Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AC1 > Cardio > Flashcards

Cardio Flashcards

1
Q

Which risk factor has the highest proportion of attributable deaths associated with it globally?

A

High blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the demographic transition?

A

If deaths from infectious diseases and pregnancy are reduced
Life expectancy rises
The population undergoes the ‘demographic transition’
People are a lot more likely to develop chronic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe difference in population structure between countries with high and low mortality rates

A

High mortality: pyramid structure with high numbers of young people and few older people
Low mortality: population spread more evenly distributed over all age ranges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What effects are increasing levels of acculturation, urbanization and affluence having on the epidemiological transition of cardiovascular disease?

A

Increased rates of smoking, fat intake and salt intake

Resulting in higher rates of hypertension and atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is primordial prevention?

A

Focuses on causes of unequal distribution of health damaging exposures, susceptibilities and health protective resources across social groups
Addresses questions of why socioeconomic position is oassociated with health
Prevent appearance of the mediating risk factor in the population,
Focus on social organisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is primary prevention?

A

Reduction of incidence of disease among healthy individuals by
Removing primary causative agent
Interrupting transmission of an infective agent
Protecting individual from environmental hazards
Improving host resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is secondary prevention?

A

Early detection of pre-clinical disease (screening)

Treatment to prevent progression or recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is tertiary prevention?

A

Treatment of established disease to prevent complications or relieve distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the population strategy for disease prevention?

A

Decreasing occurrence of risk factors
Population mean shifted left on bell curve
So overall reduction in number of cases of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the high risk strategy for disease prevention?

A

People thought to be at high risk of disease are targeted to reduce risk factors
Cases of disease are treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are advantages and disadvantages of the population strategy of disease prevention?

A

Attempts to control determinants of incidence rather than cases
Population based
More radical
More permanent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are advantages and disadvantages to the high risk strategy of disease prevention?

A

Extension of traditional clinical approach
Does not produce lasting population changes
Needs to be repeated from generation to generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What factors are driving the increase in incidence of ischaemic heart disease?

A

Diet: Shift from simple to processed foods, Rise of fat production and consumption, Rise of soft drinks
Physical Inactivity: Rise of cars, Rise of obesity (alongside underweight)
Cultural change: Supermarketisation, Lifestyle, Advertising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the nutrition transition?

A

People eat more: Meat, Fats, Sugar, Salt, Soft drinks, Energy dense foods
People eat less: Staples, Fruit and vegetables, Fibre, Water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the components of the recent strategy to reduce population salt intake?

A

Communication: Public Awareness Campaigns, Consumers, Food industry, Decision makers, Media, Health Professionals
Reformulation: Setting Targets, Benchmarking food categories, Labelling, Industry Engagement, Motivation, Costs & Benefits, Consumer awareness, Wider support, Corporate responsibility, Voluntary vs Regulatory
Monitoring: Population salt intake, Urinary sodium, Dietary surveys! Reformulation progress, Salt content of foods (databanks; self-reporting by industry; market surveys), Effectiveness of communication, Measuring awareness of campaigns, Measuring attitudes and behaviour changes
Research: Epidemiology, Nutrition, Public Health, Food technology, Behavioural, Evaluation, Policy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What downstream changes can be made to reduce population salt intake?

A

Legislative and fiscal changes

Mandatory reformulation – effective and reducing inequalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What upstream interventions can be put into place to reduce population salt intake?

A

Social marketing, awareness, health promotion, behavioural

Politically more likely but fewer benefits and potentially widen inequalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What different imperatives are there for implementing a population reduction in salt intake?

A

Preventative: Population salt reduction programs are both feasible and effective
Economic: Salt reduction programs are cost-saving
Political: Policies are powerful, rapid, equitable, cost-saving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the top 3 leading causes of death for males and females globally?

A

Male: ischaemic heart disease, stroke, COPD
Female: stroke, ischaemic heart disease, lower respiratory tract infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where do thiazide diuretics have their effects? And what are these effects?

A 
Act at distal convoluted tubule
Inhibit Na+/Cl- co-transport from lumen
Increase sodium & water excretion
Increase potassium loss
Vasodilate by potassium channel activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some adverse effects of thiazide diuretics?

A

Gout
Low potassium & low sodium
Raised glucose & cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name 2 thiazide diuretics

A

Bendroflumethiazide

Hydrochlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name 4 potassium sparing diuretics

A

Aldosterone antagonists: Spironolactone, Eplerenone

Epithelial Na+ channel blocker (ENaC): Amiloride, triamterene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How are potassium sparing diuretics used?

