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Med school > Cardiac > Flashcards

Cardiac Flashcards

1
Q

State the pressures through the major vessels and chambers of the heart: Pulmonary artery Right atrium Right ventricle Left atrium Left ventricle Aorta

A

Pulmonary artery: 25/9

Right atrium: 2/0

Right ventricle: 25/0

Left atrium: 8/5

Left ventricle: 120/5

Aorta: 120/80

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2
Q

Describe myocardial muscle cells

A

branched, striated, single nucleus, attached to each other by intercalated discs

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3
Q

What is the delay in seconds at the AV node?

A

Approx 0.13 seconds

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4
Q
A
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5
Q
A
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6
Q

What type of channels cause the steady incline (no resting potential) of the pacemaker action potential?

What are they permiable to?

What stimulates their opening?

A

Funny channels

Permiable to both K and Na

Stimulated by hyperpolarisation of the cell

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7
Q

In non-pacemaker cells, what channels sustain the depolarisation causing the plateau phase?

A

Calcium channels

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8
Q

A shorter plateau phase with less calcium does what to contraction force?

A

reduces the force

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9
Q

Regardless of channels open, what will effect the force of contraction?

A

The length of the muscle fibres

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10
Q

Upon arrival of an action potential voltage gated ____ type Ca channels open, causing an influc of about __% of calcium.

A

L type channels

10% of calcium required enters

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11
Q

The influx of calcium induces the opening of ___ Ca channels which release the remain 90% of calcium from the ______________.

A

RyR channels

Sarcoplasmic reticulum

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12
Q

What two things binding causes the muscle cell to contract?

A

Ca and troponin

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13
Q

Ca and toponin unbinding causes relaxation.

Ca is pumped back into the SR (ATP dependant).

The ____ transporter exchanges 3 Na for 1 Ca.

Na gradient maintained by ______.

A

NCX antiporter

Na/K/ATPase

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14
Q

Describe Starlings Law

A

Independant of HR, the stretch of the myocytes increases the force of contraction.

Related to the overlap of the actin and myosin.

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15
Q

Longer muscle fibres are more _______ to Ca, causing a left shift in the dose - concentration curve

A

More sensitive to Ca causing increased tension/force at the same levels of calcium.

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16
Q

Parasympathetic action on the heart causes __ to bind to _______ receptors, causing a ______ in heart rate.

A

Parasympathetic action on the heart causes Ach to bind to muscarinic receptors, causing a decrease in heart rate.

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17
Q

Sympathetic increase causes ___ to bind to ___ receptors causing an _______ in heart rate by the SA node, and an increase in ______ by the cardiac muscles

A

Sympathetic increase causes NE to bind to Beta receptors causing an increase in heart rate by the SA node, and an increase in contractility by the cadiac muscles.

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18
Q

NE or E increases ______ causing the opening of ___ channels, increasing the speed of depolarisation.

A

cAMP

Funny channels

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19
Q

On parasympatheitic activation, Ach causes an increase in the opening of ___ channels and a decrease in the opening of ___ channels, hyperpolarising the cells, reducing the rate of depolarisation.

A

K

Calcium channels

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20
Q

Elastic arteries increase in diameter during systole. The following recoil enables what?

A

The maintainance of BP during diastole

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21
Q

BP =

A

CO x SVR (Ohms law)

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22
Q

CO =

A

HR x SV

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23
Q

Short term control of MAP is via what means?

Long term control is by?

A

Neural control

Blood vessels and kidneys

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24
Q

Neural cardiac control comprises of ______ feedback.

A

Negative

  1. detector
  2. afferent pathways
  3. coordinating centre
  4. efferent pathways
  5. effector
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25
Q

Which barareceptor is the most important in cardiac feedback?

A

carotid bodies

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26
Q

Carotid bodies transmit via the ________

Aortic bodies via the _________

A

Glossopharangeal nerve

Vagus nerve

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27
Q

State the sequence of events in the barareceptor reflex

A
  1. Increase pressure detected in carotid bodies
  2. Increase firing to CNS
  3. Coordination in vasomotor medullary centre
  4. Efferent increase in vagal tone and decrease sympathetic drive
  5. Decrease HR and vaso/veno dilation reduced MAP
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28
Q
A
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29
Q

Barareceptor signals feed into the _______ of the rostral medulla

A

Nucleus tractus solitaris

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30
Q

What hormonal controls exists in the maintainance of BP?

A

RAAS system

Vasopressin

Atrial natriuretic peptide

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31
Q

State the process of the RAAS

A
  1. JGA in nephron detects drop in pressure or macula densa in distal tubule detects low NA causing release renin
  2. Renin converts angiotensinogen (from liver) to angiotensin I (inert peptide)
  3. Angiotensin I converted to Angiotensin II by ACE in lungs
  4. Angiotensin II causes
    • vasoconstriction
    • aldosterone release causing insertion of aquaporins in CD retaining H2O
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32
Q

AT1 receptors cause what responses?

