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Myocardial ischaemia and cardiomyopathy Flashcards

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1
Q

Describe ECG characteristics for escape rhythm (nodal rhythm)

A

Regular RR interval

Absent P wave or P wave after QRS complex

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2
Q

What is a toxin that can trigger DADs? Describe the 5 step mechanism.

A

Digoxin

  • Blocks the Na+/K+ ATPase
  • Na accumulates inside the cell
  • Increased Na blocks Na+/Ca+ exchanger
  • Ca+ can’t leave the cell
  • Resting membrane potential increases towards threshold
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3
Q

What is eccentric hypertrophy and what stimulus leads to this?

A

Thin walls and large cavities = chamber enlargement

Sarcomeres added in series increase myocyte cell length

Stimulus = volume overload

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4
Q

Describe ECG characteristics for third degree AV block

A

RR interval is regular

PP interval is regular but some blocked by QRS complex

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5
Q

Differentiate transmural and diffuse subendocardial myocardial infarctions.

A

Transmural
- full thickness of ventricle wall
- distribution of coronary artery
- associated with acute coronary AS plaque rupture and superimposed thrombosis

Subendocardial
- inner 1/3 to 1/2 ventricle wall
- not acute
- associated with diffuse stenosing coronary AS and global reduction in blood flow

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6
Q

Outline role of carotid sinus massage

A

Detecting arrhythmias or diagnosing carotid sinus syndrome.

Carotis sinus hypersensitivity = exaggerated response to pressure applied to the carotid sinus

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7
Q

Morphology of sudden cardiac death (secondary to IHD)

A

marked atherosclerosis

coronary thrombosis

LV hypertrophy

myocardial scarring, no acute infucktion

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8
Q

ECG characteristics of ventricular tachycardia

A

> 3 ectopic beats in succession

Sharp R waves with shoulders that may be P or T waves

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9
Q

Define chronic IHD (ischaemic cardiomyopathy)

A

Patients who insidiously develop congestive cardiac failure as a consequence of ischaemic damage.

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10
Q

Define delayed after-depolarizations (DADs)

A

Waves in the membrane potential that occur after full repolarisation.

Associated with high intracellular calcium concentrations - can raise the cell’s membrane potential to threshold.

This can lead to fast HR.

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11
Q

How does angiotensin II play a role in cardiac remodelling?

A
  • Up regulating AT1 receptors and TGF-beta1
  • Activating fibroblasts
  • Promoting synthesis of collagen

Leading to fibrosis

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12
Q

Define early after depolarizations (EADs)

A

Waves in the membrane potential that occur during repolarisation.

Caused by abnormal reactivation of ion channels or when repolarisation is slowed down (long QT interval).

Can lead to torsades de pointes, tachycardia and other arrhythmia

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13
Q

ECG characteristics of atrial flutter and atrial fibrillation.

A

Atrial flutter
- Sawtooth pattern (regular PP interval)
- Regular RR interval

Atrial fibrillation
- RR interval irregular
- no visible P waves

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14
Q

Outline pulmonary edema in terms of HF

A

Most severe form of left HF

Right ventricular output > left
Pressure backs up
Fluid leak into pulmonary interstitial spaces
Hypoxia and poor O2 exchange

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15
Q

Define pulmonary hypertensive heart disease

A

RV enlargement secondary to pulmonary hypertension caused by disorders that affect the lungs or pulmonary vasculature

(exclude RV dilatation/ hypertrophy due to LV and congenital heart disease)

Acute follows massive pulmonary embolus

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16
Q

Effect of HF on Frank-Starling curve

A

HF + treatment (inotropic agents such as digoxin) = reduced SV over EDP

HF = reduced (again) SV over EDP

Reduced SV per EDP = decreased contractility = reduced cardiac performance at a given preload

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17
Q

Outline systemic edema in terms of HF

A

Unresolved left failure: eventually leads to right sided failure by venous congestion in the systemic circulation

