Brainscape's Knowledge GenomeTM

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


See full index

Year 3 > Cardio > Flashcards

Cardio Flashcards

1
Q

causes of MI

A

CAD, aortic stenosis, hypertrophic cardiomyopathy, tachyarrhythmias, cocaine use, anaemia, thyrotoxicosis

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

causes of cardiovascular non-ischemic chest pain

A

pericarditis, aortic dissection

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

causes of upper GI chest pain

A

gastro-oesophageal reflux disease, gallstones, peptic ulcers, pancreatitis

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

causes of respiratory chest pain

A

pulmonary embolism, pneumothorax, pneumonia, pleurisy

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

causes of musculoskeletal chest pain

A

costochondritis, Herpes Zoster, shingles

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

diagnosing visceral and somatic pain (in history taking)

A

visceral: diffuse, poorly localised
somatic: localised

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

def angina

A

discomfort in chest and/or jaw, shoulder, back, arm caused by myocardial ischaemia. most common cause in CAD

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

symptoms/characteristics typical angina

A
  1. discomfort in chest and/or jaw, shoulder, back, arm
  2. symptoms bought on by exertion
  3. symptoms relieved within 5 minutes (rest or GTN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

def atypical angina

A

chest discomfort that meets 2/3 characteristics of typical angina

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

risk factors for CAD

A

age, gender, diabetes, hyperlipidaemia, smoking, hypertension

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

def dyspnoea

A

shortness of breath

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

what do you look for on an ECG?

A
  • heart rate
  • rhythm (sinus-rhythm starting at the P wave): PR interval 120-200 ms
  • axis: QRS complex upright
  • QRS complexe: les than 120 ms
  • Q waves
  • isoelectric ST interval
  • T waves: less than 5mm in height in limb leads and less than 15 mm in chest leads
  • QT interval should be less than half the preceding RR interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ECG indictions of CAD

A
  • Q waves: more than 40 ms wide, 2 mm deep, 25% of depth of QRS complex, seen in leads V1-3
  • Left bundle branch block: broad QRS (more than 0.12 sec), dip S wave in V1, no Q wave in V5/V6
  • ST depression, T wave flattening or inversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

types of angina

A

stable, unstable, decubitus angina (lying flat), variant (prinzemetal) angina

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

ECG: difference between ischemic and infarcting endocardium

A

ischemic: depressed ST
infarcting: elevated ST + inverted T waves

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

branches of left coronary artery

A

Lad
circumflex
obtuse marginal
diagonal

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

branches of right coronary artery

A

right marginal

poster descending artery

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

venous drainage of heart

A 
oblique vein of left atrium
great cardiac vein
left marginal vein
posterior vein of left ventricle
middle cardiac vein 
small cardiac vein 
--> coronary sinus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

markers of cardiac cell death

A 
troponin (T or I) 2-12 hours after MI (peak at 24-48 hours after MI) and can be elevated for up to 2 weeks post MI
creatine kinase (non specific to cardiac cells)

Increase Proportionally to cardiac death and mortality

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

where are troponin T and I found in cells

A

actin filaments

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

causes of ventricular fibrillation

A
  • IRRITABLE VENTRICULAR CELLS: Cad, electrolyte abnormalities (low Ca, high K, low Mg)
  • SCAR: MI, cardiomyopathy (infection, genetic disorders, CAD)
  • ELECTROCUTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

different types of Ventricular tachycardia

A

focal

reentrant

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

causes of focal vtach

A

cell irritation due to

  • hormones
  • low oxygen
  • stretch

(CAD, electrolyte abnormalities)

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

causes of reentrant vtach

A

scar (MI, hypertrophic and dilated cardiomyopathy)

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

Afib ecg: what does it look like?