A
  • Vasoconstriction
    • arterioles > venules
  • Aldosterone release
  • Intra-renal
    • efferent arteriole, Na+ retention
  • Sympathetic stimulation
  • Thirst and vasopressin secretion
  • Endothelin and vasodilator prostanoids
  • ↑ Cellular growth – myocardium, fibroblasts
  • Superoxide production
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33
Q

AT2 receptors cause what response?

A
  • Vasodilation
  • Decreased cell growth
  • Apoptosis
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34
Q

What is arginine vasopressin/ADH?

A

an 8 amino acid peptide secreted by magnocellular neurons in paraventricular and supraoptic nuclei of
hypothalamus with nerve endings in posterior
pituitary

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35
Q

What does ADH do?

A
  • regulates water excretion by kidney (V2 receptors) by altering permeability of collecting duct to water (aquaporins)
  • vasoconstriction (V1 receptors) - higher concentrations
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36
Q

What is ANP?

A
  • 28 amino acid peptide (ANP – A-type)
  • Secreted from cardiac atria in response to atrial stretch
  • Causes Arteriolar vasodilatation
  • Natriuretic (sodium excretion) and diuretic (increased urine production)
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37
Q

What local controls exist in the control of BP?

A
  • Autoregulation (myogenic, metabolic)
  • Nitric oxide
  • Endothelin
  • Prostanoids
  • prostacyclin (PGI2), PGE2
  • thromboxane (TXA2)
  • Other – kinins, histamine
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38
Q

Nitric Oxide is released by ____ cells in response to increased ____ ____.

In smooth muscle it causes and increase in _____ resulting in relaxation.

A

endothlial cells in reponse to sheer strees.

causes an increase in cGMP.

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39
Q

What is endothelin and what does it do?

A
  • 21 AA peptide synthesised by endothelium
  • Very potent vasoconstrictor
  • Long lasting vasoconstriction
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40
Q

What is the time course of compensatory mechanisms in shock?

A
  • Sympathetic nervous system
  • Immediate
  • Angiotensin II and vasopressin
  • 10 min to 1 h
  • Volume recovery mechanisms
  • 1h to 48h or longer
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41
Q

Flow = ?

A

F = ΔP/R

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42
Q

flow is inversely proportional to?

A

Length of the vessel

Viscosity of the blood

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43
Q

Flow is proportional to?

A

The pressure difference

The 4th power of the radius

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44
Q

Blood viscosity depends on?

A

Blood viscosity depends on:

  • the concentration of erythrocytes in the blood (hematocrit)
  • plasma viscosity
  • erythrocyte deformability and flow velocity
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45
Q

What increases the probability of turbulent flow?

A

Large diameter + high velocity + high blood density –
higher probability of turbulent flow

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46
Q

Velocity =

A

Velocity =
Volume flow/Cross sectional
area

So the capilarries have a massive cross sectional area but lower velocity compared to the aorta

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47
Q

How big are capillaries?

A

Diameter: 3-8 μm (Erythrocytes 7.2 μm)

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48
Q

Capillaries are made up of?

A

Endothelial cells, basement membrane ± pericytes

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49
Q

What methods of transport are used across capillary walls?

A

Liquid
• Hydrostatic pressure
• Colloid osmotic pressure
Molecules
• Diffusion
• Filtration
• Vesicular transport, transcytosis

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50
Q

Ficks law states?

A

Fick’s law
Rate of diffusion =

P x area x concentration difference

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51
Q

Permiability coeeficient =

A 
Permeability coefficient (cm/s)=
Diffusion coefficient (cm2/s)/Wall thickness(cm) = distance
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52
Q

What is the net filtration equation?

A
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53
Q

What is the net reabsorption equation?

A

(Pc - Pif) - (oncotic c - oncotic if)

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54
Q

What factor of Pc sensitive to?

A

Pc is sensitive to changes in the venous
pressure including central venous pressure

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55
Q

Endothelial permiability can increase due to what three factors?

A

Burns
Allergy
Infection

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56
Q

Colloid osmotic pressure may decrease due to what?

A

Malnutrition or starvation

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57
Q

What control functions does the endothelial perform?

A
  • Control of vascular diameter
  • Control of exchange
  • Entry/exit of immune cells
  • Coagulation
  • Tumour growth/metastasis
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58
Q

where is the majority of the blood in the circulation

A

Heart and lungs 16 %
Systemic circulation 84 %:
-64 % in veins
-13 % in arteries
-7 % in arterioles & capillaries

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59
Q

Flow = ?

A

diff P/R

so flow is inverseley proportional to radius

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60
Q

diff P =

A

R x flow

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61
Q

State the Hagen-Poiseulle equation and discuss its meaning

A

The H-P equation states the determinants of resistance.

n - viscosity

Most important being that resistance is inverseley proportional to the radius of the tube to the power of 4. This means that if the radius decreases by 2 the resistance increases by 16.

