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Definitions > Cardio > Flashcards

Cardio Flashcards

1
Q

What is shock?

A

State of circulatory failure that results in inadequate organ perfusion and tissue oxygenation to meet the demands of tissues

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2
Q

What are the 4 types of shock?

A
  • Hypovolaemic - caused by inadequate circulating blood volume
  • Distributive - state of profound vasodilation of the circulation resulting in reduced perfusion pressure and inappropriate distribution of blood despite adequate CO. E.g septic, neurogenic
  • Cardiogenic - compromise of cardiac pumping => decr CO
  • Obstructive - reduced cardiac filling not related to hypovolaemia
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3
Q

Describe the fast response cardiac action potential (atrial and ventricular muscle and Purkinje fibres)

A

Phase 0 (upstroke/ depolarisation) - Na in (fast Na+ current)
Phase 1 (early rapid partial depolarisation) - Na channels close, voltage-sensitive transient K channels open (ITO, K out)
Phase 2 (plateau) - Ca in (L-type). Balances K out
Phase 3 (Repolarisation) - Ca channels close, K out (Ikr, delayed rectifier K current)
Phase 4 (resting potential) = -85mV, K out = Na and Ca in

Ventricular muscle AP = 250ms, 200ms is ARP, 50ms is RRP

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4
Q

Describe the slow response/ pacemaker AP (SAN and AVN)

A

Phase 4 = MP from -65mV to threshold potential of -40mV, by slow spontaneous depolarisation by fall in K+ permeability (decr K efflux) and incr inward sodium funny current. T-type Ca open.
- Or HCN channel - activated by hyperpolarisation and contributes to diastolic depolarisation of pacemaker cells. Enhanced by SNS; inhibited by PSNS
Phase 0 (depolarisation) = opening of L-type Ca2+, Ca in (peak MP 20mV)
Phase 3 (repolarisation) = inactivation of funny, T and L-Ca, incr in K+ permeability (K out)

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5
Q

Pacemaker depolarisation rates

A

SAN = 100-110 impulses/min
AVN = 40-60 impulses/min
Bundle of His = 40 impulses/min
Purkinje fibres = 15-30 impulses/min

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6
Q

Conduction rates

A

SAN = 0.05m/s
Atrial pathways = 1m/s
AVN = 0.05m/s
Bundle of His = 1m/s
Purkinje system = 4m/s
Ventricular muscle = 1m/s

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7
Q

Troponin subunits

A

Trop-C - binds Ca2+ during muscle activation and exposes actin site for X-bridge formation

Trop-T - binds troponin to tropomyosin

Trop-I - binds to actin, inhibits actin-myosin interaction at rest

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8
Q

Excitation-coupling in cardiac muscle cells

A

All or nothing response
1. Depolarisation, influx of ‘activator’ Ca2+ via L-type channels
2. Small amount of Ca11+ binds RyR2 on SR and induces release of large amount of Ca (CICR)
3. Ca binds with trop-C to produce contraction
4. Cytoplasmic Ca extruded from cells via sarcolemmal Na/Ca exchanger (NCX. 20%) or taken back into the SR via SERCA (80%) regulated by phospholamban

Regulation
- SNS (B1) => activation of adenyl cyclase + PKA => phosphorylation of L-type channels, RyR2, contractile proteins and SERCA => incr Ca2+ influx and augmented Ca2+ release, altered Trop-C affinity for Ca2+ and incr Ca2+ reuptake into SERCA => incr force of contraction, incr rate of X-bridge cycling, (opening Ca channels and phosphorylation of myosin) and incr relaxation (via phospholamban and trop I)

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9
Q

Frank-Starling’s Law

A

Strength of ventricular contraction is dependent on the length of the resting fibres, i.e incr preload => incr SV (up to a point)

Normal heart has operating range of sarcomere lengths of 1.8-2.2um. If >2.2um, contraction starts to decrease (occurs in failing heart)

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10
Q

Cardiac cycle

A

At average resting HR of 72bpm, cardiac cycle 0.8s. Systole 0.3s, diastole 0.5s

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11
Q

Ventricular myocytes

A

Those that depolarise last are the first to depolarise. Ventricular depolarisation proceeds from the epicardial to endocardial surface