A

irregularly irregular heart rate

-no distinct P waves

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

risk factors for Atrial fibrillation

A

diseased atrial tissue

  • age
  • inflammation
  • enlarged atria (high BP, valve disease, lung disease, Afib)

hormonal abnormalities (thyroid)

alcohol abuse

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

complications post MI

A

-decreased contractibility
—> embolism (ventricular thrombus)
—> cardiogenic shock (decrease contractibility —> hypotension—> decrease vessel perfusion —> ischemia —> decrease contractibility)

-electrical instability (arrhythmia)

-tissue necrosis causing inflammation
—>pericarditis
—>cardiac tamponade (rupture of cardiac muscle causing blood to fill space between pericardium and serous sac)
—>mitral regurgitation (rupture of papillary muscles)
—>hypoxemia + stress on pulmonary vessels

–> congestive heart failure

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

Def orthostatic

A

Relating to or caused by an upright posture

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

Stages of hypertension

A 
Grade 1 (mild): 140-159/90-99
Grade 2 (moderate): 160-179/100-110
Grade 3 (severe): >180/>110
Isolated systolic hypertension: >140/<90
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Types of hypertensive crisis, BP measurement, symptom and management

A

Hypertensive urgency:

  • BP: >180/>110 mmHg
  • symptoms: no target organ damage, headaches, nosebleeds, SoB, severe anxiety
  • management: oral medication, outpatient

Hypertensive emergency:
-BP: >180/>120 mmHg
-symptoms: target organ damage, chest pain, SoB, numbness/weakness, vision change, difficulty speaking, back pain
Management: IV medication, (vasodilator, Ca channel blockers, beta blockers), intensive care BUT reduce BP over 24-48 hours (25% over first few hours) to minimise ischemia

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

Assessment cardiovascular risk and target organ damage in hypertension

A

QRISK2 risk assessment
Urinalysis: protein, albumin:creatinine ratio, Haematuria
Blood test: FBC, glucose, electrolyte, creatinine, eGFR, total and HDL cholestérol
ECG
Fundoscopy for hypertensive retinopathy

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

Grade of hypertensive retinopathy

A

– Grade 1 – tortuosity of the retinal arteries with increased reflectiveness (silver wiring)
– Grade 2 – grade 1 plus the appearance of arteriovenous nipping, produced when thickened retinal arteries pass over the retinal veins
– Grade 3 – grade 2 plus flame-shaped haemorrhages and soft (‘cotton wool’) exudates due to small infarcts
– Grade 4 – grade 3 plus papilloedema (blurring of the optic disc)

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

Pharmacological Management of hypertension

A

Aged <55:
A -> A+C -> A+C+D -> (resistance hypertension): A+C+D+other diuretics, alpha or beta blockers + consider sealing expert advice

Aged >55 or black person of African or Caribbean family origin of any age:
C -> A+C -> A+C+D -> (resistance hypertension): A+C+D+ (IF K=4.5) low dose spironolactone OR (IF K> 4.5) alpha or beta blocker + consider sealing expert advice

A: ACEi or ARB
C: Ca channel blocker (CCB)
D:thiazides like diuretics

IN PREGNANCY:
-labetalol, nifedipine or methyldopa

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

Pathophysiology of increase BP

A

Usually due to increase peripheral resistance (PR)(increased arteriolar vasoconstriction)
-increased sympathetic action (constriction of muscles)
-decreased blood flow to kidneys: release of renin (RAAS citation causing increase in PR) + aldosterone (increase absorption if H2O + Na+ causing increase in CO)
—> increase in BP causes decrease blood flow to kidneys (iCloud circle)

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

What are the end organ damage in hypertension

A

Eyes hypertensive retinopathy (papilloedema, flame haemorrhage, cotton wool spot, hard exudate, arteriovenous nicking)

Brain: hypertensive cerebrovascular disease, haemorrhage/infarction, seizures, vascular dementia

Heart/blood vessels: LVH, IDH (w/ or w/out HF), pulmonary oedema, MI, atherosclerosis, aneurysms, sorti dissections

Kidneys: hypertensive nephropathy (shrunken kidneys), CKD

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

Examples of causes of secondary hypertension

A

Common:
Renal parenchyma disease
Renal artery stenosis
Primary aldosteronism

Uncommon:
Phaeochromoytoma
Cushing’s syndrome

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

Def orthopnoea

A

SoB when lying flat

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

Describe the waveforms of JVP and what they correspond to

A
  • A wave: atrial contraction
  • C wave: closure of tricuspid valve
  • X descent: atrial relaxation
  • V wave atrial filling during systole
  • Y descent: passive ventricular filling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Classification of murmurs based on intensity

A

Grade 1: can only be heard if listen intensely for some time
Grade 2: faint murmur heard immediately on auscultation
Grade 3: loud murmur with no palpable trills
Grade 4: loud murmur with a palpable thrill

