Cardiac Diseases Flashcards
1
Q
Heart layers [review]
A
epicardium = outer surface myocardium = middle, muscular contracting layers endocardium = inner, lines the inner chambers and heart valves
2
Q
Heart valves [review]
A
AV valves: bicuspid (mitral) on the left, tricuspid on the right.
Semilunar valves: pulmonic (RV and pulmonary arter) and aortic (LV and aorta)
3
Q
Cardiac Conduction [review]
A
SA node (pacemaker) (60-100BPM) to
Right and Left Atria to
AV node (50BPM if SA stops working) to
Bundle of His (40BMP if others dysfxn) to
Right and Left bundle branches to
Purkinje Fibers (ventricular contraction)
4
Q
1st heart sound [review]
A
“Lub” - AV valves shut at the beginning of systole - sound is the interruption of laminar flow (blood against a closed valve)
5
Q
2nd heart sound [review]
A
Semilunar valves shut at the end of systole d/t falling pressure
- *physiologic split** = artic valve closes earlier than pulmonic by .02-.04 seconds in exp, and .04-.06 in insp - helps sides keep together
- – pulmonic opens sooner, closes later
6
Q
Atherosclerosis
A
- *most commonly on coronary arteries - or other larger vessels
- hardened plaque - fibrofatty lesions internally lining vessels
- most common cause of CAD = inflammation from ATO
- progression of ATO means vessel can’t dilate as well
- advanced: calcification or rupture
7
Q
Atherosclerosis: inflammation
A
Deposits attract bacteria and then inflammatory response.
- Same risk factors of HD initiate chemical response for inflammation (smoking, HTN, lipoproteins, hyperglycemia)
8
Q
Organisms that could contribute to atherosclerosis
A
chlamydia pneumoniae, Herpes simplex virus, Cytomegalovirus
9
Q
Atherosclerosis: r/t morbidity and mortality
A
- responsible for most cases of MI and CVA
- Principle cause of death in the US and Western Europe
- Potential sequelae: MI, CVA, gangrene in extremities, sudden cardiac death
10
Q
Atherosclerotic Lesion dvlpmt: fatty streaks
A
- occurs in all ages.
- kids at 1-2yo, if homozygous dominant for hypercholesterolemia
- Contains foam cells: T cells and macrophages filled with lipids
- results in disorganized layers of cells: smooth muscle from tunica media migrates into tunica intima
11
Q
Atherosclerotic Lesion dvlpmt: Fibrous Plaques
A
- CT, smooth muscle cells full of lipids, macrophages, lymphocytes
- thickens and may occlude the lumen, often w/ necrosis and calcification
PROCESS: Plaque expands => Artery gets inflamed => fibrous capsule forms => separates plaque from lumen => decreased blood flow, increased BP
12
Q
Atherosclerotic Lesion dvlpmt: Complicated lesion
A
- Degenerated plaque may rupture
- Softer lesions more likely to rupture
- Ulcerations, cracks serve as sites for platelet adherence and aggregation. Can result in thrombus => occlusion => MI
13
Q
Common Sites of Atherosclerosis (list)
A
(All Arteries)
- Aorta
- Femoral A
- Popliteal A
- Tibial A
- Coronary As
- Carotid As
- Cerebral As
14
Q
Common Sites of Atherosclerosis (description)
A
- more common at bifurcations where there is more force
- In legs: more common w/ DM or smokers
- In coronary As: more common in epicardial portions
- New lesions may occur at sites of CABG b/c tissue is less smooth after surgery
15
Q
Atherosclerosis: risk factors
A
- Males over 45, Females over 55 or early menopause
- Family Hx of premature CHD, AMI, Sudden death
- HTN
- High LDLs/ Low HDLs
- High triglycerides
- DM
- Obesity & inactivity
- Low birth weight
16
Q
Atherosclerosis risk factors: Hyperlipidemia
A
( high levels of fats in blood)
- Clear assc. w/ CAD and Hypercholesterolemia
- risk increases with high LDL cholesterol
- cause: dietary, genetic, overproduction, deficient removal, DM, renal disease, alcoholism, hypothyroidism, corticosteroids, estrogens….