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12
Q

P wave

A

Atrial depolarisation
80-100ms
<2.5mm
Positive in II and aVF, biphasic in V1

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13
Q

QRS complex

A

Ventricular depolarisation
60-100ms

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14
Q

T wave

A

Ventricular repolarisation
100-250ms
<5mm height

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15
Q

PR interval

A

Time take for excitation to spread through the atria, AVN and bundle of His.
Start of P wave to start of Q wave
0.12-0.2s

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16
Q

QRS interval

A

Time taken for excitation to spread through the ventricles
0.06-0.12s

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17
Q

QT interval

A

Duration of ventricular depolarisation and repolarisation. Varies inversely with HR. Start of Q wave to end of T wave.
QTC = QT/sqrt RR (<0.44s men, <0.46s in women, >350ms in both)

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18
Q

ST segment

A

End of S wave to beginning of T wave. Represents the period when the ventricles are depolarised.
<2mm deviation from isoelectric V1-3.
<1mm deviation from isoelectric elsewhere

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19
Q

Major determinants of myocardial O2 demand

A
  1. Wall tension/ stress (30-40%)
  2. HR (15-50%)
  3. Contractility (10-15%)
  4. Basal metabolism (25%)
  5. External work (10-15%)

O2 requirement for electrical or activation work ~0.7mL/min per 100g or tissue

High O2 consumption - 9.8ml/min/100g

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20
Q

Ventricular volume

A

130mL standing
160mL lying
- Atrial contraction accounts for 1/5 of end diastolic ventricular volume.
- End of systole 60mL remains in each ventricle (heart usually only eject 60% of EDV)

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21
Q

Determinants of volume of blood ejected from ventricles

A

Preload
Afterload
Myocardial contractility
(HR)

22
Q

Preload

A

Degrees of stretch of ventricular muscle fibres at the end of ventricular filling (represented by EDV). Incr preload incr SV

Factors effecting
- Cardiac factors (HR, atrial contraction, compliance, after load, valve disease, external compression)
- Systemic factors (VR, changes in aortic pressure)

23
Q

Afterload

A

LV wall stress developed during ventricular ejection and reflects force that has to be generated before the muscle is shortened.
- Increased afterload => decr SV

Slope of line connecting LVEDV and end systolic point is index (Ea line).

Resistance to ventricular ejection:
- myocardial wall stress/ intrinsic factors (La place)
- input impedance/ extrinsic factors (Hagen-Poiseuille)

24
Q

Myocardial contractility

A

Intrinsic ability of the myocardial cells to develop force at a given fibre length, independent of preload and afterload.

Slope of ESPVR line is index of contractility (Ees).

25
Q

Compliance

A

Ratio of a volume change to corresponding pressure change, or the slope of the EDPV relationship.

Stiffness is the inverse of compliance.

26
Q

End-systolic PVR line

A

Slope is index of contractility (Ees - end systolic elastance).

Steeper gradient = positive inotrope

27
Q

Index of mechanical energy and work

A

Volume of PV loop = external work of ventricle = stroke work

Triangle formed from end systolic pressure line, end diastolic pressure line and line representing is-volumetric relaxation = internal work and correlated to the heat generated (potential energy)

Total mechanical work + heat generated = total pressure volume area (correlated well with O2 consumed during single contraction)

28
Q

Arteriolar function

A

Main component of peripheral resistance
- Alter TPR
- Alter vascular resistances of individual organs
- Alter capillary hydrostatic pressure + distribution of total body water between intravascular, interstitial and intracellular compartments

29
Q

Resistance formula

A

8nL/pi.r^4

n= blood viscosity
L = length
r = radius

30
Q

MAP

A

= DBP + (SBP - DBP)/3

= Peripheral run off x TPR

31
Q

LaPlace’s Law

A

Describes pressure volume relationships of spheres
Wall tension = (Pressure x Radius)/ ventricular wall thickness

32
Q

Three types of capillaries, and function

A
  • Continuous - most common, in muscle, brain and CT. Tight junction. E.g BBB
  • Fenestrated - renal glomeruli, intestinal mucosa and choroid plexus. Large pores/ fenestrations
  • Discontinuous/ sinusoidal - type of fenestrated capillary in bone marrow and lymph nodes, large enough to allow RBCs and WBCs to pass. In liver and spleen which lack tight junctions completely.

