left atrium to left ventricle

BLOOD BACK UP: LEFT ATRIUM

DYSRYTHMIAS such as afib pulmonary HTN and edema

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17
Q

mitral valve regurgitation

A

BACK UP BLOOD: LEFT ATRIUM

  • backflow from left ventricle to left atrium during ventricular systole

-AFIB eventually increase pul pressure.

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18
Q

tricuspid valve regurgitation

A

Blood back up in the right atrium

Blood will backflow from the right ventricle into the right atrium

May be caused by dilation and failure of right ventricle

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19
Q

Fetal circulation at birth

A
  • newborn takes first deep breath and lungs expand

-The blood that was diverted into the ductus arterosis, now goes through the lungs for oxygen

Changes in pressure in the left atrium close the foramen ovale and ductus Arteriosus

-Foramen ovale closes quickly at birth
-ductus arteriosus takes 10-15 hrs to close fully.

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20
Q

Shunt

A

tube placed in the body to redirect blood flow.

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21
Q

Patent ductus arterosis

A

PDA fails to close, blood shunts from the aorta into the pulmonary artery and into the lungs
ETI- preterm infants, teratogen exposure, genetics
Complications- HF and respiratory distress.

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22
Q

Atrial Septal defect (ASD)

A

AN opening in the septum between the L and R atrium.
-Blood will shunt left to right increasing work load for the atrium
Complications- Atril fibrillation, pulmonary htn

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23
Q

Ventricular septal defect

A

opening between the ventricular septum.
you get a left to right shunt initially.
-However if big enough it move right to left.

ETI- incomplete separation during birth.
Clinical: murmurs,CHF

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24
Q

Tetralogy of fallot (TOF)

A

Patho- there is right to left shunting across the VSD
EPI- most common cyanotic congenital heart defect

CM: Cyanosis, irritable, TET SPELLS: hypoxia during times of stress or increase in work when crying or eating.

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25
Q

What are the four defects present in TOF?

A
  1. Pulmonary stenosis
  2. Ventricular septal
    defect
  3. overiding of aorta
  4. Right ventricle hypertrophy
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26
Q

circulatory shock

A

failure of CV system to perfuse organs & tissues
not enough oxygenate blood goes to the body.

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27
Q

obstructive shock

A

an obstruction of the flow of blood through great veins, heart or lungs
- causes are dissecting aortic aneurysm, cardiac tamponade, most common is PE (pulmonary embolism)

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27
Q

hypovolemic shock

A

Diminished blood volume cases.
-inadequate filling of vascular compartment causes can be hemorrhagic blood loss,
dehydration, burn survivors

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27
Q

Cardiogenic

A

wheen the heart fails to pump sufficiently. frequently seen with MI, dysrhythmias, and heart surgery

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28
Q

Types of disruptive shocks and what do they cause?

A

Cause:Massive dilation
anaphylactic shock
neurogenic shock
septic shock

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29
Q

Anaphylactic shock

A

Severe allergic reaction that cause vasodilation and increase capillary penetration.
-due to drug or food consumption

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30
Q

neurogenic shock

A

due to the loss of sympathetic nervous ssystem generally with a person after a spinal injury of t6 and above.

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31
Q

septic shock

A

severe infection activates the system inflammatory response w/ hypotension despite fluid resuscitation

32
Q

shock complications

A

Acute respiratory distress syndrome
acute renal failure
GI ischemia or poor GI motility due to redistribution of blood flow
DIC
Multiple organ failure

33
Q

How is HF classified

A

Stage, functional ability, and Left ventricular ejection fraction (LVEF)

34
Q

Left ventricular ejection fraction

A

% of blood that leaves the LV and pumped into the body w/ each contraction ( think percent of SV)

FORMULA
(end diastolic volume - end systolic volume/ end diastolic volume)

35
Q

Stages of HF

A

Stage A- at high risk for HF (no sx or structural change)
Stage B- Pre-HF (structural change but no sx)
Stage C- Symptomatic HF
Stage D- Advanced HF

36
Q

Classes of HF

A

1= no limitation
4= SEVERE limitations

37
Q

HFrEF

A

LVEF≤40

38
Q

HFimpEF

A

Previous LVEF ≤ 40% recent LVEF ≥40%

39
Q

HFmrEF

A

LVEF 41%-49%

40
Q

HFpEF

A

LVEF≥ 40%

41
Q

Left Heart Failure Pulmonary Pathogenesis

A

-increased LV pressure, which causes backup of blood/pressure in the left atrium.
-backup of blood continues to pulmonary veins
-increases pulmonary pressure, increased hydrostatic pressure and fluid filtration.
-results in pulmonary congestion/edema

42
Q

Left heart failure perfusion pathogens

A
  • decrease cerebral perfusion, fatigue and potential cognition issues
    -decreased renal perfusion
    -weak pulses hypotension
    -decreased muscle perfusion: decreased activity tolerance.
43
Q

Right heart failure etiology

A

left sided heart failure
-pulmonary hypertension
-COPD
-CAD RIGHT VENTRICLE MI
HEART VALVE DISEASE

