Cardiology - Miscellaneous Flashcards by Jen P

Effect of diabetes on cardiac?

higher CAD risk
abnormal LV systolic and diastolic dysfunction
coronary MICROVASCULAR disease
endothelial dysfunction
autonomic dysfunction

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Thiamine deficiency (Beri Beri) effects of cardiac system?

High output failure

Dilated cardiomyopathy

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Hyperhomocysteinaemia effects on cardiac system?

Premature atherosclerosis

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Obesity effects on cardiac system?

- Excessive LV filling presure on exertion

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HypERthyroidism effect on cardiac system?

SVT
HTN
AF (in 15%)
Means-Lerman Scratch: systolic pleuropericardial rub at left 2nd ICS on EXPIRATION

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Means-Lerman Scratch

= systolic pleuropericardial rub at left 2nd ICS on EXPIRATION

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Hypothyroidism effects on cardiac disease

decreased cardiac output
decreased stroke volume
decreased HR
decreased pulse pressure

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Cardiac Tumours:

What is the most common cancer to metastasise to the heart?

Metastatic melanoma

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Cardiac Tumours:

What is Carney Complex?

Carney Complex: mutation in tumour suppressor PRKAR1A
Autosomal Dominant
Blue naevi
Myxoma
Endocrine overactivity
- Cushing's
- Testicular tumor
- Pituitary adenoma

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Cardiac Tumours:

What mutation is seen in Carney Complex?

Mutation in tumour suppressor gene PRKAR1A

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What clinical features would represent an atrial myxoma?

AF
Mid-diastolic murmur with ‘tumour plop’
Embolism

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What murmur do you hear with an atrial myoxoma?

Mid-diastolic murmur with ‘tumour plop’

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If a Carney Complex atrial myxoma what is the problem with surgical resection?

Carney complex myxoma often recur.

Normal myxoma recurrence in 5-15% after resection

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What is Loeffler’s Endocarditis?

Eosinophilic endocardial disease

Associated with restrictive cardiomyopathy

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What is Fabry’s Disease and how is it related to the heart?

X linked recessive deficiency of alpha-galactosidase A.

Associated with restrictive cardiomyopathy

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What is Kaussmaul’s sign?

INCREASE in JVP on inspiration

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Is carotid sinus hypersensitivity more common in males or females?
Which age group?

Males more common
Increased age

Also more commonly right-sided hypersensitivity

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On carotid massage when is it diagnostic for carotid sinus hypersensitivity?

Reproducible on massage and if:

Asystole >3 seconds (indicates cardioinhibitory CSH)
Decrease in SBP of >50mmHg independent of HR (indicates vasodepressor CSH)

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When would you do a pacemaker in carotid sinus hypersensitivity?

If it is cardioinhibitory (ie carotid sinus massage reproduces symptoms and has asystole >3 seconds)

or if mixed carotid sinus hypersensitivity

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A patient has syncope/dizziness/falls on turning their head or tight fitted collars….what do you think of?

Carotid sinus hypersensitivity

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How does DIGOXIN work? (5 ways)

1) Cardiac Glycoside: direct VASOCONSTRICTION in smooth muscle (arterial and venous)

2) POSITIVE Inotrope:
Direct inhibition of membrane bound NaK-ATPas –> increases intracellular Ca
- associated increase in slow inward Ca current during action potential

3) SLOWED conduction
4) INCREASED REFRACTORY PERIOD by stimulation of vagal tone
5) PARASYMPATHETIC PROPERTIES: hypersensitises carotid baroreceptor and stimulates central vagal nuclei

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Causes of supratherapeutic digoxin level:

1) renal impairment
2) MI and acidosis –> suppression of Na/K ATPase
3) Hypothyroidism –> decreased renal excretion
4) Drugs

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Drugs that INCREASE digoxin level

Verapamil/Diltiazem
Erythromycin
Tetracyclines
Paroxetine

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Drugs that DECREASE digoxin level

Study These Flashcards

Rifampin

Visual changes in digoxin toxicity

``` Yellow-green distortion Xanthopsia (yellow halo around eyes) Transient scotoma Decreased acuity Photophobia ```

GIT complications of digoxin toxicity

General (anorexia / n+v / diarrhoea) | Mesenteric ischaemia after rapid IV infusion

Cardiac complications of digoxin toxicity

palpitations syncope peripheral oedema bradycardia + hypotension

Neuro complications of digoxin toxicity

``` drowsiness/fatigue/confusion neuralgia and headache paraesthesia and neuropathic pain hallucinations seizures ```

