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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
risk factors HF cont.. \*\*\*STABLE ANGINA NOTT A RISK FACTOR\*\*\*\*
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
26
other risk factors HF
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
27
heart failure classifications
left side - blood backs up in pulmonary system right side - blood backs up systemic circulation
28
left side HF Poorly controlled HTN is most common cause of left sided HF
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
29
right side HF COPD most common cause of right HF Pulmonary hypertension
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
heart flow
attached
31
Heart failure: Reduced Ejection Fraction (HFrEF) [Systolic HF] EF \< 40% impaired contractile function
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
Hear failure: Preserved Ejection Fraction (HFpEF) [Diastolic HF] HTN common cause pulmonary congestion\*\*
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
what is normal ejection fraction (EF)?
55-65%
34
comparing EF
see attached
35
chronic vs acute HF
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
what is ventricular remodeling in HF? ENLARGEMENT AND DILATION OF THE LEFT VENTRICLE
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
what is S3 gallop?
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
HF and other diseases
below
39
cardiac muscle cell dysrhythmias
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
cardiac conduction - action potential
Na and K ATP causes action potential repolarization - T wave depolarize - light turns on add picture
41
normal electrical conductivity sinus rhythm starts from SA node!
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
normal sinus ARRHYTHMIA \*\* P-P intervals are different
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
what is a dysrhythmia?
Abnormality of the cardiac rhythm Problem with impulse generation or conduction Why is it significant? --- affects CO
44
cardiac output
see below
45
what causes dysrhythmias?
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
sinus rhythms
Sinus rhythm Sinus arrhythmia Sinus tachycardia Sinus bradycardia Paroxysmal supraventricular tachycardia
47
sinus brady
* Originates in SA node * Regular, rate \< 60 bpm * Rhythm normal * Normal PR interval and QRS
48
causes sinus brady
hypokalemia vagal response digoxin toxicity (HF med) late hypoxia medications myocardial infarction
49
clinical manifestations sinus brady
decrease CO = decreased O2 perfusion
50
tx symptomatic sinus brady
s/s brady - dizzy, LOC, hard to arouse ## Footnote * atropine: anticholinergic * If drug not effective: PACEMAKER
51
sinus tachy
sinus tachy more often than brady occurrence ## Footnote * Originates in SA node * Heart Rate 100 -150 BPM * Rhythm = regular * P waves similar (may be partially hidden) * Normal PR interval and QRS
52
causes sinus tachy
catecholamines - exercise, pain, strong emotions fever FVD \*\*\*sometimes 1st symptom medications - epi, albuterol substances hypoxia
53
tx sinus tachy
based on cause!! hypovolemia - fluids fever - antipyretics pain - pain meds beta blockers - decrease HR and myocardial O2 consumption
54
paroxysmal (occasional) superventricular tachy (PSVT) \*\*originates above AV node\*\*
* 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
PSVT causes
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
clinical s/s PSVT
palpitations chest pain fatigue lightheadedness or dizziness dyspnea
57
premature atrial contractions (PACs)
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
atrial dysrhythmias
atrial flutter atrial fibrillation
59
atrial flutter
* 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
causes atrial flutter
CAD cardiomyopathy heart valve disease congenital heart disease inflammation of heart - myocarditis high blood pressure other conditions - lung disease/overactive thyroid electrolytes
61
atrial fibrillation (AF)
* Multiple irritable spots in the atria * IRREGULARLY IRREGULAR (both atrial and ventricular) * HR 100-175 bpm * No identifiable ”P” wave * “fibrillation” waves
62
clinical manifestations A Fib
palpitations heart racing fatigue dizziness chest discomfort SOB poss assymptomatic
63
a fib causes
electrolyte imbalances hypoxia CVD
64
a fib complications
decreased cardiac output heart failure embolus - stroke
65
tx of A Fib
* The most common type of treated dysrhythmia * Pharmacological * Rate control: Beta blockers, CCB, digitalis, amiodarone * Stroke Prevention: anticoagulants, antiplatelets * Non-pharmacological * Abalation, cardioversion
66
ventricular dysrhythmias
Premature Ventricular contractions (PVCS) VTACH VFIB
67
premature ventricular contractions (PVCs)
* 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
subtypes of PVCs
bigeminy trigeminy quadrigeminy
69
VTACH
* 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
VTACH
* 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
ventricular fibrillation - VFIB
* 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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