17
Q
Atherosclerosis risk factors: Smoking
A
- Accelerates Ath
- 3-5x risk of CAD
- 70% death rate
BUT! Cessation lowers risk to that of non-smokers within ONE YEAR.
18
Q
Atherosclerosis risk factors: Diabetes Mellitus
A
Basically, metabolism of fat is affected.
- 4x risk of MI
- risk of gangrene in LE
- females more prone
- often hand in hand w/hyperlipidemia
- Goal: control blood sugar and BP
19
Q
Atherosclerosis risk factors: Hypertension
A
can be a silent killer
- Risk 5x greater when 160/95
BUT: this is the MOST TREATABLE aspect of the disease
20
Q
Atherosclerosis risk factors: Obesity and inactivity
A
Obesity assc w/ hypertriglyceridemia, hypercholesterolemia, glucose intolerance, HTN
Inactivity may lower HDLs
21
Q
Coronary Artery Disease: mortality and risk
A
- leading cause of death and disability in the US
- 1/3 males, 1/10 females under 60 - post menopause =
- 800000 new AMIs yearly
- 540,000 recurrences yearly
- BUT! Mortality is declining d/t:
- CPR and better hospital care
- management of HTN
- Lower cholesterol diets
- use of antibiotics
22
Q
Manifestations of CAD: Sudden Cardiac Death
A
- w/in an hour
- first sign of trouble in 25% of cases
- 350,000 deaths annually
- peaks for infants (born with heart defects) and adults 45-75
- more frequently in the AM
23
Q
Sudden Cardiac Death: Causes
A
90% direct result of lethal dysrhythmias: V tach, V fib, bradycardia, asystole
Major factors:
- 75% d/t CAD
- 25% d/t myocardial abnormalities (hypertrophy, dilation, valvular disease)
Occurs with:
- 75% or greater narrowing of Coronary As (stent needed)
- Old AMI
- acute thrombosis at site of fissured plaque
- note: 90% of Carotid cases: no symptoms until 90% narrowing d/t circle of willis
24
Q
SCD: treatment
A
if untreated, irreversible brain damage in 3-5 minutes and death
Treatment:
- CPR
- defibrillation, pacing for bradyarrhythmia, drugs
- Electrophysiologic testing to ID drug therapy needed
- implanted cardioverter/defibrillator
- resection of diseased myocardium
25
CAD: description
- atherosclerosis narrows/obstructs the coronary As
| - Decreased perfusion of myocardial tissue, inadequate O2 supply
26
CAD: outcomes
- Symptoms occur when there is inadequate blood supply (ischemia)
- L. main artery = "widowmaker." CAD significant if occlusion is reduced 50% here, or 75% in any other major branch.
- Leads to: HTN, angina, dysrhythmia, MI, CHF, death
27
CAD: Collateral circulation
CC = more than one artery supplies a muscle with blood.
- present in coronary As (especially in older folks)
- but it takes time to develop
- CAD in younger people is more likely to be lethal!!
28
CAD: Treatment
Treat the underlying condition.
- Occlusion more than 70% requires a stent
- Patients may go to cardiac rehab to help develop collateral circulation
29
Angina: description
- Chest pain from myocardial ischemia
- caused by imbalance b/t O2 supply and demand
- provoked by exertion or anxiety
- lasts several minutes, alleviated by rest.