If tube length and viscosity increase by 2 so will the resistance.

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62
Q

State flow rate equation and discuss its meaning

A

Blood flow is:

proportional to pressure difference

proportional to the 4th power of the radius

inversely proportional to the length of the vessel

inversely proportional to the viscosity of the blood

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63
Q

What increases the liklihood of turbulent flow?

A

Large diameter vessels

High velocity

High blood density

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64
Q

state the velocity equation

A

velocity = volume flow/cross sectional area

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65
Q

state the cross sectional area or the aorta and the capillaries

A

aorta 3.cm

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66
Q

state the diameter of capillaries and red blood cells

A

caps 3-8 micrometers

rbcs 7.2 micrometers

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67
Q

what are capillaries made of?

what methods do liquid and molecules use to pass through them?

A

endothelail cells, BM, pericytes

liquid - hydrostatic pressure and colloid osmotic pressure

molecules - diffusion, filtration, vesicular transport, trancytosis

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68
Q

state Fick’s law and what it describes

A

ficks states the rate of diffusion

rate of diff = permiability coefficient x area x concentration difference

where…

P (cm/s) = diff coeff (cm2/s) / wall thickness (cm)

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69
Q

what is the oxygen extraction ration?

A

the fraction of oxygen delived to the microcirculation that is taken up by the tissues

ussually 20 mL/dL - 5 mL/dL = 15mL/dL % ext ratio

heart = 60% so its sensitive to global oxygen delivery

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70
Q

capillaries:

filtration %?

reabsorption %?

lymphatics %?

lymph volume?

A

filtration 100%

reabsorption 80-90%

lymph 10-20%

lymph volume 2-3 litres

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71
Q

where do the lymphatics drain into?

A

right lymphatic duct drains right arm and chest - enters venous circuit in the bifurcation of the subclavian and jugular vein.

thoracic duct runs from the cisterna chyli into the same bifurcation of the same on the left.

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72
Q

what may cause oedema?

A

permiability increase (burns, allergy, inf)

hydrostatic pressure increase (high BP, cardiac)

Lymph (obstruction - elephantitis due to filaria worm)

colloid osmotic decrease (malnutrition)

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73
Q

what stimulates NO release in the vessels and what does it do?

A

shear stress and activation by acetylcholine induce the release of NO (endothelian nitric oxide synthase), which diffuses into the smooth muscle, which converts cGTP to cGMP which causes relaxation of the vascular smooth muscle

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74
Q

where do immune cells tend to exit the circulation

A

immune cells mainly leave the blood in the venule side of the circulation due to p selectin enabling the attachment and diapedisis through the vessel.

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75
Q

definitions of:

aneurysm

varix

ectasia

A

aneurysm: localised dilation in CV system
varix: enlrged dilated tortuous (not straight) vein, artery, lymph
ectasia: widening of any canal or hollow organ (eg bile duct)

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76
Q

what is a berry aneurysm

A

in circle of willis, caused by HT and/or atherosclerosis superimposed on the congenital weakness of deficiency in the media causing a subarachnoid bleed

77
Q

dissecting aneurysm is what?

A

medial degeneration or “cystic medial necrosis” not due to inflam or atheroma. Normally genetic, HT, bicuspid aortic valve, coarctation, familial.

78
Q

factors effecting primary hypertension

A

genestics and lifestyle (obesity, alcohol, activity, diet/salt, stress, drugs, cholesterol, smoking

79
Q

causes of secondary hypertension

A
  • kidneys - renal failure
  • adrenals - cushings = inc cortisol
  • coarctation of the aorta
  • hyperaldosteronism
  • drugs - contraceptive pill
  • pregnancy
  • phocytochromatoma - adrenaline secreting tumor
80
Q

How do loop and thiazide diuretics diuretics act?

A

Loop - on the thich ascending loop by inhibituing the Na/K/2 Cl transporter

thiazides act in the diluting segment of the distal tubule by inhibiting the Na/Cl transporter

For chronic issues thiazide is better

81
Q

how do alpha blockers work?

A

by blocking the alpha receptors from binding with NE in veins and arteries, preventing contraction =

decreased systematic vascular resistance via areterial and venous dialtion.

compensatory Na and water retention may occur

eg prazosin

82
Q

how do beta blockers work?

A

derease sypathetic drive via B1 receptors in heat, reducing cardiac output.

can also reduce peripheral resistance, decrease renin secretion, vasodilation

83
Q

how do ACE inhibitors work?

A

decrease:

vasocconstriction

aldosterone secretion

sympathetic stimulation.

increase kinin mediated vasodilation

-prils.

84
Q

how to angiotensisn II inhibitors work?

