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Phase 1 Cardio > Phsyiology > Flashcards

Phsyiology Flashcards

1
Q

What is hemopoesis?

A

Formation of blood cellular components. All blood components are derived from haematopoeitic stem cells.

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2
Q

What is anaemia?

A

Too few blood cells - low Hb levels

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3
Q

What is hypoxia?

A

Low levels of oxygen in your body tissues

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4
Q

What is polycythaemia?

A

Increase in RBC in the body
Primary - abnormality in bone marrow that form RBC
Secondary - disorder outside the bone marrow that causes overstimulation of normal bone marrow - overproducing RBC

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5
Q

What is thrombosis?

A

Blood clot

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6
Q

What are corpuscular issues that cause anaemia?

A

Issues can happen with:
- Membrane
- Haermoglobin - thalassemia, sickle cell etc
- Enzymes

This is mainly haemolysis

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7
Q

What are extra corpuscular issues that cause anaemia?

A
  • reduced production
    Iron, B12,Folate deficiency, chemotherapy
  • increased destuction/loss
    Bleeding, haemolyiss, auto/alloimmune, mechanical, other
  • redistribution (hyperslenism)
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8
Q

What is sickle cell disease?

A

Diff in

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9
Q

What is Acute chest syndrome?

A
  • chest, pain, fever, dyspnoea, cough
  • diff from pneumonia
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10
Q

What is innate immunity?

A
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11
Q

What is adaptive immunity?

A
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12
Q

What is humoral and cellular immunity?

A
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13
Q

What is the lymphoid journey?

A
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14
Q

What are abnormalities of the WBC?

A

Neutrophil leukocytosis/ neutropenia
•Eosinophilia/eosinopenia
•Basophilia
•Monocytosis/ monocytopenia
•Lymphocytosis/ lymphopenia
•Myeloid malignancies (AML, MDS, MPN)
•Lymphoid/plasma cell malignancies ( ALL, Lymphoma-T/B/NK , HG-LG,Hodgkin/Non-Hodgkin, multiple myeloma)

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15
Q

Describe RBS

A
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16
Q

Describe WBC

A
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17
Q

Describe platelets

A
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18
Q

What is the structure of platelets?

A

Plasma membrane
•Cytoskeleton
•Dense tubular system
•Secretory granules
alpha ( e.g.VWF,PF4,plasminogen)
dense ( e.g. serotonine)
lysosome
peroxisome

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19
Q

What occurs in platelet activation?

A
  1. Initiation
    Endothelial injury-collagene/vWF-PLT monolayer (PLT GPVI,GPIb-IX-V receptors)-PLT shape change/tethering/spreading/rolling/
    adhesion
  2. Propagation
    Granular release (ADP,TXA2),PLT activation (GPIIb-IIIa –fibrinogen receptor),aggregation
  3. Stabilisation
    Primary PLT thrombus/white clot-coagulation cascade –thrombin- fibrin network
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20
Q

What are the different types of bleeding?

A

PLT and haemophilia

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21
Q

What is PLT type of bleeding?

A

thrombocytopenia/thrombocytopathy)
•Hx of skin & mucosal bleeding (GI,GU), early post-procedural bleeding (minutes)
•Petechial rash
•WF disease,ITP,congenital thrombocytopathy,
•medication,liver disease, renal failure

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22
Q

What is haemophilia type of bleeding?

A

factor deficiency)
•Hx of muscle/joint bleeding, late post-procedural bleeding ( hours, days)
•Large suffusions,haematomas
•Haemophilia A,B,C

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23
Q

What occurs in the cardiac action potential?

A
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24
Q

What is ohms law?

A

V = I R
V = voltage
I = current
R = resistance

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25
Q

What do the P wave, QRS complex and T wave represent?

A

P wave = atrial depolarisation
QRS complex = ventricular depolarisation
T wave = ventricular repolarisation

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26
Q

What is diff between Atrial fibrillation and Atrial flutter?

