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438 Cards in this Set
- Front
- Back
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Name the 3 structures in the carotid sheath
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Internal jugular vein (lateral)
Common carotid artery (medial) Vagus nerve (posterior) **VAN |
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Draw the heart
Label: RCA, LCA, CFX, LAD, PD, acute marginal artery |
P. 244
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SA and AV nodes are supplied by what artery?
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Usually RCA
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The inferior portion of the left ventricle is supplied by what artery?
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80% of the time, the RCA supplies it via the PD
20% of the time, PD arises from CFX |
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What does it mean to be right dominant in coronary anatomy?
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RCA supplies inferior portion of left ventricle via PD
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What does the acute marginal artery supply?
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Right ventricle
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What does the circumflex artery supply?
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Posterior left ventricle
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What does the LAD supply?
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Apex and anterior interventricular septum
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What does the PD supply?
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Posterior septum
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Where does coronary artery occlusion most commonly occur?
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LAD, which supplies anterior interventricular septum
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When do coronary arteries fill?
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During diastole
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What is the most posterior part of the heart?
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Left atrium
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What does enlargement of the left atrium cause?
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Dysphagia (due to compression of the esophageal nerve)
Hoarseness (due to compression of the recurrent laryngeal nerve, a branch of the vagus) |
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Draw the chest and 4 locations to auscultate
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P. 245
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What can you hear in the aortic area?
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Systolic murmur
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Name 3 things aortic systolic murmur indicates
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Aortic stenosis
Flow murmur Aortic valve sclerosis |
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What can you hear in the pulmonic area?
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Systolic ejection murmur
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Name 2 things a pulmonic systolic ejection murmur indicates
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Pulmonic stenosis
Flow murmur (ex. atrial septal defect) |
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How does ASD present aurally?
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ASD commonly presents with a pulmonary flow murmur (increased flow through pulmonary valve) and a diastolic rumble (increased flow across tricuspid)
Murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilatation of the pulmonary artery |
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What can you hear in the tricuspid area?
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Pansystolic murmur
Diastolic murmur |
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Name 2 things a pancystolic tricuspid murmur indicates
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Tricuspid regurgitation
VSD |
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Name 2 things a diastolic tricuspid murmur indicates
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Tricuspid stenosis
ASD |
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What can you head in the mitral area?
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Systolic murmur
Diastolic murmur |
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Name something a systolic mitral murmur indicates
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Mitral regurgitation
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Name something a diastolic mitral murmur indicates
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Mitral stenosis
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What can you hear at the left sternal border?
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Diastolic murmur
Systolic murmur |
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Name 2 things a diastolic left sternal border murmur indicates
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Aortic regurgitation
Pulmonic regurgitation |
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Name something a systolic left sternal border murmur indicates
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Hypertrophic cardiomyopathy
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What is the equation for cardiac output?
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CO = Stroke volume x Heart rate
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What is the Fick principle?
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CO = rate of O2 consumption / (arterial O2 content - venous O2 content)
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What is the equation for MAP?
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Cardiac output x total peripheral resistance
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How can you estimate MAP?
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2/3 diastolic pressure + 1/3 systolic pressure
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What is pulse pressure and what is it proportional to?
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= Systolic pressure - diastolic pressure
Proportional to stroke volume |
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Give an equation for stroke volume
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= CO/HR = EDV - ESV
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Describe how/why CO changes during exercise
When does it decrease? |
CO increases initially as a result of an increase in SV
After prolonged exercise, CO increases as a result of increase in HR If HR is too high, diastolic filling is incomplete and CO decreases |
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Name 3 things that affect stroke volume
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Contractility
Afterload Preload |
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How does stroke volume change with preload, afterload, and contractility?
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Stroke volume increases when:
Preload increases Afterload decreases Contractility increases |
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Name 4 things that increase contractility (and SV)
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Catecholamines (increased activity of Ca pump in SR)
Increased intracellular calcium Decreased extracellular sodium (decreased activity of Na/Ca exchanger) Digitalis (increased intracellular Na, resulting in increased Ca) |
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Name 5 things that decrease contractility (and SV)
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Beta blockade
Heart failure Acidosis Hypoxia/hypercapnea Non-dihydropyridine Ca channel blockers |
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Name 4 things that increase myocardial O2 demand
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Increased afterload
Increased contractility Increased heart rate Increased heart size (increased wall tension) |
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Name 3 times SV increases
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Anxiety
Exercise Pregnancy |
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A failing heart has a ______ SV
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Decreased
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Preload = Ventricular ______
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End Diastolic Volume
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Afterload = ________
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Mean Arterial Pressure (proportional to peripheral resistance)
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What do venodilators do to preload?
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Decrease preload
Ex. nitroglycerin |
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What do vasodilators do to afterload?
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Decrease afterload
Ex. hydralazine |
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Name 3 things that increase preload
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Exercise (slightly)
Increased blood volume (overtransfusion) Excitement (sympathetics) |
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What is the force of contraction proportional to?
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Initial length of cardiac muscle fiber (preload)
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Draw the Starling curve
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P. 246
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Give an equation for ejection fraction
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= SV/EDV = (EDV-ESV)/EDV
Index of ventricular contractility |
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What is ejection fraction normally?
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>= 55%
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Give an equation for deltaP
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Delta P = Q x R = Flow x Resistance
Similar to Ohm's law: DeltaV = IR |
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Give an equation for resistance
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= Driving pressure / flow
= Delta P / Q = 8n (viscosity) x length / pi r^4 |
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How are resistances related in series?
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R1 + R2 + R3...
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How are resistances related in parallel?
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1/Rtotal = 1/R1 + 1/R2 + 1/R3 ...
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What is the relationship between resistance and viscosity?
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Directly proportional to viscosity
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What is the relationship between resistance and radius?
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Inversely proportional to r^4
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What is viscosity due to?
Name 3 times it increases |
Mostly hematocrit
Increases in: polycythemia, hyperproteinemic states (multiple myeloma), hereditary spherocytosis |
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What accounts for most of the total peripheral resistance?
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Arterioles
(regulate capillary flow) |
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Draw the curve of CO vs. EDV for different blood volumes and inotropy
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P. 247
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Draw the cardiac cycle graph (P vs V)
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P. 248
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Draw aortic pressure vs. time
Add LV pressure, LA pressure, heart sounds, ventricular volume, jugular venous pulse, ECG |
P. 248
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Name the 5 phases of the left ventricle
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Isovolumetric contraction
Systolic ejection Isovolumetric relaxation Rapid filling Reduced filling |
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What is isovolumetric contraction of LV?
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Period between mitral valve closure and aortic valve opening
Period of highest O2 consumption |
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What is systolic ejection of LV?
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Period between aortic valve opening and closing
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What is isovolumetric relaxation of LV?
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Period between aortic valve closing and mitral valve opening
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What is rapid filling of LV?