A

Weak agents
Useful in combination with other drugs
Useful against aldosterone excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are side effects of potassium sparing diuretics?

A

High serum potassium and low sodium

Gynaecomastia (spironolactone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What effect does B1 receptor stimulation have on the heart?

A 
Inotropic effect (contraction)
Chronotropic effect (rate)
AV nodal conduction (velocity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What effect does B2 receptor stimulation have?

A

Smooth muscle relaxation

GI, vascular, bronchial, ciliary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the signalling cascade that occurs on stimulation of B1 receptors

A

Coupled to Gs protein
Leads to increased adenylate cyclase activity, so increased cAMP
This activates protein kinase A which phosphorylates L type calcium channels resulting in increased expression at cell surface
This leads to increased contractility and pacemaker activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the signalling cascade that occurs on stimulation of B2 receptors

A

Coupled to Gs protein
Leads to increased adenylate cyclase activity, so increased cAMP
This leads to activation of protein kinase A which phosphorylates:
sarcolemma so decreased calcium influx, sarcolplasmic reticulum so increased calcium uptake, myosin light chain kinase so decreases contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name a cardio selective beta blocker

A

Atenolol

B1 specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are beta blockers used to prevent?

A

Heart attacks and strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are side effects of beta blockers?

A 
Bronchospasm
Lethargy 
Heart failure 
Raynaud’s 
Bad dreams 
Explosive diarrhoea
Reduced HDL-cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name some calcium channel blockers

A

Nifedipine
Diltiazem
Verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where does digoxin exert its effects?

A

Na/K ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where are L type calcium channels located? And what is their function?

A

Vascular smooth muscle
Cardiac myocytes & sinoatrial & atrioventricular nodes
Renal tubules
Regulate influx of calcium into cells
Stimulate smooth muscle and cardiac myocyte contraction
Contribute to pacemaker currents and action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What effects do calcium channel blockers have?

A

Vascular smooth muscle relaxation
Decreased myocardial force generation
Decreased heart rate
Natriuresis & diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which calcium channel blockers are used to decrease blood pressure? And which are used primarily to reduce cardiac work?

A

BP: nifedipine, amlodipine, lercanidipine
Cardio: verapamil, diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are side effects of verapamil?

A 
Heart failure
Heart block 
Peripheral oedema
Constipation
Facial flushing 
Headaches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are side effects of diltiazem?

A 
Facial flushing
Headaches
Peripheral oedema
Heart failure
Heart block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are Dihydropyridines?

A

Arterio-selective dilator & natriuretic

E.g. nifedipine, amlodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are side effects of nifedipine and amlodipine?

A

Marked facial flushing
Headaches
Peripheral oedema
Polyuria (exacerbate prostatism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

In what pathological states might the RAAS system be activated?

A

Heart failure
Sepsis
Severe blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Give 4 examples of ACE inhibitors

A

Captopril, enalapril, lisinopril, ramipril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are side effects of ACE inhibitors?

A

Cough,
Angio-oedema
Caution in renal artery stenosis
Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Name 3 angiotensin receptor blockers

A

Losartan, valsartan, candesartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name some side effects of angiotensin receptor blockers

A

Caution in renal artery stenosis
Hyperkalaemia
Myalgia
Raised CPK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name 2 alpha blockers

A

Prazosin

Doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe the signalling cascade of alpha 1 receptors

A

Act via Gq which leads to increased activity of phospholipase c
This leads to production of IP3 and DAG from PIP2
This leads to increased calcium release from stores and therefore smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Phenoxybenzamine?

A

Non selective irreversible alpha blocker

Used to treat hypertension, particularly caused by phaeochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are side effects of alpha blockers?

A

First dose hypotension

Postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are contraindications to ACE inhibitor use?

A

Pregnancy, renovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are contradictions to use of rate limiting calcium channel blockers?

A

Heart block, CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is a contraindication to use of diuretics?

A

Gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are contraindications to beta blocker use?

A

Asthma, COPD, Heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are contraindications to alpha blocker use?

A

Incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are blood pressure targets for patients under 80 years old?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What would be a first choice antihypertensive for a patient under 55?

A

ACE inhibitor or ARB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What would be a first choice antihypertensive for a patient over 55 or black patient, African/Caribbean origin of any age?

A

Calcium channel blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the step 2 choice of antihypertensive if mono therapy is not successful at reducing blood pressure to an acceptable level?

A

ACE inhibitor/ARB and calcium channel blocker combined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the step 3 choice of antihypertensive if step 2 combination has failed to control blood pressure adequately?