- No myocardial necrosis (cells are HUNGRY not dead)
- Sequelae: AMI, death
30
Angina: Oxygen supply and demand
- Symptoms occur when O2 demand > supply
- Determinants of O2 demand: HR, contractility, Ventricular wall tension
- also physiological states increase demand: exercise, emotional stress, increased SNS activity
31
Angina: Causes
O2 imbalance caused by:
- Atherosclerotic Heart Disease
- Hypertrophic cardiomyopathy
- Aortic Stenosis (low CO to feed myocardium)
- coronary artery spasm
- conditions that increase myocardial O2 consumption
- At any time, heart is extracting near maximal O2.
Most people have both incr. demand AND decreased supply
32
Angina: goal of treatment
provide relief, correct the imbalance, prevent progression to reduce risk of MI
- often w/ use of nitroglycerine
- Increase oxygen supply to the heart, decrease demand
33
Types of Angina
- Classic Angina: stable or unstable
- Stable: relatively constant pattern of pain: pain => rest (+ nitroglycerine) => relief
- Unstable: recent onset, ANY change in pattern, part of a continuation
- 20% progress to MI within 3 months
- Variant/ Prinzmetal's: Pain during rest OR demand. V-arrhythmia caused by CA spasm
34
Angina: Health history
The most powerful tool for diagnosis. Ask lots of Qs.
| Describe: COLDSPA, changes, etc.
35
Angina: typical manifestation
- exertional discomfort
- several minutes duration, relieved by rest (more than 20 min? suspect...)
- In sternum, but can be in various places
- Can radiate to back, epigastrium, jaw... (may present diff in males and females)
- "tightness, heaviness, choking senseation."
- provoked by walking uphill/stairs, arm work, sex, exercise in cold weather, emotions, big meal
36
Angina: physical findings
- Incr. HR, Incr. BP
- S3 or S4 can be heard
- systolic murmor d/t mitral regurgitation
- Rule out: GERD, PUD, PE, MI, cholecystitis, asthmatic bronchitis
37
Angina: EKG measurements
EKG during an attack:
- ST segment depression = ischemic injury
- ST segment elevation = infarction (watch out for "tombstones"
- T wave inversion can occur during episode of pain
38
Angina: diagnostic testing
- EKG
- Stress test (watch out for an MI)
- Cardiac enzymes (normal in angina)
- Cardiac catheterization: diagnosis about patency of coronary As
39
Coronary Arteriography
Cardiac Cath = gold standard
- most precise means to document CAD
- Measures L ventr. fxn (LVF)
- - LVEDP or LVEDF, EF
- For patients with severe angina, chest pain, MI in progress
40
Angina: pharm management
- Nitrates: vasodilation
- Beta blockers: block B1 receptors, reducing contractilit
- Calcium channel blockers: more for Prinzmetal/ vasospasms
Antiplatelet therapy
- Unstable angina: daily ASA
- Hospitalized: may need IV heparin and ASA
41
Angina: surgical procedures
- Percutaneous Transluminal Coronary Angioplasty (PTCA): arteries dilated with catheter
- Laser angioplasty: laser probe advanced through a cannula, for small occlusions- laser heat vaporizes plaque
- Atherectomy: using a drill to pulverize plaque - for patients with PAD, but increased risk of traveling debris
- Vascular stent: in conjunction with PTCA to eliminate risk of closure
- CABG: saphenous or mammary veins attached between ascending aorta and stenotic coronary artery
42
Acute Myocardial Infarction: morbidity and mortality
- 30% of all cardiac death
- 750K hospitalizations and kills >500K
- CAD diagnosed in 7 million Americans (cause most MIs)
43
Causes of MI
*most Thrombotic occlusion + CAD : an already small lumen vulnerable to any crack or additional clotting
Other causes
- Inefective endocarditis emboli: lining of heart inflamed and roughened
- Thrombi from prosthetic valves: foreign material
- Atrial thrombi (with A fib - atrial quivering, blood not flowing)
- vasospasm from cocaine/amphetamine use
- small vessel disease in DM or collagen vascular disease
- trauma
44
MI: description
- myocardial tissue is Abruptly and Severely deprived of O2
- can lead to necrosis of tissue (diff from angina)
- infarction evolves over several hours (earlier response better)
- physical changes 6 hours later, enzymes come in and do further damage, infarcted area blue and swollen
