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326 pharm 1 > cardiovascular patho mod 6 > Flashcards

cardiovascular patho mod 6 Flashcards

1
Q

CAD

A

Coronary arteries branch from the aorta
Arteries become CLOGGED d/t atherosclerosis

**left anterior descending artery #1

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2
Q

problems of the heart (3)

A
  1. Electrical (conduction)
  2. Plumbing (ARTERY BLOCKAGE, spasm, or valve issues)
  3. Pump (heart muscle)
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3
Q

CAD umbrella term for what?

A

heart disease/cardiovascular disease
- coronary artery disease/coronary heart disease =
heart attack

congenital heart failure
heart failure
arrythmia

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4
Q

non-modifiable risk factors CAD

A

Age - increased
family history
gender - male, then same after menopause
ethnicity - black, Hispanic , native Americans
genetics

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5
Q

modifiable risk factors CAD

A

***HYPERLIPIDEMIA
HTN
smoking
diabetes - insulin resistance, increased HLD
obesity/inactivity - android obesity (apple)
diet
depression/stress

DASH DIET

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6
Q

etiology CAD

Patho: Ischemic Heart Problems – “a plumbing issue”

A

Etiology: Atherosclerosis develops in the arteries supplying the myocardium = ARTERY BLOCKAGE

The blockage causes decreased tissue perfusion
Is ENDOTHELIAL DYSFUNCTION

The heart must work harder to pump the blood

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7
Q

endothelial dysfunction

A

Vessels aren’t necessarily blocked but become narrowed when they are supposed to dilate

Causes: DM, HTN, HPL, smoking

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8
Q

angina — main symptom CAD

A

May be asymptomatic

Eventually, as coronary arteries continue to narrow, the decreased blood flow may cause chest pain/ANGINA

COMPLETE OCCLUSION = myocardial infarction

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9
Q

stable angina

**mistaken for indigestion

A

STABLE angina- coronary blood flow is diminished but NOT BLOCKED

There is an imbalance between oxygen supply and demand

Is brought on by EXERTION
Is relieved with REST
Usually only last 2-5 minutes

Most often caused by ATHEROSCLEROSIS

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10
Q

angina

A

It is important to EXCLUDE the heart being the cause of the chest pain BEFORE exploring non-cardiac causes

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11
Q

atypical angina in women

A

Discomfort
Hot or burning
Tenderness

Location
Not always the chest

Other symptoms
Indigestion
Heart burn
Nausea
Fatigue/weakness
Lightheadedness
Dyspnea

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12
Q

angina, pain, and MI

A

Chest pain not brought on by exertion
Chest pain may radiate to other areas
Pain not relieved in 2-5 min
Often accompanied by N/V, SOA, diaphoresis
Risk for myocardial infarction increased

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13
Q

what to do with stable angina?

s/s not better after 5 mins – call 911

A

EDUCATION - remember rest and relaxation

DECREASING DEMAND
Nitrates
Prevent/treat further atherosclerosis
TEACH ABOUT myocardial infarctions

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14
Q

3 types of heart failure

A

Left versus right-sided
Systolic versus diastolic
Preserved versus reduced

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15
Q

what is cardiomyopathy

A

disease that affects myocardium

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16
Q

cardiomyopathy — leads to heart failure

A

Disease that affect the myocardium

Usually idiopathic, can be caused by ischemia, hypertension, inherited disorders, infections, toxins, myocarditis, auto-immune condition

Lead to heart failure

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17
Q

causes dilated cardiomyopathy

A

ischemia, ETOH, decreased valve EF

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18
Q

restrictive cardiomyopathy (amyloid)

A

R side HF
resistant to filling, rigid

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19
Q

hypertrophic cardiomyopathy

A

deadly arrhythmias, HTN

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20
Q

what is heart failure?

A

Heart failure is a chronic, progressive condition in which the heart muscle is unable to pump enough blood to meet the body’s needs for blood and oxygen.