A

competatiive antagonist of angiotensisn at AT1 receptors, causing:

decreased:

vasoconstriction

aldosterone release

sympathetic stimulation

* no kinin effects

-sartans

85
Q

what are the principles of drug treatment in HT?

A
  • only one drug from one class
  • commence with monotherapy
  • avoid contraindicated agents
  • if BP change inadequate:
    • increase initial dose OR
    • add another class of drug
86
Q

discuss combined therapy in HT

A
  • needed for more chronic lowering
  • combines drugs with different actions
  • inteferes with reflex compesations
  • may be able to use lower doses to avoid side effects
87
Q

most common HT drug classes include

A
  • ACE Is
  • ATII antagonists
  • diuretics
  • calcium chhannel blockers
  • beta blockers
  • alpha 1 blockers
88
Q

define atherosclerosis

A

an intimal lesion that can weaken the media, a focal accumulation of:

lipid

inflammation

fibrosis

89
Q

risk factors for IHD?

A
  • age and gender
  • hyperlipidemia
  • smoking
  • HT
  • diabtes
  • exercise
  • stress
  • alcohol/diet
  • oral pill
90
Q

atherosclerotic components:

ECM

Shoulder

Core

Periphery

A

ECM - collagen, elastin, proteoglycans

Shoulder - MACs, SM, T cells, Liable to crack.

Core - lipid, cholesterol, foam cells, plasma proteins, pos thrombus

Periphery - neovascularisation

91
Q

Possible outcomes of athersclerosis

A
  • thrombus
  • ulceration
  • emboli
  • rupture
  • calcification
  • stable plaque
92
Q

define the two types of angina

A

stable - caused by trasient ischemia , onset at exertion, alleviated by rest. No necrosis.

unstable - occurs at rest, caused by disrupted plaques, on route to an MI

93
Q

what is the difference between stable and vulnerable plaques?

A

stable - thicker fibrous plaque, smaller lipid core,

vulnerable opposite

94
Q

what are wavy fibres?

A

a histological finding where non-infarcted fibres pull on infarcted fibres. occur approx 4 hours post infarct at borders.

95
Q

what serum markers would you see in an MI?

A
  • 1st is myoglobin and CK which declines fast
  • Troponn is the key marker as it remians high for days
96
Q

sudden death causes in an MI?

A
  • often caused by inducing ventricular arrhythmia

or

  • long QT - loss of K channels
  • Brugada - sodium channels effected - early RV depolarisation
  • Commotio cardis - blunt non penetrating blow
  • WPW - accessory pathway
97
Q

interventions for MI?

A
  • angiogram
  • PTCA- percutaneous transluminal coronary angioplasty
  • stent
  • CABG - use saphenous veins normally, can be mammary or radial arteries.
98
Q

what is tricuspid aortic sclerosis?

A

age related dystophic calcification of the cusps of the aortic valve as a result of age related wear and tear. There is no commisure fusion

99
Q

what murmurs can be heard during systole?

A
  • aortic stenosis
  • pulmonary stenosis
  • mitral regurg
  • tricuspid regurg
  • VSD
  • mitral valve prolapse
100
Q

what is rheumatic fever?

A

a multisystem disease after a group A streptococcal infection cuasing an immune reaction affecting the heart, joints andd soft tissues.

a long latent period occurs between rheumatic fever and rheumatic heart disease

101
Q

acute rheumatic fever can affect which layers of the heart?

A

All.

  • myocarditis: produces aschoff’s bodies
  • endocarditis: vegetations
  • pericarditis: fibrinous
102
Q

what are aschoff’s bodies?

A

found in the myocardium - indoicative of RHD

central zone of degenerate collagen with a surrounding lymphohistocytic infiltrate

103
Q

what rumurs occur in diastole?

A
  • aortic regurg
  • pulmonary regurg
  • mitral stenosis
  • patent ductus arteriosus
104
Q

what is the pathogenesis of infective endocarditis?

A

enothelial damage + thrombus = circculating organisms = vegetations

105
Q

what occurs in right to left shunts?

A

cyanosis, clubbing, paradoxical emboli

106
Q

what occurs in left to right shunts?

A

inncreased pulmonary blood flow

107
Q

congenital heart disease -

what is concordance AV connection?

A

normal R-R and L-L AV connectiions

108
Q

congenital heart disease -

what is discordant AV connection?

A

RA-LV

LA-RV connection

109
Q

congenital heart disease -

what is double inlet?

A

RA and LA enter either LV or RV

110
Q

congenital heart disease -

absent one connection?

A

RV or LV not connected to their corrosponding atria

111
Q

congenital AV defects -

what is isometric AV connection?

A

when the RA or LA is joined by an ambiguous connection

112
Q

what is truncus arteeriosus?

A

a single great artery arising from both ventricles

113
Q

ventricular wall stress =

A

ventricular wall stress =

ventrivular radius x pressure / 2 x wall diameter

114
Q

what factors may affact the La PLace law?

