Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

phase 2a clinical > cardiovascular system > Flashcards

cardiovascular system Flashcards

1
Q

atherosclerosis definition

A

pathology of arteries in which there is deposition of lipids in the arterial wall, with surrounding fibrosis and chronic inflammation

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

risk factors for atherosclerosis

A 
age
tobacco smoking
high serum cholesterol
obesity
diabetes
hypertension
family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

distribution of atherosclerosis

A

found within peripheral and coronary arteries

focal distribution along artery length

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

structure of atherosclerotic plaque

A

contains lipid, necrotic core, connective tissue, fibrous cap

eventually plaque occludes the vessel lumen causing ischaemia or ruptures, forming a thrombus

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

inflammation and atherosclerosis

A

LDL’s pass in and out of arterial endothelial cells
in excess they accumulate in the arterial wall and undergo oxidation and glycation
damage to endothelial cells leads to endothelial dysfunction

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

adhesion of leukocytes in atherosclerosis

A

chemoattractants are released from the endothelium and send signals to leukocytes

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

progression of atherosclerosis

A 
fatty streaks
intermediate lesions
fibrous plaques
plaque rupture
plaque erosion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

fatty streaks

A

appear at early age (<10)

consist of aggregations of lipid-laden macrophages and T cells in the intimal layer of the vessel wall

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

intermediate lesions

A

layers:

  • lipid laden macrophages (Foam cells)
  • vascular smooth muscle cells
  • T lymphocytes
  • adhesion and aggregation of platelets to vessel wall
  • isolated pools of extracellular lipid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

fibrous plaques

A

impedes blood flow
prone to rupture
covered by dense fibrous cap (collagen and elastin) laid down by smooth muscle cells that overlies lipid core and necrotic debris
may be calcified
smooth muscle cells, macrophages, foam cells, T cells

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

plaque rupture

A

constantly growing and receding
the cap is resorbed and redeposited
if balance is shifted in favour or inflammatory conditions it becomes weak and it ruptures
highly thrombotic plaque constituents are exposed (basement membrane, collagen, necrotic tissue)
thrombus formation

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

plaque erosion

A

fibrous cap does not disrupt
luminal surface under the clot may not have endothelium present but is smooth muscle cell rich
exposed thrombogenic subendothelial basement membrane to blood

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

treatment for coronary artery disease

A

percutaneous coronary intervention- stent implantation

restenosis was a limitation

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

restenosis

A

recurrence of abnormal narrowing of an artery or valve after corrective surgery

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

drug elution

A

anti-proliferative and inhibits healing

works by reducing smooth muscle cell proliferation so reduced the regrowth after placement of a stent

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

other useful drugs in atherosclerosis

A

aspirin- inhibits platelet cyclo-oxygenase but can cause excessive bleeding

statins- reduce cholesterol synthesis

clopidogrel- inhibitor of receptor on platelets

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

ECG

A

electrocardiogram is a representation of the electrical events of the cardiac cycle

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

ECGs can identify:

A 
arrhythmias
MIs
pericarditis
chamber hypertrophy
electrolyte disturbances
drug toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pacemakers of the heart

A

SA node
AV node
ventricular cells

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

pacemakers of the heart: SA node

A

dominant pacemaker

intrinsic rate is 60-100 beats/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

pacemakers of the heart: AV node

A

back up pacemaker

intrinsic rate of 40-60 beats/min

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

pacemakers of the heart: ventricular cells

A

back up pacemaker

intrinsic rate of 20-45 beats/min

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

ECG: impulse conduction

A

sinoatrial node -> AV node-> bundle of His -> bundle branches -> purkinje fibres

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

ECG: calibration

A

25mm/s

0.1mV/mm

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

ECG: PQRST

A

p wave= atrial depolarisation
QRS= ventricular depolarisation
T wave= ventricular repolarisation

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

ECG: PR interval

A

atrial depolarisation and delay in AV junction (AV node to bundle of His)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ECG paper

A

horizontally:

  • one small box= 0.04 seconds
  • one large box= 0.2 s

vertically:
-one large box= 0.5mV

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

ECG leads

A

measure difference in electrical potential between two points

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

ECG: bipolar leads

A

two different points on the body

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

ECG: unipolar leads

A

one point in the body and a virtual reference point with zero electrical potential, located in the centre of the heart

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

12 lead ECG, type of leads

A

3 standard limb leads

3 augmented limb leads\6 precordial leads

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

ECG: Rule 1 (PR interval length)

A

PR interval should be 120-200 milliseconds (3-5 small squares)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

ECG: Rule 2 (QRS width)

A

width of QRS complex should not exceed 110ms ( or 3 small squares)

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

ECG: Rule 3 (QRS in leads I and II)

A

QRS complex should be dominantly upright in leads I and II

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

ECG: Rule 4 ( QRS and T)

A

QRS and T waves tend to have same general direction in the limb leads

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

ECG: Rule 5 (waves in aVR)

A

all waves are negative in lead aVR

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

ECG: Rule 6 (R and S waves growing)

A

R wave must grow from v1 to at least V4

S wave must grow from V1 to at least V3 and disappear in V6

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

ECG: Rule 7 (ST segment)

A

ST segment should start isoelectric except in V1 and V2, where it may be elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ECG: Rule 8 (P waves)

A

P waves should be upright in I,II and V2-V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ECG: Rule 9 (Q waves)

A

should be no Q wave (or only a small Q , less than 0.04s in I,II and V2-6

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

ECG: Rule 10 ( T waves)

A

T wave must be upright in I,II and V2-6

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

ECG: P wave

A
  • always positive in I and II but negative in aVR
  • <3 small squares in duration
  • <2.5 squares in amplitude
  • commonly biphasic in V1
  • best seen in II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