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21
Q

how is cardiac output affected by HF

A

decreased

Heart failure results in decreased cardiac output, decreased myocardial contractility, increased preload, increased afterload

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22
Q

development of HF

A

volume overload - fluid to lungs
impaired ventricular filling - during diastole
weakened ventricular muscle
decreased ventricular contractility - during systole

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23
Q

etiology HF - major causes

A

REPEATED ISCHEMIC EPISODES – ischemic cardiomyopathy
Myocardial infarction ± papillary muscle rupture (RAAS system)
Chronic HTN
COPD (RVF)
Dysrhythmias - ischemia
Valve disorders; mitral insufficiency, aortic stenosis
Pulmonary Embolus (RVF)

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24
Q

risk factors HF

**STABLE ANGINA NOT A RISK FACTOR***

A

HYPERTENSION —- Greatest risk factor
- DM can also contribute

Within 6 months of MI
- 22% men
- 46% women
- Diagnosed at later age – estrogen is
cardioprotective
Men and postmenopausal women have same risk of CV disease
Higher incidence in Black/African-Americans
Genetics

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25
Q

risk factors HF cont..

***STABLE ANGINA NOTT A RISK FACTOR****

A

Age: increases with age; most common reason for hospitalization in people age 65 years and older.

Ethnicity: Black/African Americans are at higher risk than Caucasians.

Family history and genetics
Diabetes
Ischemic heart disease
Obesity
HTN
Lifestyle factors: Smoking and sedentary lifestyle

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26
Q

other risk factors HF

A

COPD
Severe anemia
Congenital heart defects
Viruses:
—-Although uncommon, certain viral infections can cause myocarditis, which weakens the heart muscle.
Alcohol abuse/Drug Abuse
Kidney conditions:
—-Excess blood volume, edema, HTN, and
accumulation of nitrogenous waste, which can
weaken the heart

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27
Q

heart failure classifications

A

left side - blood backs up in pulmonary system

right side - blood backs up systemic circulation

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28
Q

left side HF

Poorly controlled HTN is most
common cause of left sided HF

A

Left sided HF
Congestion in LEFT chambers
LV increases in size (LVH)
Backflow into pulmonary veins
Congestion in LUNGS

Findings
Cough, crackles, wheezes - pulmonary edema
Frothy sputum, may be blood tinged
Paroxysmal nocturnal dyspnea (PND)
Orthopnea - can’t breath laying flat

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29
Q

right side HF

COPD most common cause of right HF
Pulmonary hypertension

A

Right sided HF
Often due to COPD with cor pulmonale
Congestion in RIGHT chambers
RV increases in size (RVH)
Backflow into vena cava, decreased to the lungs
Congestion in jugular veins, liver, lower extremities

Findings
JVD
Dependent edema
Weight gain
Hepatosplenomegaly

30
Q

heart flow

A

attached

31
Q

Heart failure: Reduced Ejection Fraction (HFrEF) [Systolic HF]

EF < 40%
impaired contractile function

A

Determined by patient’s ejection fraction  EF < 40%

Caused by IMPAIRED contractile function, increased afterload, cardiomyopathy, and mechanical problems
Left ventricle loses ability to generate pressure to eject blood

Weakened muscle cannot generate stroke volume and then lowers cardiac output

LV fails, blood backs up, causes fluid backup and accumulation

32
Q

Hear failure: Preserved Ejection Fraction (HFpEF) [Diastolic HF]

HTN common cause

pulmonary congestion**

A

Inability of the ventricles to relax and fill during diastole
HTN is the primary cause of HFpEF
Being female, older age, diabetes, and obesity are all other risk factors for HFpEF

LV is stiff and noncompliant leading to high filling pressures  leads to decreased stroke volume and decreased cardiac output

Reduced CO leads to fluid congestion

EF is normal or only moderately decreased (40-49%)

33
Q

what is normal ejection fraction (EF)?

A

55-65%

34
Q

comparing EF

A

see attached

35
Q

chronic vs acute HF

A

Progressive
Chronic
+ Episodes of “decompensated” HF

Acute:
New or worsening signs/symptoms
Frequent visits to the ER
Hospitalization
Less common- new onset HF (20%)

36
Q

what is ventricular remodeling in HF?

