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Patho > Alteration of Cardiac Function > Flashcards

Alteration of Cardiac Function Flashcards

1
Q

Seven Principal Mechanism of Heart Disease

A

Ischemia
Pump Failure
Restriction of flow
Regurgitant flow
Shunted flow
Disorder of cardiac conduction
Rupture of heart or major vessel

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2
Q

Inadequate Blood supply to heart muscle

A

Ischemia (most important)

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3
Q

Inability of heart to contract adequately or to empty properly

A

Pump Failure (Heart Attack - secondary)

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4
Q

Valve disease or hypertension

A

Restriction of Flow

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5
Q

Valve disease with back-flow

A

Regurgitated Flow

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6
Q

Congenital defects with diversion of flow from one chamber to another

A

Shunted Flow (Ex. ASD, VSD)

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7
Q

Uncoordinated impulse or blocked conduction pathways

A

Disorder of Cardiac Conduction

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8
Q

Great Vessels of the Heart

A
  • Superior and inferior Vena Cave enter Right atrium bringing Unoxygenated Blood
    – Gonna go to the right ventricle then to the right and left Pulmonary Arteries to lung for Oxygenation
  • Pulmonary veins take O2 blood from lungs to left atrium => left ventricle => systemic side Aorta (Ascending (head and neck) or Descending (chest and lower body)
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8
Q

Penetration of heart or ruptured aneurysm, with loss of circulatory continuity

A

Rupture of Heart or Major Vessel

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9
Q

Distribution of Coronary Blood Flow

A

Left Anterior
- Descending: Disturbance=> Myocardial necrosis
- Right Coronary: Disturbance=> electrical abnormality
- Circumflex

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10
Q

Anterior 2/3 of intraventricular septum, most of left ventricle, cardiac apex, papillary muscle

A

Descending

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11
Q

Right ventricle, SA node, Posterior left ventricle, posterior 1/3 of intraventricular septum

A

Right Coronary

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12
Q

Lateral left ventricular wall

A

Circumflex

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13
Q

Ischemic Heart Disease (introduction)

A
  • Imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nitration requirement (narrowing of blood vessels)
  • 90% of death of IHD are result of Obstructive Atherosclerotic disease of coronary arteries
  • Can also be result of
    – Increased cardiac workload
    – Diminished blood volume (eg. shock)
    – Diminished oxygenation (eg. pneumonia)
    – Diminished oxygen carrying capacity (eg. CO poisoning)
  • Mortality reduced by 50% since 1963 as result of intervention that reduce risk factors and surgical approaches
    Current major risk factors: diabetes, obesity, smoking
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14
Q

Ischemic Heart Disease (Consequence, Involve, Progression)

A
  • Consequence of inadequate coronary perfusion relative to myocardial demand (usually caused by narrowing or occlusion and new superimposed thrombus or vasospasm)
  • May involve any coronary artery. but LAD (left anterior descending- close to origin)
    – Narrowing most sever in first several cm after vessel origin
    Occlusion:
  • When <70% occlusion => asymptomatic
  • When >70% occlusion => represent critical stenosis and will be symptomatic with exercise
  • Occlusion of 90% will be symptomatic at rest
    Rate of atherosclerosis development is important, Slow development may permit formation of collateral circulation (when develop rapidly it has higher morality rate)
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15
Q

Clinical Manifestation of IHD

A
  • Angina Pectoris (chest pain with no damage to heart)
  • Myocardial infarction (heart attack with damage to heart)
  • Dysrhythmias (Interfere w/conduction of heart - heart disease in right side)
  • Chronic IHD with Congestive Failure (damage in myocardia)
  • Sudden Cardiac Death
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16
Q

Angina Pectoris (often first sign of ischemia)

A
  • Develop when blood/oxygen supply is inadequate to meet demand for myocardial contractility
  • Cardiac muscle cannot develop an oxygen debt during stress and replay it later (it doesn’t store glycogen - anaerobic metabolism is impossible for it - only 30-40 sec)
    – Reversible episodes of discomfort or pressure induced by exercise or cold; relieved by rest, nitroglycerin (control vessel dilator, enhances circulatory flow)
    – Heaviness to sever pain in chest wall to left side, shoulder, neck, or jaw (for 5-10 min)
  • No myocardial cell death, no increase in serum enzymes (the pain is from ischemic release of adenosine, bradykinin, or other stimulator of autonomic nerves)
  • Patient pain description: not hot, sharp, fleeting
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17
Q