ECG: right atrial enlargement

A

tall (>2.5), pointed P waves

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

ECG: left atrial enlargement

A

notched, bifid P wave in limb leads

M for mitrale

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

ECG: short PR interval

A

wolff-parkinson-white syndrome

accessory pathway allows early activation of the ventricle

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

ECG: long PR interval

A

first degree heart block

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

ECG: QRS complex

A
  • non-pathological Q waves present in I,II aVL, V5 and V6
  • pathological >25% amplitude of subsequent R wave
  • R waves in V6
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

ECG: ST segment

A

flat- isoelectric

elevation or depression by 1mm or more is considered normal

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

ECG: T wave

A
  • normal is asymmetrical, first half having a more gradual slope than the second
  • should be at least 1/8, but less than 2/3 of the amplitude of R wave
  • abnormal= symmetrical, tall, peaked, biphasic or inverted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ECG: QT interval

A
  • measured in lead aVL as it doesn’t have prominent U waves
  • 0.35-0.45s
  • decreased when heart rate increases
  • HR=70bpm, QT <0.4s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

ECG: U wave

A
  • related to after depolarisations, which follow repolarisations
  • small, round, symmetrical and positive in lead II
  • same direction as T wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

ECG: rule of 300 or 1500, for determining heart hate

A

count number of large boxes between QRS complexes and divide this into 300 (smaller boxes with 1500)

e.g. 300/4= 75bpm

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

ECG: 10 second rule for determining heart hate

A

ECGs record 10 seconds of rhythm per page
count number of beats present on ECG
multiply by 6

better for irregular rhythms

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

ECG: the QRS axis

A

represents overall direction of the hearts electrical activity

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

ECG: abnormalities in the QRS axis

A

ventricular enlargement

conduction blocks

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

ECG: determining the axis

A

quadrant approach

equiphasic approach

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

ECG: quadrant approach

A

QRS complex in leads I and aVF
determine if they are positive or negative
combination should place the axis into one of the 4 quadrants

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

ECG: equiphasic approach

A

most equiphasic QRS complex
identified lead lies 90 degrees away from the lead
QRS in this second lead is positive or negative

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

ECG: right bundle branch block

A
  • RBB is blocked so septal depolarisation from left to right (what normally occurs)
  • left ventricular depolarisation down LBB, no RV depolarisation yet
  • RV depolarisation from the LV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

ECG: left bundle branch block

A
  • LBB is blocked to septal depolarisation from right to left
  • RV depolarisation, no LV depolarisation yet
  • LV depolarisation from RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

angina definition

A

a symptom which occurs as a consequence of restricted coronary blood flow

almost exclusively secondary to atherosclerosis

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

angina and coronary arteries

A

epicardial= main exterior arteries e.g. LAD, circumflex etc.
small vessels= microvessels
symptoms occur when diameter falls below 75%

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

angina pathophysiology

A

Oxygen supply/demand mismatch:

  • impairment of blood flow by proximal stenosis
  • increased distal resistance
  • reduced oxygen carrying capacity of blood- anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

electro-hydraulic analogy: healthy, rest

A

resistance of the epicardial arteries is negligible and so the flow through the system is determined by the resistance of the microvascular vessels

flow around 3ml/s

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

electro-hydraulic analogy: healthy, exercise

A

more flow is needed to meet metabolic demand so microvascular resistance falls so flow increases

flow is increased 5 fold (15ml/s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

electro-hydraulic analogy: disease, rest

A

compensated
epicardial disease causes the resistance of the epicardial vessel to increase
compensation occurs by reduction of microvascular resistance, maintaining flow @ 3ml/s

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

electro-hydraulic analogy: diseased, exercise

A

decompensated
microvascular resistance falls to try to increase flow, however it will ‘max out’
flow can therefore not meet metabolic demand- myocardium is ischaemic

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

types of angina

A

stable angina
unstable angina
crescendo angina
microvascular angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

angina non-modifiable risk factors

A

gender
family history
personal history
age

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

angina modifiable risk factors

A 
smoking
diabetes
hypertension
hypercholesterolaemia 
sedentary lifestyle
stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

angina precipitants (supply)

A 
anaemia
hypoxaemia 
polycythaemia 
hypothermia
hypovolaemia
hypervolaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

angina precipitants (demand)

A 
hypertension
tachyarrhythmia
hyperthyroidism
hypertrophic cardiomyopathy 
cold weather
emotional stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

angina incidence

A 
men= 35/100,00/year
women= 20/100,000/year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

angina prevalence

A 
men= 5% (5000/100,000)
women= 4% (4000/100,000)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

angina mortality

A

annual= 1.2-2.4%
cardiac death= 0.6-1.4%
MI=0.6-2.7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

angina history taking

A 
chest pain/discomfort:
-heavy, central, tight, radiation to arms/jaw/neck
-precipitated by exertion
-relieved by rest/GTN
(from above):
-3/3= typical angina
-2/3= atypical angina
-1/3 or 0/3= non-anginal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

angina differential diagnosis (*=important)

A

*pericarditis/myocarditis
*pulmonary embolism
chest infection
*aortic dissection
*gastro-oesophageal (reflux/spasm/ulceration)
*MSK
*psychological
MI??