A

A fib:
- random atrial activity
- random ventricular capture
- irregularly irregular rhythm

Flutter:
- organised atrial activity - 300/min
- ventricular capture at ratio to atrial rate (2:1 = 150bpm)
- Usually regular/ irregular if ratio varies

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27
Q

What is the PR interval?

A

Allow atria to contract before ventricular systole
120-200ms (3-5 squares)

Long - suggests heart block 1st degree
Delayed AV conduction

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28
Q

What is the difference between ECG electrodes and leads?

A

Electrode
•Physical connection to patient in order to measure potential at that point
•10 electrodes to record a 12 lead ECG

Lead
•Graphical representation of electrical activity in a particular ‘vector’
•Calculated by the machine from electrode signals

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29
Q

What is the difference between bipolar and unipolar leads?

A

Bipolar lead
•Measures the potential difference (voltage) between two electrodes
•One electrode designated positive, the other negative

•Unipolar lead
•Measures the potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative)
•Sometimes known as augmented leads

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30
Q

What does a neutral electrode do?

A

Neutral electrode
- Reduces artefact – not directly involved in ECG measurement

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31
Q

What is the resting membrane potential like in the heart?

A

Membrane of heart muscle cell
•Normally only permeable to K+
•Potential determined only by ions that can cross membrane

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32
Q

How is a negative membrane potential created?

A

Negative membrane potential
•K+ ions diffuse outwards (high to low concentration)
•Anions cannot follow
•Excess of anions inside the cell
•Generates negative potential inside the cell

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33
Q

What are the myocyte membrane pumps?

A

Myocyte membrane pumps
•K+ pumped IN to cells
•Na+ and Ca2+ pumped OUT of cells
•Against their electrical and concentration gradients
•Therefore requires active transport (Na+-K+ pump)
•Requires ATP for energy

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34
Q

What is the Nernst equation?

A

E= 60log (conc outside/conc inside)

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35
Q

What is each phase of the cardiac action potential?

A

Phase 4 - resting potential
Phase 0 - depolarisation - Na+
Phase 1 - Initial repolarization - K+
Phase 2 - plateau - Ca+/K+
Phase 3 - repolarisation - K+
Phase 4 - maintenance of resting potential

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36
Q

What is the reason for all the electrical activity?

A

Contraction of the heart muscles requires delivery of Ca2+ ions to the cytoplasm

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37
Q

What occurs in excitation-contraction coupling?

A

Step 1: Ca influx
Step 2: Amplification of Ca with Na
Step 3: Ca induced Ca release

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38
Q

What is Troponin-tropomyosin actin complex?

A

•Calcium binds to troponin
•Conformational change in tropomyosin reveals myosin binding sites
•Myosin head cross-links with actin
•Myosin head pivots causing muscle contraction

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39
Q

What are specialist conduction tissues?

A
  • SAN
  • AVN
  • His/purkinje system
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40
Q

What is the phase 4 slope affected by?

A
  • autonomic tone
  • drugs
  • hypoxia
  • electrolytes
  • age
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41
Q

What is the autonomic control of the heart?

A

Sympathetic stimulation
•Increases heart rate (positively chronotropic)
•Increases force of contraction (positively inotropic)
•Increases cardiac output

•Parasympathetic stimulation
•Decreases heart rate (negatively chronotropic)
•Decreases force of contraction (negatively inotropic)
•Increases cardiac output

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42
Q

What is sympathetic stimulation affected by?

A

Controlled by:
•Adrenaline and noradrenaline + type 1 beta adrenoreceptors
•Increases adenylyl cyclase  increases cAMP

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43
Q

What is parasympathetic stimulation affected by?

A

•Controlled by:
•Acetylcholine
•M2 receptors – inhibit adenyl cyclase  reduced cAMP

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44
Q

What does the AV node do?

