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CV HY Physio
Day 7
| Question | Answer |
|---|---|
| How does acidosis affect contractility and stroke volume in the heart? | Decreases both contractility and SV |
| How does hypoxia affect contractility and stroke volume in the heart? | Decreases both contractility and SV |
| How does hypercapnea affect contractility and stroke volume in the heart? | Decreases both contractility and SV |
| What causes stroke volume to increase in anxiety? | Catecholamine surge |
| What happens to stroke volume in pregnancy? | Increases (b/c have a higher volume of blood) |
| What are the treatment goals and corresponding drug classes for managing an MI? | Decrease amt of O2 consumption: 1. Decrease afterload (ARB/ACE-i*) 2. Decrease contractility and HR (Beta blockers) 3. Decrease preload (nitrates- venous dilators) *ACE-i and ARB decrease both preload and afterload |
| How does increased contractility shift the Starling curve? | L shift |
| How does CHF shift the Starling curve? | R shift (decreased contractility, so for a given preload, you are pushing out less blood) |
| How will adding digitalis to a CHF picture affect the Starling curve? | It will shift it L (increases contractility), but not as far L as the normal curve is. |
| What is the normal ejection fraction? | >/= 55% (this decreases in heart failure) |
| Which part of the vascular tree accounts for most of the total peripheral resistance? | Arterioles (regulate capillary flow) |
| Viscosity mostly depends on which component of blood? | Hematocrit |
| How does exercise affect total peripheral resistance? | Decreases it (arterioles in skeletal m dilate to supply exercising m fibers) |
| How does a narcotic overdose affect ionotropy (contractility)? | Decreases it (just like heart failure) |
| What causes the 4th heart sound (which is normally not audible in adults)? | Filling of the ventricle by atrial systole. Atrial systole contributes to, but is not essential for, ventricular filling. |
| What happens to the PR interval in heart block? | It is increased (conduction velocity thru AV node is slowed, so time for impulse to get from atria to ventricles is increased) |
| What happens to the PR interval with an increased heart rate? | It decreases |
| What does the QT interval represent? | The entire period of depolarization and repolarization of the ventricle (note that the repolarization of the atrium is buried in the QRS complex) |
| What does the QRS complex represent? | Depolarization of the ventricle |
| What does the P wave represnt? | Depolarization of the atrial m |
| What does the ST segment represent? | Period when the entire ventricle is depolarized; it is isoelectric |
| What does the T wave represent? | Ventricular repolarization (marks the end of the contraction) |
| What causes the first heart sound? | Turbulence of blood flow against the newly closed AV valves (mitral/tricuspid). Marks the beginning of systole. |
| Which AV valve closes first? | Mitral valve (may hear splitting) |
| What causes the second heart sound? | Turbulence of blood flow against the newly closed aortic and pulmonic valves. Marks beginning of diastole. |
| What does the dicrotic notch represent? | Pressure goes back up when aortic valve has closed due to elasticity of aorta which allows for filling of the coronary aa |
| Name two diseases that present with loss of the dicrotic notch. | Marfan's and syphilis (lose elasticity of the aorta) |
| What causes the third heart sound which is normal in children, but associated with disease in adults? | Rapid flow of blood from the atria into the ventricles |
| What type of disease process does an S3 indicate? | Volume overloaded heart (e.g., dilated ventricles) |
| What type of disease process does an S4 indicate? | Left ventricular hypertrophy (L atrium pushing against a stiff L ventricular wall) |
| Wide splitting is associated with which disease processes? | Pulmonic stenosis or R bundle branch block |
| Fixed splitting is associated with which disease process? | ASD |
| Paradoxical splitting (reversal of the normal closure sequence with pulmonic closure occuring before aortic; during inspiration the second sound is single, and during expiration the second sound splits) is associated with which disease processes? | Aortic stenosis or L bundle branch block |
| An S3 is normal in which populations? | Pregnant women and children |
| Mitral regurgitation is associated with which extra heart sound? | S3 |
| Which extra heart sound may be heard after an MI? | S4 |
| How are cardiac myocytes electrically coupled to each other? | Via gap junctions |
| During what phase of the ventricular action potential does myocyte contraction take place? | Phase 2 |
| What turns on the I funny channel in Phase 4 of the pacemaker action potential? | Repolarization |
| Which antiarrhythmics inhibit phase 0 of the pacemaker action potential? | CCBs and beta blockers |
| Which EKG change indicates a recent MI? | T wave inversion |
| What causes a U wave on an EKG? | Hypokalemia and bradycardia |
| What kind of QRS pattern will SA, AV, Bundle of His, and Purkinje rhythms have? | Narrow QRS |
| What kind of QRS pattern will ventricular rhythms have? | Wide QRS |
| How do T waves correlate with K levels? | High T wave= high K, flat T wave= low K |
| What is the speed of conduction from fastest to slowest: atria, AV node, purkinje, ventricles | Purkinje > atria > ventricles > AV node |
| What is the order of predominance of pacemaker activity: AV, bundle of His/Purkinje/ventricles, SA | SA > AV > bundle of His/Purkinje/ventricles |
| Ventricular tachycardia characterized by shifting sinuosidal waveforms; prolonged QT wave predisposes | Torsades de pointes |
| Why is torsades de pointes so dangerous? | Can progress to v-fib (syncopal episodes and sudden death) |
| What is the cause of congenital long QT syndromes? | Defects in cardiac sodium or potassium channels |