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

angina examination

A 
often seem normal or near normal
signs of risk factors:
-smoking
-diabetes
-hypertension
-high cholesterol 
signs of complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

angina basic investigations: 12 lead ECG

A

often appear normal

can be signs of ischaemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

angina basic investigations: echo

A

will seem normal

can be signs of previous infarcts or give alternative diagnoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

angina basic investigations: pre test probability

A

calculates probabilities of obstructive coronary disease by categorising patients according to their gender, age and typical pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

angina diagnosis: treadmill test

A

induce ischaemia while walking uphill at a fast pace
look for ST segment depression
detects a late stage of ischaemia

unsuitable if:

  • can’t walk
  • unfit
  • BBB
  • young female
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

angina diagnosis: CT angiogram

A
  • high negative predictive value
  • ideal for excluding CAD in younger, low risk individuals
  • limited in tachycardia, AF or calcified disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

angina diagnosis: invasive angiogram

A

traditionally purely anatomical

some modern functional testing techniques such as FFR (pressure gradient across stenosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

angina diagnosis: stress echo

A

functional test

dynamic imaging with and without pharmacological stress, looking for regional wall motion abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

angina diagnosis: SPECT/myoview

A

radio-labelled tracer taken up by metabolising tissues
1st scan under stress, if perfusion defect bring back for a 2nd
a rest scan to see if its fixed defect (scar) or reversible (ischaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

angina diagnosis: cardiac MRI

A

same principle as stress echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

choosing an angina diagnosis test

A
  • pre test probability of CAD
  • invasive vs non-invasive
  • allergies
  • sensitivity/specificity
  • radiation
  • patient choice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

angina primary prevention

A 
reducing the risk of CAD and it's complications
antihypertensives
statins and lipid modulating therapies
diabetic therapy
smoking cessation
general diet advice
plenty of exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

angina secondary prevention

A

risk factor modification
lifestyle changes similar to primary
pharmacological to reduce symptoms and risk of cardiovascular events
interventional such as surgery and PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

angina treatment: beta blockers

A

1st line anti-anginal
beta 1 specific
reduce heart rate and contractility by antagonising the sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

angina treatment: beta blocker side effects

A

bradycardia
tiredness
erectile dysfunction
cold hands and feet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

angina treatment: beta blocker contraindications

A 
excess bradycardia
severe heart block
severe bronchospasm
asthma 
coronary spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

angina treatment: nitrates

A

1st line anti-anginal
primary venodilators (systemic veins)
reduce preload of the heart and therefore the work of the heart and O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

angina treatment: calcium channel antagonists

A

1st line anti-anginal
arterodilators (systemic arteries) decreasing BP and afterload of the heart
so reduce energy needed for same CO
dilating coronary arteries antagonises spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

angina treatment: antiplatelets

A 
e.g. aspirin
reduce events
cyclo-oxygenase inhibitor:
-decrease prostaglandin synthesis (thromboxane)
-decrease platelet aggregation

causes gastric ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

angina treatment: statins

A

HMGCoA reductase inhibitors
reduces events
reduces LDL cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

revascularisation

A

restore coronary artery and increase the flow

performed when medication fails or when risk of disease is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

types of revascularisation

A

percutaneous coronary intervention (PCI- stenting)

coronary artery bypass graft (CABG- surgery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

PCI pros

A

less invasive
convenient
repeatable
acceptable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

PCI cons

A

stent thrombosis
restenosis
disease is complex
dual anti-platelet therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

CABG pros

A

prognosis

deals with complex disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

CABG cons

A 
invasive
risk of stroke or bleeding
can't do it if frail
one-time treatment
length of stay
time of recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

When to use PCI or CABG

A

STEMI- PCI
NSTEMI_ mainly PCI but also CABG
stable-PCI or CABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

acute coronary syndromes

A

a spectrum of acute cardiac conditions from unstable angina to MI
all associated with sudden reduced blood flow to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

acute coronary syndromes: the big five risk factors

A 
smoking
hypertension
diabetes mellitus
hypercholesterolaemia 
family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

acute coronary syndromes: other risk factors (not the big five)

A 
CKD
peripheral arterial disease (PAD)
inflammatory conditions
ethnicity
stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

unstable angina clinical classification

A

cardiac chest pain at rest
cardiac chest pain with crescendo pattern
new onset angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

unstable angina diagnosis

A

history
ECG
troponin (no significant rise)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

acute MI

A

supply of blood to the heart is suddenly blocked

usually causes permanent cardiac muscle damage, although this may not be detectable in small MIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

ST elevation MI (STEMI)

A

sudden complete blockage of a coronary artery

can usually be diagnosed on ECG at presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

non ST elevation MI (NSTEMI)

A

severely narrowed coronary artery but it isn’t 100% blocked

retrospective diagnosis made after troponin results are available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Q wave MI vs non-Q wave MI

A

a way of defining MI on the basis of whether pathological Q waves develop on the ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

non-Q wave MI

A

no new Q waves
poor W wave progression
ST elevation
biphasic T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Q wave MI

A

large Q waves
STEMI (or MIs associated with left bundle branch block) are larger infarcts so more likely to lead to pathological Q wave formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

MI: symptoms

A

cardiac chest pain:

  • unremitting
  • severe (can be mild or absent)
  • occurs at rest
  • sweating, shortness of breath, nausea/vomiting
  • 1/3 occur in bed at night
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

MI: mortality

A

early:

  • 30% outside hospital
  • 15% inside hospital

late:

  • 5-10% in first year
  • 2-5% annually thereafter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