Function of capillaries is delivery and removal of nutrients and metabolite to tissues by diffusion. And distribution of fluid between intravascular and extravascular compartments by bulk flow across a semipermeable capillary wall

33
Q

Four Starling forces

A
  • Capillary hydrostatic pressure (Pc) - prime force moving fluid out into interstitial space
    => Art end = 35mmHg, venous end = 15mmHg
    => Pc proportional to post capillary resistance/ pre capillary resistance
    => Incr by elevated venous pressure (e.g standing or HF)
  • Interstitial hydrostatic pressure (Pif) - opposes Pc, but normally very low
    => = 0mmHg
  • Plasma oncotic pressure (πp) - produced by high albumin conc in capillary (draws fluid in)
    => = 28mmHg
  • Interstitial fluid oncotic pressure (πif) - some protein present, moves fluid out of capillary
    => = 3mmHg

NET filtration pressure (NFP) = (Pc-Pif) - (πp - πif)
=> Art end = 10mmHg, venous end = -10mmHg

Bulk flow across capillary wall = k x NFP
- Art end - bulk flow out of vessel into ISF = filtration (net loss from filtration = 4L/day, reabsorbed by lymphatics)
- Venous end - bulk flow into the vessel from ISF = absorption

34
Q

Endothelium substances

A
  • Prostacyclin - inhibits plt adhesion and aggregation and vessel constriction
  • NO - vasodilator, incr cGMP => decr Ca2+ => muscle relaxation and vasodilation
    => NO production stimulation by Ach, ATP, bradykinin, serotonin, substance P and histamine
  • Endothelin - potent vasoconstrictor
35
Q

Vein function

A
  • Low pressure, high volume capacitance system.
  • Low resistance pathways for return of blood to the heart
  • Act as capacitance vessels that maintain the filling pressure of the heart
36
Q

Determinants of venous return to the heart

A
  • Pressure gradient for venous return (MFSP - mean RA pressure)
  • Venous valves
  • Pumps (skeletal muscle + respiratory)
  • Effect of ventricular contraction and relaxation
  • Venomotor tone
  • Posture
37
Q

Arterial baroreceptor reflex (high pressure baroreceptor)

A

Most important mechanism of short-term regulation of BP

Main sensors (mechanoreceptors)
- Carotid baroreceptor (more sensitive) - in carotid sinus
- Aortic baroreceptor - lies in transfers arch of aorta
=> Afferent pathways in the glossopharyngeal and vagus nerves with integrating centres in the medulla
=> Efferent pathways are the cardiac parasympathetic and cardiovascular sympathetic nerves
=> Effector organs - heart and peripheral blood vessels
=> Hormonal - ADH

  • Effect immediate in seconds (i.e changes in posture)

Baroreceptors - sense stretch (static) and rate of change of stretch (dynamic)

38
Q

Cardiopulmonary (low pressure) baroreceptors

A

Detect change in volume which cause stretching.

  • In RA + great veins
  • Distention => stretch detected by mechanoreceptors
  • Integration centre in medulla/ hypothalamus
  • Efferent pathways are cardiac PSNS and SNS
  • Hormonal efferents - ANP, RAAS, AT-II and aldosterone
39
Q

Peripheral chemoreceptors

A
  • In the carotid and aortic bodies
  • Stimulated by hypoxia and hypercapnia
    => Net effect - rise in peripheral resistance and HR
  • Chemoreceptors drive further increase in sympathetic output
40
Q

NTS (nucleus tractus solitarius)

A

Main site of termination of the glossopharyngeal and vagus nerves, as well as second order afferent nerves of other receptors.
Relays afferent sensory information from the baroreceptors by polysynaptic pathways to other structures in the medulla

41
Q

RVLM (rostral ventrolateral medulla)

A

Groups of neurons (vasomotor area) is major source of excitatory input to sympathetic nerves controlling the peripheral blood vessels.
- Tonically active
- Results in incr CO and PVR
- Neurotransmitter = glutamate
- Tonic activity inhibited by baroreceptor reflex

42
Q

CVLM (caudal ventrolateral medulla)