Classic (Stable) Angina

A
  • Pain relieved by rest or nitrates
  • Caused by a fixed atherosclerotic narrowing (70%-90%) of a coronary artery
  • Occurs when oxygen demand increase due to exertion emotional stress or heavy meals. Consistent within individual (each episode is the same with the past episode)
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18
Q

Unstable Angina (Crescendo Angina)

A
  • Advancing ischemic heart disease
  • Every attack different even within an individual
  • 30% will have MI (Medical emergency) within 3 months; CCU (gets worse)
    – May be caused by transient formation of platelets aggregates in coronary artery region narrowed by atherosclerosis; this further decrease O2 supply to myocardium
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19
Q

Prinzmetal (Variant) Angina

A
  • Pain occurs almost exclusively at rest or during sleep
  • Vasospasm of one or more coronary arteries, even in the absence of atherosclerosis
  • Respond to nitroglycerin and calcium channel blocker
  • Frequently causes dysrhythmias (hyper contraction of blood vessel)
  • May occur in normal (10-15%) coronary arteries or diseased (85%) arteries in regions adjacent to an atherosclerotic narrowing
    1) Hyperactivity of sympathetic nervous system
    2) Increased calcium flux in arterial smooth muscle
    3) Abnormal thromboxane production (hormone causing platelet aggregation and arteriole constriction)
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20
Q

Silent Ischemia

A
  • No physical discomfort (identify damage in autopsy or EKG)
  • Chronic ischemia often due to increase in BP induced by mental stress (detected in physical exam by rapid extra heart sound)
  • Frequent in diabetics due to autonomic neuropathy and in elderly ( more common in women)
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21
Q

Treatment of Ischemic Heart Disease

A
  • Slow/arrest atherosclerosis (drugs, eg., HMG-CoA reductase inhibitors/statin) - slow down rate of accumilation
  • Control signs/symptoms (pharmacotherapy; behavioral correction-don’t smoke, don’t work in cold (vasoconstriction slows heart))
    – Want to reduce myocardial workload => oxygen consumption:
    — BP, HR, Contractility, Left ventricular volume
  • Re-establish myocardial flow (surgery)
    – PTCA Angioplasty - Catheter or balloon Coronary artery bypass graft or Sten
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22
Q

Myocardial Infarction

A
  • 10% under 40 years, 45% before age 65
  • Premenopausal women generally protected, post-menopausal women catch up to males in risk. IHD is most common cause of death in older women
  • Blacks and white equally affected (Asian less affected)
  • Diabetics (all eventually develop atherosclerosis and ischemia), including premenopausal females, at high risk for early MI.
  • 10% of MIs occur in the absence of occlusion disease (vasospasm)-kill just as rapidly
  • Rapid occlusion MOST lethal; thrombosis can develop within minutes of endothelial injury (platelets=>RBC=>occlusion)
  • Necrosis MOST common in subendocardial zone (coagulation necrosis)
  • Sudden cardiac death is generally due to arrhythmia with ventricular fibrillation
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23
Q

Acute Myocardial Infarction

A
  • About onset of pain
  • Nausea related to pain
  • Cool, clammy and pain skin due to sympathetic vasoconstriction
  • Tachycardia
  • Weakness and fatigue (in women a key symptom)
  • Feeling of anxiety, impending doom
  • Pain can spread to jaw, neck, arms, back, and stomach
    Aspirin can help if the clot didn’t already form as it will prevent platelet aggregation
  • ST segment will be elevated in EKG (difference in patient EKG determine where damage is-this is why circulation is important)
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24
Q

Myocardial Infarction

A

Loss of coronary blood flow either sudden or gradual
- Acute ischemia: Usually coronary thrombosis superimposed on atherosclerotic plaque…30% die within few weeks due to MI
- Chronic ischemia: Slow and progressive narrowing of artery, myocardial cells adapt to hypoxia and get anastomoses

