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Pathophysiology 2.0 > Pathophysiology of Cardiac Disease - Lect 8 > Flashcards

Pathophysiology of Cardiac Disease - Lect 8 Flashcards

1
Q

Which layer of the heart is at increased risk of ischemia? Explain why.

A

Sub-endocardial layer

has a good blood plexus of blood vessels

BUT …

due to diastole collapsing the BVs from increased pressure = decrease BF

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2
Q

Which branches of cardiac blood vessels are most susceptible to atherosclerosis?

A

proximal epicardial parts &

intramural branches

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3
Q

What are the causes of ischaemia in relation to the CVS?

A
  1. Progressive atherosclerosis stenosis
  2. erosion of atheromatous plaque with superimposed thrombosis
  3. emboli from infective endocarditis or cardiac valvular disease
  4. low coronary arterial perfusion due to
    • shock from haemorrhage
    • severe aortic valve disease
    • severe anaemia
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4
Q

What is interesting about coronary BF?

A

is independent of aortic pressure

as is ensures auto-regulatory mechanisms

uses 60% consumption O2 at rest = cannot withstand an increase in CO as consumption cannot rise that much more

fills during diastole

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5
Q

what % of occlusion needs to occur to result in ischaemia?

A

75-80%

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6
Q

What parts of the heart does the Left Circumflex supply?

A

left atrium and left ventricle

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7
Q

What parts of the heart does the Left Anterior Descending Artery supply?

A

the right ventricle, left ventricle and interventricular septum

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8
Q

What parts of the heart does the Right Marginal Artery supply?

A

right ventricle and the apex

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9
Q

What parts of the heart does the Right Coronary Artery supply?

A

right atrium and right ventricle

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10
Q

What is the blood flow pattern to the subepicardial and subendocardial tissue in the left ventricle?

A
  1. Is far more dependant on diastolic flow to meet O2 demands
  2. has a much lower blood flow during diastole (as the opening of the atrial semilunar valve opens and covers the opening to the coronary bvs
  3. is far more susceptible to ischaemia
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11
Q

What is the blood supply to the intramuscular wall of the heart?

A

is from the penetrating arteries arising from the coronary arteries

forms a plexus via the anastomosis of the epicardial and endocardial plexi

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12
Q

Does the heart undergo aerobic or anaerobic metabolism? State why.

A

AEROBIC

  • has poor ATP reserves
  • has less mitochondria - only ~30% of myofibre volume
  • relies on O2 supply to produce energy
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13
Q

When does cell death in the myocardium occur?

A

occurs when …

  • tissue ATP reserves are very low
  • can no longer under glycolysis
  • membrane damage and calcium influx
  • BF can be re-established ONLY if ischaemia is brief
  • if prolonged = CANNOT reperfuse
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14
Q

What is the major fuel sources of the myocardium?

A
  1. Fatty Acids = most desired
  2. Glucose
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15
Q

What is the definition of Acute Myocardial Infarction (AMI)?

A

area of necrotic myocardium resulting from sudden absolute or relative reduction in coronary blood supply

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16
Q

What is the cause of Acute Myocardial Infarction?

A

thrombosis superimposed on …

OR haemorrhage within …

an atheromatous plaque in the coronary circulation

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17
Q

What are the clinical features of Acute Myocardial Infarction?

A

signs and symptoms

  • severe chest pain (sudden then gradual build-up, lasts hrs)
  • profuse sweating = autonomic NS
  • Angina (also chest pain but is nonspecific)
  • is silent in 10% of patients
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18
Q

What disease is the leading cause of mortality in the USA?

A

Acute Myocardial Infarction

wooooooo YAYYYYY

more than 500,000 people die per year

but maybe not this year = COVID BABY

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19
Q

What is the morphology of an Acute Myocardial Infarction?

A

depends on the location and size of infarction

  • site of occlusion in coronary artery = L vs R have dif prognosis & main vs distal branches also have dif prog
  • Anatomical pattern of blood supply = left vs right dominance
  • presence or absence of anastomotic circulation within coronary tree= large arteries do not anastomose vs small do = if in large blood supply is only thru that artery
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20
Q

What are the clinical measures which can determine the location of the Acute Myocardial Infarction?