MI: risk factors

A 
higher age
diabetes
renal failure
left ventricular systolic dysfunction
smoking
obesity
high cholesterol
etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

acute coronary syndromes: causes

A

majority= rupture of atherosclerotic plaque and consequent arterial thrombosis

uncommon= coronary vasospasm, drug abuse, artery dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

formation of a thrombus

A

endothelial injury (exposes subendothelial collagen),
initial adhesion of platelets (GPIb on platelets binds to VWF, assisting binding to collagen),
stable adhesion and aggregation (GPIIb/IIIa, soluble platelet agonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

troponin as an investigation

A

highly sensitive marker for cardiac muscle injury but not specific as it is a protein released in other forms of muscle injury (regulates actin-myosin contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

when is troponin also tested positive

A 
gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

after MI troponin

A

rises for 4-8 hours, peaking at 12-18 hours

back to normal in 10-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

troponin: hsTnT, Rohe assay

A

make sure one measurement taken at least 6 hours after pain,

if not elevated 6 hours after pain- no MI
if it is elevated, repeat after 3 hours
if significant rise or fall (alongside other diagnostic factors) MI confirmed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

acute coronary syndromes: initial management

A

999- to get to hospital fast
paramedics- look for ST elevation (contact primary PCI centre)
take aspirin 300mg immediately
pain relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

initial management of an MI

A

MONA

Morphine
Oxygen
Nitrates
Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

acute coronary syndromes: hospital management

A 
diagnosis
bed rest
oxygen therapy if hypoxic
pain relief
aspirin
beta blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

acute coronary syndromes: pharmacological treatment

A

P2Y12 inhibitors
GPIIb/IIIa antagonists
anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

acute coronary syndromes: P2Y12 inhibitors

A

P2Y12 causes amplification of platelet activation

so inhibitors used in combination with aspirin as dual anti-platelet therapy

130
Q

acute coronary syndromes: GPIIb/IIIa antagonists

A

GPIIb/IIIa causes amplification of platelet activation

used in combination with aspirin and P2Y12 inhibitors in patients undergoing PCI

131
Q

acute coronary syndromes: anticoagulants

A

target formation and/or activity of thrombin

inhibit both fibrin formation and platelet activation

132
Q

acute coronary syndromes: pharmacological secondary prevention

A 
lifelong aspirin
P2Y12 inhibitors for one year or longer in high risk patients
lifelong statins
ACE inhibitors
beta blockers
133
Q

acute coronary syndromes: complications to treat after

A

heart failure
diuretics
implantable defibrillator
heart transplant

134
Q

thrombosis

A

blood coagulation inside a vessel

135
Q

arterial thrombosis

A

thrombus formed inside an artery

high pressure system, platelet rich

136
Q

arterial thrombosis: risks in coronary circulation

A

can cause an MI

137
Q

arterial thrombosis: risks in cerebral circulation

A

cerebrovascular accident

stroke

138
Q

arterial thrombosis: risks in peripheral circulation

A

peripheral vascular disease

gangrene

139
Q

venous thrombosis

A

thrombus formed in a vein

low pressure system, fibrin rich

140
Q

venous thrombosis: DVT

A

thrombosis in vein lying deep below the skin

141
Q

venous thrombosis: pulmonary embolus

A

dislodged thrombus occluding pulmonary vasculature

142
Q

venous thrombosis: circumstantial causes

A 
surgery
immobilisation
oestrogen (combined pill, HRT)
malignancy
long haul flights
143
Q

venous thrombosis: genetic causes

A

factor V leiden (5%)
PT20210A (3%)
antithrombin deficiency
protein C or S deficiency

144
Q

venous thrombosis: acquired causes

A

anti-phospholipid syndrome
lupus anticoagulant
hyperhomocysteinaemia

145
Q

venous thrombosis: DVT investigations

A

compression ultrasound
doppler
d dimer

146
Q

venous thrombosis: pulmonary embolus investigations

A

CT scan
CT pulmonary angiogram
V/Q perfusion scan

147
Q

venous thrombosis: treatment

A

initially: low molecular weight heparin
after: oral warfarin for 3-6 months OR DOAC for 3-6 months

148
Q

venous thrombosis: prevention

A

thromboprophylaxis: any measure taken to prevent thrombosis such as low molecular weight heparin or early mobilisation and good hydration

149
Q

anticoagulant pharmacology

A 
heparin
low molecular weight heparin
aspirin 
warfarin
new oral anticoagulant drugs
150
Q

anticoagulant pharmacology: heparin

A

glycosaminoglycan
binds directly to antithrombin and increases its activity
indirect thrombin inhibitor

151
Q

anticoagulant pharmacology: low molecular weight heparin

A

smaller molecule, less variation in dose and renally excreted
once daily, weight adjusted dose given subcutaneously

152
Q

anticoagulant pharmacology: aspirin

A

inhibits cyclo-oxygenase irreversibly

inhibits thromboxane formation and hence platelet aggregation

153
Q

anticoagulant pharmacology: warfarin

A 
orally active
prevents synthesis of active factors II, VII, IX and X
antagonist of vitamin K
prolongs prothrombin time
long half life (36 hours)
154
Q

anticoagulant pharmacology: new oral anticoagulant drugs

A 
NOAC/DOAC
orally active like aspirin and warfarin
directly acting on factor II or X
shorter half life
no blood tests or monitoring
155
Q

deep vein thrombosis and pulmonary embolism prevalence

A

25,000 a year die from these in the uk
50% preventable
premature mortality

156
Q

deep vein thrombosis: symptoms

A

non-specific

pain and swelling in the leg

157
Q

deep vein thrombosis: signs

A

tenderness
warmth
discolouration
oedema

158
Q

pulmonary embolism: symptoms

A

breathlessness
pleuritic chest pain
rapid breathing
hypotension

159
Q

pulmonary embolism: signs

A 
tachycardia
tachypnoea
pleural rub
cyanosis
right heart strain
160
Q

inherited cardiac conditions: cardiomyopathies

A

refers to primary heart muscle disease and is often genetic

161
Q

inherited cardiac conditions: hypertrophic cardiomyopathy

A

constriction of ventricles due to hypertrophy of the cardiac muscle- this can also block small coronary arteries
caused by sarcomere protein gene mutations
1 in 500 people
the fibrosis is non conduction so electrical impulses travel around, causing arrhythmias