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25
Q

Myocardial Infarction (Heart Attack)

A

Irreversible hypoxia and cellular death caused by prolonged ischemia
- Most often due to atherosclerosis via thrombosis within 1.5cm of vessel Orign
- Most often occurs with hemorrhage into <70% occlusion plaque
– Left anterior descending (40% - 50%)
– Circumflex (15% - 20%)

26
Q

Sequence in Coronary Occlusion

A
  • Atheromatous plaque (lipid, macrophages, debris) eroded or injure to endothelium (push lumen to one side) => expose subendothelial collagen to blood
  • Platelets adhere, aggregate, and are activated, releasing ADP, thromboxane A2, and serotonin
  • Formation of mature, occlusive thrombus within min of initiation
  • 50% of thrombi disappear within 24 hrs
27
Q

Initial Managements of MI

A
  • Full extent within 3-6 hr of onset => rapid admission and initiation of treatment is crucial
    – Give oxygen and aspirin, get EKG
    — False positive and negative (has MI but denies it) present diagnostic challenge
    – Pain relief is important
    – the first 24hr has the greatest risk for sudden death=> must monitor enzymes and EKG
    – Blood thinners, ACE inhibitors, beta blockers are prescribed, emergent surgery considered
    – Best read and return to activities
    50% of MU develop slowly = progressive failure (congestive heart failure)
28
Q

Enzyme Pattern in MI

A
  • Blood enzymes level indicate macromolecules (platelets,..) leaking out of ht cell through the permeable plasma membrane (want it to go down)
    Standard blood enzyme include
  • Myosin
  • Cardiac troponin T and I(generally not found in circulation but will appear within 15-30 min of MI, and peak at 48hr with it remaining elevated for 7-10 days)
  • Myoglobin
  • Creatine kinase (cardiac specific-CK(MB))
    – Will be elevated 2-4hrs, peak at 24-48 hr, and return to normal within 72
  • Lactate dehydrogenase (LDH-big enzyme)
    —Re-perfusion cause Enzyme levels to peak earlier
    This allows monitoring the progression or resolution of the MI
29
Q

Morphology:Up to 4hr

A
  • Gross (none),
  • Microscopy (loss of glycogen/LDH)
30
Q

Morphology: 4-24hr:

A

Gross:
- Gradually deepening dark area surrounded by erythema.
- Oedema
Microscopy:
- Beginning coagulation necrosis contraction bands.
- Pyknotic nuclei
- Odema
- Few acute inflammatory cells

31
Q

Morphology: 3-7 days

A

Gross:
- Pale/yellow centre with hemorrhagic border
Microscopy
- Obvious necrosis of muscles
- Hemorrhage (more if reperfusion injury)
- Plenty of neutrophils and few macrophages

32
Q

Morphology: 1-3 weeks

A

Gross
- Pale, thin (loos of tissue mass) pale grey area with red border
Microscopy
- No muscle
- Granulation tissue (second intention healing)
- Macrophages prominent capillaries
- Fibroblasts

33
Q

Morphology: 3-6 week (permanent)

A

Gross
- Small silvery white scar
Microscopy
- Replacement of granulation tissue by dense fibrosis (scar)

34
Q

Cellular Injury

A

Change happen after 8-10 sec of decreased blood flow but not seen by light microscope for 24%
- Myocardial oxygen reserve used quickly and anaerobic metabolism takes over
- Myocardial cells are sensitive to low pH so lactic acidosis exacerbates problem => electrolyte disturbance

35
Q

Cellular Death

A

After 20 min of myocardial ischemia; irreversible hypoxic injury
- Glycogen for anaerobic ATP production is consumed within sec of onset of ischemia

36
Q

Complication of MI

A

Dependent on size and location infarct, survival duration
- Abnormal myocardial contraction
- Myocardial rupture
- Cardiogenic shock (40% loss of cardiac cells)
- Dysrhythmias (up to 90%); often with sudden death; salvo PVCs
- Mural thromboemboil
- Ventricular aneurysm
- Papillary muscle dysfunction
- Progressive heart failure
around 30% will re infarct within 60days