A

ECG = good guide to site of infarction via changes in the peaks and waves

angiograms = confirm blockage after 3 - 4 hrs of pain episode

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21
Q

How is Acute Myocardial Infarctions diagnosed?

A

as serum cardiac enzyme and proteins released from damaged tissue blood tests can determine if lvls are elevated e.g. …

Cardiac muscle troponin = most reliable early indicator but still not as specific as wanted can also be released by other muscles

creatine kinase = not immediate and not specific

transient leukocytosis = occurs 1 to 3 days after infarction and not specific enough

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22
Q

What are the different marco- and micro-scopic changes that occur throughout the progression of MI up to 18 hours?

A

UP to 18 hrs

  • sig. changes in either macro or micro
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23
Q

What are the different marco- and micro-scopic changes that occur throughout the progression of MI 24 hours to 48 hours?

A

macroscopic

  • pale oedematous muscle

microscopic

  • oedema
  • acute inflammatory cell infiltration
  • necrosis of myocytes
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24
Q

What are the different marco- and micro-scopic changes that occur throughout the progression of MI after 3 to 4 days

A

macroscopic

  • yellow rubbery centre with a haemorrhagic border

microscopic

  • obvious necrosis & inflammation
  • early granulation
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25
Q

What are the different marco- and micro-scopic changes that occur throughout the progression of MI after 1 to 3 weeks

A

microscopic

  • progressive fibrosis

macroscopic

  • infarcted area paler and thinner than uninfected ventricle
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26
Q

What are the different marco- and micro-scopic changes that occur throughout the progression of MI after 3 to 6 weeks?

A

microscopic

  • dense fibrosis

macroscopic

  • silvery scar becoming tough and white
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27
Q

When do symptoms of myocardial infarction appear?

A

when the artery has an occlusion between 75 - 85 %

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28
Q

What are the 3 main types of coronary arterial obstructions that occur? What are their relative % of cases

A
  1. Left Anterior Descending Artery Obstruction = 50%
  2. Right coronary artery obstruction = 30%
  3. Circumflex artery obstruction = 20%
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29
Q

Describe briefly what occurs in a Left Anterior Descending Artery Obstruction.

A

Left Anterior Descending Artery Obstruction. (c. 50%)

  • artery of “sudden death”
  • anterior infarction
  • ECG changes in the anterior chest leads
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30
Q

Briefly describe what occurs in a Right Coronary Artery Obstruction.

A

Right Coronary Artery Obstruction (c. 30%)

  • inferior infarction
  • ECG changes in leads II, III & aVF
  • can involve posterior septum
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31
Q

Briefly describe what occurs in a Circumflex Artery Obstruction.

A

Circumflex Artery Obstruction (c. 20%)

  • lateral infarction
  • ECG changes in leads I and aVI
  • as well as chest leads V4-6
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32
Q

Describe the basic steps which lead to either chronic ischemic heart disease or acute coronary syndrome.

A
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33
Q

What is Coronary Dominance? Which one is associated with a worse prognosis?

A

tendency to have slightly different blood supply to the posterior ventricular wall

if it is from right = RIGHT DOMINANCE = ~60-70%

if it is from left = LEFT DOMINANCE = ~20%

can be from both left and right = ~10%

Left = worse prognosis as it supplies left ventricle

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34
Q

What are the different complications associated with a myocardial infarct? (hint = 12)

A
  1. Sudden Death
  2. Arrhythmias
  3. Persistent Pain
  4. Angia
  5. Mitrial incompetence
  6. Pericompetence
  7. Pericarditis
  8. Cardiac Rupture
  9. Mural Thrombosis
  10. Ventricular aneurism
  11. Dressler’s syndrome
  12. Pulmonary emboli
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35
Q

What is the interval of time and the mechanism of action in which sudden death occurs?

A

Interval = within hours

Mechanism = often ventricular fibrillation

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36
Q

What is the interval of time and the mechanism of action in which arrhythmia occurs?

