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Disease Mechanisms > Ch 12: The Heart > Flashcards

Ch 12: The Heart Flashcards

1
Q

what is congestive heart failure

A

inability to effectively pump blood to meet metabolic demands of peripheral tissue
can lead to ischemic heart disease (IHD) and hypertension (HTN)

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2
Q

what is the mechanism of the progression to congestive heart failure

A

increased mechanical work (due to pressure overload, volume overload, or trophic signals) leads to cellular hypertrophy from increase DNA ploidy (replication without division)

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3
Q

what does pressure overload of the heart lead to

A

sarcomeres assemble parallel
leads to concentric wall thickness and increase in mass

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4
Q

what does volume overload of the heart lead to

A

sarcomeres assemble in series which leads to ventricular dilation and an increase in mass

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5
Q

what happens during hypertrophy of the heart in terms of capillaries

A

increase in tissue size but no increase in capillary numbers
leads to decrease in oxygen and nutrient supply

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6
Q

what happens during hypertrophy of the heart in terms of increase in mass/heart rate/contractility

A

as mass/HR/contractility go up, so do metabolic demands

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7
Q

what happens during hypertrophy of the heart in terms of increase in fibrous tissue deposition

A

increased resistance to diastolic filling

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8
Q

what happens during hypertrophy of the heart in terms of increased gene expression

A

more cell growth and protein expression

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9
Q

what is forward failure/effects of left sided CHF

A

low cardiac output

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10
Q

what is backward failure/effects of left sided CHF

A

left sided CHF leads to increased ventricular volume and pressure
this increased pressure and volume backs up to the pulmonary veins and leads to congestion/edema within the pulmonary system

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11
Q

what two things are used to assess extent of congestive heart failure

A

brain natriuretic peptide (BNP) and ECG

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12
Q

what occurs in left sided congestive heart failure:
-causes
-mechansim
-compensation mechanisms

A

usually caused by ischemic heart disease (IHD), hypertension, aortic and mitral valvular disease, or primary myocardial disease
blood backs up into left ventricle which leads to inadequate tissue perfusion
compensation: catecholamine release, RAAS, and ADH

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13
Q

what happens in regards to the kidneys when we have myocardial dysfunction (decreased CO and BP)

A

decreased perfusion to kidneys
increase in angiotensin 2 and aldosterone
cause retaining of sodium and water, increased BP and HR
ventricular remodeling

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14
Q

what is systolic left sided congestive heart failure

A

inability to pump
reduced contractibility of left ventricle leads to decreased CO and BP
inadequate tissue perfusion

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15
Q

what is diastolic left sided congestive heart failure

A

inability to fill
left ventricle stiff and cannot relax during diastole
leads to pulmonary congestion that gets worse with more demand
can be caused by hypertension from diabetes, obesity, and b/l renal artery stenosis

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16
Q

what is right sided congestive heart failure

A

inability of the right side of heart to pump blood to the lungs
usually caused by left sided CHF or lung disorders (cor pulmonale)
affects brain and kidney

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17
Q

what is backward failure/effects of right sided CHF

A

systemic and venous congestion

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18
Q

what is forward failure/effects of right sided CHF

A

low cardiac output

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19
Q

how does left sided heart failure effect the heart

A

leads to left ventricular hypertrophy
may also cause left atrium dilation

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20
Q

how does left sided heart failure effect the lungs and what do patients present with

A

pulmonary congestion and edema with wet heavy lungs
dyspnea (trouble breathing on exertion) which leads to orthopnea (shortness of breath while lying down), paroxysmal nocturnal dyspnea, and dyspnea at rest

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21
Q

how does left sided heart failure effect the kidneys

A

retention of salt and water which leads to increase of interstitial fluid and blood volumes
prerenal azotemia (buildup of toxins in blood)

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22
Q

how does left sided heart failure effect the brain

A

only seen in advanced stages of CHF
cerebral hypofusion (not enough blood to the brain) leads to hypoxic encephalopathy (brain injury due to not enough oxygen)
leads to irritability, loss of attention span, and restlessness that can lead to stupor (daze) and coma

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23
Q

what are the overall effects of right sided HF

A

engorgement of systemic and portal venous systems
little pulmonary congestion

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24
Q

what are the effects of right sided HF on heart

A

hypertrophy of right atrium and ventricle

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25
Q

what are the effects of right sided HF on liver and portal system

A

ascites, congestive heptaomegaly, and passive congestion (nutmeg liver) all lead to centrilobular necrosis and cardiac sclerosis or cirrhosis (cirrhosis of liver due to heart condition)

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26
Q

what is the effect of right sided HF on the spleen

A

congestive splenomegaly

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27
Q

what is the effect of right sided HF on the kidney

A

more pronounced congestion than left sided HF

28
Q

what are the effects of right sided HF on the subcutaneous tissue

A

peripheral edema and anasarca

29
Q

what is the effect of right sided HF on the brain

A

hypoxic encephalopathy

30
Q

what is ischemic heart disease

A

a group of syndrome caused by lack of oxygen, nutrients, and removal of wastes
most are due to coronary atherosclerosis (coronary artery disease)
can also be caused by coronary emboli, myocardial vessel inflammation, or vascular spasm
usually begins silent then causes a sudden onset of symptoms

31
Q

what three coronary vessels are most involved in coronary artery disease

A

left anterior descending
right coronary artery
left circumflex artery

32
Q

what are four clinical manifestations of ischemic heart disease

A

angina pectoris (chest pain)
myocardial infarction (MI - heart attack)
chronic IHD with heart failure
sudden cardiac death (SCD)