44
Q

Right heart failure pathogenisis

A

Right ventricular dysfunction in either systolic or diastolic
-decreased in blood to the pulmonary circulation
-back up of blood into the right atrium
-right atrial and ventricular enlargement
-back up from overload right atrium into venous system circulation.
- hepatomegaly and splenomegaly
-ascites and peripheral edema
-GI tract congestion

45
Q

left sided failure manifestations

A

cyanotic
fatigue
dizziness
tachypnea
confusion
orthopnea
increase respiration rate

46
Q

Right sided HF

A

JVD
EDEMA
SPLEENGOMEGALY
HEPATOMEGALY
FATIGUE
SWELLING IN HANDS AND FINGERS

47
Q

PRELOAD

A

blood and pressure coming into the heart

48
Q

CONTRACTILITY

A

strength of heart contraction

49
Q

AFTERLOAD

A

pressure in systemic arterial circulation

50
Q

Frank Starling law

A

Frank-Starling Law - an increase in
ventricular filling enhances the systolic
performance of the heart and cardiac
output, up to a point then it begins to fallllllll

51
Q

Atrial Natriuretic peptide (ANP)

A

Produced by atrial stretch

52
Q

What does ANP and BNP promote

A

venous and atrial vasodilation

reduce preload and afterload

52
Q

B-TYPE Natriuretic peptide (BNP)

A

produced by ventricular stretch

53
Q

myocardial contractile cells

A

involved in contracting the heart make up 99% of heart

54
Q

myocardial conducting cells

A

used to conduct electrical current to the heart and notify the heart to contract

55
Q

What is the cardiac conducting system?

A
  1. (Sinoatrial)SA node
    -initiates cardiac action potential
    2.inter nodal pathways
    -conducting through atria
  2. Atrioventricular node(AV)
    -conduction from atria to septum
    4.Bundle of HIS
    -conduction through septum
    5.Bundle branches
    -conduction split to L and R ventricles
    6.perkinge fibers
    -conduction through ventricles
56
Q

Normal Electrical Flow

A
  1. Impulse generated at SA node pacemaker of the heart
  2. Impulse travels to the AV node
  3. AV node connects and passes impulse to the purkinje system which transmits the electrical activity of the ventricles to contract
  4. An ECG is a graphic recording of electrical activity
57
Q

qrs-wave

A

Ventricular contraction (depolarization)

58
Q

p-wave

A

atrial contraction (depolarization)

59
Q

T wave

A

ventricular repolarization

60
Q

Two causes of dysrhythmias

A

Impulse formation issues
impulse conduction issues

61
Q

Impulse formation issues

A

myocardial contraction and conduction cells generating inappropriate self -depolarization

62
Q

impulse conduction issues

A

problems with normal conduction

63
Q

Generation of dysrhythmias

A

hypoxia, electrolyte imbalances
-cardiac surgery
-reduced coronary blood flow MI

64
Q

types of dysrhythmias

A

supraventricular
-ventricular
- conduction issues/heart blocks

65
Q

Supraventricular

A

originate above the ventricles
sinus tachycardia & brady cardia
AFIB
atrial flutter

66
Q

ventricular dysrhythmias

A

originate in ventricles
ventricular fibrillation
ventricular tachycardia
premature ventriuclar complexes

67
Q

conduction issues/ heart block

A

Conduction issues typically related to A/V node or other areas in conduction system

  • Possibly life threatening
68
Q

AFIB

A

Irregular rhythm
Etiology:Structural heart changes (cardiomyopathy, valves, surgery, etc) Other medical conditions such as hyperthyroid, sleep apnea, age) ETOH and certain medications
MOST COMMON SUSTAINED DYSRHYTHMIA
High risk of stroke due to atrial blood pooling in left atrial appendage.

69
Q

Ventricular tachycardia

A

rapid regular ecotopic ventricular contractions
Can degenerate into vfib
ETI- Mycardial ischemia
infarction
electrolyte issues/ imbalance

70
Q

Torsades du points

A

Type of VT with regular oscillating polymorphic pattern
-Can degenerate into VFIB, cardiac arrest
- Etiology:
- Long QT time, as seen on ECG (from medications, electrolyte
imbalances, or congenital)
 Must be addressed immediately

71
Q

VFIB

A

Asynchronous discharge of multiple ventricular ectopic foci
-No coordinated ventricular contraction; effective Pumping action of
the heart stops
-Etiology:
- Myocardial ischemia, infarction, sustained VT
- Electrolyte disorders / imbalances
-Certain medications
- Life threatening Emergency
24

72
Q

Premature ventricular contraction

A

Ectopic ventricular beat
-typically random and infrequent
ETI-
HF, myocardial ischemia, electrolyte imbalances caffeine tobacco

73
Q

Conduction disorders

A

first degree
second degree
-type 1
type 2
third degree

74
Q

first degree

A

PR interval is longer than normal

75
Q

Second dregree type 1

A

PR interval is normal but gradualy increases until pr interval is misssed

76
Q

second degree type 2

A

condcution is randomly missed often needs pacemaker

77
Q

Third degree

A

complete heart block
ventricles are firing on their own no coordination
life threatening

Patho key terms 1-3 (8 decks)

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