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Intergrated physiology and pharmacology > ALL THINGS HEART <3 > Flashcards

ALL THINGS HEART <3 Flashcards

1
Q

What happens in the P,QRS and T wave?

A

P- atrial depolarisation
QRS- ventricular depolarisation
T- ventricular repolarisation

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2
Q

What are the 2 implications of long QT syndrome?

A

1.Triggered activity-
delay in repol means Na+ channels are activated again (after threshold reached) additional beat produced as a result, causing V.T and possible V.F
2.Re-entrant excitation
triggering of extra electrical activity in certain areas and time in the cardiac muscle- if the electrical activity backs up on itself- generates more A.Ps, causing V.T and possibly V.F

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3
Q

Symptoms of long QT

A

Syncope and palpitations

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4
Q

Treatment for long QT and its side effect

A

Beta blockers- atenolol etc. Can cause asthma, because it increases the risk of bronchoconstriction

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5
Q

What are the 3 main types of long QT and which channels are affected

A

LQT1- IKs, LQT2-IKr- both loss of function mutations, plateau is prolonged because not enough K+ is leaving the cell
LQT3-INa- gain of function mutation, Na+ channels open and don’t close, depol for longer

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6
Q

Symptoms for short QT

A

Syncope, palpitations and arrhythmias

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7
Q

What are the 2 types of short QT?

A

GoF- IKr,IKs and Ik1- too much K+ leaving the cell, repol too quick
LoF- Ica- channels open and close too early or don’t function normally

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8
Q

Treatments for short QT

A

Implanted defibrillator, K+ channel blockers may be effective

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9
Q

What are the 4 phases of the cardiac cycle?

A
  1. Inflow
  2. Isovolumetric contraction
  3. Outflow
  4. Isovolumetric relaxation
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10
Q

Brief summary of each phase

A 
1-rapid ventricular filling
diastasis
atrial contraction
2-ventricles contract
first heart sound
3-rapid ejection
decreased ejection
4-dicrotic notch
pressure in ventricles fall
second heart sound
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11
Q

What is happening to the valved in each of these phases

A

1-opening of AV valves
2-closing of AV valves
3-opening of SL valves
4-closing of SL valves

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12
Q

Which factors affect how much tension the cardiac muscle can produce

A
  1. Preload- the initial sarcomere length (EDV)

2. Afterload- opposing force and arterial pressure creates the afterload

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13
Q

What is isotonic contraction?

A

Contraction of the cardiac muscle focuses only on afterload

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14
Q

What is contractility and what causes it to increase

A

It is the innate ability of the heart to contract. In general contractility increases when more cross bridges form per stimulus
NA causes an increase in maximum force and velocity. Reducing time between beats also increases contractility.

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15
Q

What is the Fick principle?

A

The O2 content of the pulmonary vein is derived from the pulmonary artery blood and O2 uptake across the lungs

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16
Q

How do you measure cardiac output to the lungs?

A
  1. O2 uptake rate by volume and O2 content of expired air
  2. O2 (PA)- a catheter
  3. O2 (PV)- peripheral arterial blood
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17
Q

Other ways of measuring cardiac output to the lungs

A

Indicator solution
Thermodilution
Ultrasound

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18
Q

What controls cardiac output?

A

Intrinsic- homeometric and heterometric
Extrinsic- parasympathetic- chronotropic (negative) and sympathetic- chronotropic and ionotropic (positive)
Humoral (positive)

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19
Q

Blood flow=?

A

difference in pressure/ resistance

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20
Q

Transmural pressure=?

A

Tension/radius

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21
Q

Compliance=?

A

change in volume/ change in pressure

22
Q

What is the Windkessel effect?

A

The elastic nature of the arteries helping to dampen down large fluctuations in blood pressure- expand during systole, recoil during diastole

23
Q

How is tissue fluid formed?

A

Formed through the balance of fluid being transferred between the capillaries and tissue

24
Q

What forces balance- causing the net production of TF?

A 
Hydrostatic pressure (favouring fluid out of the capillaries)
Oncotic pressure (favouring fluid into the capillaries)
25
Q

What does TF formation depend on?

A
  1. difference in H.P
  2. difference in oncotic pressure
  3. capillary filtration coefficient
26
Q

What does the auto regulation of circulation consist of?

A

Myogenic regulation- keeps blood flow in vessels constant
Metabolite regulation- concentrations of metabolites
Flow= (pressure in arteries-pressure in veins)/ resistance

27
Q

What does the extrinsic control of circulation consist of?

A

Autonomic
Humoral
Local agents

28
Q

4 examples of local agents

A

Prostaglandins- vasodilator
Serotonin- vasoconstrictor
Histamine- vasodilator
Endothelium derived relaxing factor- vasodilator

29
Q

What does an ECG record?