A

ACE inhibitor/ARB and calcium channel blocker and thiazide diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

If steps 1-3 antihypertensive son have failed to control blood pressure, what condition is present? What do you do about it?

A

Resistant hypertension

Consider further diuretic, alpha/beta blocker, expert advice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What did the sprint trial show relating to blood pressure?

A

More intensive management of high blood pressure (SBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What should be attempted before starting antihypertensive therapy in patients with high blood pressure?

A

Moderate reduction in dietary salt intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What long term effects can hypertension have on the heart?

A

Increased LV mass, with or without chamber dilatation (left
ventricular hypertrophy, LVH)
Left atrial abnormalities
Myocardial ischaemia
Systolic and diastolic LV dysfunction (heart failure)
Atrial and ventricular arrhythmias
Sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are clinical consequences of hypertensive heart disease?

A 
Angina pectoris
Asymptomatic heart failure
Cardiac dysrhythmias 
Acute Coronary Syndromes
Symptomatic heart failure
Myocardial infarction
Sudden death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What neurohormonal factors contribute to cardiac damage in hypertension?

A

Activation of RAAS
Enhanced adrenergic activity
Increased production/reduced catabolism of biologically active molecules (cytokines, growth factors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What haemodynamic factors contribute to cardiac damage in hypertension?

A

Increased peripheral resistance
Increased wall stress
Decreased coronary reserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What vascular factors contribute to cardiac damage in hypertension?

A 
Endothelial dysfunction
Vascular remodelling
Decreased vascular compliance
Increased vascular reactivity
Coronary and Peripheral vascular atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What myocardial changes contribute to cardiac damage in hypertension?

A

eft ventricular remodelling
Foetal gene expression
Myocyte hypertrophy
Alteration in extracellular matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How does hypertensive heart disease lead to oedema?

A

Passive venous congestion due ventricular dysfunction and high arterial pressure
This leads to increased aldosterone production and thus Na and water retention and therefore oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

How does hypertensive heart disease result in dyspnoea?

A

Increased pulmonary venous pressure due to ventricular dysfunction leads to increased ventricular filling pressure and increased atrial pressure
This results in increased pulmonary capillary pressure which leads to interstitial oedema
This decreases lung distensibility and increases O2 consumption, therefore leading to shortness of breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Name some common presenting symptoms of congestive heart failure

A 
Dyspnoea at rest
Dyspnoea on exertion
Effort intolerance
Fatigue and weakness
Orthopnoea
Paroxysmal nocturnal dyspnoea
GI complaints
73
Q

Name some signs of congestive heart failure

A 
Resting tachycardia
Third heart sound
Vascular congestion
Peripheral oedema
Hypotension
Organomegaly (e.g. liver)
Pleural effusion
Cachexia
74
Q

Describe management steps for hypertensive heart disease

A

Effective management of high BP to regress LVH
ACE-I or ARB for LV systolic dysfunction
ARB for LV diastolic dysfunction
Beta-blockers in presence of IHD and arrhythmias (AF)
Heart failure: ACE-I first line (ARBs alternative), beta-blockers (3rd gen, nebivolol) prolong survival, if congestive symptoms, loop diuretics or anti-aldosterone
Manage other CV risk factors (statins, aspirin, anti-diabetics)
AF: combine anti-coagulation (vitamin K antagonists, apixaban, dabigatran, rivaroxaban)
Ventricular arrhythmias, specialist input for diagnosis and management

75
Q

What is hypertensive kidney disease?

A

Hypertensive nephrosclerosis is a blood pressure-related pathologic process marked by a progressive decline in renal function

76
Q

What are some modifiable risk factors for the progression of renal disease?

A 
Hypertension
Albuminuria/Proteinuria
Dyslipidemia
Hemoglobin A1C
Smoking
Anemia
Ca and P04
77
Q

What are some non modifiable risk factors for the progression of renal disease?

A

Age
Ethnicity
Gender

78
Q

How do ACE inhibitors effect renal filtration?

A

Efferent arteriole dilation due to combined effect of bradykinin and a decrease in angiotensin II leads to decrease in GFR

79
Q

What is hypertensive retinopathy?

A

Spectrum of microvascular signs in the retina pathophysiologically related to elevated blood pressure

80
Q

What are the grades of hypertensive retinopathy?

A

Mild (grade I-II): arteriolar narrowing, arteriovenous nicking, arteriolar wall opacity (silver-wiring)
Moderate (grade III): Mild retinopathy and one or more of: retinal haemorrhage (blot, dot, or flame-shaped), microaneurysms, cotton-wool spot, hard exudates
Malignant (grade IV): Moderate retinopathy and optic disc swelling and macular oedema (papilloedema)

81
Q

What calibration should an ECG be set to?