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

Tests and investigations in diagnosis of HF

A 
ECG
Chest X ray
Blood tests:
-BNP
-NT-proBNP
-Renal, liver, thyroid and lipid function profile
-HbA1c
-FBC
Trans thoracic echo (exclude valve disease, assess left ventricular function, detect intracardiac shunts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What produces the sound of heart murmurs

A

Turbulent blood flow:

  • low viscosity of blood
  • decreased radis of vessel/valve
  • increased velocity of blood through morphologically normal structures
  • regurgitation against incompetent valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Causes of murmurs due to decreased blood viscosity

A

Anaemia

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

Causes of murmurs due to decreased diameter of vessel, valve, or orifice

A

Valvular stenosis
Coarctation of the aorta
Ventricular septal defect

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

Causes of murmurs due to increased velocity of blood through normal structures

A

Hyper dynamic states (ie sepsis, hyperthyroidism)

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

Causes of murmurs due to regurg acros an incompetent valve

A

Valvular regurg

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

Initial treatment of acute HF

A
  • IV diuretic therapy
  • increase dose of the diuretic the patient is already on
  • monitor closely weight, renal function and urine output during diuretic therapy
  • do not offer routinely opiates, nitrates inotropes or vasopressors
  • do not offer sodium nitroprusside
  • consider inotropes or vasopressors in people with reversible cardiogenic shock
  • if person in cardiogenic pulmonary oedema with severe dyspnoea and acidaemia OR respiratory failure OR reduced consciousness OR physical exhaustion : NIV
  • consider ultrafiltration for people with confirmed diuretic resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Treatment of acute HF after stabilisation

A
  • Treat underlying cause
  • montor renal function, electrolytes, HR; BP and overall clinical status
  • offer surgical aortic valve replacement therapy if severe aortic stenosis or mitral vale regurg

HF with preserved LV function ( EF > 45%)

  • diuretics
  • tract co-morbidities

HF with impaired systolic function ((EF <45%)

  • diuretics
  • beta blockers (first line)
  • ACEi (first line)
  • aldosterone receptor antagonist (second line)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

HF symptoms

A

—> SoB

  • orthopnoea
  • on exertion/at rest
  • paroxysmal nocturnal dyspnoea

—> tiredness/fatigue

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

HF signs

A
  • pulmonary oedema/pleural effusion
  • raised JVP
  • pitting oedema
  • ascites
  • tachycardia
  • S3 gallop
50
Q

Which beta blocker is not licenced for HF

A

Atenolol

51
Q

AF management

A

In new onset:
-If life threatening haemodynamic instability: Emergency electrical cardio version
-If no life threatening haemodynamic instability: rate (beta blockers or rate limiting Calcium channel blocker) or rhythm control
—> electrical or pharmacological cardioversion (flecainide or amiodarone)

If in AF for more than 48 hours: anticoagulate, long term rhythm control and rate control

52
Q

What is the Frank-Sterling curve

A

Relationship between the volume of blood in the heart at the end of diastole (pre-load/end diastolic volume) and the force of contraction of the ventricle

Stroke volume/EDV

(If myocardial cells stretched: increase force and velocity of contraction
BUT only until 15 mmHG pressure)

53
Q

Causes of mitral valve regurg

A

Rheumatic heart disease
IHD (papillary muscle rupture)
Valvular vegetation (endocarditis)
Dilated left atrium

54
Q

What is ejection fraction and what is a normal value?

A

Measurement of how much blood is being pumped out of the heart with each contraction. It is measured in percentage (stroke volume/end diastolic volume)
Normal value: 50-70%

55
Q

What are the phase of the action potential

A

0: rapid depolarisation
1: early repolarisation
2: plateau phase
3: repolariasation
4: resting membrane potential

56
Q

How long is the cardiac AP

A

300 ms

57
Q

Ion channel activity during cardiac AP

A

Sodium (short but intense)
Calcium (long )
Potassium (delayed, repolarisation)

58
Q

Properties of cardiac AP

A
  1. Long duration and refractory period:
    - prevent premature re-excitation (which is different to skeletal muscle)
    - long refractory: inactivation of Na channels and persistence of K channels
  2. Fast conduction velocity (for uniform activation, esp in His-Purkinje system)
  3. Pacemaker activity
59
Q