A
  • aortic valve stenosis = ↑ pressure
  • valvular regurg or systolic heart failures = ↑ radius
  • compensatory wall changes (hypertrophy) and HCM ↓ wall stress
115
Q

what are the features of the heart blocks?

A
  • 1st degree - PR >0.2 seconds
  • 2nd degree type 1 - PR prolongues then drops a QRS
  • 2nd degree type 2 - no prolongation of PR but drops a QRS
  • 3rd degree - no relationship between P wave and QRS but both are reqular in rhythm
116
Q

What drugs may be prescribed to treat heart failure?

A
  • digoxin
  • loop diuretics
  • ACE I’s
  • spirinolactone
  • beta blockers
117
Q

how does digoxin work?

A
  • cardiac glycoside
  • acts on the Na/K/ATPase
  • ↓ Ca removal from cell by reducing the Na gradient
  • ↑ Ca in cell which ↑ Ca in SR
  • ↑ Ca released from SR on arrival of action potention = ↑ force of contration
  • Also ↑ refractory period by slowing the conduction thorugh the AV node
  • ↑ vagal tone
118
Q

how does spirinolactone work?

A
  • K+ sparing which acts on CD
  • aldosterone antagonist
  • acts on the Na/K/ATPase pump
  • ↓ Na reabsorption
  • ↓ K secretion
  • ↓ H2O reabsorbed
119
Q

Describe the process of physiologic splitting of the second heart sound in A2 and P2

A
  • lungs inflate = ↓ intrathoracic pressure
  • ↓ resistance in pulmonary vessels = ↑ blood flow in them = “hangout” where blood continues through the pulmonary valve a bit after systole
  • back pressure against the P valve causes it to close a bit later
  • preload ↓ a bit ↓ LV filling meaning Aorta may close a bit earlier
120
Q

when is S3 heard, what may cause it?

A
  • early in diastole
  • “kentucky”
  • caused by abrupt limitation of in flow to the ventricle causing vibration of heart and blood
    • ↓ compliance in ventricles and ↑ atrial pressure
    • predictive of MI in CP
    • mitral regurg - mechanism not clear
121
Q

when is S4 heard and what causes it?

A
  • late in diastole
  • atrial kick into poorly compliant ventricle causing sudden deceleration of blood
    • LV hypertrophy due to HT
    • aortic stenosis
    • hypertrophic cardiomyopathy
122
Q

what might cause the paradoxical splitting of S2 on expiration?

A

aortic stenosis

LBBB

123
Q

widened splitting of the heart sounds may occur ?

A
  • heard on expiration
  • A2 early of P2 late
  • caused by delayed shutting of P2
    • RBBB
    • pulmonary stenosis
  • Plus
    • LV pacing
      • VT
      • mitral regurg
124
Q

what causes fixed and widened splitting of S2?

A
  • constant on expiration and inspiration
  • ASD causes an increase in blood flow to the right heart = late closure of pulmonary valve
125
Q

what is the treatment for decompensated CHF?

A

L M N O P

  • lasix (frusemide)
  • morphine (venodilates to reduce preload, ↓ sympathetic NS)
  • nitrates - venodilates to ↓ preload
  • oxygen
  • posture
126
Q

what is the treatment for unstable VT with haemodynamic compromise?

A

cardioversion

127
Q

what is the treatment for stable VT?

A
  • cardioversion with lidocaine IV
  • ↓ automaticity through the his-purkinje system by increasing the conducting threshold.
  • blocks Na influx into the cells
128
Q

define VT?

A
  • heart rate 100-250 bpm
  • absent p wave and pr interval
  • qrs wide and bizarre >0.12
129
Q

beta blockers specific for CHF are?

A

metoprolol

carvedilol

bisoprolol

130
Q

management for CHF includes?

A
  • ↓ salt
  • ↓ weight
  • ↓ fluid
  • no smoking or alcohol
131
Q

symptoms and signs of left heart failure include?

A
  • symptoms
    • pulm oedema
    • SOB - OE, PND, OP
    • fatigue
    • exercise intolerance
  • signs
    • LV heave
    • pulsus alterans - strong/wea/strong
    • mitral regurg - systolic murmor - thrill
    • loud P2 due to inc pulm pressures
    • crackles
    • wheeze - congested lungs compress airways
132
Q

symptoms and signs of right heart failure?

A
  • symptoms
    • periph oedema
    • sacral oedema
    • hepatosplenomegally
    • anorexia - hepato cong
  • signs
    • S3 gallop - systolic failure
    • S4 gallop - diastolic failure
    • tricuspid regurg - systolic murmor
    • RV heave
    • kussmaul sign - paradoxical JVP rise on inspiration due to inc RA pressure
    • increased JVP
133
Q

what are the instructions and mechanisms behind taking BP?