A

1 mV = 10mm calibration

Paper speed 25mm/second

82
Q

Describe QRS waveform nomenclature on an ECG

A 
Initial negative wave = Q (q)
First positive wave = R (r)
Negative wave after R = S (s)
Any second positive wave = R’ (r’)
Entirely negative wave = QS (qs)
LARGE DEFLECTIONS =UPPER CASE
small deflections = lower case
83
Q

Which areas of the myocardium are represented by the precordial leads V1-6?

A

V1, V2: RV wall
V3, V4: IV septum (transition zone)
V5, V6: LV wall

84
Q

What causes the progressive increase in positive deflection of the QRS complex from V1-V6?

A

Increasing muscle thickness

85
Q

What are the normal dimensions of a QRS complex?

A

Min height: 8mm

Max height: R

86
Q

What drug may cause ST depression?

A

Digoxin

87
Q

What may cause t wave inversion?

A

Left ventricular hypertrophy

88
Q

Describe normal p wave morphology

A

Always +ve V3-6
+ve or biphasic V1-2, If biphasic +ve > -ve
Duration

89
Q

What is a normal PR interval?

A

3-5 small squares

90
Q

In an MI, how quickly should percutaneous coronary intervention be performed? And how quickly should thrombolysis be given?

A

90 mins from medical contact for PCI

30 mins for thrombolysis

91
Q

What is Virchows triad for determining risk of deep vein thrombosis?

A

Abnormal blood flow
Endothelial injury
Hypercoagulability

92
Q

Which leg is a dvt more likely to occur in?

A

Left - right common iliac artery crosses origin of left common iliac vein

93
Q

What factors in a history would make you suspicious of a dvt?

A

Paralysis, paresis or recent orthopedic casting of lower limb
Recently bedridden (over 3 days) or major surgery within past 4 weeks
Localised tenderness in deep vein system
Swelling of entire leg
Calf swelling 3 cm greater than other leg
Pitting edema greater in symptomatic leg
Collateral non varicose superficial veins
Active cancer or cancer treated within 6 months

94
Q

What are differential diagnoses for a dvt?

A 
Baker's cyst
Cellulitis
Muscle damage
Superficial venous thrombosis
Post phlebitic syndrome
External venous compression
95
Q

What is the wells criteria?

A

Calculates risk of PE
Clinical signs and symptoms of DVT (3 points)
PE is number 1 diagnosis (3 points)
Heart Rate >100 (1.5 points)
Immobilisation (>3 weeks) or surgery within 4 weeks (1.5 points)
Previous objective PE/DVT diagnosis (1.5 points)
Haemoptysis (1 point)
Malignancy, treatment within 6 months (1 point)

96
Q

What are differences between a VQ scan and a CTPA for imaging PE?

A

CTPA: Fast and fairly accurate. Often not a perfect scan in real life. Very unlikely to pick up amniotic fluid embolism. CTPA picks up other causes. High radiation dose
VQ scan: higher negative predictive value, good for peripheral defects. Chest radiograph needs to be normal

97
Q

What precautions should be used when imaging women of child bearing age?

A

ALARA: As low as is reasonably achievable
High dose test: use 10 day rule if possible. Image within 10
days of commencing period. Radiation damage to fetus in early pregnancy is an all or nothing response
Do a pregnancy test or be sure that they are not pregnant
In a true emergency the priority may be to do the scan

98
Q

What may be presenting signs and symptoms of an aortic aneurysm?

A

Severe back pain

Hypotensive

99
Q

How can you tell if a patient has a critically ischaemic leg?

A

Cold, pulseless
Short distance claudication
Rest pain
Gangrene

100
Q

What are options for assessing an ischemic leg?

A

Doppler ultrasound
MRA
CTA

101
Q

What are indications for renal artery intervention?

A

Resistant hypertension
Worsening renal function. No point if glomerular sclerosis has already set in (kidneys less than 9cm or obviously echogenic and scarred)
Flash pulmonary oedema

102
Q

What is a resting membrane potential?

A

Potential difference that exists across the membrane of excitable cells

103
Q

What are the most important ions in determining membrane potential?

A

Sodium, potassium and chloride ions

104
Q

What are ion concentrations outside of cells?

A

Na: 140
K: 4
Cl: 115
Ca: 2

105
Q

What are ion concentrations inside cells?

A

Na: 10
K: 160
Cl: 3
Ca: 0.0001

106
Q

Which ions are membranes permeable to during resting membrane potential?