Different types of arrhythmias depending on categories

A

Abnormal pacemaker/triggered activity

  • early afterdepolarisation
  • delayed afterdepolarisation

Re-entry

60
Q

What is the difference between pacemaker and triggered activity

A

Pacemaker: spontaneous
Triggered: set of after being excited by a stimulation

61
Q

Pathophysiology of early after depolarisation and the medical issue it underlies

A

Decreased outward K currents: prolonges AP (+ can lead to re-activation of L-Type Ca channels)

Medical issue: long QT syndrome (genetic or acquired: anti histamines, anti cancer)

62
Q

Pathophysiology of delayed afterdepolarisation

A

Cellular calcium overload

  • spontaneous Ca release from SR
  • activates depolarising membrane currents

Medical issue: HF

63
Q

Pathophysiology of re-entry arrhythmia

A
  • unidirectional block (AP can propagate in one direction but not the other)
  • slow conduction (cell excitability is decreased)
  • short AP (shortens refractory period, increase activation of K channels)

Medical issue: post MI

64
Q

What is Ca induced Calcium release and how does it work

A

Ca entry on Ca current triggers SR release

L-Ca channel: infux of Ca into cell
Ca activates RyR charnels

Uptake into SR by SERCA (ATPase): influences by availability of Ca and by phosphorylation of phospholamban (during sympathetic stimulation)
NCX (exchange 1 Ca for 3 Na)

65
Q

Def inotropic

A

Influencing the contractibility of muscular tissue

66
Q

Def lusitropy

A

Relaxation of cardiac muscle

67
Q

Effect of catecholamines on cardiac muscle

A

Inotropic: Increase L-Ca current (more trigger and loading)
Lusitropic: increase SERCA (increased SR Ca) via phosphorylation of phospholamban

68
Q

What are peripheral signs for infective endocarditis

A 
Splinter haemorrhages
Clubbing
Janeway lesions 
Osler’s nodes
Roth spots
Petechiae
69
Q

Diagnostic criteria for infective endocarditis

A

Modified Duke criteria:

  • 2 major criteria
  • 1 major criteria and 3 minor criteria
  • 5 minor criteria

BE FIV(E) PM

Major criteria:
-+ blood culture
- evidence of endocardial involvement:
A. + echo (vegetation, abscess or valve dehiscence)
B. New valvular regurg

Minor criteria:

  • Fever
  • Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
  • Vascular phenomena (maj arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions)
  • Predisposition (heart condition or IVDU)
  • Microbiological evidence (+ blood culture but not meeting major criteria or serologic evidence of active inf w/ org consistent with IE)
70
Q

Which beta blockers can be used in treatment of HF

A

Bisoprolol
Carvedilol
Nebivolol
Metoprolol (modified release)

71
Q

Components of the CHADS2 score

A 
Congestive HF
Hypertension 
Age> 75
DMT2
Stroke or TIA symptoms
72
Q

Chest pain history timing differentials

A

Seconds: Musculoskeletal/non cardiac
Minutes: ACS, GORD, musculoskeletal
Hours: all
Days (dull, persistent): not ACS

73
Q

Chest pain history associated symptoms differentials

A

Nausea/vomiting: ACS, upper GI pathology
Sweating/clammy: ACSS, PE, aortic dissection
SoB: ACS, resp causes
Hypotension/syncope: PE, ACS, aortic stenosis

74
Q

ECG paper:

Time of small square and big square

A

Small: 0.04 sec
Big: 0.2 sec

75
Q

Which leads on ECG look at:

  • inferior part of the heart
  • lateral part
  • anterior
  • septal
A 
Inferior: II, III and aVF
Lateral: V5, V6, aVL, I
Anterior: V1, V2
Septal: V3, V4
AVR: right atrium (always neg deflection)
76
Q

How long should each part of the ECG be?

A

PR interval: 3-5 small squares/ 120-200 ms
QRS complex: < 3 ss/ <120ms
QT interval: female 350-470ms/ male 350-450ms (no more than 2 big squares)

77
Q

Diagnostic investigations for angina chest pain

A

(Resting 12 lead ECG (if can’t exclude stable/unstable angina from clinical history))

(Go down first, second, third line of results are inconclusive/non-diagnostic)
First line: 64 slice CT coronary angiography: significant CAD
Second line: non invasive functional testing: reversible myocardial ischemia
—> MPS/ with SPECT
—> stress echo
—> first pass contrast enhanced magnetic perfusion
—> MRI for stress wall motion abnormalities
Third line: invasive coronary angiography

78
Q

Type of systolic murmurs

A

Tricuspid/mitral regurgitation
Aortic/pulmonary stenosis
Mitral valve prolapse

79
Q

Types of diastolic murmurs

A

Tricuspid/mitral stenosis

Aortic/pulmonary regurgitation

80
Q

Which valves close on S1? On S2?