A

Transmits cardiac impulse between atria and ventricles
•Delays impulse
•Allows atria to empty blood into ventricles
•Fewer gap junctions
•AV fibres are smaller than atrial fibres
•Limits dangerous tachycardias

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45
Q

What is automaticity?

A
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46
Q

What does the refractory period do?

A

•Prevents excessively frequent contraction
•Allows adequate time for heart to fill

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47
Q

What is thrombosis?

A

Thrombosis
- Formation of clot (thrombus) inside blood vessel
- Platelets have a central role in arterial thrombosis
•Heart attack (myocardial infarction)
•Stroke
•Sudden death

•Antiplatelet medications can be life-saving

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48
Q

What is atherogenesis?

A
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49
Q

What is atherothrombosis?

A
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50
Q

What happens to platelets first?

A

Shape change
Smooth discoid- speculated +psuedopodia
- increases SA
- increases possibility of cell-cell interactions

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51
Q

What do glycoprotein 2b/3a (GPIIb/IIIa) do?

A

•Platelet activation
•Increases number of receptors
•Increases affinity of receptor for fibrinogen
•Fibrinogen links receptors, binding platelets together (platelet aggregation)

•Also known as integrin aIIbb3

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52
Q

What happens after an atherosclerotic plaque rupture?

A

After atherosclerotic plaque rupture
•Platelets adhere to damaged vessel wall
•Collagen receptors bind to subendothelial collagen which is exposed by endothelial damage
•GPIIb/IIIa also binds to von Willebrand factor (VWF) which is attached to collagen
•Soluble agonists are also released and activate platelets

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53
Q

What does aspirin do?

A

Inhibits amplification pathway

54
Q

What does platelet activation lead to?

A

This leads to:
•Shape change
•Cross-linking of GPIIb/IIIa
•Platelet aggregation

55
Q

What happens to arachnoid acid?

A

Converted into prostaglandins by COX

56
Q

What does Cox 1 and 2 do?

A

COX-1
Mediates GI mucosal integrity
Thromboxane A2-mediated platelet aggregation
COX-2
Mediates inflammation
Involved in prostacyclin production, which inhibits platelet aggregation and affects renal function

57
Q

What does aspirin inhibit?

A

Aspirin
Low dose aspirin inhibits COX-1 and high dose aspirin inhibits both COX-1 and COX-2

58
Q

What does ADP activate?

A

ADP activates P2Y1
-Causes platelet activation
-Results in GPIIb/IIIa fibrinogen cross-linking and aggregation

ADP activates P2Y12
-Sustains platelet activation and aggregation

59
Q

What do dense granules do?

A

Dense granules release ADP, which causes further activation

Activation of GPIIb/IIIa also amplifies platelet activation

60
Q

What does thrombin do?

A

Thrombin activates protease-activated receptors (PAR) on platelets

This leads to platelet activation and release of ADP, which amplifies this activation

61
Q

What does inhibition of translocase and activation of scrambles lead to?

A

Inhibition of translocase and activation of scramblase leads to expression of aminophospholipids on the outer platelet membane, which allows assembly of prothrombinase complex and generation of thrombin

62
Q

What is platelet procoagulant activity?

A

activated platelets catalyse thrombin generation, creating an amplification loop that also links with coagulation (the production of fibrin)

63
Q

What are the anti-fibrinolytic factors?

A
64
Q

What feature do platelets have?

A

Platelets have pro-inflammatory and prothrombotic interactions with leukocytes and release inflammatory mediators from a granules

65
Q

How do antithrombotic drugs work?

A
66
Q

What measurements must you know on an ECG?

A

5 big squares = 1s

67
Q

What do deflections show?

A

Positive
Negative
Baseline

68
Q

What is the SAN known as?

A

Pacemaker of the heart

69
Q

How long is QRS complex?

A

Less than 120ms (3 small squares)
Prolonged - bundle branch block most common cause
- issues with ventricles
William marrow ?

70
Q

How long is the QT interval?