A

Membrane is relatively permeable to K+ and Cl-

Membrane is relatively impermeable to Na+ and Ca++

107
Q

Which ion pump is key to resting membrane potential?

A

Sodium (pumps outside) and Potassium (pumps inside)
Electrogenic: 3 sodium for 2 potassium, therefore deficit of positive ions inside cell
Generates large concentration gradients for the ions

108
Q

Which ion channels are key to the action potential?

A

Fast Na channels: When open there is rapid influx of sodium, Close when MP is less negative that -55mV for a few
milliseconds
L-type Ca channels (slow sodium-calcium channels): Take longer to open and cause influx of positive ions
K channels: Large amounts of potassium diffuse out of cell

109
Q

What is Wolff-Parkinson-White syndrome?

A

Pre excitation syndrome
Abnormal accessory connection pathway between the atria and ventricles (bundle of Kent) which stimulate premature ventricular contraction - supraventricular tachycardia

110
Q

In diastole, what determines the resting membrane potential?

A

Selective membrane permeability to K+

K+ concentration gradient (inside > outside)

111
Q

Describe the sino atrial nodal action potential

A

Phase 4: inward Na pacemaker funny current
Phase 0: upstroke inward Ca current
Phase 3: downstroke outward K current

112
Q

Describe the atrial and ventricular action potential

A

Phase 4: resting membrane potential
Phase 0: upstroke inward Na current
Phase 1: Na inactivation, K and Cl outward current
Phase 2: plateau, inward Ca current L type
Phase 3: repolarisation, K outward current

113
Q

What is Brugada syndrome?

A

Reduction in Na+ channel activity
Inherited loss of function mutation of Na-channel, leading to altered spread of heart beat and ventricular fibrillation
Also reduction in Ca2+ channel activity, altering length of plateau of the cardiac action potential

114
Q

What is cardioplegia?

A

Intentional and temporary cessation of cardiac activity, primarily for cardiac surgery
Depolarisation opens Na+ channels in short term, long term
depolarisation reduces number of Na+ channels available
As a result action potential may be reduced or fail if external [K+] is raised

115
Q

What is excitability in relation to a cardiac myocyte?

A

Amount of inward current required to bring a myocardial cell to threshold potential

116
Q

What is the basis for the refractory period?

A

Na+ inactivation gates close with depolarisation
Na+ channels are closed so there can be no inwards current
The cell is thus refractory

117
Q

What happens if a cardiac action potential is too short?

A

Re-entrant excitation may occur, with risk of ventricular fibrillation

118
Q

How does B1 stimulation lead to increased heart rate? Which receptor has the opposing effect?

A

Pacemaker potential sped up so action potentials fire more quickly
Acetyl-choline acting at M2 muscarinic receptors

119
Q

How does an action potential lead to myocyte contraction?

A

Ca2+ entry during plateau phase through L-type voltage gated Ca2+ channels (enhanced by adrenaline and noradrenaline)
Releasing Ca2+ from intracellular stores in sarcoplasmic reticulum (also enhanced by adrenaline and noradrenaline)
Ca2+ activates contraction by binding to troponin C on myofilaments of contractile apparatus, permitting cross bridge formation

120
Q

What are some causes of conduction disease in the heart?

A

Intrinsic: Idiopathic degenerative fibrosis, Ischaemia, Cardiomyopathies, Infiltrative diseases e.g. sarcoidosis, haemochromatosis, Congenital abnormalities
Extrinsic Causes: Autonomic dysfunction, Hypothyroidism, Electrolyte abnormalitites e.g. hyperkalaemia, Drugs e.g. digoxin, beta-blockers, calcium channel blockers, Cardiac surgery

121
Q

What types of sino atrial nodal bradycardias are there?

A

Sinus bradycardia
Sinus arrest
Sinus node exit block
Junctional escape rhythm

122
Q

How might you see a junctional escape rhythm on an ECG?

A

Look for p waves in inferior leads and V1

Retrograde p wave after QRS complex

123
Q

What are the different types of atrioventricular nodal bradycardias are there?

A

1st degree AV block: PR interval over 0.2ms
Mobitz 1/Wenkebach: Each beat, pr interval lengthens until one beat is not conducted
Mobitz 2: 2:1 3:1 4:1 patterns of conduction, pr interval is fixed
Complete heart block

124
Q

What are the types of tachycardias?

A 
Supraventricular tachycardia (SVT): narrow complex
Ventricular tachycardia (VT): wide complex
125
Q

What are the different types of supraventricular tachycardias?