A
  • Depressor effect on the CVS - reduces peripheral resistance and cardiac contractility
  • Tonically inhibitors RVLM cells by GABA release
43
Q

Central parasympathetic neurons

A
  • Cell bodies of efferent vagal parasympathetic cardiac nerves located in nucleus ambiguus in the ventrolateral medulla and the dorsal vagal nucleus
  • Receive baroreceptor input from eh NTS and discharge with each cardiac cycl
44
Q

Long term regulation of arterial BP

A
  • Involves kidneys, renal handling of Na + H2O and regulation of blood volume
  • RAAS most important renal body fluid mechanism
45
Q

Threshold

A

Minimum membrane potential for an AP to occur

46
Q

Excitability

A

Ability of cardiac muscle to generate an AP during:
- ARP (250ms) - cell not excitable due to closure of Na+ channels, will not reopen until -50mW
- RRP (50ms) - can excited cell to generate AP with supra maximal stimulus, but will be slower and weaker conduction (slop of phase 0 less steep and peak less high)

47
Q

Irritability

A

Elevated RMP - diminished potential between resting and threshold
- More likely to reach AP threshold as less difference. Therefore aberrant discharge/ arrhythmias more likely
- Some Na+ channel may still be closed
=> Phase 0 less steep
=> Phase 1 less high

48
Q

Myocardial O2 supply

A

Depends on coronary blood flow + arterial O2 content

CorBF = (AoP - LVP)/ CVR
AoP = Aortic pressure
LVP = LV pressure
CVR = coronary vasculare resistance (governed by Haagen-Poiseuille law, R = 8nl/πr4)
- normal cbf 250ml/min (5%CO), resting o2 demand 25ml/min

  • HR - ↑HR -> ↓diastolic time -> ↓coronary perfusion
  • Metabolic autoregulation - exercise -> ↑myocardial metabolic activity -> release vasodilator substances (adenosine, NO) -> ↑radius -> CBF
  • Sympathetic innervation - SNS -> coronary vasoconstriction (but overridden by metabolic autoregulation)
  • Viscosity - ↑viscosity -> ↓flow

Arterial O2 content
DO2 = CO x 1.34 x [Hb] x SaO2 + 0.003 x paO2

DO2 = rate of oxygen delivery in ml/min (usually 15ml/kg/min)

  • Normal O2 content in blood 20ml O2/100ml blood.
  • O2 extraction ratio at rest is already high ~75%
49
Q

Oxygen content

A

CvO2 (mixed venous blood) can be measured from pulmonary artery catheter
CvO2 = ([Hb] x 1.34 x SpO2) + (PvO2 x 0.003)

CaO2 = ([Hb] x 1.34 x SO2) + (PaO2 x 0.003)

1.34ml/g= Hufners constant - max amount of Hb-bound O2 per unit of blood

0.003 = solubility constant (mL/dL/mmHg) , or 0.03ml/L/mmHg. Thus in every L of maximally oxygen-saturated blood, there is only 3ml/L of dissolved O2.

[Hb]

50
Q

Regional Blood flow

A

At rest
CO = 5L/min (70ml/kg)
Liver = 1500ml/min (30%)
Kidney = 1000ml/min (20%)
Skeletal muscle = 750ml/min (15%)
Brain = 750ml/min (15%)
Skin = 500ml/min (10%)
Heart = 250ml/min (5%)
Other = 250ml/min (5%)

51
Q

Oxygen content vs pressure

A

Partial pressure (PaO2) = amount of O2 dissolved in plasma (i.e not bound to Hb), aka oxygen tension

Content dissolved = partial pressure x solubility

Oxygen saturation (SaO2) = percentage of all the available heme binding sites saturates with O2

Oxygen content (CaO2) = how much O2 is in the blood. (Total bound to Hb + total dissolve in plasma)

52
Q

Hyperkalaemia ECG changes

A
  • Peaked T waves
  • P wave widening/flattening, PR prolongation
  • Bradyarrhythmias: sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow AF
  • Conduction blocks (bundle branch block, fascicular blocks)
  • QRS widening with bizarre QRS morphology

With worsening hyperkalaemia… (> 9.0 mmol/L):
- Development of sine wave appearance (pre-terminal rhythm)
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm
- Asystole

Definitions (14 decks)

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