A

S1: tricuspid/mitral
S2: aortic/pulmonary

81
Q

Why do we listen to the different places on the chest wall for the heart sounds

A

Places we expect the blood to travel towards

82
Q

Describe an aortic/pulmonic stenosis murmur

A 
Systolic ejection murmur 
S1 then nothing
EC (ejection click)
Crescendo descrenscendo murmur
S2

(Radiates to the carotid: only for aortic stenosis murmur)

83
Q

Describe a mitral(/tricuspid) regurgitation murmur

A

Holo/pan sysolic murmur
S1
Flat murmur: no change in intensity
S2

Radiates to axilla (mitral)

84
Q

Treatment of unstable angina and NSTEMI

A
  1. Aspirin 300mg
  2. clopidogrel/ticagrelol + glycoprotein inhibitors (for people at high risk)
  3. Unstable angina: LMWH
    NSTEMI: LMWH, PCI/thrombolyis, angiography/CABG or Fondaparinux (if not planning angiography w/in 24h)

Post MI: ACEi, dual antiplatelet therapy (aspirin + another), beta blocker, statin

85
Q

Treatment for acute STEMI

A
  1. Aspirin +clopidogrel/ticagrelol
  2. PCI (percutaneous coronary intervention) or fibrinolysis
    - give PCI if presenting w/in 12 hours of onset of unprompted if can be delivered w/in 120 minutes of the time fibrinolysis could have been given
  3. After PCI: anti-platelets, ai thrombin drugs? Look into this
86
Q

How does ACS present

A 
Silent ischemia (in the elderly, T2DM)
Stable angina 
Unstable angina
NSTEMI
STEMI
Heart failure
Sudden death
87
Q

How can an ECG be normal in ACS

A

Ischemia in circumflex artery (need V7-V9 lead)
Isolated RV ischemia (V3R and V4R leads)
Transient episodes of bundle branch block

88
Q

What is the drug treatment for ACS

A

Anti-ischemic agents (beta blockers, nitrates, Ca channel blockers, nicorandil, ivabridine, ranolazine)

Antiplatelet agents (aspirin, P2Y12 receptor inhibitors)

Anticoagulants (LMWH, factor Xa inhibitors, inhibitors of coagulation)

89
Q

Long term management of ACS

A 
Aspirin for life + another antiplatelet therapy (for 12 months)
Statins 
Beta blockers (if LVEF<40%)
ACEi (to all)
Aldosterone antagonists (if LVEF<35%)
Secondary prevention (lifestyle)
90
Q 
Which arteries are blocked in
Inf
Ant
Lateral
MI?
A

Inf: RCA
Ant: LAD
Lateral: circumflex

91
Q

Consequences of Vfib

A

No pulse

Not enough oxygen circulating

92
Q

Signs and symptoms of Vtach

A 
pulse >120 BPM
Palpitations
SoB
Chest pain 
Lightheaded/dizzy/syncope

ECG: regular R waves in absence of atrial rhythm, can be broad complex (>3ss) or narrow complex (<3ss)

93
Q

What does GRACE score calculate?

A

Estimate admission-6 month mortality for patients with ACS

Takes into account
Age, HR/pulse, systolic BP, creatiine, cardiac arrest on admission?, ST segment deviation on ECG?, abnormal cardia enzymes?, Killip class (CHF,JVP, pulmonary oedema, cardiogenic shock)

94
Q

What does CRUSADE score calculate?