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Period just after mitral valve opening
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What is reduced filling of LV?
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Period just before mitral valve closure
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What is S1 sound?
Where is it loudest? |
Mitral and tricuspid valve closure
Loudest at mitral area |
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What is S2 sound?
Where is it loudest? |
Aortic and pulmonary valve closure
Loudest at left sternal border |
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What is S3?
What is it associated with? |
In early diastole during rapid ventricular filling phase
Associated with increased filling pressures and more common in dilated ventricles (but normal in kids) |
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What is S4?
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"Atrial kick"
In late diastole High atrial pressure Associated with ventricular hypertrophy Left atrium must push against stiff LV wall |
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Name the 3 waves of JVP
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a wave - atrial contraction
c wave - RV contraction (tricuspid valve bulging into atrium) v wave - increased atrial pressure due to filling against closed tricuspid valve |
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Draw S2 splitting
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P. 248
Aortic valve closes before pulmonic Inspiration increases this difference |
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Draw wide splitting
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P. 248
Associated with pulmonic stenosis |
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Draw fixed splitting
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Associated with ASD
P. 248 |
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Draw paradoxical splitting
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Associated with aortic stenosis
P. 248 |
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Explain normal splitting
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Inspiration leads to drop in intrathoracic pressure which increases capacity of pulmonary circulation
Pulmonic valve closes earlier because of decreased return to left heart |
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Explain wide splitting
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Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)
Delay in RV emptying causes delayed pulmonic sound regardless of breath - exaggeration of normal splitting |
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Explain fixed splitting
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Seen in ASD
ASD leads to left to right shunt and therefore increased flow through pulmonic valve such that regardless of breath, pulmonic closure is greatly delayed |
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Explain paradoxical splitting
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Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block)
Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound - therefore on inspiration, the later P2 and earlier A2 sounds move closer to one another "paradoxically" eliminating the split |
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What heart sounds do mitral/tricuspid regurgitation make?
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Holosystolic , high-pitched "blowing murmur"
Mitral - loudest at apex and radiates toward axilla Tricuspid - loudest at tricuspid are and radiates to right sternal border |
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Draw mitral/tricuspid regurgitation heart sounds
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P. 250
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What causes mitral vs. tricuspid regurgitation?
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MR often due to ischemic heart disease, mitral valve prolapse, or LV dilation
TR due to RV dilation or endocarditis Rheumatic fever can cause both |
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What is "pulsus parvus et tardus"?
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Pulses weak compared to heart sounds
Can lead to syncope Often due to age-related calcific aortic stenosis |
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What heart sounds does aortic stenosis make?
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Crescendo-descrescendo systolic ejection murmur following ejection click
LV >> aortic pressure during systole Radiates to carotids/apex |
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Draw aortic stenosis heart sounds
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P. 250
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What heart sounds does VSD make?
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Holosystolic, harsh-sounding murmur
Loudest at tricuspid area |
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Draw VSD heart sounds
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P. 250
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What heart sounds does mitral prolapse make?
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Late systolic murmur with midsystolic click
Most frequent vascular lesion Loudest at S2 Usually benign Can predispose to infective endocarditis |
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Draw mitral valve prolapse heart sounds
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P. 250
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What heart sounds does aortic regurgitation make?
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Immediate high-pitched "blowing" diastolic murmur
Wide pulse pressure when chronic Often due to aortic root dilation, bicuspid aortic valve, or rheumatic fever |
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Draw aortic regurgitation heart sounds
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P. 250
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What heart sounds does mitral stenosis make?
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Follows opening snap
Delayed rumbling late diastolic murmur LA >> LV pressure during diastole Often occurs secondary to rheumatic fever |
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Draw mitral valve stenosis heart sounds
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P. 250
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What heart sounds does PDA make?
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Continuous machine-like murmur
Loudest at time of S2 |
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Draw PDA heart sounds
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P. 250
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When do abnormal heart sounds increase intensity on inspiration?
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When defect is on right side of heart because more blood flows into RA
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When do abnormal heart sounds increase intensity on expiration?
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When defect is on left side of heart because more blood flows into LA
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Describe calcium's role in cardiac muscle contraction
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Cardiac muscle contraction is dependent on extracellular calcium, which enters the cells during plateau of action potential and stimulates calcium release from the cardiac muscle sarcoplasmic reticulum (calcium-induced calcium release)
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Name 3 ways cardiac muscle differs from skeletal muscle
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Cardiac muscle action potential has a plateau, which is due to Ca influx
Cardiac nodal cells spontaneously depolarize, resulting in automaticity due to If channels Cardiac myocytes are electrically coupled to each other by gap junctions |
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Draw the ventricular action potential and label the 4 phases
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P. 251
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Describe the phases of the ventricular action potential
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Phase 0 = rapid upstroke - voltage gated Na channels open
Phase 1 = initial repolarization - inactivation of voltage gated Na channels; voltage gated K channels begin to open Phase 2 = plateau - Ca influx through voltage gated Ca channels balances K efflux; Ca influx triggers Ca release from SR and myocyte contraction Phase 3 = rapid repolarization - massive K efflux due to opening of voltage gated slow K channels and closure of voltage gated Ca channels Phase 4 = resting potential - high K permeability through K channels |
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Where does the pacemaker action potential of heart occur?
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SA and AV nodes
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What are the key differences between pacemaker and ventricular action potentials?
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Phase 0 = upstroke - opening of voltage gated Ca channels; these cells lack fast voltage gated Na channels, results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles
Phase 2 = plateau is absent Phase 3 = inactivation of the Ca channels and increased activation of K channels --> increased K efflux Phase 4 = slow diastolic depolarization - membrane potential spontaneously depolarizes as Na conductance increases (If different from INa above) |
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What accounts for the automaticity of SA and AV nodes?
What determines heart rate? |
Phase 4
Slope of phase 4 in SA node determines heart rate |
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What effect do ACh and catecholamines have on cardiac pacemaker?
Sympathetic stimulation? |
ACh decreases the rate of diastolic depolarization and decreases heart rate
Catecholamines increase depolarization and increase heart rate Sympathetic stimulation increases the chance that If channels are open |
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Draw the cardiac pacemaker action potential
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P. 251
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What does the P wave on ECG represent?
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Atrial depolarization
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What does the PR interval on ECG represent?
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Conduction delay through AV node (normally < 200 msec)
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What does the QRS complex on ECG represent?
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Ventricular depolarization (normally < 120 msec)
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What does the QT interval on ECG represent?
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Mechanical contraction of the ventricles
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What does the T wave on ECG represent?
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Ventricular repolarization
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What does the ST segment on ECG represent?
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Isoelectric, ventricles repolarized
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What does the U wave on ECG represent?
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Caused by hypokalemia, bradycardia
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Where is atrial repolarization on ECG?