37
Q

Reperfusion Injury

A

Goal is to restore blood flow within critical window of time
- Achieved by thrombolysis (spa) or surgery
Factor contributing to Reperfusion Injury
- Mitochondrial dysfunction
- Myocyte hyper contraction-sarcomers cannot relax (w/calcium => contract can’t release)
- Free radical produced within minutes and damage membrane
- Leukocyte aggregation-occludes microvasculature
- Platelet and complement activation

38
Q

Cardiac Rupture

A

Result of necrosis of the full thickness of cardiac wall
- Happens in 1-5% of MIs
- Maximal weakness in standard MI is 7-10 days post occlusion
- Rupture of ventricular wall leads to cardiac tamponade (leakage of blood in heart=> every contraction more blood leakage into pericardial space) and rapid death

39
Q

Saphenous leg vein (bypass graft)

A

Center to anastomose with LAD; Y shaped for circumflex
Changes into artery => generate atherosclerosis

40
Q

Cardiac Stent

A

Used often in acute MI or chronic angina
- Stent installed by interventional radiologist
– Relatively safe; long-term risk include re-stenosis, hemorrhage, thrombi
– May improve long term survival; certainly improve morbidity

41
Q

Cardiac Valve Disease

A
  • Can be congenital (1-2% of live birth) or acquired
  • Classified: Both process may occur in same valve
    – Stenotic (failure of valve to open completely; Impaired forward flow)
    — Usually result of chronic process (eg., calcification)
    – Regurgitant: do not close completely (close floppily), permitting back flow of blood
    Turbulent blood flow through defective valve lead to murmurs and shortened RBC life
  • Defect in extracellular matrix of valve is common
42
Q

Normal Aortic valve

A
  • 3 thin delicate cusps 1-2% have leaflets
    – Smooth intimacy with no atherosclerosis
43
Q

Normal Tricuspid Valve

A
  • Thin, delicate leaflets attached via chord tendinae to papillary muscles of ventricle
44
Q

Valve Stenosis

A

Valve physically narrowing and failing to open effectively
- forward blood flow impeded
- Causes hypertrophy

45
Q

Valve Regurgitation

A

Valve cusp can’t close fully and blood leaks thru
- Get enlarged heart
- Left valves is more often involved due to higher pressure

46
Q

Valve Stenosis Effects

A

Stenosis most commonly post inflammatory (mitral) or Senile calcification (aortic)
- Mitral stenosis is almost always result of rheumatic fever ( group A, Beta-hemolytic strep)
– Calcified bacterial colonies on valve cusp
- Aortic stenosis with calcification result from aging
Cause:
- Increase ejection resistance (can’t open all the way)
- Increase work on left heart
- Decreased ejection volume
- Increased ejection time, thus slowed beat, weak pulse, narrowed pulse pressure
- Increased left ventricle thickness
- Dyspnea, vertigo, fatigue

47
Q

Valve Regurgitation Effect

A
  • Rheumatic fever
  • Bacterial endocarditis with valve vegetation (common in iv drug users)
  • At risk patient take antibiotics before dental work
  • Cardiac infarction with necrosis of papillary muscle (valve collapses)
    -Mitral prolapse relatively common in young females; discovered by accident as it is asymptomatic
  • Increased systolic pressure (more blood in system)
  • Decreased diastolic pressure (pressure space)
  • Widened pulse pressure
  • Increased cardiac volume, larger stroke volume
  • Increased left heart size (by dilation)
  • Water-hammer pulse (sound like pistol shot)
48
Q

Valve Repair

A

Artificial Valve: ball valve; use only when you have to (become anemic)
Biological Valve: first option

49
Q

Endocarditis

A

Microbial infection of valve (a vascular, translucent connective tissue) or lining endocardium
- Caused by bacteria (Strep virdans or Staph. aureus)
– Most common cause is the seeding of blood with microbes (eg. dental work)
- Classified as acute or subacute according to pace of clinical progression