A

interval = first few days

Mechanism = N/A

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37
Q

What is the interval of time and the mechanism of action in which Persistent pain occurs?

A

interval = 12 hrs to few days

Mechanism = progressive myocardial necrosis (if big is an extension of infarct)

38
Q

What is the interval of time and the mechanism of action in which Angina occurs?

A

interval = immediate or delayed

mechanims = ioschaemia of non-infarcted muscle

39
Q

Cardiac failure

A

interval = variable

mechanism = ventricular disfunction following muscle necrosis, arrhythmias

40
Q

What is the interval of time and the mechanism of action in which Mitral incompetance occurs?

A

interval = 1st few days

mechanism = papillary muscle disfunction

41
Q

What is the interval of time and the mechanism of action in which Pericarditis occurs?

A

Interval = 2 to 4 days

mechanism = transmural infarct and pericardial inflammation

42
Q

What is the interval of time and the mechanism of action in which Cardiac Rupture occurs?

A

interval = 3 to 5 days

mechanism = weakening of wall after necrosis, acute inflammation

43
Q

What is the interval of time and the mechanism of action in which mural thrombosis occurs?

A

interval = 1 week or more

mechanism = abnormal endothelial surface following infarction

44
Q

What is the interval of time and the mechanism of action in which Ventricular Aneurism occurs?

A

interval = 4 weeks or more

mechanism = stretching newly formed scar tissue

45
Q

What is the interval of time and the mechanism of action in which Dressler’s syndrome occurs?

A

interval = weeks to months

mechanism = autoimmune

is when there is too much fibrosis of muscle which means there is not enough muscle to pump the heart

46
Q

What is the interval of time and the mechanism of action in which Pulmonary Embolisms occurs?

A

interval = 1 week or more

mechanism = DVT in lower limb

47
Q

When a Mural Thrombosis heals how does the tissue change?

A

goes from many layers of thrombosis on infarcted tissue ( looks like a coagulation of shit in bottom sink) to a healed injury which has a resemblance to normal tissue but is fibrous

48
Q

What are the clinical features of Chronic Ischaemic Heart Disease (CIHD)?

A
  • angina
  • impaired ventricular function after previous infarction = can lead to ventricular and congestive heart failure
  • unstable or crescendo angina
  • may present severe or rapidly progressive chest pain
49
Q

What are the morphological feature of Chronic Ischaemic Heart Disease (CIHD)?

A
  • most patients have extensive coronary arterial atheroma
  • usually have to or 3 major coronary arteries with stenosis
50
Q

What do postmortem studies of Chronic Ischaemic Heart Disease (CIHD) indicate?

A
  • rupture of fibrous cap and lipid-rich atheromatous plaques
  • angiograms of
    • irregular contours of RCA
    • complete obstruction of circuflex branch
51
Q

What is the aetiology of Sudden Cardiac Death?

A

Acute cardiac failure due to ischaemic heart disease

52
Q

What are the post-mortem finding is Sudden Cardiac Death?

A

coronary artery stenosis with or without signs of previously healed infarctions

coronary thrombosis (55% of cases)

ventricular arrhythmias

any form of cardiomyopathy

53
Q

What are the typical forms of cardiomyopathy found in Sudden Cardiac Death?

A

ruptured atherosclerotic aneurysms of abdominal aorta

dissecting aortic aneurysms

pulmonary emboli

aortic stenosis

54
Q

What is Sudden Cardiac Death also referred to as -?- when what occurs?

A

Sudden Adult (or Arrhythmic) Death Syndrome (SADS)

is what SCD is called when there is no known cause.

55
Q

What are the preventative measures used to treat Sudden Cardiac Death?

A
  • defibrilators = in ventricular contraction has stopped
  • CPR
  • Implanted defibrillator (if history of arrhythmia)
  • early mobilisation after surgery prevents DVT
  • anticoagulant therapy given prophylactically to reduce risk of thrombosis and embolism e.g. asprin and warfarin
56
Q

What does DVT stand for?

A

Deep Vein thrombosis

57
Q

What is the basic definition of Heart failure?