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Masked by QRS complex
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Draw an ECG
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P. 253
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Draw a diagram of heart electrical conductance
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P. 253
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Draw the action potential at each point of heart electrical conductance
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P. 253
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What is torsades de pointes?
What can it progress to? |
Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG
Can progress to V-fib |
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What predisposes to torsades de points?
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Anything that prolongs the QT interval
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What is Wolff-Parkinson-White Syndrome?
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Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node
Ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave on ECG May result in reentry current leading to supraventricular tachycardia |
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Draw atrial fibrillation ECG
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P. 254
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Describe atrial fibrillation ECG
What can atrial fibrillation lead to? Treatment? |
Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes
Can result in atrial stasis and lead to stroke Treat with warfarin |
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Draw atrial flutter ECG
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P. 254
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Describe atrial flutter ECG
Treatment? |
Rapid succession of identical, back-to-back atrial depolarization waves
Identical appearance accounts for the "sawtooth" appearance of the flutter waves Attempt to convert to sinus rhythm - use class IA, IC, III antiarrhythmics |
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Draw 1st degree AV block ECG
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P. 254
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What happens in 1st degree AV block?
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PR interval is prolonged (> 200 msec)
Asymptomatic |
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Draw 2nd degree Mobitz type I AV block ECG
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P. 254
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What happens in 2nd degree Mobitz type I AV block?
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Progressive lengthening of the PR interval until a beat is "dropped" (a P wave not followed by QRS)
Usually asymptomatic |
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Draw 2nd degree Mobitz type II AV block ECG
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P. 255
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Describe 2nd degree Mobitz type II AV block
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Dropped beats that are not preceded by a change in the length of the PR interval (as in type I)
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What happens in 2nd degree Mobitz type II AV block?
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Abrupt, nonconducted P waves result in pathologic condition
Often found as 2:1 block where there are 2 P waves to 1 QRS response May progress to 3rd degree block |
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Draw 3rd degree (complete) AV block ECG
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P. 255
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Describe 3rd degree (complete) AV block
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Atria and ventricles beat independently of each other
Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes Atrial rate is faster than the ventricular rate |
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How is 3rd degree (complete) AV block treated?
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Pacemaker
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What disease can result in 3rd degree (complete) AV block?
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Lyme disease
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Draw ventricular fibrillation ECG
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P. 255
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Describe ventricular fibrillation
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Completely erratic rhythm with no identifiable waves
Fatal arrhythmia without immediate CPR and defibrillation |
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What 2 systems increase MAP?
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Sympathetic
Renin-angiotensin |
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How does the sympathetic system sense low MAP?
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Medullary vasomotor center senses decreased baroreceptor firing
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What does the sympathetic system do to increase MAP?
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Beta 1 (increases heart rate, increases contractility) = increases CO
Alpha 1 (venoconstriction increases venous return) = increases CO Alpha 1 (arteriolar vasoconstriction) = increases TPR |
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How does the renin-angiotensin system sense low MAP?
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JGA senses low MAP as effective circulating volume
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What does the renin-angiotensin system do to increase MAP?
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Angiotensin II (vasoconstriction) = increases TPR
Aldosterone (increases blood volume) = increases CO |
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What is ANP?
When is it released? What does it do? |
Diuretic
Released from atria in response to increased blood volume and atrial pressure Causes generalized vascular relaxation Constricts efferent renal arterioles, dilates afferent arterioles |
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How does the aortic arch transmit information?
What does it respond to? |
Transmits via vagus nerve to medulla
Responds ONLY to increased BP |
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How does the carotid sinus transmit information?
What does it respond to? |
Transmits via glossopharyngeal nerve to medulla
Responds to decreased and increased BP |
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Name 2 ways baroreceptors work
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Hypotension
Carotid massage |
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What happens to baroreceptors in hypotension?
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Decreased arterial pressure --> decreased stretch --> decreased afferent baroreceptor firing --> increased efferent sympathetic firing and decreased efferent parasympathetic stimulation --> vasoconstriction, increased HR, increased contractility, increased BP
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When is baroreceptor response to hypotension especially important?
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Severe hemorrhage
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What happens to baroreceptors in carotid massage?
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Increased pressure on carotid artery --> increased stretch --> increased afferent baroreceptor firing --> decreased HR
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Name 2 areas chemoreceptors work
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Peripherally
Centrally |
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What do peripheral chemoreceptors respond to?
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Carotid and aortic bodies respond to decreased PO2 (< 60 mmHg), increased PCO2, and decreased pH of blood
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What do central chemoreceptors respond to?
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Respond to changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2
Do not directly respond to PO2 |
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What reaction are central chemoreceptors responsible for?
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Cushing reaction
Increased ICP constricts arterioles --> cerebral ischemia --> hypertension (sympathetic response) and reflex bradycardia Note: Cushing triad = hypertension, bradycardia, respiratory depression |
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Which organ gets the largest share of systemic cardiac output?
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Liver
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Which organ gets the highest blood flow per gram of tissue?
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Kidney
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Which organ has a large arteriovenous O2 difference?
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Heart
Increased O2 demand is met by increasing coronary blood flow, not by increased extraction of O2 |
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Draw the chambers of the heart and their normal pressures
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P. 257
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What is PCWP?
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Pulmonary capillary wedge pressure
Good approximation of left atrial pressure Measured with Swan-Ganz catheter |
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What happens to PCWP in mitral stenosis?
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PCWP > LV diastolic pressure
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Define autoregulation
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How blood flow to an organ remains constant over a wide range of perfusion pressures
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Name the factors that determine autoregulation in the heart
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Local metabolites - O2, adenosine, NO
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Name the factors that determine autoregulation in the brain
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Local metabolites - CO2 (pH)
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Name the factors that determine autoregulation in the kidneys
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Myogenic and tubuloglomerular feedback
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Name the factors that determine autoregulation in the lungs
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Hypoxia causes vasoconstriction
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Name the factors that determine autoregulation in skeletal muscle
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Local metabolites - lactate, adenosine, K+
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Name the factors that determine autoregulation in the skin
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Sympathetic stimulation most important mechanism - temperature control
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How is pulmonary vasculature unique?
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Hypoxia causes vasoconstriction so that only well-ventilated areas are perfused
In other organs, hypoxia causes vasodilation |
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Name the 4 Starling forces
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Capillary pressure - pushes fluid out of capillary
Interstitial fluid pressure - pushes fluid into capillary Plasma colloid osmotic pressure - pulls fluid into capillary Interstitial fluid colloid osmotic pressure - pulls fluid out of capillary |
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Give an equation for net filtration pressure
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= [(Pc - Pi) - (pi c - pi i)]
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Give an equation for net fluid flow
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= (Pnet)(Kf)
Where Pnet = net filtration pressure Kf = filtration constant (capillary permeability) |
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Name 4 mechanisms of edema
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Increased capillary pressure (increased Pc; heart failure)
Decreased plasma proteins (decreased pi c; nephrotic syndrome, liver failure) Increased capillary permeability (Increased Kf; toxins, infections, burns) Increased interstitial fluid colloid osmotic pressure (Increased pi i; lymphatic blockage) |
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Name 5 causes of early cyanosis ("blue babies")
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Right to left shunts:
Tetralogy of Fallot (most common cause) Transposition of great vessels Truncus arteriosus Tricuspid atresia Total anomalous pulmonary venous return |
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Name 3 causes of late cyanosis ("blue kids")
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Left to right shunts:
VSD (most common congenital cardiac anomaly) ASD (loud S1; wide, fixed split S2) PDA (close with indomethacin) |
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What is Eisenmenger's syndrome?
