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BRS1 - Valentine > Cardiovascular disorder > Flashcards

Cardiovascular disorder Flashcards

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1
Q

What are cardiomyopathies?

A

Disorders that affect the cardio myocytes or cardiac muscle function

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2
Q

Give examples of cardiomyopathies?

A
  • Heart failure
  • Tako Tsubo syndrome
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
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3
Q

What is the definition of heart failure and what could it lead to?

A

Heart unable to maintain adequate circulation for metabolic requirements of the body

this can lead to:

  • Preserved ejection fraction (HFpEF): where Ejection fraction is more than or equal to 50% and theres reduced diastolic function
  • Reduced ejection fraction (HFrEF): where EF is 40% or more and there’s reduced systolic function
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4
Q

Describe what happens to the heart in HFrEF (systolic)

A

ECCENTRIC cardio myocyte growing; left ventricle is more dilated

Can be treated pharmacologically

not enough strength to pump blood

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5
Q

What happens in HFpEF

A

Concentric increase in left muscle muscle mass

Have problem relaxing (Diastolic)

Pharmacological interventions aren’t very useful

Hypertension maybe most lijkely cause

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6
Q

What are the underlying causes of heart failure

A

Secondary to:

  • cardiac damage (ischaemia, myopathy )- HFrFR
  • hypertension- HFpEF
  • valve disease
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7
Q

What are the effects of heart failure on cardiac output and the life expectancy

A
  • Reduced cardiac output - venous blood accumulation as a result
  • Poor prognosis- 50% mortality rate in 5 years
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8
Q

What are the general symptoms of Heart failure; are they sufficient to confirm diagnosis? If not what is

A

General symptoms:

  • Breathelssness, fatigue
  • Fluid retention caused by cardiac dysfunction

not sufficient hence need markers in blood to confirm like”

Atrail natriuretic peptide or BNP levels

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9
Q

What are the ECG findings and diagnosis of Heart failure - what is the significance

A

Enlarged QRS complex

however this is not specific and this ECG result can be caused by Atrila fibrillation or Hypertrophy

need BNP levels with ECG TO CONFIRM

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10
Q

What is Dilated Cardiomyopathy

A

Cardiomegaly and dilation, systolic dysfunction with hypo-contraction

i.e- this is a type heart failure with reduced ejection fraction

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11
Q

What is the underlying cause of Dialted cardiomyopathy

A

Congenital - 20-50% familial

secondary to Anterior MI

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12
Q

What is it’s (dilated cardiomyopathy)effects on cardiac output and life expaectancy

A

Reduced cardiac output - and ejection fraction lower than 40%

end stage annual mortality of 10% to 50%

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13
Q

What investigations would you perform and what ECG findings would you see on Dilated cardiomyopathy

A

General symptoms:

  • Dyspnoea, fatigue

ECG findings - no specific feature the abnormalities similar to Left ventricular hypertrophy

enlarged QRS complex

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14
Q

What is the definition of Hypertrophic cardiomyopathy

A

Unexplained left ventricular hypertrophy- primarily affects the interventricular septum

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15
Q

What are the causes of Hypertrophic cardiomyopathy

A

Congenital; usually familial, autosomal dominant inheritance

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16
Q

What are the effects of hypertrophic cardiomyopathy on cardiac output and life expectancy

A

Reduce cardiac output

can cause sudden cardiac death during exercise

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17
Q

What investigations would you need to perform on someone you suspect to have Hypertrophic cardiomyopathy

A

Same as Dialted cardiomyopathy

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18
Q

What is Tako tsubo syndrome

A

Left ventricular syndrome where the apex balloons (like a Japanese octopus pot)

symptoms Mimic MI especially in ECG readings but there aren’t MI markers in blood

Broken heart syndrome- occurs later in life due to stressful event/trauma

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19
Q

What causes Tako tsubo syndrome

A

Stressful event

women are mor predisposed to it

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20
Q

What are the effects of Tako tsubo syndrome on cardiac output and life expectancy