A 
Sinus tachycardia 
AV nodal re-entrant tachycardia (AVNRT) 
AV re-entrant tachycardia (AVRT) 
Atrial tachycardia – focal or re-entrant 
Atrial fibrillation
126
Q

How do you spot an atrioventricular nodal re entrant tachycardia on an ECG?

A

Retrograde atrial activity

127
Q

Describe the mechanism of re entrant loop tachycardias

A

2 pathways for electrical activity, slow and fast through AV node
Slow has a short refractory period
If fast is still refractory, slow pathway conducts and then retrograde activity goes back up the fast which then reactivates the atria

128
Q

What does atrial flutter look like on an ECG?

A

Macro re entrant tachycardia
Sawtooth appearance between QRS complexes
No clear isoelectric line

129
Q

What types of ventricular tachycardias are there?

A

Normal heart: Right ventricular outflow tract - monomorphic
Torsades: Brugada/CPMVT (catecholaminergic polymorphic VT)
Structural heart disease: IHD – monophormic, HCM (hypertrophic cardiomyopathy)/ARVC (arrythmogenic right ventricular cardiomyopathy)

130
Q

What different mechanisms can underly arrhythmias?

A

Enhanced automaticity: ectopy or focal tachycardias from atria or ventricles. Elevated extracellular potassium, Low intracellular pH, Catecholamine excess, Ischaemia
Triggered activity: impulse initiation caused by after-depolarizations which occur in presence of a previous AP. When they reach threshold potential, new AP is generated, source of a new triggered response, leading to self-sustaining triggered activity
Re-entry: electrical wave front in heart gets caught in a loop. At least two pathways or presence of barrier which may be anatomic, pathologic or functional. Unidirectional Block: block can be physiologic (premature depolarization or increased heart rate) or pathologic (changes in repolarization). Slow conduction must be present to prevent collision of leading edge of wave front into the trailing edge

131
Q

What is phase 4 of a cardiac ventricular action potential?

A

Resting phase (resting membrane potential)
Phase cardiac cells remain in until stimulated
Associated with diastole portion of heart cycle

132
Q

What is phase 0 of the cardiac action potential?

A

Opening of fast Na channels and rapid depolarization
Drives Na+ into cell (inward current), changing membrane potential
Transient outward current due to movement of Cl- and K+

133
Q

What is phase 1 of the cardiac action potential?

A

Initial rapid repolarization
Closure of fast Na+ channels
Phase 0 and 1 together correspond to the R and S waves of the ECG

134
Q

What is phase 2 of the cardiac action potential?

A

Plateau phase sustained by balance between the inward movement of Ca+ and outward movement of K +
Has long duration compared to other nerve and muscle tissue
Normally blocks any premature stimulator signals
Corresponds to ST segment of ECG

135
Q

What is phase 3 of the cardiac action potential?

A

Repolarization, K+ channels remain open, Allows K+ to build up outside cell, causing the cell to repolarize
K + channels finally close when membrane potential reaches certain level
Corresponds to T wave on ECG

136
Q

What disorders of cadiac impulse formation are there?

A

No signal from pacemaker site
Development of ectopic pacemaker: May arise from conduction cells (most are capable of spontaneous activity), Often a result of other injury (ischemia, hypoxia)
Development of oscillatory after depolarisations: Can initiate spontaneous activity in non pacemaker tissue, May be result of drugs (digitalis, norepinephrine) used to treat other cardiopathologies

137
Q

What is the biggest problem in using anti arrhythmic drugs?

A

Anti-arrhythmics are pro-arrhythmic as well
Eg: Treatment of a non-life threatening tachycardia may cause fatal ventricular arrhythmia
Must be vigilant in determining dosing, blood levels, and in follow-up when prescribing antiarrhythmics

138
Q

What are different mechanisms of action of anti arrhythmic drugs?

A 
Na+ channel blockade 
β-adrenergic receptor blockade
Prolong repolarisation 
Ca2+ channel blockade
Adenosine 
Digitalis glycosides
139
Q

What is the mechanism of action of class 1 anti arrhythmic drugs?

A

Na channel blockers
1A: Mod.block Ph.0; slow conduction; increase APD
1B: Min.block Ph.0; slow conduction; shorten Ph3 repolarisation
1C: Marked block Ph.0; slow conduction; no change APD or repolarisation. Increased suppressionof Na channels

140
Q

Give examples of class 1 anti arrhythmic drugs

A

1A: Quinidine, Procainamide
1B: Lidocaine, Phenytoin
1C: Flecainide, Encainide

141
Q

Give an example of a class 2 anti arrhythmic drug

A

Propranolol

142
Q

What is the mechanism of again of class 2 anti arrhythmic drugs?