| Name a congenital long QT syndrome that presents with severe congenital sensorineural deafness. | Jervell and Lange-Nielsen syndrome |
| What is the treatment for torsades de pointes? | Push Mg |
| Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing the AV node. | Wolf-Parkinson-White syndrome (may result in re-entrant supraventricular tachycardia) |
| Delta wave on EKG (small upstroke b/f the QRS complex) | Wolf-Parkinson-White syndrome |
| What drug should NEVER be given to treat Wolf-Parkinson-White syndrome? | Adenosine (give procainamide and amiodarone instead) |
| EKG: irregularly irregular with no discrete P waves | A fib: can result in atrial stasis and lead to stroke. Treat with Beta blocker or CCB, and proplylax against thromboembolism with warfarin. "Bag of worms atria" |
| Why don't we treat a new a fib with cardioconversion? | B/c 48 hours is long enough for a clot to form. Contraction may dislodge clot leading to a stroke. |
| EKG: sawtooth waves; rapid succession of identical, back to back p waves | Atrial flutter: Use class IA, IC, or III antiarrhythmics |
| EKG: prolonged PR interval (>200ms=1 big box); may be caused by Borrelia burgdorferi; asymptomatic | AV block (1st degree) |
| EKG: Progressive lengthening of the PR interval until a beat is dropped (P wave not followed by a QRS complex); usually asymptomatic | 2nd degree Mobitz type I (Wenckebach). Type "won" gives you a "warning" b/f dropping a beat. |
| EKG: dropped beats that are not preceded by a change in the length of the PR interval | Mobitz type II |
| Aria and ventricles beat independently of each other. P waves bear no relation to QRS complexes. May be caused by Lyme disease. | 3rd degree (complete) heart block; treat with pacemaker |
| EKG: completely erratic rhythm with no identifiable waves; fatal without immediate CPR and defibrillation | V fib |
| What stimulates the renin angiotensin system? | Juxtoglomerular apparatus which senses decreased mean arterial pressure (effective circulating volume) |
| What substance is relased from the atria in response to increased blood volume and atrial pressure to produce vascular relaxation? | ANP |
| How does ANP affect the kidneys? | Constricts efferent renal arterioles and dilates afferent arterioles (via cGMP), promoting diuresis and contributing to the "escape from aldosterone" mechanism |
| What does the aortic arch respond to? | Only INCREASED BP |
| Via what nerve does the aortic arch transmit? | Vagus n (CN 10) |
| What does the carotid sinus respond to? | Decreases and increases BP |
| Via what nerve does the carotid sinus transmit? | Glossopharyngeal n (CN 9) |
| Which receptors are important in the response to hemorrhage? | Baroreceptors |
| What is carotid massage used to treat? | supraventricular tachycardia (do NOT use in elderly b/c of stroke risk); if carotid massage doesn't work, use adenosine |
| What changes do peripheral chemoreceptors respond to? | Decreased oxygen (<60mmHg), increased carbon dioxide, and decreased blood pH |
| What changes do central chemoreceptors respond to? | changes in pH and carbon dioxide in brain interstitial fluid; do NOT directly respond to oxygen changes |
| Patient with hypertension, bradycardia, and respiratory depression | Cushing triad: cuased by a cranial lesion with elevated intracranial pressure; mediated by central chemoreceptors |
| In what organ is blood extraction always 100% | Heart |
| How is increased oxygen demand met in the heart? | Increased coronary blood flow (NOT increased exctraction of O2-- it's already 100%!) |
| What is pulmonary capillary wedge pressure a good approximation of? | L atrial pressure |
| What happens to PCWP in mitral stenosis? | PCWP > LV diastolic pressure |
| What is a Swan-Ganz catheter used to measure? | PCWP(L atrial congestion and L end diastolic pressure) |
| What is unique about hypoxia in the lungs? | Causes vasoconstriction |
| Why does adenosine trigger vasodilation? | Body senses free adenosine as a low energy state b/c all of the phosphates have been broken down |
| What is the function of capillary pressure (Pc)? | Pushes fluid out of capillary; will be higher at early part of capillary (more fluid than colloid at the beginning, so you tend to push fluid out of capillary into interstitium) |
| What is the function of interstitial fluid pressure (Pi)? | Pushes fluid into capillary |
| What is the function of plasma colloid osmotic pressure (πc)? | Pulls fluid into the capillary |
| What is the function of interstitial fluid colloid osmotic pressure (πi)? | Pulls fluid out of capillary |
| How does heart failure affect capillary pressure (Pc)? | Increases it |
| How does nephrotic syndrome affect plasma colloid osmotic pressure (πc)? | Decreases it (lose protein) |
| How does liver failure affect plasma colloid osmotic pressure (πc)? | Decreases it (reduced synthesis of protein) |
| How do toxins, infections, and burns affect capillary permeability (Kf=filtration constant=capillary permeability) | Increases it (this is why you become edematous with sepsis) |
| How does lymphatic blockage affect interstitial fluid colloid osmotic pressure (πi)? | Increases it (built up proteins pull fluid out of capillaries) |
| What causes the different presentation seen in pitting and non-pitting edema? | Pitting edema has an excess of fluid in the absence of colloid (usually gravity-dependent). Non-pitting edema has lots of colloid in the interstitium which balances out excess fluid in the interstitium so no depression can be made in the skin. |
| What is the source of collateral circulation in an occlusive/ischemic event? How does it work? | Coronary microvessels are a network of arterioles that act as passageways to major vessels and can supplement blood flow to the myocardium distal to occluded vessels by vasodilating and diverting blood flow to ischemic areas. |
Created by:
sarah3148
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