Left ventricular output > right
Pressure backs up
Fluid accumulates in systemic tissue

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18
Q

List 4 common tachycardias

A

Sinus tachycardia
Ventricular tachycardia
Premature ventricular complex
Torsades de pointes

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19
Q

Describe ECG characteristics for second degree Mobitz type 1 AV block

A

Regular RR interval

PR interval increasing until QRS complex skipped, repeat

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20
Q

List 3 non-ischaemic cardiomyopathies

A
  • Dilated (most common non-ischaemic)
  • Hypertrophic
  • Restrictive
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21
Q

Define congestive heart fialure

A

Pathophysiological state resulting from impaired cardiac function whereby the heart cannot output enough blood sufficient to meat the metabolic demands of the organs and tissues of the body

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22
Q

3 types of pacemakers

A

Single chamber
Double chamber
Rate responsive

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23
Q

Define hypertensive heart disease

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A

LV hypertrophy in absence of other CV pathology but history of hypertension

  • heart weight > 20% of predicted (500g)
  • LV concentric hypertrophy
  • coronary artherosclerosis
  • heart failure leads to LV dilation
24
Q

Chronic heart disease morphology

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A

moderate/severe stenosis by atherosclerosis and sometimes complete occlusion

discrete healed grey-white scars

may have pericardial adhesions

25
Describe ECG characteristics for second degree Mobitz type 2 AV block
RR interval regular or irregular PR mostly constant. QRS may be dropped consistantly or randomly
26
Describe familial hypercholesterolaemia
Autosomal dominant Affects how cholesterol (LDL) is cleared Accelerates premature atherosclerotic CVD by 15-20 yrs 1 in 250 people
27
What is concentric hypertrophy and what stimulus leads to this?
Thick walls and small cavities = wall thickening Sarcomeres added in parallel increase myocyte cell width Stimulus = pressure overload
28
Define re entry
A type of cardiac arrhythmia that occurs when an electrical impulse continues to circulate in a closed loop. A transient block = area of myocardium with delayed transmission of signal. In this area, contraction occurs after the rest of the myocardium has finished contracting. Once the signal is passed through the transient block, it stimulates the rest of the myocardium to contract again = ectopic beat.
29
Describe mycoyte remodelling post MI
Eccentric hypertrophy - regional dilation; change to spherical rather than elliptical - apoptosis and fibrosis; thinning of infarct zone
30
Mechanism of ANP/BNP in reducing BP
Vasodilation Decrease sodium reabsorption Inhibit SNS Increase water and salt excretion Decrease cardiovascular response All = decrease BP
31
Clinical picture of left HF (8)
Dyspnoea Cough orthopnoea Paroxysmal nocturnal dyspnoea Productive cough with pink frothy sputum Tachypnoea Pale, possibly cyanotic Clammy and cold skin Crackles/wheezes
32
What is a premature ventricular complex?
Short runs of inappropriate activity where the heart beat is initiated by Purkinje fibers in the ventricles rather than SA node. Impulse has to travel from myocyte to myocyte = wide complex QRS. Ventricles contract before atria have optimally filled the ventricles, therefore, ejection is suboptimal and circulation is inefficient
33
When is cardiac rupture most likely to occur post infarction?
4 days post infarction due to disintegration of myofibers
34
List classes of heart failure based on level of patient activity
Class I - no physical limitations Class II - slight limitations in physical activity. Symptomatic at ordinary physical activity Class III - marked limitations in physical activity. Symptomatic at less than ordinary physical activity Class IV - inability to carry on physical activity without discomfort. Angina may be present at rest.
35
How are BNP/ANP and angiotensin II related in heart failure.