A

Measure of time to ventricular repolarisation
Onset of QRS end of T

Men - 350-440ms
Women 350-460ms

71
Q

What causes the deflections?

A

+ve electrode at +ve source = positive deflection
Current flow towards lead

+ve electrode at -ve source = negative deflection
Current flow away from lead

72
Q

What does Right leg lead do?

A

Neutral electrode - reduces artefact - not directly involved in ECG measurement

73
Q

What are the cardiac cycle phases?

A

LV contraction
- isovolumetric contraction
- maximal ejection
LV relaxation
- start relaxation and reduced ejection
- isovolumetric relaxation
- Rapid LV filling and suction
- Slow LV filling (diastasis)
- atrial booster

74
Q

What occurs in systole?

A

Ventricular contraction

Wave of depolarisation arrives,
•Opens the L-calcium tubule, {ECG: Peak of R},
•Ca2+ arrive at the contractile proteins,
•LVp rises > LAp:
•MV closes: M1 of the 1st HS,
•LVp rises (isovolumic contraction) > Aop,
•AoV opens and Ejection starts.

75
Q

What occurs in diastole?

A

Ventricular relaxation

  • LVp peaks then decreases.
    •Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR.
    •“phase of reduced ejection”.
    •Ao flow is maintained by aortic distensibility.
    •LVp < Ao p, Ao. valve closes, A2 of the 2nd HS.
    •“isovolumic relaxation”, then “MV opens”.
76
Q

What happens in Ventricular filling?

A

LVp < LAp, MV opens, Rapid (E) filling starts.
•Ventricular suction (active diastolic relaxation), may also contribute to E filling (esp. ex. ?S3).
•Diastasis (separation): LVp=LAp, filling temporarily stops.
•Filling is renewed when A contraction (booster), raises LAp creating a pressure gradient.(path, S4)

77
Q

What is the difference between physiological and cardiologic systole?

A

Physio:
1. Isovolumetric contraction
2. Maximal ejection

Cardio:
1. M1 to A2
2. Only part of isovolumetric contraction (includes maximal and reduced ejection phases)

78
Q

What is the difference between physiologic and cardiologic diastole?

A

Physiologic
1. Reduced ejection
2. Isovolumetric relaxation
3. Filling phases

Cardio
1. A2 to M1 interval (filling phases included)

79
Q

Define preload

A

Load present before LV contraction has started

80
Q

Define Afterload

A

Load after ventricle starts to contract

81
Q

What is LV filling pressure?

A

Difference between LAp and LV diastolic pressure

82
Q

What is the all or none principle?

A

The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 m.
•The physiologic LV volume changes are affected when the sarcomere lengthens from 85% of LMAX to LMAX! ?
•Steep relationship: length-dependent activation.

In the cardiac sarcomere, at 80% of the optimal length, only 10% of the maximal force is produced!

83
Q

What does increased diastolic heart volume lead to?

A

Increasing diastolic heart volume, leads to increased velocity and force of contraction (Frank 1895).
•This is the positive inotropic effect.

84
Q

Define contractility

A

Contractility (inotropic state): the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load)

85
Q

Define elasticity

A

Elasticity, is the myocardial ability to recover its normal shape after removal of systolic stress.

86
Q

Define compliance

A

Compliance is the relationship between the change in stress and the resultant strain.(dP/dV).

87
Q

Define diastolic distensibility

A

Diastolic distensibility is the pressure required to fill the ventricle to the same diastolic volume.

88
Q

Where is contractility and compliance reflected?

A

The pressure-volume loop reflects contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship.

89
Q

What is the difference between isometric and istotonic contractions?

A

Iso = the same (Greek),
•Metric = length (Greek),
•Tonic = contractile force (Greek),
•The force-velocity curve may be a combination of initial isometric conditions followed by isotonic contraction.
•The isometric conditions can be found during isovolumic contraction, isotonic contraction is totally impossible in the heart, given the constantly changing load.