ENLARGEMENT AND DILATION OF THE LEFT VENTRICLE

A

A weakened heart muscle

  • Secretion of molecular substances
  • Angiotensin II, aldosterone, endothelin, TNF-alpha, catecholamines, insulin-like growth factor, and growth hormone
  • Provoke genetic changes, apoptosis, and hypertrophy of cardiac myocytes, as well as collagen deposits and myocardial fibrosis.

These molecules cause changes lead to ENLARGEMENT AND DILATION OF THE LEFT VENTRICLE
Worsens HF

37
Q

what is S3 gallop?

A

common in HF, low pitched sound hear after S2

During rapid filling of the ventricle in the early part of diastole
High ventricular end-diastolic volume
Increased pressure within ventricles

In adults older than age 40 years an S3 is abnormal and indicative of heart failure.

38
Q

HF and other diseases

A

below

39
Q

cardiac muscle cell dysrhythmias

A

electrical
- automaticity - generate electrical impulse
- excitability - respond to ourside impulse and change
- conductivity - receive electrical impulse and
conducts it

contract/shorten
- contractility - shorten in response to impulse

40
Q

cardiac conduction - action potential

A

Na and K ATP causes action potential

repolarization - T wave
depolarize - light turns on

add picture

41
Q

normal electrical conductivity

sinus rhythm starts from SA node!

A

Rate: 60-100
Rhythm: Regular

P waves:
Upright & rounded
One before every QRS

Regular rhythm
PR interval: 0.12-0.20 sec
QRS: < 0.12 sec (narrow)

42
Q

normal sinus ARRHYTHMIA

** P-P intervals are different

A

A degree of variability in the heart rate
Common in young people
HR fluctuates with respiration or autonomic nervous system

no change CO, still 60-100, narrow QRS

43
Q

what is a dysrhythmia?

A

Abnormality of the cardiac rhythm
Problem with impulse generation or conduction
Why is it significant? — affects CO

44
Q

cardiac output

A

see below

45
Q

what causes dysrhythmias?

A

Inappropriate automaticity –***K+

  • A cell initiates action potentials when it isn’t supposed to
  • myocardial ischemia

Triggered activity

  • An extra impulse is generated during or just after repolarization
  • SNS stim

Re-entry

  • Cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
  • electrolyte imbalance
46
Q

sinus rhythms

A

Sinus rhythm

Sinus arrhythmia

Sinus tachycardia

Sinus bradycardia

Paroxysmal supraventricular tachycardia

47
Q

sinus brady

A
  • Originates in SA node
  • Regular, rate < 60 bpm
  • Rhythm normal
  • Normal PR interval and QRS
48
Q

causes sinus brady

A

hypokalemia

vagal response

digoxin toxicity (HF med)

late hypoxia

medications

myocardial infarction

49
Q

clinical manifestations sinus brady

A

decrease CO = decreased O2 perfusion

50
Q

tx symptomatic sinus brady

A

s/s brady - dizzy, LOC, hard to arouse

  • atropine: anticholinergic
  • If drug not effective: PACEMAKER
51
Q

sinus tachy

A

sinus tachy more often than brady occurrence

  • Originates in SA node
  • Heart Rate 100 -150 BPM
  • Rhythm = regular
  • P waves similar (may be partially hidden)
  • Normal PR interval and QRS
52
Q

causes sinus tachy

A

catecholamines - exercise, pain, strong emotions

fever

FVD ***sometimes 1st symptom

medications - epi, albuterol

substances

hypoxia

53
Q

tx sinus tachy

A

based on cause!!

hypovolemia - fluids

fever - antipyretics

pain - pain meds

beta blockers - decrease HR and myocardial O2 consumption

54
Q

paroxysmal (occasional) superventricular tachy (PSVT)