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Uncorrected VSD, ASD, or PDA causes compensatory vascular hypertrophy, which results in progressive pulmonary hypertension
As pulmonary resistance increases, the shunt reverses from L-->R to R-->L which causes late cyanosis (clubbing and polycythemia) |
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Name the 4 parts of tetraology of Fallot
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Pulmonary stenosis (most important determinant for prognosis)
RV hypertrophy Overriding aorta (overrides the VSD) VSD See P. 258 |
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Describe what happens in tetralogy of Fallot
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Early cyanosis caused by R to L shunt across VSD - exists because of the increased pressure caused by stenotic pulmonic valve
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What does the heart of Tetralogy of Fallot look like on Xray?
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Boot shaped
Due to RV hypertrophy |
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What causes Tetralogy of Fallot?
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Anterosuperior displacement of the infundibular septum
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What do patients do to improve symptoms of Tetralogy of Fallot?
|
Squat
Compression of femoral arteries increases pressure, thereby decreasing the R to L shunt and directing more blood from RV to the lungs Compression --> resistance --> pressure |
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Describe transposition of great vessels
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Aorta leaves RV and pulmonary trunk leaves LV --> separation of systemic and pulmonary circulation
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How do kids with transposition of great vessels live?
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Not compatible with life unless a shunt is present to allow adequate mixing of blood (VSD, PDA, PFO)
Without surgery, most kids will die in first few months of life |
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What causes transposition of great vessels?
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Failure of aorticopulmonary septum to spiral
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What is infantile coarctation of aorta?
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Aortic stenosis proximal to insertion of ductus arteriosus (preductal)
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What is adult coarctation of aorta?
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Aortic stenosis distal to ductus arteriosus (postductal)
Associated with notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities |
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What is coarctation of aorta associated with?
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Turner's Syndrome
Bicuspid aortic valve Can result in aortic regurgitation |
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Draw coarctation of the aorta
|
P. 259
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What is patent ductus arteriosus?
|
In fetal period, shunt if R to L (normal)
In neonatal period, lung resistances drop and shunt becomes L to R with subsequent RV hypertrophy and failure (abnormal) |
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What does PDA sound like?
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Continuous, "machine-like" murmur
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|
|
What keeps PDA patent?
|
PGE synthesis and low O2 tension
|
|
|
What does indomethacin do to PDA?
|
Closes it
**ENDomethacin |
|
|
Draw PDA
|
P. 259
|
|
|
What defect is associated with 22q11 syndromes?
|
Truncus arteriosus
Tetralogy of Fallot |
|
|
What defect is associated with Down syndrome?
|
ASD
VSD AV septal defect (endocardial cushion defect) |
|
|
What defect is associated with congenital rubella?
|
Septal defects
PDA Pulmonary artery stenosis |
|
|
What defect is associated with Turner's syndrome?
|
Coarctation of aorta
|
|
|
What defect is associated with Marfan's syndrome?
|
Aortic insufficiency (late complication)
|
|
|
What defect is associated with offspring of diabetic mother?
|
Transposition of great vessels
|
|
|
Define hypertension
|
BP>= 140/90
|
|
|
Name 5 risk factors for hypertension
|
Age
Obesity Diabetes Smoking Genetics (Black > White > Asian) |
|
|
How much hypertension is primary?
|
90%
Primary (essential): Related to increased CO or increased TPR |
|
|
How much hypertension is secondary?
|
10%
Mostly secondary to renal disease |
|
|
What is malignant hypertension
|
Severe and rapidly progressing
|
|
|
Name 7 things hypertension predisposes to
|
Atherosclerosis
LV hypertrophy Stroke CHF Renal failure Retinopathy Aortic dissection |
|
|
Name 4 hyperlipidemia signs
|
Atheromas
Xanthomas Tendinous xanthoma Corneal arcus |
|
|
What are atheromas?
|
Plaques in blood vessel walls
|
|
|
What are xanthomas?
|
Plaques or nodules composed of lipid-laden histiocytes in the skin, especially in the eyelids (xanthelasma)
|
|
|
What are tendinous xanthomas?
|
Lipid deposit in tendon, especially Achilles
|
|
|
What is corneal arcus?
|
Lipid deposit in cornea, nonspecific (arcus senilis)
|
|
|
What is Monckeberg arteriosclerosis?
|
Calcification in the media of the arteries, especially radial or ulnar
Usually benign; "pipestream" arteries Does not obstruct blood flow; intima not involved |
|
|
What is arteriosclerosis?
|
Hyaline thickening of small arteries in essential hypertension
Hyperplastic "onion skinning" in malignant hypertension |
|
|
What is atherosclerosis?
|
Fibrous plaques and atheromas form in intima of arteries
|
|
|
Define aortic dissection
|
Longitudinal intraluminal tear forming a false lumen
|
|
|
What is aortic dissection associated with?
|
Hypertension or cystic medial necrosis (component of Marfan's)
|
|
|
How does aortic dissection present?
|
Tearing chest pain radiating to the back
CXR shows mediastinal widening False lumen occupies most of the descending aorta Can result in aortic rupture and death |
|
|
In what kind of vessels does atherosclerosis occur?