162
Q

inherited cardiac conditions: dilated cardiomyopathy

A

dilated ventricles due to thinner walls
cytoskeletal gene mutation
systole is ineffective
presents with heart failure symptoms

163
Q

inherited cardiac conditions: arrhythmogenic cardiomyopathy

A

significant rhythm disturbance
desmosome gene mutations
myocardium replaced with fibrous and fatty tissue- causing arrhythmias

164
Q

inherited cardiac conditions: channelopathy

A

inherited arrhythmia
caused by ion channel protein gene mutations (K+, Na+ or Ca2+)
structurally normal heart
recurrent syncope

165
Q

inherited cardiac conditions: channelopathy ECG

A

long QT
short QT
brugada (ST elevation)
tachycardia triggered by adrenaline

166
Q

inherited cardiac conditions: sudden arrhythmic death syndrome (SADS)

A

usually refers to normal heart and arrhythmia

167
Q

inherited cardiac conditions: familial hypercholesterolaemia

A

inherited abnormality of cholesterol metabolism

leads to serious premature coronary and other vascular disease

168
Q

inherited cardiac conditions: aortic aneurysm

A

aortovascular syndromes include marfan, loeys-dietz and vascular ehler danlos

169
Q

inherited cardiac conditions: family testing

A

ICCs are usually dominantly inherited- 50% risk of inheritance
risk needs to be assessed for each individual

170
Q

tamponade

A

compression of the heart by an accumulation of fluid in the pericardial sac
causes hypotension

171
Q

pericardial effusion

A

too much fluid within the pericardium

172
Q

chronic pericardial effusion

A

allows adaption of the parietal pericardium

compliance reduces the effect on diastolic filling of the chambers- rarely causes tamponade

173
Q

acute pericardial effusion

A

effusion onset is quick and parietal pericardium can’t adapt

volume needed to cause cardiac tamponade is lower

174
Q

acute pericarditis

A

inflammatory pericardial syndrome with or without effusion

175
Q

acute pericarditis: clinical diagnosis

A

2/4 at least of the following:

  • chest pain (85-90%)
  • friction rub(33%)
  • ECG changes(60%)
  • pericardial effusion (up to 60%)
176
Q

pericarditis: epidemiology

A

80-90% is idiopathic

5% of A&E attendances with chest pain

177
Q

pericarditis: aetiology

A 
viral
bacterial
autoimmune
neoplastic
metabolic
traumatic and iatrogenic
other
178
Q

pericarditis: viral cause

A

most common cause in developed world

enterovirus, herpes virus, adenovirus

179
Q

pericarditis: caused by TB

A

90% HIV +ve in developed countries

17-40% constrictive pericarditis

180
Q

pericarditis: clinical presentation

A

severe, sharp pleuritic chest pain, with rapid onset- relieved by sitting forward, exacerbated by lying down
dyspnoea
cough

181
Q

pericarditis: differential diagnosis

A 
pneumonia
pulmonary embolus
gastro-oesophageal reflux
MI
aortic dissection
pneumothorax
182
Q

pericarditis: investigations

A 
clinical examination 
ECG
bloods
chest xray
echo
183
Q

pericarditis: clinical examination

A

pericardial rub
sinus tachycardia
fever
beck’s triad: hypotension, muffled heart sounds, raised jugular venous pressure

184
Q

pericarditis: ECG

A

diffuse ST segment
concave ST segment
no reciprocal ST depression
PR depression

185
Q

pericarditis: bloods

A

FBC- modest WBC increase
ESR
troponin

186
Q

pericarditis: chest xray

A

often normal in idiopathic
pneumonia
modest enlargement of cardiac silhouette

187
Q

pericarditis: management

A

sedentary activity until resolution of symptoms
NSAIDs
aspirin
colchicine

188
Q

pericarditis: prognosis

A

have good long term prognosis
15-30% develop recurrence
colchicine reduced recurrence rate by 50%

189
Q

pericarditis: major complications

A 
fever >38 degrees
subacute onset
large pericardial effusion
cardiac tamponade
lack of response to aspirin or NSAIDs after a week of therapy
190
Q

pericarditis: minor complications

A

myopericarditis
immunosuppression
trauma
oral anticoagulant therapy

191
Q

heart failure

A
  • a state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
  • a syndrome and not a diagnosis on its own
192
Q

heart failure incidence/prevalence

A

incidence= 63,000 cases/year (29,000 females, 34,000 males)

prevalence= 878,000 total ( 405,000 female, 473,000 male)

mean age= 71-76 years

193
Q

heart failure aetiology

A

most common cause= myocardial dysfunction

others= hypertension, cardiomyopathy, valvular

194
Q

heart failure risk factors

A 
old age
african decent
men before women reach menopause
obesity
people who previously have had an MI
195
Q

heart failure pathophysiology

A

when the heart begins to fail RAAS and sympathetic nervous system try to compensate to maintain cardiac output
However when heart failure progresses these mechanisms are overwhelmed- decompensation

196
Q

heart failure pathophysiology mechanisms

A

venous return- preload
outflow resistance- afterload
sympathetic system activation
RAAS

197
Q

systolic failure

A

reduced ejection fraction
inability of the left ventricle to contract normally, resulting in a decrease in cardiac output
caused by ischaemic heart disease, MI and cardiomyopathy

198
Q

diastolic failure

A

preserved ejection fraction
inability of the ventricles to relax and fill fully, decreasing stroke volume and so decreasing CO
caused by chronic hypertension which increases afterload so heart pumps against more resistance

199
Q

acute heart failure

A

new onset or decompensation of chronic heart failure
characterised by pulmonary and/or peripheral oedema
w/ or w/o signs of peripheral hypotension