A
  • no one talk
  • Pt legs uncrossed
  • cuff size 80% of arm circumference
  • cuff level with heart
  • palp first to ensure you avoid auscultatory gap
134
Q

what are the main drugs used to treat HT?

A

A A A B C D

  • alpha adrengergic antagonists
  • ACE I’s
  • ARB’s
  • beta blockers
  • Ca channel blockers
  • diuretics
135
Q

how do calcium channel blockers work?

A
  • normally calcium binds with calmodulin causing stimulation of myosin light chains
  • causes myosin and actin to interact = contraction
  • Ca channel blockers ↓ Ca into cells =
  • ↓ Ca released from SR =
  • ↓ smooth muscle contraction
136
Q

define normal BP and stages of HT

A
  • normal = <120/<80 mmHg
  • pre-HT = 120-139/80-89
  • HT stage 1 = 140-159/90-99
  • HT state 2 = >160/>100
137
Q

what are the endocrine causes of secondary HT?

A

Pheochromacytoma

  • catecholamine secreting tumor of the adrenal gland medulla
  • release norepinephrine and epinephrine
  • causes intermittent chronic vasoconstriction, tachycardia, throbbing headache, palpitaions and sweating

adrenalcorticoid excess

  • eg aldosteronism due to adrenal adenoma
  • adrenal bilateral hyperplasia
  • secondary aldosteronism due to excess ang II due to renin secreting tumor
  • cushings disease causing cosrtisol excess

thyroid issues

138
Q

what are the renal causes of secondary HT?

A
  • renal parenchymal disease causes fluid retention due to nephron failure
  • renovascular HT due to renal artery stenosis - decreased flow to nephron = RAAS activation
139
Q

what are some of the consequences of poorly managed HT?

A
  • heart failure
  • myocardial ischaemia and MI
  • AAA
  • stroke
  • nephrosclerosis and renal failure
  • retinopathy
140
Q

On fundoscopic eye exam what stages of damage can you see?

A
  1. silver wiring due to ↑ reflection from atherosclerosis
  2. venous nipping due to hypertrophied arteries occluding veins
  3. flame haemorrhages - burst small vessels
  4. papilloedema - swelling of optic discs, blurring or margins = raised ICP
141
Q

how do statins work?

A
  • competative inhibitors of HMG CoA reductase, the rate limiting step in cholestorol synthesis
  • this lowers chlesterol by
    • ↓ hepatocyte cholestorol ↑ LDL receptor expression = ↑ LDL removal from blood
  • VLDL and ILDL also cleared
  • ↓ VLDL = ↓ LDL as it is a precursor
142
Q

other lipid lowering drugs include?

A

bile acid binding agents

  • prevents bile being reabsorbed. causes more bile to be made from bile cholesterol stores, eventual LDL excess used.
  • cholestyramine, colestipol, cholesevaram

cholesterol absorption inhibitors

  • ↓ cholesterol uptake in GIT
  • ezetimbe

Niacin

  • ↓ lipolysis, ↓ FA to liver, ↓ TAG synthesis, ↓ VLDL synthesis
  • promoyes lipoprotein lipase
  • increases HDL
143
Q

What are the troponin types looked for in MI’s?

What is there time course?

A

Tronponins I and T

appear 3-4 hours post-MI

peak at 18-36 hours

can still be detectable at day 14

144
Q

What is CKMB?

What is its time course?

What other organs can release it on damage?

A

An isoenzyme related to creating kinase, mosre specific to cardiac dammage.

Appear 3-8 hours post-MI

Peaks at 24

Normal by 48-72

Also evident in uterine, gut, prostate, diahragm and tongue damage

145
Q

What are some of the complications of an MI?

A
  • impaired contractility =
    • stroke
    • cardiogenic shock
    • CHF
  • Tissue necrosis =
    • CHF
    • wall rupture - tamponade
    • papillary muscle ischaemia - mitral regurg = CHF
  • Electrical instability =
    • arrhythmias
  • pericardial inflammation
    • pericarditis
146
Q

HOw does an MI induce cardiogenic shock?

How can this be treated?

A
  • Severe damage to LV = ↓ CO
  • ↓ organ perfusion when BP drops <90 mmHg
  • ↓ BP = ↓ coronary perfusion = worsening ischaemia
  • treated with an intra-aortic balloon pump - expands in diastole increasing intra-aortic pressure = ↑ coronary perfusion.
  • deflates in systole to reduce the afterload
147
Q

How does mitral regurg occur after an MI?

A
  • coronary vessels supply the paillary muscles
  • ischaemia causes them to become necrotic
  • rupture causes acute reguritation
  • rapidly fatal
148
Q

when might a ventricual free wall rupture occur after an MI?

A

Rare complication.

Occurs around 2 weeks post MI due to non-infacrted fibres pulling on infarted fibres, pulling them apart.

149
Q

What causes a ventricular aneurysm?