Where in the body? |
Disease of elastic arteries and large and medium-sized muscular arteries
Abdominal aorta > coronary artery > popliteal artery > carotid artery |
|
|
Name 5 risk factors for atherosclerosis
|
Smoking
Hypertension Diabetes mellitus Hyperlipidemia Family history |
|
|
How does atherosclerosis progress?
|
Endothelial cell dysfunction --> macrophage and LDL accumulation --> foam cell formation --> fatty streaks --> smooth muscle cell migration (involves PDGF and FGF-beta) --> fibrous plaque --> complex atheromas
|
|
|
Name 6 complications of atherosclerosis
|
Aneurysms
Ischemia Infarcts Peripheral vascular disease Thrombus Emboli |
|
|
Name 2 symptoms of atherosclerosis
|
Angina
Claudication Can be asymptomatic |
|
|
Draw a diagram of atherosclerosis
|
P. 261
|
|
|
Name 4 possible manifestations of ischemic heart disease
|
Angina (CAD narrowing > 75%)
Myocardial infarction Sudden cardiac death Chronic ischemic heart disease |
|
|
Name 3 types of angina
|
Stable - mostly secondary to atherosclerosis; ST depression on ECG (retrosternal chest pain with exertion)
Prinzmetal's variant - occurs at rest secondary to coronary artery spasm; ST elevation on ECG Unstable/crescendo - thrombosis but no necrosis; ST depression on ECG (worsening chest pain) |
|
|
What is myocardial infarction?
|
Most often acute thrombosis due to coronary artery atherosclerosis
Results in myocyte necrosis |
|
|
What is sudden cardiac death?
|
Death from cardiac causes within 1 hour of onset of symptoms
Most commonly due to lethal arrhythmia |
|
|
What is chronic ischemic heart disease?
|
Progressive onset of CHF over many years due to chronic ischemic myocardial damage
|
|
|
What are red infarcts?
|
Hemorrhagic
Occur in loose tissues with collaterals, such as liver, lungs, or intestine, or following reperfusion |
|
|
What are pale infarcts?
|
Occur in solid tissues with single blood supply, such as heart, kidney, spleen
|
|
|
What causes a myocardial infarction?
|
Coronary artery occlusion
LAD > RCA > Circumflex |
|
|
Name 8 symptoms of MI
|
Diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms
|
|
|
What happens in the first day of MI?
|
No visible change by light microscopy in first 2-4 hours
Contraction bands visible after 1-2 hours Early coagulative necrosis after 4 hours - release of contents of necrotic cells into bloodstream and the beginning of neutrophil emigration |
|
|
What happens in day 2-4 of MI?
|
Risk for arrhythmia
Tissue surrounding infarct shows acute inflammation Dilated vessels (hyperemia) Neutrophil emigration Muscle shows extensive coagulative necrosis |
|
|
What happens in day 5-10 of MI?
|
Risk for free wall rupture, tamponade, papillary muscle rupture, ventricular septal rupture
Due to the fact that macrophages have degraded important structural components |
|
|
What happens by 7 weeks of MI?
|
Risk for ventricular aneurysm
Contracted scar complete |
|
|
Draw the heart and tissue slides of MI on first day, day 2-4, day 5-10, 7 weeks
|
P. 262
|
|
|
How is MI diagnosed in first 6 hours?
|
In first 6 hours, ECG is gold standard
ECG changes can include ST elevation (transmural infarct), ST depression (subendocardial infarct), and pathologic Q waves (transmural infarct) |
|
|
Name 3 cardiac enzyme markers of MI
|
Cardiac troponin I
CK-MB AST |
|
|
Describe time course of cardiac troponin I
|
Rises after 4 hours
Elevated for 7-10 days More specific than other protein markers |
|
|
Describe specificity of CK-MB
|
Predominantly found in myocardium but can also be released from skeletal muscle
|
|
|
Describe specificity of AST
|
Nonspecific
Can be found in cardiac, liver, and skeletal muscle changes |
|
|
Name 3 characteristics of transmural infarcts
|
Increased necrosis
Affects entire wall ST elevation on ECG |
|
|
Name 4 characteristics of subendocardial infarcts
|
Due to ischemic necrosis of < 50% of ventricle wall
Subendocardium especially vulnerable to ischemia Due to fewer collaterals, higher pressure ST depression on ECG |
|
|
Name 7 complications of MI
|
Cardiac arrhythmia
LV failure and pulmonary edema Cardiogenic shock (large infarct - high risk of mortality) Ventricular free wall rupture Aneurysm Fibrinous pericarditis Dressler's syndrome |
|
|
What is an important cause of death before reaching the hospital in MI?
|
Cardiac arrhythmia
Common in first few days |
|
|
What happens in wall rupture in MI?
|
Ventricular free wall rupture --> cardiac tamponade
Papillary muscle --> severe mitral regurgitation Interventricular septal rupture --> VSD |
|
|
Name 3 effects of aneurysm formation in MI
|
Decreased CO
Risk of arrhythmia Embolus from mural thrombus |
|
|
What is fibrinous pericarditis?
|
Friction rub (3-5 days post-MI)
|
|
|
What is Dressler's syndrome?
|
Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI)
|
|
|
Name 3 types of cardiomyopathies
|
Dilated (congestive)
Hypertrophic Restrictive/obliterative |
|
|
What is dilated (congestive) cardiomyopathy?
Name 7 things that cause it |
Most common cardiomyopathy (90% of cases)
Etiologies include chronic Alcohol abuse, Beriberi, Coxsackie B virus myocarditis, chronic Cocaine use, Chagas' disease, Doxorubicin toxicity, and peripartum cardiomyopathy |
|
|
Name 3 findings of dilated (congestive) cardiomyopathy
|
S3
Dilated heart on ultrasound Balloon appearance on chest x-ray ** Systolic dysfunction ensues |
|
|
What is hypertrophic cardiomyopathy?
|
Hypertrophied IV septum is "too close" to mitral valve leaflet, leading to outflow tract obstruction; 50% of cases are familial, autosomal dominant (cause of sudden death in young athletes)
Disoriented, tangled, hypertrophied myocardial fibers **Diastolic dysfunction ensues |
|
|
Name 4 findings of hypertrophic cardiomyopathy
|
Normal-sized heart
S4 Apical impulses Systolic murmur |
|
|
How is hypertrophic cardiomyopathy treated?
|
Beta blocker or heart-specific calcium channel blocker (ex. verapamil)
|
|
|
Name 5 causes of restrictive/obliterative cardiomyopathy?
|
Sarcoidosis
Amyloidosis Postradiation fibrosis Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children) Hemochromatosis (dilated cardiomyopathy can also occur) |
|
|
What is congestive heart failure?
|
A clinical syndrome that occurs in patients with an inherited or acquired abnormality of cardiac structure or function, who develop a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales)
|
|
|
Name 8 abnormalities found in CHF
|
Dyspnea on exertion, Cardiac dilation, Pulmonary edema, Paroxysmal nocturnal dyspnea, Orthopnea (shortness of breath when supine), Hepatomegaly (nutmeg liver), Ankle/sacral edema, Jugular venous distention
|
|
|
What is the cause of dyspnea on exertion in CHF?
|
Failure of LV output to increase during exercise
|
|
|
What is the cause of cardiac dilation in CHF?
|
Greater ventricular end-diastolic volume
|
|
|
What is the cause of pulmonary edema, paroxysmal nocturnal dyspnea in CHF?
|
LV failure --> increase pulmonary venous pressure --> pulmonary venous distention and transudation of fluid
Presence of hemosiderin-laden macrophages ("heart failure" cells) in lungs |
|
|
What is the cause of orthopnea (shortness of breath when supine) in CHF?
|
Increased venous return in supine position exacerbates pulmonary vascular congestion
|
|
|
What is the cause of hepatomegaly (nutmeg liver) in CHF?