200
Q

chronic heart failure

A

develops slowly
venous congestion is common
arterial pressure well maintained until quite late

201
Q

heart failure symptoms

A

three cardinal symptoms= shortness of breath, fatigue ankle oedema

cold peripheries
increased weight
dyspnoea especially when lying flat

202
Q

heart failure signs

A 
tachycardia
displaced apex beat
added heart sounds and murmurs
cyanosis
hypertension
203
Q

new york heart association classification for heart failure

A 
class I: no limitation, asymptomatic 
class II: slight limitation, mild heart failure
class III: marked limitation, moderate HF
class IV: inability to carry out physical activity without discomfort, severe HF
204
Q

heart failure treatment

A 
lifestyle changes
diuretics
ACE inhibitors
beta blockers
digoxin
revascularisation
surgery
heart transplant
205
Q

causes of acute decompression of chronic heart failure

A 
uncorrected hypertension
obesity
infection
arrhythmias
excess alcohol 
NSAIDS
206
Q

heart failure complications

A 
renal dysfunction
rhythm disturbances
DVT/PE
LBBB and bradycardia 
hepatic dysfunction
207
Q

heart failure investigations:

A

blood tests
chest xray
ECG
echo

208
Q

heart failure investigations: blood tests

A

brain natriuretic peptide- secreted by myocardium in stress
FBC
U&E
epinephrine, vasopressin and renin= high

209
Q

heart failure investigations: chest xray

A

alveolar oedema
cardiomegaly
dilated upper lobe vessels of lungs
pleural effusions

210
Q

heart failure investigations: ECG

A

shows underlying causes
if ECG and BNP are normal then heart failure is unlikely
if both abnormal then do an echo

211
Q

heart failure investigations: echo

A

assess cardiac chamber dimension

look for wall motion abnormalities

212
Q

infective endocarditis

A

infection of heart valves or other endocardial lined structures w/i the heart (septal defects, pacemaker leads)

213
Q

infective endocarditis: types

A

left sided native (mitral, aortic)
left sided prosthetic
Right sided, rarely prosthetic as rare to have those valves replaced

214
Q

infective endocarditis: pathogenesis

A

have an abnormal valve
regurgitant or prosthetic valves are more likely to get infected
introduce infectious material into blood stream

215
Q

infective endocarditis: epidemiology

A 
young= rheumatic heart disease or drug abusers
elderly= weakened immune system 
congenital heart disease
anyone with prosthetic heart valves
M:F= 2:1-9:1
216
Q

infective endocarditis: incidence

A

0.6-6/100,000 people/year

10 year survival= 60-90%

217
Q

infective endocarditis: presentation

A

signs of systemic infection (fever, sweats)
embolisation (stroke,pulmonary embolus, bone infections, MI)
valve dysfunction (heart failure)

218
Q

infective endocarditis: diagnosing criteria

A

definite IE= 2 major, 1 major+3minor or 5 minor
possible IE= 1 major, 1 major+3minor or 5 minor

major= bugs grown from culture, evidence of endocarditis on echo 
minor= predisposing factors, fever, vascular or immune phenomena and equivocal blood cultures
219
Q

infective endocarditis: echos

A

TTE= transthoracic echo, safe, non invasive, no discomfort, but poor images so lower sensitivity

TOE=transoesophageal echo, excellent pictures, uncomfortable, risk of perforation or aspiration

220
Q

infective endocarditis: peripheral signs of spread and embolism

A

bruises, infarcts (10-15%)
splinter haemorrhages
osler’s nodes (small, tender, purple nodules on the pulp of digits)
roth spots on fundoscopy

221
Q

infective endocarditis: diagnosis

A

bloods
ECG
TTE/TOE

222
Q

infective endocarditis: blood tests

A

cultures can be negative in 2-5% of patients
certain organisms require longer incubation

WBC rarely helpful
C-reactive protein (inflammation marker) is almost always present

223
Q

infective endocarditis: diagnosis with TTE/TOE

A

TTE is crucial for detecting vegetation but sensitivity is still only 60%

TOE sensitivity is 90-95%

224
Q

infective endocarditis: treatment

A

antimicrobials for 6 weeks depending on the culture
treat complications such as heart failure, abscess drainage, stroke rehab
surgery

225
Q

infective endocarditis: surgery

A
  • when the infection cannot be cured with antimicrobials
  • to fix complications such as aortic root abscess or valve damage
  • remove infected devices
  • remove large vegetations before they embolise
226
Q

infective endocarditis: prevention

A

NICE recommends not to give prophylaxis
ESC consider prophylaxis in high risk patients
talk to patient and dentist

227
Q

tetralogy of Fallot

A

ventricular septal defect
pulmonary stenosis
hypertrophy of right ventricle
overriding aorta

228
Q

tetralogy of Fallot: physiology

A

the stenosis of RV outflow leads to RV being higher pressure than the left
blue blood passes from RV to LV so patients are blue

229
Q

tetralogy of Fallot: epidemiology

A

10% of all congenital heart defects
1/1000 live births
15% have associated genetic abnormality

230
Q

tetralogy of Fallot: treatment

A

surgical repair
a shunt between R subclavian artery and R pulmonary artery to increase pulmonary blood flow

often get pulmonary valve regurgitation in adult life so redo surgery required

231
Q

ventricular septal defects

A

abnormal connection between the two ventricles
common- 20% of all congenital heart defects
1-4/1000 of live births

232
Q

large ventricular septal defects: physiology

A

very high pulmonary blood flow in infancy
breathless, poor feeding, failure to thrive
require fixing in infancy
can lead to eisenmengers syndrome