A

Reduced cardiac output- 40%

5% mortality rate

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21
Q

What are the general symptoms and investigation results of Tako tsubo syndrome

A

Chest pain

increased cardiac biomarkers

Normal blood vessels

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22
Q

What are the ECG findings for Tako tsubo syndrome

A

ST segment elevation

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23
Q

What are the conduction abnormalities - give examples

A

Atrail arrhythmia- Atrial fibrillation or Wolf Parkinson white syndrome

Ventricualr arrhythmia - Ventricular fibrillation or Torsade de pointes

Tachycardias- sinus or atrial tachycardia

conduction block: AV block or bundle branch block

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24
Q

Define conduction abnormallty

A

Disorders that affect bioeelectrical transmission along the heart

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25
What is the normal range for the cardiac axis
-30 to +90 degrees
26
What is the PR interval
Slow conduction through AV node should not be more than 0.2s
27
What is the QT interval and it's significance
Shows total duration of ventricualr depolarisation and repolarisation High QT interval can lead to heart failure also QT interval depends on heart rate:- High rate will have lower QT and low heart rate will have high QT. Hence it must be corrected using QTc using Bazetts equation
28
What does the QRS complex shows?
Ventricular depolarisation should be less than 0.12s large QRS complex shows more muscle mass
29
What is Atrial fibrillation and what can it lead to if it becomes untreated
Disorganised electric activity and contraction in atria. MULTIPLE ectopic beats not all blood is pumped out of atria- can form embolism and go to the Brain
30
What are the underlying causes of atrial fibrillation
Ectopic focus develop in atria- can be associated with pulmonary veins
31
What is the effect of atrial fibrillation on cardiac output and life expectancy
Modest decline in cardiac output increased risk of heart failure and stroke
32
What are the ECG findings for atrial fibrillation
Absent p waves, irregularly irregular rhythm and fibrialltory waves this is becuase not all waves of depolarisation pass to AVN; and dont know which focus passes AP down. no atrial contraction.
33
What is WPW Syndrome
This causes tachycardia and abnormal cardiac electrical conductance this is due to accessory conduction pathway (through left bundle of Kent or the right atria-less common-) between atrial and ventricles.
34
What are the effects of WPW on cardiac output and life expectancy
Cardiac output unchanged Normal life expectancy
35
What are the ECG findings for WPW syydrome
Pre-excitation- QRS complex of ECG: AP occurs sooner than expected- doesnt pass through AVN Biphasic/inverted T waves- AP stil come from bundle of Kent. Hence early depolarisation cancels out repolarisation
36
What are the symptoms and treatment of WPW
Symptoms: chest pain and palpitations- like most other conduction abnormalities s Treamtent- surgically or radiographically remove bundle of Kent or right atrial accessory pathway origin DONT GIVE: ACEI, BB, CCB or Digoxin
37
What is the definition of AV block and how many different types do we have?
Impaired electrical conduction through AV node Type 1, 2 or 3: worst at type 3
38
What is the underlying cause of AV block
Fibrosis or calcification of conduction system in Type 1- this occurs in AV node in Type 2 or 3- this occurs in purkinje system or bundle of HIS
39
What is the effect of AV block on cardiac output
Decreases it
40
What are the ECG findings for each type of AV block
Type 1- longer PR interval Type 2- longer PR interval but ther'e's 1 beat loss of AV conduction Type 3- complete and persistent loss of conduction form atria to the ventricle; hence AVN generates its own AP
41
What is Bundle branch block?
Impaired electrical conduction to the right or left branches or fascicles of the bundle of HIS
42
What is the underlying causes of bundle branch blocks
LBBB- ischaemia/heart disease RBBB- benign or asymptomatic
43
What is the effect of bundle branch block on cardiac output
LBBB- usually lower cardiac output
44
What are the ECG findings for bundle branch blocks and in fascicles
RBBB and LBBB: widened QRS complex Fascicles blockage: * POSTERIOR fascicles - left cardiac axis deviation * anterior- right cardiac axis deviation
45
What is MI and distinguish it from angina
MI: acute coronary syndrome- cardiac tissue damage due to coronary artery blockage. Heart muscle is necrosed Angina: pain or discomfort starting from chest and radiating outwards. No cardiac markers. Bradykinin causes pain Unstable angina: if this occurs at rest - normally caused by STEMI Stable angina- caused by exertion but pain stops at rest Vasospactic - same as unstable
46
What is the effect of MI on cardiac output and life expectancy
Depends on site of blockage but it will most likely decrease cardiac output high mortality if untreated
47
What are the ECG findings for MI
ST elevation (STEMI): caused by complete blockage NSTEMI: caused by partial blockage the lead seen on is dependent on where the blockage is