|
Increased central venous pressuring --> increased resistance to portal flow
Rarely, leads to "cardiac cirrhosis" |
|
|
What is the cause of ankle/sacral edema in CHF?
|
RV failure --> increased venous pressure --> fluid transudation
|
|
|
What is the cause of jugular venous distention in CHF?
|
Right heart failure --> increased venous pressure
|
|
|
What leads to right heart failure most often?
|
Left heart failure
|
|
|
Isolated right heart failure is due to what?
|
Cor pulmonale
|
|
|
Name 6 embolus types
|
Fat
Air Thrombus Bacteria Amniotic fluid Tumor |
|
|
What are fat emboli associated with?
|
Long bone fractures and liposuction
|
|
|
What can amniotic fluid emboli lead to?
|
DIC, especially postpartum
|
|
|
Name 3 signs of pulmonary embolus
|
Chest pain
Tachypnea Dyspnea |
|
|
Where do 95% of pulmonary emboli arise from?
|
Deep leg veins
|
|
|
Name 3 things that predispose to deep venous thrombosis
|
Virchow's triad:
Stasis Hypercoagulability (ex. defect in coagulative cascade proteins) Endothelial damage (exposed collagen provides impetus for clotting cascade) |
|
|
Name 7 signs of bacterial endocarditis
|
Fever (most common symptom)
Roth's spots (round white spots on retina surrounded by hemorrhage) Osler's nodes (tender raised lesions on finger or toe pads) New murmur Janeway lesions (small erythematous lesions on palm or sole) Anemia Splinter hemorrhages on nail bed |
|
|
What can cause new murmur in bacterial endocarditis?
|
Valvular damage
|
|
|
Which valve is most frequently involved in bacterial endocarditis?
|
Mitral valve
Tricuspid valve endocarditis is associated with IV drug abuse |
|
|
Name 4 complications of bacterial endocarditis
|
Chordae rupture
Glomerulonephritis Suppurative pericarditis Emboli |
|
|
What blood cultures are necessary to diagnose bacterial endocarditis?
|
Acute - S. aureua (high virulence); large vegetations on previously normal valves; rapid onset
Subacute - viridans streptococcus (low virulence); smaller vegetations on congenitally abnormal or disease valves; sequela of dental procedures; more insiduous onset |
|
|
Name 2 things that may cause nonbacterial endocarditis
|
Malignancy
Hypercoagulable state (marantic/thrombotic endocarditis) |
|
|
Name a bug present in colon cancer
|
S. bovis
|
|
|
Name a bug present on prosthetic valves
|
S. epidermidis
|
|
|
Be able to identify splinter hemorrhage and acute bacterial endocarditis photos
|
P. 266
|
|
|
What is Libman-Sacks endocarditis?
What is it associated with? When is it seen? |
Verrucous (wartlike), sterile vegetations occur on both sides of the valve
Can be associated with mitral regurgitation and, less commonly, mitral stenosis Seen in lupus (**SLE causes LSE) |
|
|
What causes rheumatic fever?
|
RF is a consequence of pharyngeal infection with group A beta-hemolytic streptococci
|
|
|
What are early deaths in rheumatic fever due to?
Late sequelae? |
Early deaths - myocarditis
Late sequelae - rheumatic heart disease, which affects heart valves mitral > aortic >> tricuspid (high-pressure valves affected most) |
|
|
Name 3 cell things associated with rheumatic fever
|
Aschoff bodies (granuloma with giant cells)
Anitschkow's cells (activated histiocytes) Elevated ASO titers |
|
|
How is rheumatic fever caused?
|
Immune mediated (type II hypersensitivity)
Not direct effect of bacteria |
|
|
Name 7 signs of rheumatic fever
|
**FEVERSS:
Fever, Erythema marginatum, Valvular damage (vegetation and fibrosis), ESR increased, Red-hot joints (migratory polyarthritis), Subcutaneous nodules (Aschoff bodies), St. Vitus' dance (chorea) |
|
|
What is cardiac tamponade?
|
Compression of heart by fluid (blood, effusions, etc.) in pericardium, leading to decreased CO
Equilibration of diastolic pressures in all 4 chambers |
|
|
Name 5 findings of cardiac tamponade
|
Hypotension
Increased venous pressure (JVD) Distant heart sounds Increased HR Pulsus paradoxus |
|
|
What is pulsus paradoxus?
Name 5 times it is seen |
Kussmaul's pulse
Decrease in amplitude of pulse during inspiration Seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup |
|
|
Name 3 kinds of pericarditis
|
Serous
Fibrinous Hemorrhagic |
|
|
Name 4 causes of serous pericarditis
|
SLE
Rheumatoid arthritis Viral infection Uremia |
|
|
Name 3 causes of fibrinous pericarditis
|
Uremia
MI (Dressler's syndrome) Rheumatic fever |
|
|
Name 3 causes of hemorrhagic pericarditis
|
TB
Malignancy (ex. melanoma) |
|
|
Name 5 findings of hemorrhagic pericarditis
|
Pericardial pain
Friction rub Pulsus paradoxus Distant heart sounds ECG changes with ST-segment elevation in multiple leads |
|
|
How does pericarditis resolve?
|
Can resolve without scarring or lead to chronic adhesive or chronic constrictive pericarditis
|
|
|
What is syphilitic heart disease?
What can it result in? |
Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent dilation of the aorta and valve ring
May see calcification of the aortic root and ascending aortic arch - leads to "tree bark" appearance of the aorta Can result in aneurysm of the ascending aorta or aortic arch and aortic valve incompetence |
|
|
What are the most common primary cardiac tumors in adults?
|
Myxomas
90% occur in atria (mostly LA) Usually described as "ball-valve" obstruction in the LA - associated with multiple syncopal episodes |
|
|
What are the most frequent primary cardiac tumors in kids?
|
Rhabdomyomas
Associated with tuberous sclerosis |
|
|
What is the most common cardiac tumor?
|
Metastases (melanoma, lymphoma)
|
|
|
What is a sign of cardiac tumors?
|
Kussmaul's sign:
Increase in jugular venous pressure on inspiration |
|
|
What is telangiectasia?
|
Arteriovenous malformation in small vessels
Dilated vessels on skin and mucous membranes |
|
|
What is hereditary hemorrhagic telangiectasia?
|
Osler-Weber-Rendu syndrome
Presents with nosebleeds and skin discolorations |
|
|
What is Raynaud's disease?