A

Beta blockers; decrease adrenergic input

No effect APD, suppress Ph.4 depolarisation

143
Q

What is the mechanism of action of class 3 anti arrhythmic drugs?

A

Prolong repolarisation/refractory period

Mainly K+ channel blockade

144
Q

Give examples of class 3 anti arrhythmic drugs

A

Bretylium

Amiodarone

145
Q

What is the mechanism of action of class 4 anti arrhythmic drugs?

A

Ca channel blockers. Slow conduction and increase effective refractory period in normal tissue (A-V node) and Ca dependent slow responses of depolarised tissue (atria, ventricle, Purkinje)

146
Q

Give examples of class 4 anti arrhythmic drugs

A

Verapamil

Diltiazem

147
Q

Give examples of anti arrhythmic drugs which don’t fit into the 4 classes

A

Adenosine, Digoxin, Anticoagulants

148
Q

What is quinidine?

A 
1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory period 
Fast Na channel blocker - class 1A
149
Q

What is Procainamide?

A

Fast Na channel blocker anti arrhythmic
Increases refractory period but side effects
Class 1A

150
Q

What is Disopyramide?

A

Fast Na channel blocker anti arrhythmic
Extended duration of action, used only for treating ventricular arrthymias
Class 1A

151
Q

How does lidocaine work as an anti arrhythmic drug?

A

Blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmias
Class 1B

152
Q

How does phenytoin work as an anti arrhythmic drug?

A

Anticonvulsant that also works as antiarrhythmic similar to lidocane - Na channel blockade
Class 1B

153
Q

What is Mexiletine?

A 
Oral lidocaine derivative, similar activity
Can be used as class 1B anti arrhythmic
154
Q

What is Flecainide?

A

Slows conduction in all parts of heart
Inhibits abnormal automaticity
Class 1C anti arrhythmic - Na channel blocker

155
Q

What is propafenone?

A

Class 1C anti arrhythmic drug, Na channel blocker
Also slows conduction
Weak β – blocker
Also some Ca2+ channel blockade

156
Q

How do beta blockers work as anti arrhythmic drugs?

A

Class 2
Blockade of myocardial β–adrenergic receptors
Direct membrane-stabilizing effects related to Na+ channel blockade
Slows SA node and ectopic pacemaking
Can block arrhythmias induced by exercise or apprehension

157
Q

What is the mechanism of action of Amiodarone?

A

Class 3 anti arrhythmic

Prolongs action potential by delaying K+ efflux but many other effects characteristic of other classes

158
Q

What is the mechanism of action of ibutilide?

A

Class 3 anti arrhythmic drug, K channel blocker

Slows inward movement of Na+ in addition to delaying K+ influx

159
Q

What is bretylium?

A

Class 3 anti arrhythmic drug, k channel blocker
First developed to treat hypertension but found to suppress ventricular fibrillation associated with myocardial infarction

160
Q

What is the mechanism of action of verapamil as an anti arrhythmic drug?

A

Ca channel blocker
Slow rate of AV-conduction in patients with atrial fibrillation
Blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardia

161
Q

What is the mechanism of action of Flecainide?

A

Class 1C anti arrhythmic
Depress rate of rise of AP without change in refractoriness or APD in normally polarised cells
Decreases APD, decreases automaticity, conduction in depolarised cells
Marked block of open Na channels (decreases Ph. 0); no change
repolarisation
Used primarily for ventricular dysrhythmias but effective for atrial too
Suppresses premature ventricular contractions
Associated with significant mortality; thus, use limited to last resort applications like treating ventricular tachycardias

162
Q

How do beta blockers affect the heart to act as class 2 anti arrhythmics? Metoprolol, Esmolol (short acting), Sotalol (also Class III), Acebutolol, Bisoprolol, Nebivelol

A

Slow A-V conduction
Prolong A-V refractory period
Suppress automaticity

163
Q

How does propranolol act as an anti arrhythmic?

A

Main mechanism of action is block of beta receptors
Decrease Ph 4 slope which decreases automaticity
Local anesthetic effect by block of Na channels (membrane stabilisation) at higher doses
Increases refractory period in depolarised tissues
Increases A-V nodal refractory period

164
Q

In which arrhythmic conditions is propranolol used?