33
Q

what is angina pectoris

A

paroxysmal (sudden spasm) and recurrent attacks of substernal or precordial chest discomfort
aka “chest pain”

34
Q

what are the three types of angina

A

stable (typical)
preinzmetal variant
unstable (crescendo)

35
Q

what is stable (typical) angina

A

most common
caused by imbalance of perfusion and demand
presents as pain with exertion of increase in demand
pain is crushing or squeezing that radiates
treated with: rest or vasodilators

36
Q

what is prinzmetal variant angina

A

episodic ischemia caused by coronary artery spasm

37
Q

what is unstable (crescendo) angina

A

caused by plaque disruption, thrombus, or vasospasm
prolonged pain greater than 20 mins occurring at rest

38
Q

what is a myocardial infarction:
-define
-who is most susceptible
-which area of heart is most susceptible

A

death of cardiac muscle due to prolonged ischemia (heart attack)
most occur in those over 65
most occur in the left ventricle

39
Q

what are four risk factors for a MI

A

increase age
male gender
postmenopausal women
increased atherosclerosis

40
Q

what is the mechanism of most MIs

A

atherosclerotic plaque is disrupted which activates steps 1-3 of hemostasis
vessel becomes completed occluded

41
Q

what are the less common mechanisms of MIs

A

vasospasms due to atherosclerosis, platelet aggregation, or drug ingestions (cocaine)
emboli
vessel disorders, hematologic abnormalities, amyloid deposition, and vascular dissection

42
Q

what is a transmural infarction

A

occlusion of epicardial vessels (coronary arteries) which leads to necrosis of ventricular wall

43
Q

what is a subendocardial (nontransmural) infarction

A

plaque becomes disrupted which leads to a thrombus becoming lysed
leads to necrosis of 1/3rd-1/2 half of ventricular wall

44
Q

what are the three clinical manifestations of MIs

A

rapid, weak pulse
diaphoresis (sweating)
dyspnea (difficulty breathing)

45
Q

what are the 2 ECG changes seen in MIs

A

ST segment deviations and T wave inversions

46
Q

what are the 2 common myocardial proteins in the blood that are tested for during an MI

A

troponin 1 and troponin T

47
Q

explain how myocardial proteins become elevated in the blood during an MI

A

onset of MI
plasma membrane of dead myocytes becomes leaky
troponin leaks out of cell and into the blood circulation
numbers peak 24-48 hours after event

48
Q

what are the two methods to treat MIs

A

reperfusion: catheterization and coronary bypass

49
Q

what is catheterization

A

a reperfusion method to treat a MI
catheter is placed (usually into the femoral vein) up into the heart to help identify occluded area
then a stent or balloon angioplasty is done to open up the occluded vessel

50
Q

what is coronary bypass

A

a reperfusion method used to treat a MI
heart surgery which makes a new path around the occluded artery

51
Q

what are 8 complications of an MI

A

arrhythmias
CHF + cariogenic shock
mural thrombus
myocardial rupture
papillary muscle dysfunction
pericarditis
ventricular aneurysm
chamber dilation

52
Q

what is an arrhythmia or dysrhythmia

A

abnormalities of the myocardial conduction system
can be sustained or sporadic (paroxysmal)

53
Q

what are the two main causes of arrhythmias or dysrhythmias

A

structural changes in the conduction system
intrinsic myocyte electrical instability

54
Q

explain structural changes in the conduction system which leads to arrhythmias or dysrhythmias

A

ischemic injury (most common)
hypertrophy or inflammation - both lead to irregular depolarization

55
Q

explain intrinsic myocyte electrical instability which leads to arrhythmias or dysrhythmias

A

mutations in ion channels lead to irregular depolarization or repolarization

56
Q

where can arrhythmias or dysrhythmias originate from

A

issues with atrium (supraventricular) or ventricular
conduction system or with myocyte themselves

57
Q

what are some manifestations of arrhythmias and dysrhythmias

A

tachycardia (rapid heart beat)
bradycardia (slow heart beat)
irregular rhythm with normal ventricular contration
chaotic depolarization without ventricular contraction
no electrical activity (asystole)

58
Q

what happens if you have sustained arrhythmia and what are the three things it can present with

A

loss of adequate cardiac output which leads to:
lightheadedeness
syncope (loss of consciousness)
sudden cardiac death

59
Q

what is sudden cardiac death (SCD) and what are some of its causes

A

unexpected death from cardiac causes
usually due to lethal arrhythmias like asystole or ventricular fibrillation (VF) (irregular heartbeat that affects ventricles)

60
Q

what is sick sinus syndrome

A

SA node is damaged which leads to bradycardia

61
Q

what is atrial fibrillation

A

malfunctioning atrial cells lead to independent and sporadic depolarizing
leads to irregular HR

62
Q

what is heart block and what causes it

A

heart block: heart beats slowly or abnormally
caused by AV node dysfunction
can lead to first, second, or third degree heart block

63
Q

what is long QT syndrome

A

prolonged QT segments (ventricular depolarization and depolarization)
makes you more susceptible to serious ventricular arrhythmias

64
Q

what is hypertensive heart disease

A

heart disease caused by chronic blood pressure elevation
affects LV, LA, and coronary arteries

65
Q

what is the mechanism of hypertensive heart disease

A

hypertension leads to increase demands, pressure overload, and ventricular hypertrophy

66
Q

what causes left-sided hypertensive heart disease

A

systemic hypertension

67
Q

what causes right-sided hypertensive heart disease

A

pulmonary hypertension (cor pulmonale) - if there is too much pressure in your lungs, the right side of your heart has to pump harder to overcome that pressure and get blood into the lungs

Disease Mechanisms (19 decks)

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