What is Raynaud's phenomenon? |
Decreased blood flow to the skin (small vessels) due to arteriolar vasospasm in response to cold temperature or emotional stress - Most often in fingers and toes
Called Raynaud's phenomenon when secondary to a mixed connective tissue disease, SLE, or CREST syndrome |
|
|
Name 3 characteristics of Wegener's granulomatosis
|
Triad of symptoms affecting small vessels:
Focal necrotizing vasculitis Necrotizing granulomas in the lung and upper airway Necrotizing glomerulonephritis |
|
|
Name 8 symptoms of Wegener's granulomatosis
|
Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea, hemoptysis, hematuria
|
|
|
Name 4 findings of Wegener's granulomatosis
|
c-ANCA = strong marker of disease
Chest X-Ray = large nodular densities Hematuria Red cell casts |
|
|
Name 2 treatments of Wegener's granulomatosis
|
Cyclophosphamide
Corticosteroids |
|
|
Name 3 ANCA-positive vasculitides besides Wegener's granulomatosis
|
Microscopic polyangiitis
Primary pauci-immune crescentic glomerulonephritis Churg-Strauss syndrome |
|
|
What is microscopic polyangiitis?
|
Like Wegener's but lacks granulomas
p-ANCA Small vessels |
|
|
What is primary pauci-immune crescentic glomerulonephritis?
|
Vasculitis limited to kidney
Pauci-immune = paucity of antibodies Small vessels |
|
|
What is Churg-Strauss syndrome?
|
Granulomatous vasculitis with eosinophilia
Involves lung, heart, skin, kidneys, nerves; often seen in atopic patients; small vessels p-ANCA |
|
|
What is Sturge-Weber disease?
|
Congenital vascular disorder that affects capillary-sized blood vessels (small)
Manifests with port wine stain on face and leptomeningeal aniomatosis (intracerebral AVM) |
|
|
What is the most common form of childhood systemic vasculitis?
|
Henoch-Schonlein purpura
|
|
|
Name 5 signs of Henoch-Schonlein purpura
|
Skin rash on buttocks and legs (palpable purpura)
Arthralgia Intestinal hemorrhage Abdominal pain Melana |
|
|
When does HSP occur?
What is it caused by/associated with? |
Follows URIs
IgA immune complexes Association with IgA nephropathy Small vessels Multiple lesions of same age |
|
|
Name the common triad of HSP
|
Skin
Joints GI |
|
|
What is Buerger's disease?
Who gets it? |
Also known as thromboangiitis obliterans
Idiopathic, segmental, thrombosing vasculitis of small and medium peripheral arteries and veins Seen in heavy smokers |
|
|
What do medium-vessel diseases cause?
|
Thrombosis/infarction of arteries
|
|
|
Name 4 symptoms of Buerger's disease
What can this lead to? |
Intermittent claudication
Superficial nodular phlebitis Cold sensitivity (Raynaud's phenomenon) Severe pain in affected part - may lead to gangrene and autoamputation of digits |
|
|
What is the treatment for Buerger's disease?
|
Smoking cessation
|
|
|
What is Kawasaki disease?
|
Acute, self-limiting disease of infants/kids - strong association with Asians
Necrotizing vasculitis of small/medium-sized vessels - may develop coronary aneurysms |
|
|
Name 4 symptoms of Kawasaki disease
|
Fever
Congested conjunctiva Changes in lips/oral mucosa ("strawberry tongue") Lymphadenitis |
|
|
What is polyarteritis nodosa?
|
Characterized by necrotizing immune complex inflammation of medium-sized muscular arteries
Typically involves renal and visceral vessels Lesions are of different ages |
|
|
Name 10 symptoms of polyarteritis nodosa
|
Fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, neurologic dysfunction, cutaneous eruptions
|
|
|
Name 3 findings of polyarteritis nodosa
|
Hepatitis B seropositivity in 30% of pts
Multiple aneurysms Constrictions on arteriogram Typically NOT associated with ANCA |
|
|
Name 2 treatments of polyarteritis nodosa
|
Corticosteroids
Cyclophosphamide |
|
|
What is Takayasu's arteritis?
|
Known as "pulseless disease" - affects medium and large arteries
Granulomatous thickening of aortic arch and/or proximal great vessels Associated with increased ESR Primarily affects Asian females <40 years old |
|
|
Name 7 signs of Takayasu's arteritis
|
Fever
Arthritis Night sweats Myalgia Skin nodules Ocular disturbances Weak pulses in upper extremities |
|
|
What is temporal arteritis (giant cell arteritis)?
|
Most common vasculitis that affects medium and large arteries, usually branches of carotid artery
Focal, granulomatous inflammation Affects elderly females |
|
|
Name 3 symptoms of temporal arteritis
|
Unilateral headache
Jaw claudication Impaired vision (occlusion of ophthalmic artery that may lead to irreversible blindness) |
|
|
Name 2 findings of temporal arteritis
|
Associated with increased ESR
Half of patients have systemic involvement and polymyalgia rheumatica |
|
|
What is the treatment for temporal arteritis?
|
High-dose steroids
|
|
|
Draw the Cardiac Output diagram and 5 cardiac drugs that affect it
|
P. 271
|
|
|
Name 5 categories of antihypertensive drugs
|
Diuretics
Sympathoplegics Vasodilators ACE inhibitors Angiotensin II receptor inhibitors |
|
|
Name 2 diuretic antihypertensives
|
Hydrochlorothiazide
Loop diuretics |
|
|
Name 6 sympathoplegic antihypertensive drugs
|
Clonidine
Methyldopa Reserpine Guanethidine Prazosin Beta-blockers |
|
|
Name 6 vasodilator antihypertensive drugs
|
Hydralazine
Minoxidil Nifedipine, verapamil Nitroprusside Diazoxide |
|
|
Name 3 ACE inhibitor antihypertensive drugs
|
Captopril
Enalapril Fosinopril |
|
|
Name an angiotensin II receptor inhibitor antihypertensive drug
|
Losartan
|
|
|
What are 6 adverse effects of hydrochlorothiazide?
|
Hypokalemia
Mild hyperlipidemia Hyperuricemia Lassitude Hypercalcemia Hyperglycemia |
|
|
What are 4 adverse effects of loop diuretics?
|
Potassium wasting
Metabolic alkalosis Hypotension Ototoxicity |
|
|
What are 3 adverse effects of clonidine?
|
Dry mouth
Sedation Severe rebound hypertension |
|
|
What are 2 adverse effects of methyldopa?
|
Sedation
Positive Coombs' test |
|
|
What are 4 adverse effects of reserpine?
|
Sedation
Depression Nasal stuffiness Diarrhea |
|
|
What are 3 adverse effects of guanethidine?
|
Orthostatic and exercise hypotension
Sexual dysfunction Diarrhea |
|
|
What are 3 adverse effects of prazosin?
|
1st dose orthostatic hypotension
Dizziness Headache |
|
|
What are 4 adverse effects of beta-blockers?
|
Impotence
Asthma Cardiovascular effects (bradycardia, CHF, AV block) CNS effects (sedation, sleep alterations) |
|
|
What are 6 adverse effects of hydralazine?
|
Nausea
Headache Lupus-like syndrome Reflex tachycardia Angina Salt retention |
|
|
What are 5 adverse effects of minoxidil?
