cardiovascular patho mod 6 Flashcards
CAD
Coronary arteries branch from the aorta
Arteries become CLOGGED d/t atherosclerosis
**left anterior descending artery #1
problems of the heart (3)
- Electrical (conduction)
- Plumbing (ARTERY BLOCKAGE, spasm, or valve issues)
- Pump (heart muscle)
CAD umbrella term for what?
heart disease/cardiovascular disease
- coronary artery disease/coronary heart disease =
heart attack
congenital heart failure
heart failure
arrythmia
non-modifiable risk factors CAD
Age - increased
family history
gender - male, then same after menopause
ethnicity - black, Hispanic , native Americans
genetics
modifiable risk factors CAD
***HYPERLIPIDEMIA
HTN
smoking
diabetes - insulin resistance, increased HLD
obesity/inactivity - android obesity (apple)
diet
depression/stress
DASH DIET
etiology CAD
Patho: Ischemic Heart Problems – “a plumbing issue”
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
endothelial dysfunction
Vessels aren’t necessarily blocked but become narrowed when they are supposed to dilate
Causes: DM, HTN, HPL, smoking
angina — main symptom CAD
May be asymptomatic
Eventually, as coronary arteries continue to narrow, the decreased blood flow may cause chest pain/ANGINA
COMPLETE OCCLUSION = myocardial infarction
stable angina
**mistaken for indigestion
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
angina
It is important to EXCLUDE the heart being the cause of the chest pain BEFORE exploring non-cardiac causes
atypical angina in women
Discomfort
Hot or burning
Tenderness
Location
Not always the chest
Other symptoms
Indigestion
Heart burn
Nausea
Fatigue/weakness
Lightheadedness
Dyspnea
angina, pain, and MI
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
what to do with stable angina?
s/s not better after 5 mins – call 911
EDUCATION - remember rest and relaxation
DECREASING DEMAND
Nitrates
Prevent/treat further atherosclerosis
TEACH ABOUT myocardial infarctions
3 types of heart failure
Left versus right-sided
Systolic versus diastolic
Preserved versus reduced
what is cardiomyopathy
disease that affects myocardium
cardiomyopathy — leads to heart failure
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
causes dilated cardiomyopathy
ischemia, ETOH, decreased valve EF
restrictive cardiomyopathy (amyloid)
R side HF
resistant to filling, rigid
hypertrophic cardiomyopathy
deadly arrhythmias, HTN
what is heart failure?
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.
how is cardiac output affected by HF
decreased
Heart failure results in decreased cardiac output, decreased myocardial contractility, increased preload, increased afterload
development of HF
volume overload - fluid to lungs
impaired ventricular filling - during diastole
weakened ventricular muscle
decreased ventricular contractility - during systole
etiology HF - major causes
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)
risk factors HF
**STABLE ANGINA NOT A RISK FACTOR***
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
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
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
heart failure classifications
left side - blood backs up in pulmonary system
right side - blood backs up systemic circulation
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
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
heart flow
attached
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
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%)
what is normal ejection fraction (EF)?
55-65%
comparing EF
see attached
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%)
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
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.
HF and other diseases
below
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
cardiac conduction - action potential
Na and K ATP causes action potential
repolarization - T wave
depolarize - light turns on
add picture
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)
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
what is a dysrhythmia?
Abnormality of the cardiac rhythm
Problem with impulse generation or conduction
Why is it significant? — affects CO
cardiac output
see below
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
sinus rhythms
Sinus rhythm
Sinus arrhythmia
Sinus tachycardia
Sinus bradycardia
Paroxysmal supraventricular tachycardia
sinus brady
- Originates in SA node
- Regular, rate < 60 bpm
- Rhythm normal
- Normal PR interval and QRS
causes sinus brady
hypokalemia
vagal response
digoxin toxicity (HF med)
late hypoxia
medications
myocardial infarction
clinical manifestations sinus brady
decrease CO = decreased O2 perfusion
tx symptomatic sinus brady
s/s brady - dizzy, LOC, hard to arouse
- atropine: anticholinergic
- If drug not effective: PACEMAKER
sinus tachy
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
causes sinus tachy
catecholamines - exercise, pain, strong emotions
fever
FVD ***sometimes 1st symptom
medications - epi, albuterol
substances
hypoxia
tx sinus tachy
based on cause!!
hypovolemia - fluids
fever - antipyretics
pain - pain meds
beta blockers - decrease HR and myocardial O2 consumption
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”
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)
clinical s/s PSVT
palpitations
chest pain
fatigue
lightheadedness or dizziness
dyspnea
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
atrial dysrhythmias
atrial flutter
atrial fibrillation
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
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
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
clinical manifestations A Fib
palpitations
heart racing
fatigue
dizziness
chest discomfort
SOB
poss assymptomatic
a fib causes
electrolyte imbalances
hypoxia
CVD
a fib complications
decreased cardiac output
heart failure
embolus - stroke
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
ventricular dysrhythmias
Premature Ventricular contractions (PVCS)
VTACH
VFIB
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
subtypes of PVCs
bigeminy
trigeminy
quadrigeminy
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
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?
ventricular fibrillation - VFIB
- Irregular waveforms of varying shapes and sizes
- The ventricles are just ‘quivering’
- No effective contractions = NO CARDIAC OUTPUT