90
Q

What are the main components for the myocardium?

A

Contractile tissue,
•Connective tissue,
•Fibrous frame,
•Specialised conduction system.

91
Q

What are the main components for the myocardium?

A

Contractile tissue,
•Connective tissue,
•Fibrous frame,
•Specialised conduction system.

92
Q

What does the cardiac myocyte do?

A

The pumping action of the heart depends on interactions between the contractile proteins in its muscular walls.

The interactions transform the chemical energy derived from ATP into the mechanical work that moves blood under pressure from the great veins into the pulmonary artery, and from the pulmonary veins into the aorta.

The contractile proteins are activated by a signalling process called excitation-contraction coupling.

Excitation-contraction coupling begins when the action potential depolarizes the cell and ends when ionized calcium (Ca2+) that appears within the cytosol binds to the Ca2+ receptor of the contractile apparatus.

Movement of Ca2+ into the cytosol is a passive (downhill) process mediated by Ca2+ channels.

The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytosol.

93
Q

What is the working myocardial cell like?

A

Filled with cross-striated myofibrils.

•Plasma membrane regulates excitation-contraction coupling and relaxation.

•Plasma membrane separates the cytosol from extra-cellular space and sarcoplasmic reticulum.

•Mitochondria: ATP, aerobic metabolism and oxidative phosphorylation.

94
Q

What happens in myocardial metabolism?

A

Relies on free fatty acids during aerobic metabolism (efficient energy production)
•During hypoxia, there is no FFA metabolism, thus anaerobic metabolism ensues. This relied on metabolising glucose (anaerobically) producing energy sufficient to maintain the survival of the affected muscle without contraction.

95
Q

What is the ultra-structure of the myocardial working cell?

A

Contractile proteins are arranged in a regular array of thick and thin filaments (The so called Myofibrils).

•A-band: the region of the sarcomere occupied by the thick filaments.

•I-band: is occupied only by thin filaments that extend toward the centre of the sarcomere from the Z-lines. It also contains tropomyosin and the troponins.

•Z lines bisect each I-band.

96
Q

What is the functional unit of the contractile apparatus?

A

The sarcomere: the functional unit of the contractile apparatus,

•The sarcomere is defined as the region between a pair of Z-lines,

•The sarcomere contains two half I-bands and one A-band.

97
Q

What is the sarcoplasmic reticulum?

A

The sarcoplasmic reticulum is a membrane network that surrounds the contractile proteins,
•The sarcoplasmic reticulum consists of the sarcotubular network at the centre of the sarcomere and the subsarcolemmal cisternae (which abut the T-tubules and the sarcolemma).

98
Q

What is the structure of the T-tubule?

A

The transverse tubular system (T-tubule) is lined by a membrane that is continuous with the sarcolemma, so that the lumen of the T-tubules carries the extracellular space toward the center of the myocardial cell.

•Mitochondria.

99
Q

What occurs in contraction?

A

Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule.
•These heads form the crossbridges that interact with actin, after linkage between calcium and TnC, and deactivation of tropomyosin and TnI.

100
Q

What is the myosin like?

A

2 heavy chains, also responsible for the dual heads.
•4 light chains.
•The heads are perpendicular on the thick filament at rest, and bend towards the centre of the sarcomere during contraction (row.)
•alpha myosin and beta myosin.

101
Q

What is actin like?

A

Globular protein.
•Double-stranded macromolecular helix (G).
•Both form the F actin.

102
Q

What is tropomyosin like?

A

Elongated molecule, made of two helical peptide chains.
•It occupies each of the longitudinal grooves between the two actin strands.
•Regulates the interaction between the other three!

103
Q

What is troponin?

A

I: with tropomyosin inhibit actin and myosin interaction.
•T: binds troponin complex to tropomyosin.
•C: high affinity calcium binding sites, signalling contraction.
•The latter bond, drives TnI away from Actin, allowing its interaction with myosin.