- 48 hrs later: infarct grey w/ yellow streaks (neutrophils)
- 8-10 days later: granulation tissue forms (can be necrotic)
- 2-3 months: necrotic area scars - permanently changes size and shape of L ventricle
45
MI: description
- myocardial tissue is Abruptly and Severely deprived of O2
- can lead to necrosis of tissue (diff from angina)
- infarction evolves over several hours (earlier response better)
- physical changes 6 hours later, enzymes come in and do further damage, infarcted area blue and swollen
- 48 hrs later: infarct grey w/ yellow streaks (neutrophils)
- 8-10 days later: granulation tissue forms (can be necrotic)
- 2-3 months: necrotic area scars - permanently changes size and shape of L ventricle
46
MI: Location and effects
- LAD (40-50%, "widowmaker") - anterior L ventricle, apex, IV septum
- RCA: (30-40%) - contains SA and AV nodes, inferior/posterior wall of L ventricle, R ventricle
- L circumflex A (15-20%): back of heart, lateral L ventricle
Affected portion results:
- less contractility with abnormal wall motion.
- altered compliance
- Low SV and Low EF
- high LV end Diastolic Vol (results in ineffective pumping)
47
MI: Manifestations
- Q wave infarcts preceded by fatigue, chest discomfort, malaise . can involve full thickness
- Onset often early AM
- may be clinically silent (but visible on EKG): in cases of DM neuropathy, high pain threshold
48
MI: risk factors
- atherosclerosis
- CAD
- high cholesterol
- smoking
- HTN
- obesity
- physical inactivity
- impaired glucose tolerance
- stress
49
MI: manifestations
- Pain: can differ, esp b/w sexes. often intense, severe, crushing , 30-60 min, retrosternal or radiating
- Diaphoresis
- Cool, clammy, grey skin
- weakness
- sense of doom
- restlessness/confusion
- Fever r/t inflammation
- Respiratory issues
- Extremities: peripheral cyanosis, edema, pallor
- Pre-renal failure (forward effect - inadequate perfusion)
- JVD (backward effect)
50
MI: Cardiac manifestations
- Impaired L ventricular filling backward effects: pulmonary edema, SOB< tachypnea, orthopnea, crackles in bases
- Tachycardia d/t SNS (compensatory), dysrhythmias
- BP incr. initially, but may become hypotensive
- Heart displacement of PMI: soft s1, s3, s4, mitral regurgitation, friction murmur
51
intermission: How to tell between pleural and pericardial rubs?
While auscultating have them hold their breath - will only hear pericardial friction.
52
MI: Non-specific diagnostic tests
- CBC: incr. WBC to combat infection and inflammation
- Increased ESR: remember the rouleaux formation!
- Myoglobin: O2 binding protein found in striated muscle (could also be from muscular injury)
53
MI diagnostics: Creatine Kinase
- CK or CPhosphokinase: an enzyme found in heart, brain, skeletal muscle.
* look for CK- MB - primarily found in cardiac muscle
54
MI diagnostics: Troponin
* Gold standard is Troponin I*
- protein in cardiac muscle but returns to normal sooner than Troponin- T
- TT: specific antibody can detect trop-T and is specific for myocardial injury. Also stays high longer, ie for testing MI a week ago
55
MI diagnostics: AST and LDH
- Aspartate aminotransferase (AST): enzyme - but many conditions can cause elevation
- Lactic dehydrogenase (LDH): present in all metabolizing cells. Not used much anymore but can be used to assess extent of damage
56
Hemodynamic monitoring
- Central Venous Pressure (CVP): should be close to 0, looks at how well heart is performing - amt of blood returning to heart. (via a cath in the R atrium)
- CO = HR x SV: measured via a pulmonary artery cath measuring temp
- Pulmonary capillary wedge pressure (PCWP): pressure measured in pulmonary artery - indicated L V function
57
MI: complications
- Dysrhythmias
- CHF
- Cardiogenic shock
- Thromboembolism
- ischemic pericarditis
- Myocardial rupture
- Ventricular aneurysm (late)
58
MI: pre-hospital treatment
- EMS trained in defib
- publicly available AEDs, more people trained
- analgesia with morphine
- aspirin therapy
59
MI: Hospital treatment
- CCUs reduced mortality by 50%
- Diets: liquid to avoid aspiration
- Telemetry monitoring
- stool softeners (no vagal stim!)