233
Q

small ventricular septal defects: physiology

A

small increase in pulmonary blood flow only
asymptomatic
endocarditis risk
need no intervention

234
Q

large ventricular septal defects: clinical signs

A 
small breathless skinny baby
increased respiratory rate
tachycardia
big heart on chest xray
murmur varies in intensity
235
Q

small ventricular septal defects: clinical signs

A 
loud systolic murmur
thrill
well grown
normal heart rate
normal heart size
236
Q

eisenmenger’s syndrome

A

pathophysiology:

  • high pressure pulmonary blood flow
  • damages delicate pulmonary vasculature
  • RV pressure increases
  • shunt direction reverses and patient becomes blue

high mortality rate

237
Q

atrial septal defects

A

abnormal connection between the two atria
common
often present in adulthood

238
Q

atrial septal defects: physiology

A

slightly higher pressure in LA than RA
shunt left to right
therefore not blue
increase flow into right heart and lungs

239
Q

large atrial septal defects: physiology

A

significant increased flow through the right heart and lungs in childhood
right heart dilation
SOB on exertion
increased chest infections

240
Q

small atrial septal defects: physiology

A

small increase in flow
no right heart dilation
no symptoms
leave alone

241
Q

atrial septal defects: clinical signs

A

pulmonary flow murmur
fixed split-second heart sound
big pulmonary arteries big heart on chest xray

242
Q

atrial septal defects: treatment

A

surgical closure

percutaneous (key hole) closure

243
Q

atrioventricular septal defects

A

2/10,000 live births
common in Down’s syndrome
hole in the centre of the heart
interatrial and/or interventricular

244
Q

complete atrioventricular septal defects: physiology

A 
breathless neonate
poor weight gain
poor feeding
torrential pulmonary blood flow
needs repair or PA band in infancy
repair is surgically challenging
245
Q

partial atrioventricular septal defects: physiology

A

can present in late adulthood
presents like a small VSD/ ASD
may be left alone if there is no right heart dilation

246
Q

patent ductus arteriosus: signs

A

continuous machinery murmur
if large, big heart breathless
eisenmenger’s syndrome

247
Q

large patent ductus arteriosus: physiology

A

torrential flow from aorta to pulmonary arteries in infancy
breathless, poor feeding, failure to thrive
common in prem babies
need surgical closure

248
Q

small patent ductus arteriosus: physiology

A

little flow from the aorta to Pas
usually asymptomatic
murmur found incidentally
endocarditis risk

249
Q

patent ductus arteriosus: treatment

A

surgical or percutaneous
local anaesthetic
venous approach
low risk of complications

250
Q

coarctation of the aorta

A

narrowing of the aorta at the site of insertion of the ductus arteriosus
perfusion to lower body is reduced

251
Q

severe coarctation of the aorta

A

complete or almost complete obstruction to aortic flow
collapse with heart failure
needs urgent repair

252
Q

mild coarctation of the aorta

A

presents with hypertension
incidental murmur
should be repaired to prevent problems long term

253
Q

coarctation of the aorta: clinical signs

A

right arm hypertension
bruits over scapulae and back from collateral vessels
murmur

254
Q

coarctation of the aorta: long term problems

A

hypertension
re-corarctation requiring repeat intervention
aneurysm formation

255
Q

coarctation of the aorta: treatment

A

surgical vs. percutaneous repair

256
Q

bicuspid AV

A 
has 2 cusps instead of the typical 3
1-2% of population
M>F
severely stenotic in infancy or childhood
degenerate quicker than normal valves
257
Q

pulmonary stenosis

A

narrowing of the outflow of the right ventricle
8-12% of all congenital heart defects
valvar, sub valvar, supra valvar, branch

258
Q

severe pulmonary stenosis

A 
right ventricular failure as neonate
collapse
poor pulmonary blood flow
RV hypertrophy
tricuspid regurgitation
259
Q

mild pulmonary stenosis

A

well tolerated for many years

right ventricular hypertrophy

260
Q

pulmonary stenosis: treatment

A

balloon valvuloplasty
open valvotomy
open trans-annular patch
shunt

261
Q

atrial septal defects: primum

A

defect level of tricuspid and mitral valves

262
Q

atrial septal defects: secundum

A

enlarged foramen ovale, inadequate growth of septum secundum, or excessive absorption of septum primum

263
Q

atrial septal defects: sinus venosus

A

defect involves venous inflow of either SVC or IVC

264
Q

hypertension: prevalence

A

> 75 year olds have 50% risk of hypertension
middle age have 10-30% risk
young have 5% risk

265
Q

hypertension: main causes

A

85% of cases caused by genetics and lifestyle (obesity, excessive salt, alcohol)

266
Q

hypertension: Conn’s syndrome

A

overproduction of aldosterone due to unilateral adrenal adenoma
results in sodium and water retention which increases BP

267
Q

drugs causing hypertension

A 
NSAIDS
combined oral contraceptive
corticosteroids
ciclosporin
cold cures
SNRI antidepressants
268
Q

other causes of hypertension

A 
renal parenchymal disease
renovascular disease
endocrine
coarctation or aorta 
pregnancy
sleep apnoea
269
Q

hypertension: investigation

A

eye exam- only area where blood vessels visible so can see damage caused by hypertension

270
Q

hypertension: calcium channel blockers

A

inhibit the opening of voltage-gated calcium channels in vascular smooth muscle, reducing calcium entry and thereby calcium available for muscle contraction

271
Q

hypertension: ACE inhibitors

A

prevents the generation of angiotensin II from angiotensin I

angiotensin II is vasoconstrictor that stimulates aldosterone release enhancing reabsorption of sodium