A

The electrical activity of your heart, by measuring the voltage differences between 3 limb leads

30
Q

What does a high P wave amplitude suggest?

A

Atrial hypertrophy- enlargement of the atria- more muscle mass and thus more depolarisation resulting in a larger deflection

31
Q

What does a low T wave amplitude suggest?

A

Ventricular hypoxia- not enough O2 getting to the ventricles

32
Q

Examples of abnormal heart rate variations

A

Non-exercise tachycardia- 150-200bpm
Heart flutter- 200-300bpm
Fibrillation- 300bpm+

33
Q

What are the different types of heart block?

A

1st degree:
Slowing of conduction along pathway between the SA and AV node
Increased P-R interval
2nd degree:
Intermittent block
some SA impulses fail to evoke a QRS complex- problem between atria and ventricles-
2 TYPES- MOBITZ 1-
progressive prolongation of PR interval- resulting in a blocked p wave (thus QRS)- AV node fails- PR then resets
MOBITZ2-
disease of the His-purkinje system. May be no pattern to the conduction blockade or a fixed relationship between P waves and QRS complexes
3rd degree:
complete absence of AV conduction- ‘AV dissociation’
PR interval appears variable due to there being no relationship between the P waves and QRS complexes
Need a pacemaker fitted in the ventricles

34
Q

Characteristics of Mobitz 1 on an ECG

A

Progressive prolongation of the P-R interval
Until the AV node fails- QRS complex skipped
Cycle repeats again

35
Q

What is ‘circus movement?’

A

One of the major causes of clinical arrthymias
When an electrical signal completes an alternative circuit where it backs up on itself
Conditions:
1.Unidirectional block (due to local depol/change in functional anatomy)
2.A closed conduction loop
3.Sufficiently slow conduction

36
Q

What is atrial fibrillation?- details

A

Irregular/rapid beating of the atria
Due to many regions of re-entrant electrical activity
Symptoms= palpitations, perceived exercise intolerance, oedema of the ankles and occasionally angina
Treatment=
beta blockers, flecaindine
ECG= irregular distances between QRS complexes, no obvious P waves seen

37
Q

What is considered a normal diastolic BP?

A

Less than 80

38
Q

Difference between essential and secondary hypertension

A

Essential- risk factors involved but no clear genetic cause

Secondary- consequence of a clinical condition

39
Q

Causes of essential HT

A

Ageing
Cardiac dysfunction
Vessel abnormalities
Kidney dysfunction

40
Q

Causes of secondary HT

A

Renal disease
Renal artery stenosis (narrowing)
Tumour in adrenal gland tissue
Hormone imbalance

41
Q

2 differences in excitation-coupling in skeletal and cardiac muscle

A
  1. Initiation

2. Calcium release from S.R

42
Q

At a given preload, the velocity of shortening for cardiac muscle becomes……..with lower a afterload

A

GREATER

43
Q

At a given afterload, the velocity of shortening for cardiac muscle becomes…….with a greater preload

A

GREATER

44
Q

Whats the difference between chronotropy and ionotropy?

A 
Chronotropy= Heart rate
Ionotropy= Contractility
45
Q

What do Kinins and Angiotensin 2 do?

A

Kinins- vasodilator

Angiotensin 2- Vasoconstrictor

46
Q

What are the 3 main types of innervation of the blood vessels?

A
  1. Sympa- vasoconstriction
    - Adrenaline= n.mitter
    - widely distributed
  2. Parasympa- vasodilation
    - Acetylcholine
    - less common- erectile tissue etc.
  3. Sympa- vasodilation (skeletal muscle)
    - Acetylcholine
    - specialised system of sympathetic fibres
47
Q

What does parasympathetic control of cardiac output involve

A

Vagus nerve
Ach
Negative chronotropic effect
*(Atropine blocks action on Ach- increases heart rate)

48
Q

What does sympathetic control of cardiac output involve?

A

Cardiac nerves
Positive chronotropic and ionotropic effects
Noradrenaline

49
Q

Characteristics of Mobitz 2 on an ECG?

A

PR interval is constant from beat to beat-
every nth ventricular depolarisation is missing.
type 2 is considered more serious- more likely to progress to 3rd degree heart block

50
Q

Flourishes (lol)

A

120ml left ventricle- EDV
EDpressure - 8-12mmhg
Right EDpressure-3-6mmhg

ESV=50ML

51
Q

What is the V wave of the atria?

A

Phase 1-

peak in atrial pressure just before the mitral/tricuspid valve open

Intergrated physiology and pharmacology (19 decks)

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