104
Q

What does the myosin head do in contraction?

A
105
Q

What is the micro-anatomy for the contractile unit?

A

Z, I, A and H zones,
•Myosin,
•Actin,
•Tropomyosin,
•Troponins,
•Titins,
•Calcium,
•ATP,
•Crossbridges.

106
Q

What controls the contractile cycle?

A

Calcium ions,
•Troponin phophorylation,
•Myosin ATPase.

107
Q

What are the contractile proteins of the heart?

A

Protein - location and salient properties
1. Myosin - Thick filament - Hydrolyses ATP, interacts with Actin
2. Actin - Thin filament - Activates myosin ATP, interacts with myosin
3. Tropomyosin - Thin filament - Modulates actin-myosin interaction
4. Troponin C - Thin filament - Binds Ca2+
5. Troponin I- Thin filament - Inhibits actin-myosin interaction
6. Troponin T - Thin filament - Binds troponin complex to thin filament

108
Q

What is the Structure-function relationships in excitation-contraction coupling of working cardiac myocyte in the sarcolemma?

A

Sarcolemma - role in systole (S) - role in diastole (D)
1. Na+ channel - (S)Depolarisation, (S)Opens Ca2+ channels
2. Ca2+ channel - (S)Action potential plateau, (S)Ca2+ -triggered, Ca2+ release
3. Ca2+ pump (PMCA) - (D)Ca2+ removal
4. Na+/Ca2+ exchanger - (S)Ca2+ entry - (D)Ca2+ removal
5. Na+ pump - (D)Repolarisation, (D) Na+ gradient for Na+/Ca2+ exchanger

109
Q

What is the Structure-function relationships in excitation-contraction coupling of working cardiac myocyte in T-tubule?

A

Transverse tubule
1. Na+ channel - (S)Action potential propagation
2. Ca2+ channel - (S)Ca2+ -triggered Ca2+ release

110
Q

What is the structure-function relationships in excitation-contraction coupling of working cardiac myocyte in T-tubule?

A

SR

  1. Subsarcolemmal cisternae Ca2+ release channel - (S)Ca2+ release
  2. Sarcotubular network’s Ca2+ pump (SERCA) - (D)Ca2+ removal
111
Q

What is the Structure-function relationships in excitation-contraction coupling of working cardiac myocyte in myofilaments?

A

Myofilaments
1. Actin & myosin - (S)Contraction
2. Troponin C - (S)Ca2+ receptor
3. Other proteins - (S)Allosteric regulation

112
Q

What does contraction involve?

A

Contraction of the working cells of the myocardium involves interactions among six proteins: myosin of the thick filament, actin, tropomyosin, and the 3 components of troponin in the thin filament.

113
Q

What is contraction controlled by?

A

•These interactions are controlled by the downhill movement of Ca2+ into the cytosol (excitation-contraction coupling) and active Ca2+ transport out of the cytosol.

114
Q

What are Ca2+ influxes like?

A

•All of these Ca2+ fluxes are highly regulated, which provides for the changes in cardiac muscle chemistry that give rise to changes in myocardial contractility.

115
Q

What are the events in the CC?

A

The basic three events are:
- LV contraction,
- LV relaxation,
- LV filling.

116
Q

What is the history of the CC?

A

Wiggers suggested the diagram in 1915.
•Lewis added the ECG and the HS in 1920.

117
Q

What are the steps of the CC phases?

A

LV contraction:
- Isovolumic contraction ( b )
- Maximal ejection ( c )
•LV relaxation:
- Start of relaxation and reduced ejection ( d )
- Isovolumic relaxation ( e )
- Rapid LV filling and LV suction ( f )
- Slow LV filling (diastasis) ( g )
- Atrial booster ( a ).

118
Q

What occurs in Ventricular contraction: systole?