272
Q

hypertension: angiotensin receptor blockers

A

blocks the action of angiotensin II at peripheral receptors

273
Q

hypertension: thiazide diuretics

A

inhibit sodium reabsorption at distal tubule, reducing extracellular fluid volume which is elevated in hypertension

274
Q

hypertension: beta-blockers

A

resistant hypertension may also be treated using alpha or beta adrenoceptor antagonists

275
Q

BP response expected from 50mg atenolol

A

decrease in systolic or 10mmHg

276
Q

white coat hypertension

A

anxiety when seeing a doctor so BP increases

95% of population BP is higher when in a clinical setting

277
Q

how to measure BP at home

A

ambulatory BP monitoring: patient wears for 24 hours and measure every 20 mins
semi-automated device:
patients measures twice in morning and evening for a week

278
Q

hypertension thresholds

A

clinical= 140/90

home=135/85

279
Q

stages of hypertension

A

stage 1= low risk
clinical=140-160/90-100
home=135-150/85-95

stage 2=high risk
clinical >160/100
home= >150/95

280
Q

illnesses caused by hypertension

A 
heart failure
stroke
MI
renal failure
retinopathy
281
Q

lifestyle changes to lower blood pressure

A 
weight loss
alcohol intake reduction
salt intake reduction
smoking cessation
medication review
stress reduction
282
Q

aortic stenosis

A

normal valve area= 3-4cm2

symptoms occur when valve area is 1/4 of normal

283
Q

congenital aortic stenosis

A

occur with unicuspid, bicuspid or tricuspid valves

284
Q

acquired aortic stenosis

A

degenerative calcification

rheumatic heart disease

285
Q

aortic stenosis: pathology

A

pressure gradient develops between the left ventricle and the aorta
LV function initially maintained by compensation but when these mechanisms are exhausted the function declines

286
Q

aortic stenosis: presentation

A

syncope
angina
dyspnoea on exertion

287
Q

aortic stenosis: signs

A

slow rising carotid pulse
soft or absent second heart sound
ejection systolic murmur

288
Q

aortic stenosis: natural history

A 
onset of symptoms is poor prognostic indicator
mild to sever:
8% in 10 years
22% in 22 years
38% in 25 years
289
Q

aortic stenosis: prognosis

A

angina and AS= 50% survive 5 years
syncope+AS= 50% survive 3 years
HF+AS mean survival <2 years

290
Q

aortic stenosis: investigations

A

echo- measures left ventricular size and function and valve area

291
Q

mild aortic stenosis: area and velocity

A

area >1.5cm2

velocity= 2.6-3 m/s

292
Q

moderate aortic stenosis: area and velocity

A

1-1.5cm2

3-4m/s

293
Q

severe aortic stenosis: area and velocity

A

<1cm2

>4m/s

294
Q

aortic stenosis: management

A

dental hygiene
IE prophylaxis
surgical replacement
transcatheter aortic valve implantation

295
Q

aortic stenosis: indications for intervention

A

symptomatic patients
any patient with decreasing EF
patients undergoing CABG with severe AS

296
Q

mitral regurgitation

A

back flow from LV to LA during systole

297
Q

mitral regurgitation: aetiology

A

myxomatous degeneration
ischaemic MR
rheumatic heart disease
infective endocarditis

298
Q

mitral regurgitation: pathophysiology

A

pure volume overloads
compensation= left atrial enlargement, increased contractility
RV dysfunction due to pulmonary hypertension

299
Q

mitral regurgitation: signs and symptoms

A

soft s1 and pan-systolic murmur (auscultation)
exertion dyspnoea
heart failure

300
Q

mitral regurgitation: natural history

A

compensatory phase= 10-15 years

patients with asymptomatic sever MR have 5%/year mortality rate

301
Q

mitral regurgitation: investigations

A

ECG
CXR
ECHO

302
Q

mitral regurgitation: management

A

medication
serial echo
IE prophylaxis
surgery

303
Q

aortic regurgitation

A

leakage of blood from aorta into LV during diastole

304
Q

aortic regurgitation: aetiology

A

bicuspid aortic valve
rheumatic
infective endocarditis

305
Q

aortic regurgitation: pathophysiology

A

combined pressure and volume overload

compensatory mechanisms

306
Q

aortic regurgitation: physical examination

A

wide pulse pressure

hyperdynamic and displaced apical pulse

307
Q

aortic regurgitation: natural history

A

asymptomatic until 4th/5th decade

rate of progression= 4-6% a year

308
Q

aortic regurgitation: investigations

309
Q

aortic regurgitation: management

A

IE prophylaxis
vasodilators
serial echos
surgical treatment

310
Q

mitral stenosis

A

obstruction of LV inflow that prevents proper filling during diastole
normal area=4.6cm2
symptoms begin at areas <2cm2

311
Q

aetiology

A

rheumatic heart disease=77-99% of all cases
IE=3.3%
mitral annular calcification =2.7%

312
Q

mitral stenosis: pathophysiology

A

progressive dyspnoea (70%)
increased transmitral pressures
right heart failure symptoms

313
Q

mitral stenosis: natural history

A

disease of plateaus:
mild= 10 years after initial RHD
moderate= 10 years later
severe= 10 years later

314
Q

mitral stenosis: signs

A

right sided heart failure

pinkish-purple patches on cheeks due to vasoconstriction- mitral facies

315
Q

mitral stenosis: heart sounds

A

diastolic murmur

loud opening S1 snap

316
Q

mitral stenosis: investigations

A

ecg
cxr
echo

317
Q

mild mitral stenosis: valve area

318
Q

moderate mitral stenosis: valve area

319
Q

severe mitral stenosis: valve area

320
Q

mitral stenosis: management

A

serial echos
beta-blockers and diuretics
IE prophylaxis
surgery

phase 2a clinical (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions