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What are the clinical features of TCA overdose?

Sedation and coma
Broad complex dysrhythmias
Anticholinergic syndrome


What does this ECG show and what is it consistent with?

Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2).
Broad QRS complexes.
Positive R’ wave in aVR.

TCA overdose


What are the important points about acute vs chronic lithium toxicity?

acute overdose is usually benign if adequate hydration is maintained and renal function is normal

chronic toxicity can be difficult to manage and result in devastating neurotoxicity


What are the features of lithium toxicity (acute or chronic)?

acute ingestion or chronic accumulation
CNS: confusion -> coma, cerebella symptoms, seizure, basal ganglia symptoms (choreiform movements, Parkinson-like)
GIT: nausea, vomiting, bloating
CVS: syncope
RENAL: polyuria, polydipsia, renal insufficiency
NEUROMUSCULAR: peripheral neuropathy, myopathy
ENDOCRINE: hypothermia, hyperthermia


What are the normal and toxic lithium levels?

Lithium level:
0.7-1.2mEq/L (therapeutic)
> 1.5mEq/L (toxic)
levels can be very high following acute ingestion, but do not correlate with outcome
as clinical features determine


What is the acute resuscitation mx of Lithium overdose?

A – impaired LOC -> intubate
consider whole bowel irrigation for massive acute ingestion
activated charchoal does not bind
Liberal fluid resuscitation with normal saline


What are the specific interventions for lithium toxicity?

A – impaired LOC -> intubate
consider whole bowel irrigation for massive acute ingestion
activated charchoal does not bind
Liberal fluid resuscitation with normal saline

Avoid hyponatraemia as this will decrease lithium clearance


What is the clinical significance of and RV infarct?

Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.


Which two ECG changes are most suggestive of an RV infarct?

ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle.
ST elevation in lead III > lead II  – because lead III is more "rightward facing" than lead II and hence more sensitive to the injury current produced by the right ventricle.


What does this ECG show?

There is an inferior STEMI with ST elevation in lead III > lead II.
There is subtle ST elevation in V1 with ST depression in V2.
There is ST elevation in V4R.

RV infarct


How can leads V1 and V2 help you in spotting an RV infarct?

If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.

If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.

NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.


What is the percent survival to hospital discharge with use of an AED for a shockable rhythm?

What is the overal percent survival to hospital discharge for an out of hospital arrest?


Around 7%


Do AEDs work for hospitalised patients with cardiac arrest?

Compared to usual resuscitative measures (including external defibrillation when indicated), AED use in hospitalized patients with cardiac arrest did not improve survival in a large, multi-center observational study.


What is Hypoalphalipoproteinemia?

Hypoalphalipoproteinemia is a high-density lipoprotein deficiency, inherited in an autosomal dominant manner.


Three points about LCAT deficiency

LCAT esterifies cholesterol so you get accumulation of unesterified cholesterol
Renal failure is the major cause of morbidity and mortality
Patients get very low HDL and very high TGL, as well as corneal opacities with hepatosplenomegaly (fish eye disease)


What is the cardiac index?  How is it used?

Output from left ventricle to body surface area - in L/m

Under 1.8 = cardiac shock

Used in ICU


PCWP 25 + v-waves to 40mmHg is...



PCWP of 25 with CI 1.5

Cardiogenic shock


RA 20 mmHg PAP 40/20mmHg PCWP 20 mmHg consistent wit...



Saturation of 88% in the pulmonary artery consistent with...



PAP 50/30 PCWP of 4 consistent with...



What is the evidence of the methacholine challenge in the dx of asthma?

Highly specific HOWEVER it's sensitivity is reduced in Caucasians and non-atopic asthmatics when using the test for asthma.


What is the evidence behind methacholine and mannitol testing in the dx of asthma?

Similar sens and spec - around 75% specific, poorly sensitive but increases when two exercise tests are positive


How do you define asthma reversibility?

Reversibility is demonstrated by an increase of 12% and 200 mL after the administration of a short-acting bronchodilator.


What is the most important limitation of PEF?

A limitation of PEF is that it is dependent on effort by the patient. FEV1 is also effort dependent but less so than PEF. FEV1 is not often used in the ED except in research settings.


When is the bronchoconstriction of asthma at it's greatest?

Bronchoconstriction is highest between the hours of 4:00 am and 6:00 am (the highest morbidity and mortality from asthma is observed during this time). These patients may have a more significant decrease in cortisol levels or increased vagal tone at night. Studies also show an increase in inflammation compared with controls and with patients with daytime asthma.


What happens to pa02 and Sp02 in methaemoglobinaemia and CO2 poisoning?

In carbon monoxide poisoning SpO2 will read in the 90s despite high levels of COHb — but the PaO2 should still be high.

In methemoglobinemia, the SpO2 plateaus at about 86% with increasing levels of MetHb, but again the PaO2 will not be decreased.


What is methemoglobinemia?

presence of a higher than normal level of methemoglobin (metHb, i.e., ferric [Fe3+] rather than ferrous [Fe2+] haemoglobin) in the blood. Methemoglobin is a form of hemoglobin that contains ferric [Fe3+] iron and has a decreased ability to bind oxygen. However, the ferric iron has an increased affinity for bound oxygen.[1] The binding of oxygen to methemoglobin results in an increased affinity of oxygen to the three other heme sites (that are still ferrous) within the same tetrameric hemoglobin unit. This leads to an overall reduced ability of the red blood cell to release oxygen to tissues, with the associated oxygen–hemoglobin dissociation curve therefore shifted to the left. When methemoglobin concentration is elevated in red blood cells, tissue hypoxia can occur.


What effect does flying have on PAH?

Pulmonary hypertension — Patients with pulmonary hypertension may be at particular risk for in-flight hypoxemia, as a low inspired oxygen tension can trigger pulmonary artery vasoconstriction and exacerbate hypoxemia [22,39]. The combination of exertion and low in-flight oxygen tension may lead to further oxygen desaturation