48
What is the definition of hypertension
Clinic BP- greater that 140/90 mmHg ambulatory BP machine daytime average of greater than 135/85 mmHg taken over a period of a few months and several visits
49
What are the effects of Hypertension on Q and Life expectancy (prognosis)
Potentially reduce Q can lead to kidney disease or heart failure and Mi can lead to stroke
50
What are the ECG findings and General symptoms of Hypertension
General - asymptomatic, require BP monitoring ECG features - no specific features
51
During heart failure there's a poor ventricular contraction; describe how this can create a vicious cycle
The pathological heart muscle wall can withstand the stress and hence pump out less blood- which continues the cycle
52
What drugs directly affect afterload
Calcium channel blockers
53
What drugs are licensed for HF?
* Beta blockers * ACEI * Ang-II receptor blockers * Neprilysin inhibitor * Diuretics * Vasodialtors * Digoxin * AVP antagonist * Ivabredine (funny current inhibitor) * aldosterone antagonist
54
How can Hyperkalimia kill people
Stops heart from beating they increase the Resting membrane potential Na channels are active but they remain inactivated as they cannot overcome block
55
Define Ventricular arrhythmia fibrillation
Aryythmia originating from Bundle of HIs- purkinje system or ventricular myocytes Ventricles contract at rates of esteem 150-400bpm
56
What are the underlying causes of ventricular fibrillation
Structural heart disease, MI or congenital
57
What is the effect of ventricular fibrillation on cardiac output and life expectancy
Can lead to complete loos of cardiac output death can ensue in seconds to minutes
58
What would you find in an ECG reading for ventricular fibrillation and what are the presenting symptoms
Symptom: SYNCOPE ECG findings: Irregular deflections, difficult to identify PQRST waves
59
Define Torsade de pointes syndrome - Ventricular arrhythmia
Polymorphic ventricular tachycardia that occurs due to a **long QT interval . This causes an ectopic beat to form in ventricles** Long QT interval could be due to prolonged repolarisation caused by hypomagnesaeimia **THIS IS NOT THE ECG FINDINGS**
60
What is the underlying cause of Torsade de pointes
Congenital Acquired QT interval prolongation - due to reduced repolarisation
61
What are the effects of Torsade de pointes on cardiac output and life expectancy
Reduced cardiac output Can automatically resolve OR progresses to deadly Ventricular fibrillation
62
What are general symptoms of TORSADE DE POINTES or ECG findings
General symptoms : Chest pain, syncope ECG findings Characteristic "twisting around the point"
63
Compare and contrast Sinus Tachycardia and Atrial Tachycardia
Both: ATRIAL RATE is between 100-250 bpm Differences: * Atrial Tach: p waves NOT ALWAYS followed by QRS complexes * Sinus Tach: p waves ALWAYS followed by QRS complexes
64
What is the underlying cause for Snius Tach and Atrial Tach
Sinus Tach: Physiological Atrial Tach: ONE Ectopic source of atrial beat
65
What are the effects of STach and ATach on cardiac output and life expenctancy
Cardiac output- unchanged or SLIGHTLY decreased Little impact on life expectancy
66
What would you find on ECG for STach and ATach
STach- normal but faster atrial rate ATach- **solitary p waves seen**
67
If there's Anterior infarction, in what leads would there be ST segment elevation
V1- to V4 No reciprocal ST depression
68
If there's Lateral infraction in what leads would there be ST segment elevation and depression (leads that in opposite) where's the occlusion
ST elevation - in leads 1, aVL, V5 and V6 ST depression - Lead 2, 3 and aVF this suggests there's an occlusion in circumflex artsy or lateral branch of left anterior descending artery
69
In inferior infarction, where would you see ST segment elevation and depression where's the occlusion
ST elevation - LEADS 2,3 ad aVF ST depression- leads 1 and aVL occlusion in right ventricle
70
In Posterior infarction, where would you see ST elevation and depression
ST elevation - leads 2, 3 and aVF as well as V7-V9 ST depression , V2 and V3
71
What does a saw toothed p wave indicate
Atrial flutter
72
What does prolonged p wave indicate ?
Could indicate left atrial enlargement
73
What is the ECG reading for a first degree AV heart block?
PR interval greater than 0.20s
74
What is the ECG reading for a second degree AV block - Type 1
PR intervals become progressively longer until one P wave is completely blocked and produces no QRS complex. There's a pauses as the AV node recovers. Cycle is then repeated
75
What is ECG reading for a 2nd degree AV block- type 2
Conduction ratio (P waves: QRS complexes )- this is 2:1 or 3:! Or 4:1 QRS complexes wider atrial rate faster than ventricular rate atrial rhythm is regular but ventricular rhythm is irregular add diagrams
76
What is the ECG reading for. 3RD DEGREE AV block
P waves dissassociated from QRS complex as atria and ventricles act indpedently Atrial rate is 100bpm ventricular is less than 40bpm

BRS1 - Valentine (54 decks)

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