**originates above AV node**

A
  • HR 150-250 bpm
  • Originates in AV node
  • Usually no ”P” wave àIf present they look abnormal
  • QRS normal
  • Usually caused by a re-entry phenomenon
  • Typically begins and ends suddenly
  • Often described as “feeling like my heart is racing”
55
Q

PSVT causes

A

Over exertion

Emotional stress

Stimulants

Digitalis toxicity - digoxin

Rheumatic heart disease

CAD

WPW (Wolff-Parkinson-White) - other rhythm abnormality

Right sided heart failure (cor pulmonale)

56
Q

clinical s/s PSVT

A

palpitations

chest pain

fatigue

lightheadedness or dizziness

dyspnea

57
Q

premature atrial contractions (PACs)

A

Early p waves that usually look a little different (morphological changes)

Normal PR interval

QRS does follow the PAC

Usually has no consequences, but if frequent indicates that patient at high risk for other dysrhythmia (usually afib)

CHECK ELECTROLYTES

May need O2 for hypoxia

58
Q

atrial dysrhythmias

A

atrial flutter

atrial fibrillation

59
Q

atrial flutter

A
  • Originates in the AV node – overrides the SA node
  • Reentry impulse that is repetitive & cyclic
  • Regular atrial rhythm with an ATRIAL rate of >250 bpm
  • Ventricular rate is slower
  • P wave classical “sawtooth” appearance
  • QRS usual narrow
  • May be 2:1, 3:1, or 4:1
60
Q

causes atrial flutter

A

CAD

cardiomyopathy

heart valve disease

congenital heart disease

inflammation of heart - myocarditis

high blood pressure

other conditions - lung disease/overactive thyroid

electrolytes

61
Q

atrial fibrillation (AF)

A
  • Multiple irritable spots in the atria
  • IRREGULARLY IRREGULAR (both atrial and ventricular)
  • HR 100-175 bpm
  • No identifiable ”P” wave
  • “fibrillation” waves
62
Q

clinical manifestations A Fib

A

palpitations

heart racing

fatigue

dizziness

chest discomfort

SOB

poss assymptomatic

63
Q

a fib causes

A

electrolyte imbalances

hypoxia

CVD

64
Q

a fib complications

A

decreased cardiac output

heart failure

embolus - stroke

65
Q

tx of A Fib

A
  • The most common type of treated dysrhythmia
  • Pharmacological
  • Rate control: Beta blockers, CCB, digitalis, amiodarone
  • Stroke Prevention: anticoagulants, antiplatelets
  • Non-pharmacological
  • Abalation, cardioversion
66
Q

ventricular dysrhythmias

A

Premature Ventricular contractions (PVCS)

VTACH

VFIB

67
Q

premature ventricular contractions (PVCs)

A
  • Contraction coming from an ectopic focus in the VENTRICLES
  • It comes EARLIER than the QRS should come and doesn’t follow a normal rhythm or p-wave
  • Wide and distorted in shape compared to normal QRS
  • Causes: stimulants, ELECTROLYTES, hypoxia, fever, exercise, emotional stress and CVD
  • Treat the CAUSE
68
Q

subtypes of PVCs

A

bigeminy

trigeminy

quadrigeminy

69
Q

VTACH

A
  • Consists of 3 or more PVCs together
  • Ectopic focus within the ventricles takes controls and fires repeatedly à no atrial contractions occurring
  • SERIOUSLY decreases cardiac output
70
Q

VTACH

A
  • Associated with MI, CAD, significant electrolyte abnormalities, heart failure, drug toxicity and other bad things
  • Rate usually 150-200BPMs, usually regular
  • No p-wave evident, PR not measurable
  • Treat: ACLS à depend on pulse, patient will be symptomatic very quickly unless converts back to other rhythm
  • May need an anti-dysrhythmic medication like beta blocker or CCB
  • Electrolyte replacement
  • First question: pulse or pulseless?
71
Q

ventricular fibrillation - VFIB

A
  • Irregular waveforms of varying shapes and sizes
  • The ventricles are just ‘quivering’
  • No effective contractions = NO CARDIAC OUTPUT

326 pharm 1 (23 decks)

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