- bed rest
- gradual resumption of ambulation
- O2 therapy to avoid hypoxemia
60
AMI: Convalescence
- prevent recurrent w/ CA++ channel and betal blockers / aspirin
- anticoag for 6 months in high risk
- risk factor mod
- cardiac rehab
- propt detection of progression of CAD
61
Stenosis
Failure to OPEN
| stayclosis
62
Regurgitation
Failure to CLOSE completely
63
Causes of Valve disease
(L. much more common)
- myxomatous degeneration - weakening of CT
- Calcific degeneration
- Congenital defects
- Infective endocarditis
- CAD
- AMI
64
Which valves are open during systole?
| Which are closed
Semilunar valves are open
| Atrioventricular valves are closed
65
Which valves are open during diastole?
| Which are closed?
AV valves are open
| SL valves are closed
66
Primary valve issues in systole? (L ventricle only)
Mitral regurgitation
| Aortic stenosis
67
Primary valve issues in diastole? (L ventricle only)
Mitral stenosis
| Aortic regurgitation
68
Auscultating valve issues
Listen for WHERE and WHEN is the murmur?
Systolic sounds = "lub-shh-dub"
Diastolic sounds = "lub-dub-shh"
Sound can often resonate to Erbs point
69
Mitral valve stenosis: description and manifestations
Description: Mitral valve doesn't fully open in diastole, impeding blood flow from LA to LV.
- heard as a diastolic murmur
Manifestations:
- atrial hypertrophies resulting in A fib, clotting, and embolization
- can lead to backward effects in the lungs: pulmonary congestion and all its stuff (sounds, orthopnea, poor oxygenation, etc.)
- Less SV = Less CO => fatigue, activity intolerance, weakness
=> initiats RAAS, which increases the pressure more.
70
Mitral Valve Regurgitation
Mostly caused by mitral valve prolapse (less serious)
Mitral valve doesn't fully close in systole, allowing blood to flow back into the atria and lungs
Manifestations: Backward to lungs and forward, blood absent from L ventricle
- palpitations
- rhythm disturbances
- dizziness
- dyspnea
- chest pain
- anxiety
71
Aortic Valve Stenosis
Aortic valve doesn't fully open during systole.
Leads to LV hypertrophy, which can lead to LV failure
- head w/ systolic murmur
Manifestations:
SAD! (Syncope, Angina, Dyspnea)
Fatigue, hypotension
*low* peripheral pulse d/t low blood flow
72
Aortic valve regurgitation
Aortic valve doesn't fully close during diastole, allowing blood to flow back. LV hypertrophies - some similar SS to AV stenosis but pulse pressure WIDENS (high systolic, low diastolic) leading to bounding peripheral pulses.
73
Diagnosing Valve disease
- cardiac auscultation
- CXR (may not be visible if diastolic HF)
- Electrocardiography to see electrical activity
- coronary angiography
- MRI
- Doppler ultrasound
74
Meds for Valve disease
- Digitalis
- Diuretics
- Anticoagulants
- Beta blockers
- Calcium channel blockers
75
Surgery for valve disease
- Commissurotomy (separate flaps of mitral valve during stenosis)
- valvuloplasty
- Valve replacement: plastic, metal, animal