A

Stratified bleeding risk post MI

Looks at:
HR, systolic BP, hématocrite, creatinine clearance, sex, signs of CHF at presentation, history of vascular disease or DM

95
Q

physiological difference between a STEMI and a NSTEMI

A

STEMI: full thickness of the ventricular wall
NSTEMI: partial thickness of wall affected

96
Q

type 1 and 2 MI

A

type 1: spontaneous MI due to ruptured atherosclerotic plaque

type 2: secondary to ischemia due to either increase oxygen demand or decreased supply

97
Q

NYHA classification of heart disease

A

Class I: no limitation of physical activity
Class II: sight limitation of physical activity, comfortable at rest
Class III: marked limitation of physical activity, comfortable at rest
Class IV: inability to carry out physical activity without discomfort + discomfort at rest

98
Q

ACC/AHA stage of heart failure

A

stage A: at high risk of dvlpt of HF (no abnormalities or signs/symptoms)

stage B: dvlpt structural Heart disease that is strongly associated w/ dvlpt go HF (w/out sign/symptoms)

stage C: symptomatic HF associated with underlying structural heart disease

Stage D: advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy

99
Q

what are the 5 problems aneurysms can cause

A
  • grow
  • burst
  • embolise
  • compress other structures
  • thombose
100
Q

what is the cutoff for surgery with AAA

A

5.5 cm in men and 5 cm in women

101
Q

what is an aortic aneurysm?

A

swelling of the aorta greater than 1.5 times its normal size

102
Q

Fontaine description of peripheral arterial disease?

A

stage 1: asymptomatic
stage 2: intermittent claudication
stage 3: rest pain/nocturnal pain
stage 4: gangrene/necrosis

103
Q

signs of chronic limb ischemia

A

lower limb cold, dry skin, lack of hair
pulses diminished/absent
ulceration may occur + dark discolouration of toes or gangrene
(must examine abode for AAA)

104
Q

symptoms of acute lower limb ischemia?

A

5Ps: pain, pallor, parasthesia, paralysis, perishing cold

pain unbearable and requires opioids for relief

105
Q

aetiology of acute limb ischemia

A

embolic or thrombotic disease (i.e. previously reported symptoms of claudication)

106
Q

symptoms/signs of ruptured AAA

A 
severe epigastric pain radiating to the back 
hypotension 
tachycardia 
profound anaemia 
sudden death
107
Q

management of AAA

A
  • medical: BP, smoking, hyperlipidemia and diabetes + regular ultrasounds
  • surgical: graft, stent, endovascular repair (EVAR)
108
Q

treatment of chronic limb ischemia

A
  • comorbidities (BP, cholesterol, diabetes, smoking, diet etc)
  • low dose aspirin or other anti platelets
  • angioplasty
109
Q

when do you do surgical treatment of carotid stenosis

A

symptomatic patients (in last 6 months) >70% stenosis of ICA

110
Q

aetiology of aneurysms?

A
  • atherosclerotic
  • mycotic (infection of arterial wall)
  • infammatory
  • connective tissue disorder
  • false
111
Q

where ca you find aneurysms

A

aortic/iliac
popliteal
visceral (splenic most common)
intracerebral

112
Q

what shapes can aneurysms be?

A

fusiform

saccular

113
Q

causes of aortic dissection

A

hypertension
connective tissue disease
aneurysm
trauma of the chest

114
Q

Stanford classification of aortic dissection

A
  • type A: ascending aorta

- type B: descending aorta, distal to left subclavian origin

115
Q

causes of shock

A
  • hypovolaemia (exogenous losses)
  • cardiogenic (intrinsic cardiac pump failure)
  • obstructive ( obstruction to cardiac outflow OR restricted cardiac filling)
  • distributive (vasodilatation and malperfusion)
116
Q

examples of hypovolaemic shock

A

haemorrhage
burns
GI losses
dehydration

117
Q

examples of distributive shock

A
  • SIRS related (sepsis, pancreatitis, trauma, burns)
  • neurogenic (spinal cord injury)
  • anaphylaxis
118
Q

examples of cariogenic shock

A
  • MI/ischemia
  • arrythmis
  • acute valve pathology
119
Q

examples of obstructive shock

A
  • tension pneumothorax
  • pericardial tamponade
  • PE
120
Q

physiological response to shock

A
  • sympathetic system activated
  • adrenal catecholamine release
  • compensatory cardiovascular responses
  • sodium and H2O retention
  • coagulation system activation
  • cortisol release
121
Q

def shock

A

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion, resulting in generalised cellular hypoxia and/or inability of cells to utilise oxygen

122
Q

aetiology of shock

A
  • failure of heart to act as effective pump
  • mechanical impediments to forwards flow
  • loss of circulatory volume
  • abnormalities of peripheral circulation

Year 3 (7 decks)

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