ANP/BNP (more so BNP) are increased in patients with heart failure. BNP has anti fibrotic effect = local control of ventricular remodeling in the presence of NPR-A receptors
36
4 types of pericardial disease
1 pericardial effusion 2 haemopericardium 3 pericarditis 4 pericardial tumours
37
What is a bread and butter heart?
A heart with fibrinous pericarditis
38
3 primary cardiomyopathies 5 secondary cardiomyopathies
Primary - genetic 1 dilated (globular) 2 hypertrophic 3 restrictive (rigid) Secondary - 1 ischaemic 2 valvular 3 hypertensive 4 inflammatory 5 systemic disorders
39
Cardiac disease other than ischaemic
cardiac hypertrophy hypertensive heart disease pulmonary hypertensive heart disease
40
What is the most common form of myocarditis?
Viral myocarditis - histology shows interstitial lymphocytic infiltrates
41
Clinical picture of right HF
Pressure back up into venous system JVD Hepatomegaly Edema (legs and ankles) Abdomen - ascites
42
Describe ECG characteristics for first degree AV block
Regular RR interval PR interval delayed, but regular
43
Treatment of myocardial ischaemia?
Thrombolysis Angioplasty/stenting Coronary bypass grafts
44
Microscopic appearance of area of infarct timeline
Coagulative necrosis not detectable for 4-12 hrs 4-12 hrs beginning necrosis; haemorrhage; oedema; early neutrophilic infiltrate 24 - 73 hr total necrosis 3 - 7 days disintegration of dead myofibres and resorption by macrophages 10 days well developed phagocytosis; prominent granulation tissue 7 weeks scarring complete
45
Describe torsades de pointes?
Polymorphic ventricular tachycardia. Marked by rhythmic short and tall undefined waves. Can be caused by long QT syndrome Characteristic illusion of twisting of the QRS complex around the isoelectric baseline.
46
Define myocarditis
Inflammatory involvement of the heart muscle characterized by leukocytic infiltration and necrosis of myocytes
47
Why are blood clots likely in atrial fibrillation and atrial flutter?
Atria quiver rather than contract and therefore, fail to pump all the blood out. The blood then pools and can form clots.
48
Indications, positive finding and therapy for carotid sinus syndrome?
Syncope! Ventricular pause > 3s and/or fall in sys BP > 50mmHg defines carotid sinus hypersensitivity Cardiac pacing
49
Outline mechanisms leading to ventricular dilation
Lengthening of cardiac myocytes mediated through cardiac hypertrophy and the addition of sarcomeres Cardiomyocyte slippage due to collagen changes - collagen connections between myocytes are disrupted and side-to-side slippage occurs
50
Macroscopic appearance of area of infarct 6-12 hours to weeks (4)
Hrs: dark mottling < 10 day: hyperaemic border, central yellow area > 10 days: red gray depressed infarct, rimmed by hyperaemic zone Proceeding weeks evolves to fibrous tissue
51
What is an explanation for the attenuated response to natriuretic peptides in chronic heart failure?
NPR-A downregulation Desensitization to cGMP due to chronically high ANP and BNP
52
Outline physiological and pathological hypertrophy.
Physiological stimulus (e.g. post natal development) = insulin growth factors - leads to physiological hypertrophy Pathological stimulus (e.g. volume or pressure overload) = angiotensin II / endothelin I - leads to pathological hypertrophy
53
Describe atrial structural changes occurring during early atrial fibrillation
Cardiomyocyte remodelling is induced by stretch. Induces signal transduction that leads to increased expression of growth factors. Structural remodelling includes: dedifferentiation, myolysis, apoptosis, fibrosis, hypertrophy.
54
Outline role of ANP and BNP
Atrial natriuretic peptide and brain natriuretic peptide = regulate blood volume and vascular tone. Released in response to stretch in the atria and ventricles respectively. Antagonistic to angiotensin II Both hormones are elevated in heart failure.
55
List 3 pharmaceutical treatments and their function
ACE inhibitors and diuretics = decrease fluid load Digoxin (dobutamine) = improve contractility Beta blockers = decrease heart rate = decrease heart workload

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