Cardiology - important concepts - Sheet1 Flashcards
How does a less negative membrane potential affect excitability? What are some situations in which you may have a less negative membrane potential?
As the resting membrane potential becomes less negative, less Na channel inactivation gates are open. There are now less Na channels available to be excitable. This reduces excitability and ultimately slows contractions. This situation can be seen in ischemia, situations with high extracellular K concentrations, and is mimicked when the drug TTX is given.
Is degree of stenosis correlated with which lesions are most dangerous in unstable angina?
Nope. Not easy to tell which plaques are vulnerable, not related to degree of stenosis
What is the role of anti-coagulants and anti-platelet agents in treatment of USA/NSTEMI?
Patients are treated based on risk stratification. Low-risk patients are managed medically and these anti-thrombotics prevent thrombosis after plaque rupture, reduce chances of occlusion.
In what condition are intrramyocardial arterioreles hypertrophied?
Hypertrophic Cardiomyopathy
Best drugs to increase SVR?
Norepinephrine, phenylephrine
Best drugs to increase CO without increasing SVR?
Dobutamine and Isoproterenol (careful with iso because it can drop BP which is not good in CHF)
What is the significance of lipophilicty vs. hydrophilicty in regards to autonomic antagonists?
Lipophilic = short half-life but greater risk of CNS toxicity due to greater ability to cross BBB, hydrophilic = longer half-life and usually renally excreted (careful with pts with renal failure!)
Should you give beta-blockers to patients in cardiogenic shock? How about complete heart block?
Nope, beta-blockers are negative inotropes, so don’t give it to someone in HF until they are hemodynamically stable. They will slow conduction so don’t give it to someone in heart block until you have restored normal sinus rhythm.
Holosystolic murmur?
Mitral regurgitation
Crescendo/decrescendo systolic murmur?
Aortic Stenosis
Decrescendo, high pitched diastolic murmur?
Aortic regurgitation
Low pitched M shaped at axilla and apex?
Mitral stenosis
How does extracellular potassium change in ischemia?
More extracellular potassium in inschemia, resting membrane potential is less negative
Which layer of the heart is most susceptible to ischemic injury?
Subendocardium due to increased pressure during systole, decreased autoregulation and distance from arteries.
What is the mutation in DiGeorge? What does it cause?
deletion of 22q11, results in neural crest migration defects. presents as thymus defects, parathyroid defects, CHD and defects in formation of aortic arch
What causes the RVH in Tetralogy of Fallot?
The VSD (not the outflow tract narrowing!)
What is the acute effect of diurectics? Long term action?
Natriuresis resulting in decreased blood volume. Compensatory mechanisms result in increased renin production, sodium retention and fluid restoration. Long term though, there is a decrease in ECF. Mechanism not known, could be due to long term decrease in pulmonary vascular resistance due to increased NO production
What metric might tell you that there is a ventricular septal defect post MI?
Very high venous saturation as measured from PA (along with high pressures in RA/RV/PAWP)
Are thin wavy myoctyes necessarly a sign of infarction?
Nope, can just be ischemic. Can’t know just by looking at them
What channels are responsible for automaticity of the SA node? Purkinje fibers?
Sa node - delayed rectifier potassium channel and t-type calcium channel. purkinje - funny current
What determines conduction velocity?
Magnitude of excitatory current, speed of excitatory current, resistance to flow (ex. in acute infarct, gap jxns are closed, increasing resistance to flow between myocytes)
If there is low venous oxygen saturation, what assumption can we make about cardiac output?
Cardiac output is probably low as the tissues need to extract more oxygen from the blood due to decreased flow
What is the equation for cardiac output as calculated by the fick principle?
Cardiac output = vo2 (o2 consumption)/avo2d (difference in o2 between arterial and venous measurements0
What is the equation for systemic vascular resistance?
(SAP-RAP)/CO
What is the equation for total pulmonary resistance?
PAP/CO
What is the equation for pulmonary vascular resistance?
(PAP-LAP)/CO
What must you check before starting a patient with CHF on a phoshodiesterase 3 inhibitor?
That they are volume overloaded, because PDEIs decrease preload and afterload, can result in hypotension.
Why might you give someone with torsades des pointes isoproteronol?
It increases the HR which will shortern action potential duration and therefore the QT interval
What conditions increase risk of using anti-arrhytmics?
1: Prolonged QT 2: slow sinus node 3: av block 4: systolic dysfxn (classes I, II, and IV are negative inotropes
What is the hypothesized natriuretic hormone mechanism of HTN?
When intravsacular volume high, a hypothesized peptide blocks sodium/potassium pump resulting in increased sodium excretion in kidney but simulatneous increcased calcium concentration in vascular smooth muscle resulting in increased tone –> HTN
What is the renal sympathetic mechanism of HTN?
Increased renal sympathetic activity in HTN results in decreased renal flood flow, sodium reabsorption and RAAS activation, renal denervation - possible treatment?
What changes are seen in histology in benign HTN? Malignant HTN?>
Benign: hyaline arteriosclerosis, fibroblastic intimal hyperplasia, medial hypertrophy; Malignant: fibrinioid sclerosis, hyperplastic arteriolotiis “onion-skinning”, microangiopathic hemolytic anemia
Other organ changes seen in benign HTN? Malignant HTN?
benign: LVH, nephrosclerosis, berry aneurysms, retinal microaneurysms; malignant: acute cortical necrosis, increased ICP, retinal flame shaped hemorrahges and papilledema,
What are the criteria for metabolic syndrome?
3 of the following 5: increased abdominal adiposity, increased BP, increased fasting glucose, increased TG, decreased HDL
In which cardiomyopathy would you see intramyocardial arteriolar hypertrophy?
HCM
What is the hallmark of RCM as seen on a pressure wave form?
Rapid early diastolic filling with rapid decceleration slope