A

describes the end-result of various types of cardiac dysfunction leading to inadequate tissue perfusion

typically as a result of ischaemic diseases

e.g. ventricular dysfunction

58
Q

What is the prognosis typically for heart failure?

A

Poor (bad) ~3 years = established heart failure

59
Q

What are the typical disabling symptoms of heart failure?

A

fatigue

poor exercise

shortness of breath with light exercise

60
Q

How many Americans have heart failure? (hint = %) and what is the % of hospitalizations over 65?

A

1% - USA peeps have

20%

61
Q

How do you clinically diagnose Heart Failure?

A

very difficult as there is compensated HF

there is no simple lab test

potentially an echocardiogram (ECG)

62
Q

What is the basic or typical pathophysiology of Heart Failure?

A
  1. mechanoreceptors (baroreceptors) detect underfilling in the; left ventricle, aortic arch, carotid sinus and renal afferent arterioles which
  2. send afferent impulses to via the vagus and glossopharyngeal N. to the Cardioregulatory centre
  3. cerebral response = activation of sympathetic NS;
  • tachycardia, increase myocardial contractility, vasoconstriction of arteries and veins
  • release of renin and angiotensin = renal vasoconstriction
  • direct (non-osmotic) release of ADH from hypothalamus = increase fluid retention and thus increases BV
    *
63
Q

What is the difference between chronic and acute heart failure?

A

depends on the speed of development of underlying pathological changes

64
Q

What are the different types of heart failure? How do they differ from one another?

A
  1. Acute Heart Failure
  • within mins of myocardial infarct
  • sudden severe SOB, marked pulmonary oedema
  1. Chronic Heart Failure
  • valvular defects
  • e.g. mitral stenosis, incompetence
  • may develop over years
  • patient describes a worsening of symptoms
  1. Chronic congestive Heart Failure
  • may develop after episode of acute HF
  • e.g. Infarct
65
Q

Is heart failure one-sided?

A

Yes initially BUT ….

mwahahahah

it is infact both

ventricular failure of one occurs after the failure of another

66
Q

What is Left-sided Heart Failure?

A

is when blood fails to move from the lungs back to the heart

fluid will escape into the pulmonary system

causes pulmonary congestion and oedema

67
Q

What are the typical symptoms of Left Heart Failure?

A
  • restlessness
  • confusion
  • orthopnea (SOB = increased RR)
  • tachycardia
  • exertional dyspnea (amplified SOB with increased exertion)
  • fatigue
  • cyanosis (blushing of face)
  • paroxysmal nocturnal dyspnea
  • elevated pulmonary capillary wedge pressure
  • pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea)
  • *
68
Q

What is Right Heart Failure

A

failure to move blood from veins back to heart

cannot return blood from periphery

69
Q

What are two key characteristics of Right Heart Failure?

A

raised jugular pressure

liver enlargement (via IVC and hepatic veins as blood pools here)

70
Q

What are the further divisions the right heart failure is broken into?

A
  1. Cor pulmonale
  2. Mitral stenosis
71
Q

What is “cor pulmonale”?

A

is right heart failure which is secondary to lung disease

e.g. COAD (bronchitis and emphysema)

72
Q

How does “cor pulmonale” occur?

A

decreased lung capillary bed due to increased tissue destruction (as a result of lung disease)

normal CO pumped though smaller vessels to increase pulmonary pressure

hypoxia reflex = pulmonary vasoconstriction = further increase in pulmonary vascular resistance

right ventricular failure due to elevated pulmonary pressures

73
Q

What are the typical symptoms seen in “cor pulmonale”?

A
  • maybe secondary to chronic pulmonary problems
  • distended jugular veins
  • anorexia and complaints of GI distress
  • Weight Gain
  • dependent Oedema
  • Enlarged liver and Spleen
  • Ascites (accumulation of fluid in peritoneal cavity)
  • increased peripheral venous pressure
  • fatigue
74
Q

What is Mitral stenosis?

A

mitral = valve btw left atrium and ventricle

stenosis = narrowing of vessel

thus narrower area to drain from atrium to ventricle

75
Q

What is Congestive Heart Failure?

A
  • both right and left heart failure
  • full combination of both systemic and pulmonary signs
76
Q

What are the four major causes of heart failure?