A
  • weeks to months after the MI phagocuyes have cleared away necrotising tissue
  • this weakens the hearts wall
  • starts to bulge outwards (dyskinesia) - doesn’t rupture
  • can cause a thrombus, arrhythmias, heart failure (forward failure)
  • Continued ST elevation a sign
150
Q

what conditions may be confused with ACS?

A
  • Cardiac
    • pericarditis
    • aortic disection
  • pulmonary
    • PE
    • pneumonia
    • pnumothorax
  • GIT
    • oesophageal spasm
    • cholecystitis
    • GORD
151
Q

when considering a differential diagnosis, what mneumonic might you use?

A

VITAMIN CDE

  • vascular
  • infection/inflammation
  • trauma/toxin
  • autoimmune
  • metabolic
  • iatrogenic/idiopathic
  • neoplastic/neuro
  • congenital
  • degenerative
  • endocrine
152
Q

Label A B C D

A
153
Q

what is the main cause of mitral valve stenosis?

A
  • rheumatic heart disease
  • caused by group A streptococcal
  • Aschoff’s bodies form on valves - forms a fibrous scar.
  • thickened valves - fusion of commisures
  • shortening of chordae tendonae
154
Q

discuss the pathophysiology of mitral valve stenosis with regards to degree of stenosis, pressures in heart and consequences.

A
  • valve x-section ↓ from 4-6cm to about 2cm
  • causes
    • ↑ LA pressure
    • ↑ LA volume
    • ↑ risk of AF
    • ↑ pulm pressures = dyspnoea
155
Q

what is the main presenting symptom of mitral valve stenosis?

A
  • dyspnoea
  • often begins OE but can progress to PND, OP, and at rest
156
Q

what complications can occur with mitral stenosis?

A
  • pulmonary oedema
  • right heart failure
  • peripheral oedema
  • hepatosplenomegally
157
Q

what are Kerley B lines?

A

show on radiograph - thin linear lines in the lung interstitium due to fluid

158
Q

what treatment options are there for RHD and mitral stenosis?

A
  • long term penicillin to prevent reoccurence and further damage
  • AB’s if risk of infection - eg dental work
  • Diuretics to releive congestion
  • digoxin for AF
  • beta blockers/Ca channel blockers to slow heart rate if needed.
  • anticoagulants to prevent thrombus formation
  • surgery to repair valve
    • valvuloplasty to split valves open
    • replace valve
159
Q

list some causes of mitral regurgitation

A
  • RHD - shortens chordae tendonae
  • Inf endo - leaflet perforates
  • MI - papillary muscle dysfunction
  • calcification of annulus - age, diabetes, CKD
160
Q

what happens to blood flow and pressures in the heart with mitral regurgitation?

A
  • LV ejects blood back into LA = ↓ CO
  • ↑ LA pressure and volume
  • ↑ volume induced wall stress in LV due to ↑ volume returning from LA
  • CO must ↑ to meet demands - occurs via Frank Starling mechanism
161
Q

what MACROSCOPIC changes can be observed in the heart post-MI?

A
  • 2-12 hours dark mottling begins
  • 12-24 hours dark mottling evident
  • 1-3 days mottling with yellow infact centre
  • 3-7 days hyperaemic border. yellow centre softening
  • 7-10 days very soft yellow centre, depressed red margins
  • 10-14 red-grey borders depressed
  • 2-8 weeks grey scar spreading from border to centre
  • >2 months scarring complete
162
Q

what MICROSCOPIC changes would you expect to see post-MI?

A
  • ussually none - possibly wavy lines at border
  • 12-24 hours early coagulation necrosis, oedema, haemorrhage
  • 1-3 days coag, necrosis, pyknosis of nuclei, marginal contraction, hyper-eosinophilia, neutrophils
  • 3-7 dead myofibres disintegrate, dying neutrophils, phagoytes at border
  • 7-10 ++ phagocytosis, granulation at margins
  • 10-14 ++ granulation, new vessels, collagen laid down
  • 2-8 weeks ++ collagen
  • > 2 months dense collagen scar
163
Q

what is the main cause of mitral stenosis?

what pathological changes does it cause?

A

Mainly by rheumatic fever, rarely congenital or age related calcification.

  • causes thickening of valves
  • fusion of the commisures
  • thickened and shortened chordae tendonae.
164
Q

what is the pathophysiology of mitral stenosis?

A
  • ↑ LA pressure
  • ↑ LA volume = stretched atrial conduction pathways = AF = ↓ output and ↑ vol and pressure
  • ↑ pulmonary pressure = dyspnoea
  • ↑ likelihood of infective endocarditis
165
Q

how does mitral stenosis present?

A
  • dyspnoea on exertion, orthopnoea, nocturnal dyspnoea or at rest.
  • Conditions which ↑ CO will exacerbate symptoms (anaemia, AF, pregnancy, fever, hyperthyroidism, stress, sex)
  • May result in RHF causing JVP, peripheral oedema, hepatomegaly, ascites.