ECG findings of digoxin toxicity

``` AV block Sinus bradycardia Torsades ST reverse tick Short QT Flattened/inverted T waves ```

Dialysis of digoxin?

DON'T DIALYSE DIGOXIN TOXICITY!!! (minimal clearance)

Treatment of digoxin toxicity?

Acute: charcoal within 6-8 hours Treat K abnormality BUT DON'T USE CALCIUM (delays depolarisation and precipitates VT) Treat hypoMg Digibind (if unavailable then use phenytoin or lidocaine --> dissociates inotrope and dysrhythmic action of digoxin) Arrythmias: DON'T USE CCBs!!!! (as these increase digoxin levels)

Classic ECG findings of hypokalaemia

``` U waves Small or absent T waves Prolonged PR ST depression Long QT ``` ** "in hypokalaemia U have no Pot and no T, but a long PR and a long QT" ***

Classic ECG findings of hypothermia:

``` Bradycardia J waves 1st degree HB Long QT Atrial and ventricular arrythmias ```

JVP Physiology: | what are 'a' waves and what abnormalities might you see?

'a' waves = atrial contraction (first bump on the JVP) LARGE: due to atrial pressure (ie tricuspid or pulmonary stenosis, or pulmonary HTN) ABSENT: AF CANNON: due to atrial contractions against CLOSED tricuspid in: - complete HB - ventricular tachycardias/ectopics - single chamber pacing

JVP Physiology: | When might you see 'cannon' a waves and why do they occur?

CANNON: due to atrial contractions against CLOSED tricuspid in: - complete HB - ventricular tachycardias/ectopics - single chamber pacing

JVP Physiology: | What is the 'c' wave?

= closure of tricuspid valve NOT usually seen (2nd little bump after the 'a' wave on the JVP)

JVP Physiology: | What is the 'v' wave?

= passive filling of blood into atrium against closed tricuspid valve (3rd bump) GIANT: tricuspid regurg / RHF

JVP Physiology: | What is the 'x' descent?

= fall in atrial pressure during ventricular systole | 2nd 'trough'

JVP Physiology: | What is the 'y' descent?

= opening of tricuspid valve | final downward bit of the JVP

JVP Physiology: | What part of the JVP represents atrial contraction?

'a' wave

JVP Physiology: | What part of the JVP represents closure of the tricuspid valve?

'c' wave (not usually seen)

JVP Physiology: | What part of the JVP represents passive filling of blood into the atrium against a closed tricuspid valve?

'v' wave

JVP Physiology: | What part of the JVP represents fall in atrial pressure during ventricular systole?

'x' descent

JVP Physiology: | What part of the JVP represents opening of the tricuspid valve?

'y' descent

Who does fibromuscular dysplasia tend to affect?

Women in childbearing years

Which arteries does fibromuscular dysplasia affect?

Medium sized arteries

How does fibromuscular dysplasia present?

Usually asymptomatic RENAL: involved in 60 - 70% --> renovascular hypertension CNS: in 25-30% - -> stroke - -> sudden onset exposive headache and neck stiffness suggests FMD-associated aneurysm - -> predisposing factor in 15% of spontaneous carotid cervical dissections VISCERAL: abdo pains or ischaemic bowel LIMBS: intermittent claudication

How do you diagnose fibromuscular dysplasia?

CTA

Management of fibromuscular dysplasia?

Nil treatment if asymptomatic Antiplatelets Surgery if RENAL FMD

When is the onset of radiation cardiotoxicity?

5-20 years

With which cancer is pericardial effusion associated with radiation cardiotoxicity?

Oesophageal cancer

Which valves are associated with valvular disease relating to radiation cardiotoxicity?

Left sided valves more affected. Increased risk if also using anthracycline

With what chemotherapy agent is short term chemo cardiotoxicity associated?

5-Fluorouaracil is associated with high incidence of chest pain and ECG changes (death in 2-8%) Usually resolve within 7 days

With which chemo agents are associated with long term chemo cardiotoxicity?

Anthracyclines Trastuzumab Kinase inhibitors

Important facts about trastuzumab-induced chemo cardiotoxicity?

- increased risk of >50 YEARS OLD or if PREVIOUS ANTHRACYCLINES - REVERSIBLE - NOT dose related (so can rechallenge later)

When and what is affected in anthracycline-induced chemo cardiotoxicity?

- symptoms usually occur within a few months, but can occur up to 20 years later - subclinical decline in systolic and diastolic dysfunction

What are the risk factors for anthracycline-induced chemo cardiotoxicity?

- Cumulative dose (STRONGEST RF) - -> Incidence <1% if cumulative <400) - age at treatment - concomitant therapy with other cardiac toxics - chest radiation - pre-existing cardiac disease

How can you modify the response to anthracyclines in anthracycline-induced chemo cardiotoxicity?

- liposome encapsulation - infusion rather than bolus - structural analogues (epirubicin / mitoxantrone) - adjunctive cardioprotective agents (ie: dexrazoxone = EDTA chelator which reduces risk)

Cardiology - Miscellaneous Flashcards

(58 cards)