A
  1. ischaemic Heart Disease*
  2. Systemic hypertension*
  3. Valvular Heart Disease*
  4. Lung Disease to Right Heart Failure to Congestive Cardiac Failure

* vast majority of clinical cases are to do with 1st 3 either alone or together

77
Q

What are the basic symptoms of Heart Failure?

A

shortness of breath

pulmonary oedema

systemic venous congestion

oedema

(not all are present in all patients)

78
Q

How is heart failure typically diagnosed? What is the gold standard?

A

Echocardiogram = gold boi

there’s no routine lab tests but natriuretic peptides may become routine lab tests as increases in BNP are associated with early HF

79
Q

What is Dyspnea?

A

subjective symptom of shortness of breath or difficulty in breathing (hard to determine degree)

1st sign of HF

exact cause not understood but maybe

increase pulm BV = increase pulm BP = causes blood/fluid to move from capillary to alveoli = pulm oedema = reduced ventilation capacity due to increased perfusion

= pink frothy Sebucum

80
Q

Which type of heart failure is linked to dyspnoea?

A

Left Ventricular Heart Failure

81
Q

Why is left ventricular heart failure characterised by dyspnoea?

A

orthopnea = shortness of breath whilst supine as increase Venous return to heart from GIT and legs

paroxysmal nocturnal dyspnoea = sudden urgent SOB during sleep due to increase pulm venous pressure

recurrent alveolar haemorrhage = blood-stained sputum

82
Q

What is Systemic Venous Congestion?

A

in later stages of Heart failure

  • increase fluid retention (compensation from kidneys) = increase venous return to increase ventricular preload and volume overloading
  • increase venous blood as increase TPR due to increase Blood vol
  • early sign = distended jugular vein
83
Q

Why does systemic vascular congestion occur?

A

Due to increase blood volume and therefore TPR means that it is harder for blood to travel back to the heart as the pressure keeping the valves shut is greater than the pressure needed to open them

THUS blood especially travelling through the IVC is extremely hard and thus pools in liver

84
Q

During Congestive Heart Failure what is occurring during systemic venous congestion?

A

elarged liver from engorgment of lobular central veins and hepatic sinusoids

as IVC cannot drain into heart

can lead to hepatic ischaemia which is associate with fatty changes

85
Q

During prolonged HF what is occuring as a result of systemic venous congestion?

A
  • Liver function tests = abnormal
  • increased serum bilirubin and transamines
  • left ventricular dilation is radiological and ECG feature
  • increase CNS pressure = decrease CO
  • liver = nutmeg liver
86
Q

What is Oedema?

A

is the fluid accumulation in subcutaneous tissue specifically in the pleural, pericardial and peritoneal cavities

87
Q

what are the causes of oedema?

A

Hydrothorax (pleural effusion ot low protein transduction)

common in in congestive LHF

high systemic venous pressure

large pleural effusions

pericardial and peritoneal ascites = severe congestive HF

88
Q

What are other clinico-pathical features associated with HF?

A
  • renal or secondary renal failure = proteinuria common, not sereve
  • non-specific symptoms
    • nausea vomiting lethargy headache sleeping problems
    • prominent in elderly
89
Q

What are the causes of secondary renal failure and the non-specific symptoms that are associated with HF?

A

congestion in large venous beds of intestines

reduced cerebral BF

loss of skeletal muscle bulk

low grade amnesia

90
Q

What is valvular heart disease?

A

injury to the valves of the heart = 10% of cases of HF

Is valvular stenosis = narrowing of valves = obstruction to BF

91
Q

What are the main causes of valvular disease?

A

dilation of ventricles (increase cross-sectional area of valve orficies)

ischaemic fibrosis of left ventricle

calcific degeneration of aortic valve

scarring and calcification of cusps due to rheumatic fever

92
Q

What are problems that arise from Valvular Heart Disease?

A

valvular stenosis = via thiccening or calcification

valvular incompetance

fails to prevent reflux

infective or thrombotic nodules

impair norm mobility of valve

Pathophysiology 2.0 (19 decks)

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