50
Q

Acute endocarditis

A

Destructive tumultuous infection by virulent organism
- Has significant morbidity and morality even with appropriate antibiotic therapy

51
Q

Subacute endocarditis

A

Involve organism of lower virulence and damaged heart (clinical warning)
- Have long course but good outcome with treatment
- Septic fragment seed through body

52
Q

Infectious Myocarditis

A

Infectious and/or inflammatory processes targeting the myocardium
- Most commonly viral infection particularly coxsackieviruses A&B and enteroviruses (target cardiac muscles)
- My be present in COVID19 or Lyme disease
- Has a broad clinical expression
– Some patient are asymptomatic
– Other have life threatening cardiac arrhythmia or congestive failure
- Clinical signs or symptoms can mimic MI
- Non-infectious myocardial injury is common with cardiotoxic drugs such as anthracyclines
– Limit exercise in recovery period

53
Q

Pericardial Disease

A

Usually secondary to disease elsewhere in heart or another systemic disorder (particularly kidney disease)
- Associated with pericardial effusion-sac
– normally contain 50mL of fluid
– can contain more than 500mL if slow accumulation (too much or too fast result in cardiac tamponade)
- Primary pericarditis is viral but may result from cardiac surgery, thoracic radiation, uremia of renal organ (uric acid in blood is high)
Present clinically as atypical chest pain (not related to exertion and worse when recumbent) and prominent friction rub (increase of fluid)

54
Q

Cardiac conduct system

A

Start from the SA node in the right athrium
- Goes to the AV node in septum
– goes down to the right and left ventricle
— Purkinje fibers

55
Q

Atrioventricular Block

A

Called heart block or bundle branch block
- refer to blockage of action proteintal spreading anywhere in Purkinje fibers or bundle of his
Got three types

56
Q

First degree block

A

Each QRS follow P (depolarization) but w/extended delay

57
Q

Second degree block

A

Rare failure of P (depolarization) wave failing to cause QRS

58
Q

Third degree block

A

Complete block with loss of link between P(depolarization) wave and QRS

59
Q

Cardiac Dysrhythmias

A

Arrhythmia: All complexes normal but rhythm is irregular
Bradycardia: All complexes normal but rate is slow (<60bpm)
Tachycardia: All complexes normal but rate is high (>100bpm)
Atrial Fibrillation: Baseline irregular; ventricular response is irregular
Ventricular Fibrillation: Rapid, wide irregular ventricular complexes (can kill you)

60
Q

Arrhythmias

A

Abnormal rhythms of heart that are too slow (bradycardia) or too fast (tachycardia) (underlie sudden cardiac death without MI or plaque disruption)
- Chaotic depolarization without contract or irregular rhythms
- Can arise from anywhere in conduction system
- May be sustained or paroxysmal (occurs then stops)
- Ischemia is most commonly the cause
May be inherited as CHANNELOPATHY (mutation (at least 15) of genes for C+, K+ and/or NA+ channels) rare but very serious
Treatment primarily pharmacological

61
Q

Dysrhythmias of Impulse Formation

A
  • Sinus Bradycardia
  • Premature atrial contraction
  • Atrial tachycardia
  • Atrial flutter: 60-350 beats/min. Many p-waves, occasional QRS complex
  • Atrial fibrillation: Most common dysrhythmia (350-600 beats per minute)
    Ventricular contration is irregular and may not follow atrial depolarization
  • Ventricular Tachycardia 60-250 beats/min. Limited ventricular filling and massively reduced stroke volume
  • Ventricular bradycardia
  • Premature contractions—depolarization originating from an ectopic site. Canoccur randomly in the cardiac cycle
  • Ventricular fibrillation: Most serious; cardiac output = 0 and pulse and BP are nonexistent
    All rated with rest and drugs
62
Q

Factors contributing to Arrhythmia

A

Ischemia
Hypoxia
Acidosis
Alkalosis
Electrolyte abnormalities
Catecholamine exposure
Autonomic Influence
Drug toxicity
Overstretching of cardiac fibers
Scarred or diseased tissue
(Major intrinsic, largely acute)

Patho (17 decks)

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