On examination:

  • ↑ volume/intensity of S1 due to ↑ atrial pressure
  • High pitch opening snap after S2 (due to tense cordae tendonae
  • Decrescendo diastolic murmur – ↑duration = ↑ severity
166
Q

what are some causes of mitral regurg?

A
  • rheumatic fever
  • inf endocarditis
  • IHD - papillary muscle rupture
  • calcification of the annulus
  • ruptured chordae tendonae
167
Q

what is the pathophysiology of mitral regurg?

A
  • LV stroke volume ejected back into LA = ↓ CO into aorta
  • ↑ LA volume and pressure
  • ↓ forward flow CO
  • ↑ volume related stress on LV and back flow in atria returns to the LV
  • Overall CO must increase to meet needs – occurs via Frank Starling mechanism
168
Q

what are some causes of aortic stenosis?

A
  • age related calcification
  • RF
  • rare - congenital bicuspid aortic disease
169
Q

what is the pathophysiology of aortic stenosis?

A

Pathophysiology:

  • Normal aortic valve cross section = 3-4cm, can reduce to < 1cm in severe stenosis
  • ↑ LV pressure = concentric hypertrophy = ↓ compliance
  • ↓ compliance = ↑ diastolic pressure = ↑ LA hypertrophy

Presentation:

  • Angina – oxygen demand increases (↑ muscle mass, ↑ wall stress due to LV pressure ↑). Myocardial supply also reduced due to ↑ diastolic pressure reducing coronary blood flow.
  • Exertional syncope
  • CHF
170
Q

what are some causes or aortic regurg?

A
  • congenital marfan’s disease
  • dissecting aorta
  • syphilis
171
Q

what are some symptoms of ASD?

A
  • RBBB
  • right axis deviation
  • RV heave at left sternal edge
  • S2 splitting
  • R sided cardiomegally
  • RA arrhythmias
172
Q

what is Eisenmengers complex?

A
  • a remodelling of the right ventricle to compensate for increased volumes and pressure due to VSD.
  • causes a reversal of the L-R shunt.
  • causes cyanosis
173
Q

discuss bicuspid aortic valve disease

A
  • congenital defect found in 1:5000 births
  • can cause aortic stenosis
  • inreases LV pressure
  • often asympotomatic
  • symptoms can present later in life due to calcification of valve leaflets - sycope, angina, dyspnoea, fatigue
174
Q

what causes infective endocarditis?

A
  • organisms in blood stream
  • endocardial dysfuntion (such as fibrin deposition allowing the adherance of the organism)
  • type of bacteria depends on its means of entry:
    • oral (streps)
    • skin (s. aureas)
    • bowel (Enterococci)
175
Q

when should you suspect inf. endocarditis?

A
  • new murmur
  • fever/sepsis
  • new embolic event
  • signs of renal infarct (haematuria, glom-neph)
  • fever +
    • new valve
    • IV drugs
    • new murmur
    • cutaneous signs (splinter haem, janeway lesions, osler’s nodes, opthalmic roth spotes)
176
Q

describe the criteria for diagnosing inf. endo and its treatement

A
  • Major:
    • 2-3 cultures + over 12 hours
    • evidence of endocardial involvement
  • minor:
    • predisposition (IV drugs etc)
    • fever
    • single blood culture
    • vascular signs
  • treatment:
    • penicillins
    • phrophylaxis for high risk patients
177
Q

what conditions carry a high risk of inf. endo?

A
  • prosthetic valves
  • previous Hx
  • congenital heart diesease, inc:
    • cyonitic shunts
    • repaired defects with prosthetics
    • heart trabsplant with patho
    • RHD in indigenous AU
178
Q

what ongoing treatment is required for pts with replaced valves?

A

anticoagulation therapy

  • prosthetics - warfarin with INR levels of 2.5-3.5 for life of valve (30 years)
  • biomechanical valves - anticoags for 6 months (as the valve will reendothelialise) lasts for 10 years
179
Q

what criteria is used to assess for RF?

A
180
Q

what is the treatment for RF?

A
  • single IM benzathine penicillin G

or

  • 10 days oral penicillin
  • bed rest
  • paracetamol or nsaids for joint pain
    *
181
Q

what changes can you see in the heart due to RF?

A
  • carditis which can result in:
    • myocarditis - aschoiff bodies
    • endocarditis - vegetations
    • pericarditis - fibrinous
182
Q

what is the treatment regime for RHD?

A
  • IM benzathine penicillin each month for 10 years after most recent episode

or

  • until the age of 21
  • if moderate until 35 years old
  • if severe until 40 years old
183
Q
A
184
Q
A
185
Q
A
186
Q
A
187
Q
A
188
Q
A
189
Q
A

Med school (13 decks)

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