A

Blocks abnormal pacemakers in cells receiving excess catecholamines (pheochromocytoma) or up-regulated beta-receptors (Hyperthyroidism)
Blocks A-V nodal reentrant tachycardias, inhibits ectopic foci
Treat supraventricular tachydysrhythmias
Contraindicated in ventricular failure, also can lead to A-V block

165
Q

Give uses of beta blockers

A

Angina (non-selective or beta 1-selective): decrease O2 demand more than O2 supply, Exercise tolerance increase in angina patients
Arrhythmia (beta 1-selective, LA-action): catecholamine-induced increases in conductivity and automaticity
Congestive Heart Failure: caution with use
Glaucoma (non-selective): decrease aqueous humor formation (Timolol)
Block of tremor of peripheral origin (beta 2-AR in skeletal muscle)
Migraine prophylaxis
Hyperthyroidism: decrease cardiac manifestation (propranolol)
Panic attacks, stage fright

166
Q

What is beta blocker supersensitivity?

A

Rebound increase in sympathetic response after stopping beta blocker treatment
Effect with beta-blockers, less with beta-blockers with partial agonist activity (ie. pindolol). Gradual withdrawal

167
Q

What are contraindications to beta blocker use?

A

Asthma: Blockade of pulmonary beta 2-receptors increase in airway resistance (bronchospasm)
Diabetes: Compensatory hyperglycemic effect of exocrine pancreatic insufficiency in insulin-induced hypoglycemia is removed by block of beta 2-ARs in liver. Beta 1-selective agents preferred

168
Q

What is the mechanism of action of Amiodarone? When is it used?

A

Prolongs refractory period by blocking potassium channels
Also member of Classes IA,II,III,IV since blocks Na, K, Ca channels and alpha and beta adrenergic receptors
Serious side effects related to iodine core. Used frequently in emergency situation (ITU, A&E)
Effective against atrial, A-V and ventricular arryhythmias
Very long acting (>25 d)

169
Q

What are adverse effects of Amiodarone?

A

Cardiac: heart block, QT prolongation, bradycardia, cardiac failure, hypotension
Pulmonary: pneumonitis (leading to fibrosis)
Bluish discolouration skin, corneal microdeposition
GI tract disturbances, hepatotoxicity
Thyroid discturbances: both hypo- or hyperthyroidism

170
Q

What are mechanisms of action of verapamil?

A

Blocks active and inactivated Ca channels, prevents Ca entry
More effective on depolarized tissue, tissue firing frequently or areas where activity dependent on Ca channels (SA node; A-V node)
Increases A-V conduction time and refractory period; directly slows SA
and A-V node automaticity
Suppresses oscillatory depolarising after depolarisations due to digitalis

171
Q

What extracardiac effects does verapamil have?

A

Peripheral vasodilatation via effect on smooth muscle
Used as antianginal / antihypertensive
Hypotension may increase HR reflexively

172
Q

What are some adverse effects of verapamil?

A

Cardiac: Too negative inotropic for damaged heart, depresses contractility - Can produce full A-V block. Can’t use in HF
Extracardiac:Hypotension, Constipation, Nervousness, Gingival hyperplasia

173
Q

How does adenosine act as an anti arrhythmic?

A

Activates P1 purinergic receptors (A1) coupled to K channels, decrease CV, increase refractory peroid
Diagnosing and/or terminating PSVT or AVNRT
Activation of ACh sensitive K+ channel. Leading to hyperpolarisation of SA node, depressing the SA node
Slowing AV conduction and shortening action potential in atrium
In PSVT: reduces Calcium current in AV node, leading to depression of re-entry in PSVT

174
Q

How can potassium ions act as anti arrhythmics?

A

Depress ectopic pacemakers

175
Q

How does digoxin work as an anti arrhythmic?

A

Used to treat atrial flutter and fibrillation
AV node decreased conduction
Myocardium decreased refractory period
Purkinje fibers increased refractory period, decreased conduction

176
Q

What are side effects of adenosine?

A 
Chest tightness
Dyspnoea (especially in asthmatic pt – contraindicated)
Sudden fall in blood pressure
Flushing
Headache
177
Q

How does magnesium act as an anti arrhythmic drug?

A

Influneces Na/K ATPase, Na channels, K channels, Ca channels

Used in variety of arrhythmias to stabilise action potential

178
Q

In which arrhythmias might magnesium be the treatment of choice?

A

Torsade de pointes

Refractory VTs

179
Q

Describe how pacemakers are inserted

A

Leads are inserted via subclavian vein and advanced to chambers on right side of the heart
Two leads used, one for right atrium, other for right ventricle
Pulse generator containing microcircuitry and battery are attached to leads and placed into a pocket under skin near clavicle
Pulse generator sends signal down leads in programmed
sequence to contract atria, then ventricles

AC1 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions