Cardiology Flashcards
What is a key endothelial derived vasoconstrictor substance?
Endothelin
LVH with deep T-wave inversions in limb leads and precordial leads. Striking T-wave inversions in mid-precordial leads suggest apical HCM (Yamaguchi’s syndrome)
What is a normal PR interval?
120-200ms
On smooth muscle cells what receptors does noradrenaline activate? What does Adrenaline?
NorAd: Postjunctional α1 receptors in large arteries and α2 receptors in small arteries and arterioles resulting in vasoconstriction. Ad: alpha and beta receptors. Note: Most blood vessels express β2-adrenergic receptors on their vascular smooth-muscle cells and respond to β agonists by cyclic AMP–dependent relaxation
What are the pharmacokinetics of Sacubitril and Valsartan?
Sacubitril: Pro-Drug. Highly protein bound 97%, liver metabolism to active metabolite, 50-50 urine/faeces excretion. 11hr half-life. Valsartan: Highly protein bound 97%, not overly metabolised. 10hr half-life, 86% faeces excretion
In a patient with chronic cor pulmonale from from COPD, why wouldnt classical right heart strain patterns be seen on ECG?
Flattening of the diaphragm, downward deflection of the heart and expansion of the chest cavity all result in decreased amplitude of the ECG and not the more classical Right Ventricular Hypertrophy.
How does Ca++ and end diastolic volume relate to stroke volume? What is this law?
Starling’s law. The principle is that there is an optimal length of extension for the sarcomere which can generate maximal force and sensitivity for Ca++. This stretching occurs during relaxation or Diastole of the heart cycle. A concept dubbed ‘length-dependent activation’.
What can a blood pressure differential of >10mmHg between arms indicate?
Subclavian Artery inflammation or atherosclerosis, supra-valvular aortic stenosis, aortic coarctation, aortic stenosis.
What is Sacubitril and Valsartan?
Sacubitril: Prodrug that inhibits neprilysin (neutral endopeptidase [NEP]) through the active metabolite LBQ657, leading to increased levels of peptides, including natriuretic peptides Valsartan: Produces direct antagonism of the angiotensin II (AT2) receptors. Displaces angiotensin II from the AT1 receptor; antagonizes AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.
How do positive inotropic drugs relate to Ca++?
Inotropic medications, with regards to cardiac function increase the Ca++ exposure to the myofilament which inturn results in increased cross-bridge and increased contractility. Examples: Digoxin and Beta Adrenergic agonists (NorAdrenaline).
In a normal ECG which lateral lead would be the transitional lead(s)?
V3-4, as the vector direction becomes more positive with the increasingly prominent R waves and reduced prominence of the S waves
How does hypoxaemia affect vascular growth?
Hypoxaemia stimulates growth factor release e.g. Vascular Endothelial Growth Factor (VEGF) and Fibroblast Growth Factor (FGF). Which stimulates endothelial proliferation and tube formation. Termed: Angiogenesis. Note: While angiogeneisis can result in collateralisation, as is the case in myocardial infarct or ischaemic injury, true revascularisation with vessels with all 3 layers does not typically occur in the adult mammal.
What are some pathological causes of prominent U waves?
Dofetilide - K-channel blocker, not used in Aus. Amiodarone - Sotalol Quinidine Hypokalaemia Prominent U waves are indicative of Torsades des pointes, and precordial U wave inversion is subtle sign of ischaemia.
In assessing the jugular venous pulse wave, what does each of these letters correspond with? a? C? x? v? y?
a - Corresponds to the atrial filling and can be elevated in reduced right heart compliance. C - corresponds to the carotid pulsation or the closing of the tricuspid valve due to contraction of the ventricles. x - this is a descent and corresponds to the filling of the atria with the peak at V V - is the peak filling prior to opening of the tricuspid valve and the subsequent steep y descent with filling of the ventricles before returning to the a wave.
What is Laplace’s Law? How is it used?
Tension of the myocardial fibre = intra-cavitary ventricular pressure x ventricular radius / wall thickness
What leads can be assessed to determine if there is normal depolarisation of the atria?
p-waves in positive II and negative in aVR
What are some examples of Class IA anti-arrhythmic drugs causing QT prolongations?
quinidine, disopyramide, procainamide, tricyclic antidepressants, phenothiazines
What are some non pharmacological causes of QT prolongation?
Hypothermia, Hypocalcaemia, Intracranial bleed.
What 4 conditions is LBBB a sign of?
Coronary heart disease (frequently with impaired left ventricular function), hypertensive heart disease, aortic valve disease, and cardiomyopathy.
What are determinants of Myocardial Contractility?
A. Intramyocardial [Ca2+] ↑↓ B. Cardiac adrenergic nerve activity ↑↓ C. Circulating catecholamines ↑↓ D. Cardiac rate ↑↓ E. Exogenous inotropic agents ↑ F. Myocardial ischemia ↓ G. Myocardial cell death (necrosis, apoptosis, autophagy) H. Alterations of sarcomeric and cytoskeletal proteins ↓ 1. Genetic 2. Hemodynamic overload I. Myocardial fibrosis ↓ J. Chronic overexpression of neurohormones ↓ K. Ventricular remodeling ↓ L. Chronic and/or excessive myocardial hypertrophy ↓
What are some determinants of Preload?
A. Blood volume B. Distribution of blood volume 1. Body position 2. Intrathoracic pressure 3. Intrapericardial pressure 4. Venous tone 5. Pumping action of skeletal muscles C. Atrial contraction
What role does the cardiac isoform of the Ryanodine receptor (RyR2) play in the contractility of the heart? What is the normal inhibitory protein for this receptor? How are these involved in Heart Failure?
RyR2 controls intracellular Ca++ levels and regulates ‘Calcium Sparks’ which in turn results in Ca++ influx and subsequently contraction of the heart via Myosin-Actin interactions. Calstabin 2 inhibits RyR2, which in turn reduces the Ca++ and contractility. Phosphokinase A (PKA) dissociates Calstabin from RyR2. In states of high plasma catecholamines and cardiac sympathetic neuronal release of norepinephrine, PKA is hyperphosphorylated and results in Calstabin 2 depleted-RyR2 which in turn results in depletion of the Sacroplasmic Reticulum Ca++ and reduced cardiac contractility (heart failure) and ventricular arrhythmias.
What are some endothelial derived vasodilatory substances?
Prostacyclin Endothelium-derived hyperpolarizing factor (EDHF) Nitric oxide (NO) Hydrogen peroxide (H2O2) Impaired production or excessive catabolism may result in hypertensive states. EDHF is of unclear mechanism and appears to display gender heterogeneity.
What does deep T-wave inversion of the precordial leads (v1-6) typically indicate?
Left Anterior Descending inschaemia. Wellen’s Twaves
What is a q-wave on ECG?
Initial deflection (negative direction) on the QRS complex.
What are the 3 main nerve classes that regulate vasculature tone? What are their neurotransmitters?
Sympathetic - Adrenaline/Noradrenaline Parasympathetic - Acetylcholine Nonadrenergic/Noncholinergic - Which has 2 subgroups Nitrergic - Nitric oxide and Peptidergic - substance P, vasoactive intestinal peptide VIP, calcitonin gene-related peptide, and ATP.
What are these pressure gradients demonstrating?
Aortic Stenosis (left) as evidenced by the gradient difference between ventricle and aorta.
Mitral Stenosis as evidenced by the mitral gradient relative to the pulmonary cap wedge.