A

Wave of depolarisation arrives,
•Opens the L-calcium tubule, {ECG: Peak of R},
•Ca2+ arrive at the contractile proteins,
•LVp rises > LAp:
•MV closes: M1 of the 1st HS,
•LVp rises (isovolumic contraction) > Aop,
•AoV opens and Ejection starts.

119
Q

What occurs in Ventricular contraction: systole?

A

Wave of depolarisation arrives,
•Opens the L-calcium tubule, {ECG: Peak of R},
•Ca2+ arrive at the contractile proteins,
•LVp rises > LAp:
•MV closes: M1 of the 1st HS,
•LVp rises (isovolumic contraction) > Aop,
•AoV opens and Ejection starts.

120
Q

What occurs in ventricular relaxation: diastole?

A

LVp peaks then decreases.
•Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR.
•“phase of reduced ejection”.
•Ao flow is maintained by aortic distensibility.
•LVp < Ao p, Ao. valve closes, A2 of the 2nd HS.
•“isovolumic relaxation”, then “MV opens”.

121
Q

What occurs in ventricular filling?

A

LVp < LAp, MV opens, Rapid (E) filling starts.
•Ventricular suction (active diastolic relaxation), may also contribute to E filling (esp. ex. ?S3).
•Diastasis (separation): LVp=LAp, filling temporarily stops.
•Filling is renewed when A contraction (booster), raises LAp creating a pressure gradient.(path, S4)

122
Q

What are the differences in Physiological and cardiological systole

A

Physiologic

  1. Isovolumetric contraction
  2. Maximal ejection

Cardiologic systole

  1. From M1 to A2
  2. Only part of isovolumetric contraction (includes max and reduced ejection phases)
123
Q

What are the differences in Physiologic vs. Cardiologic Diastole?

A

Physiologic
- reduced ejection
- isovolumetric relaxation
- filling phases

Cardiologic Diastole
- A2 to M1 interval (filling phases included)

124
Q

Define preload and afterload

A

Preload: is the load present before LV contraction has started.
•Afterload: is the load after the ventricle starts to contract.

125
Q

What is starlings law of the heart?

A

Starling 1918: Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction.
•LV filling pressure: is the difference between LAp and LV diastolic pressure.
•The relationship reaches a plateau.

126
Q

What is the link between The Force-Length Interaction & Starling’s law?

A

The force produced by the skeletal muscle declines when the sarcomere is less than the optimal length (Actin’s projection from Z disc “1m” X 2).
•In the cardiac sarcomere, at 80% of the optimal length, only 10% of the maximal force is produced!

127
Q

What is the all or none principle?

A

The cardiac sarcomere must function near the upper limit of their maximal length (LMAX) = 2.2 m.
•The physiologic LV volume changes are affected when the sarcomere lengthens from 85% of LMAX to LMAX!
•Steep relationship: length-dependent activation.

128
Q

What is the frank and isovolumetric contraction?

A

The heart can, during the cycle, increase and decrease the pressure even if the volume is fixed.
•Increasing diastolic heart volume, leads to increased velocity and force of contraction (Frank 1895).
•This is the positive inotropic effect.
•Ino: Fibre (Greek); tropus: move (Greek).

129
Q

Define contractility and elasticity

A

Contractility (inotropic state): the state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load)

•Elasticity, is the myocardial ability to recover its normal shape after removal of systolic stress.

130
Q

Define compliance and diastolic distensibility

A

Compliance is the relationship between the change in stress and the resultant strain.(dP/dV).

•Diastolic distensibility is the pressure required to fill the ventricle to the same diastolic volume.

131
Q

What is the pressure-volume loop?

A

The pressure-volume loop reflects contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship.

132
Q

What is the force-velocity curve?

A

The force-velocity curve may be a combination of initial isometric conditions followed by isotonic contraction.

•The isometric conditions can be found during isovolumic contraction, isotonic contraction is totally impossible in the heart, given the constantly changing load.

Phase 1 Cardio (9 decks)

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