|
Hypertrichosis
Pericardial effusion Reflex tachycardia Angina Salt retention |
|
|
What are 6 adverse effects of nifedipine, verapamil?
|
Dizziness
Flushing Constipation (verapamil) AV block (verapamil) Nausea Edema |
|
|
What is the adverse effect of nitroprusside?
|
Cyanide toxicity (releases CN)
|
|
|
What is the adverse effect of diazoxide?
|
Hyperglycemia (reduces insulin release, hypotension)
|
|
|
What are 8 adverse effects of ACE inhibitors?
|
Hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increased renin
|
|
|
What are 2 adverse effects of losartan?
|
Fetal renal toxicity
Hyperkalemia |
|
|
What is the mechanism of hydralazine?
|
Increases cGMP --> smooth muscle relaxation
Vasodilates arterioles > veins Afterload reduction |
|
|
Name 3 clinical uses of hydralazine
|
Severe hypertension
CHF First-line therapy for hypertension in pregnancy, with methyldopa |
|
|
Name 6 toxicities of hydralazine
|
Compensatory tachycardia (contraindicated in angina/CAD)
Fluid retention Nausea Headache Angina Lupus-like syndrome |
|
|
What is the mechanism of minoxidil?
|
K+ channel opener
Hyperpolarizes and relaxes vascular smooth muscle |
|
|
What is the clinical use of minoxidil?
|
Severe hypertension
|
|
|
Name 5 toxicities of minoxidil
|
Hypertrichosis (hair growth)
Pericardial effusion Reflex tachycardia Angina Salt retention |
|
|
What should hydralazine be used with?
|
= vasodilator
Use beta-blockers to prevent reflex tachycardia Use diuretic to block salt retention |
|
|
Name 3 calcium channel blockers
|
Nifedipine
Verapamil Diltiazem |
|
|
What is the mechanism of calcium channel blockers?
|
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility
|
|
|
What calcium channel blockers are used in vascular smooth muscle?
|
Nifedipine > Diltiazem > Verapamil
|
|
|
What calcium channel blockers are used in heart?
|
Verapamil > Diltiazem > Nifedipine
|
|
|
Name 5 clinical uses of calcium channel blockers
|
Hypertension
Angina Arrhythmias (not nifedipine) Prinzmetal's angina Raynaud's |
|
|
Name 5 toxicities of calcium channel blockers
|
Cardiac depression
Peripheral edema Flushing Dizziness Constipation |
|
|
What is the mechanism of nitroglycerin, isosorbide dinitrate?
|
Vasodilate by releasing nitric oxide in smooth muscle, causing increase in cGMP and smooth muscle relaxation
Dilate veins >> arteries Decrease preload |
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Name 3 clinical uses of nitroglycerin, isosorbide dinitrate
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Angina
Pulmonary edema Aphrodisiac/erection enhancer |
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Name 5 toxicities of nitroglycerin, isosorbide dinitrate
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Tachycardia
Hypotension Flushing Headache "Monday disease" in industrial exposure: tolerance for vasodilating action during week, loss over weekend, reexposure on Monday |
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Name 3 treatments of malignant hypertension and what each does
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Nitroprusside - short acting, increases cGMP via direct release of NO
Fenoldopam - dopamine D1 receptor agonist, relaxes renal vascular smooth muscle Diazoxide - K+ channel opener, hyperpolarizes and relaxes vascular smooth muscle |
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What is the goal of antianginal therapy?
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Reduction of myocardial O2 consumption by decreasing one or more of the determinants: end diastolic volume, blood pressure, heart rate, contractility, ejection time
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What do nitrates do in antianginal therapy?
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Affect preload
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What do beta-blockers do in antianginal therapy?
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Affect afterload
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What effect on end diastolic volume do nitrates have?
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Decrease EDV
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What effect on end diastolic volume do beta-blockers have?
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Increase EDV
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What effect on end diastolic volume do nitrates and beta-blockers have?
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No effect or decrease EDV
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What effect on blood pressure do nitrates have?
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Decrease BP
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What effect on blood pressure do beta-blockers have?
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Decrease BP
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What effect on blood pressure do nitrates and beta-blockers have?
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Decrease BP
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What effect on contractility do nitrates have?
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Increase contractility (reflex response)
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What effect on contractility do beta-blockers have?
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Decrease contractility
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What effect on contractility do nitrates and beta-blockers have?
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Little/no effect
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What effect on heart rate do nitrates have?
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Increase HR (reflex response)
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What effect on heart rate do beta-blockers have?
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Decrease HR
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What effect on heart rate do nitrates and beta-blockers have?
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Decrease HR
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What effect on ejection time do nitrates have?
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Decrease ejection time
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What effect on ejection time do beta-blockers have?
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Increase ejection time
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What effect on ejection time do nitrates and beta-blockers have?
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Little/no effect on ejection time
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What effect on myocardial O2 consumption do nitrates have?
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Decrease MVO2
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What effect on myocardial O2 consumption do beta-blockers have?
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Decrease MVO2
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What effect on myocardial O2 consumption do nitrates and beta-blockers have?
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Really decrease MVO2
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How do calcium channel blockers work in antianginal therapy?
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Nifedipine is similar to nitrates in effect
Verapamil is similar to beta-blockers in effect |
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Name 2 drugs contraindicated in angina
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Pindolol
Acebutolol Partial beta agonists |
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Name 5 categories on lipid-lowering agents
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HMG-CoA Reductase inhibitors (statins)
Niacin Bile acid resins (cholestyramine, colestipol, colesevelam) Cholesterol absorption blockers (ezetimibe) "Fibrates" (gemfibrozil, clofibrate, bezafibrate, fenofibrate) |
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Fill out the table on pg. 274 involving lipid-lowering drugs
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P. 274
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Draw the production of cholesterol and where drugs affect it
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P. 274
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Draw the cardiac drug sarcomere sites of action
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P. 275
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Name 6 factors involved in excitation-contraction coupling
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Na/K ATPase
Na-Ca exchanger Voltage gated (L-type) calcium channel Calcium pump in the wall of SR Ryanodine receptors and calcium release channels in SR, closely coupled to L-type calcium channels in cell membrane Site of calcium interaction with troponin-tropomyosin system |
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Describe beta1 receptors role in cardiac sarcomere
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Beta 1 receptors are Gs and activate protein kinase A, which phosphorylates L-type and Ca channels and phospholamban, both of which increase intracellular Ca during contraction
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What is a cardiac glycoside?
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Digoxin
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What are the pharmacokinetics of digoxin?
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75% bioavailability
20-40% protein bound Half-life = 40 hours Urinary excretion |
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What is the mechanism of cardiac glycosides?
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Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger/antiport
Increase intracellular calcium --> positive inotropy Also stimulates vagus nerve |
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Name 2 clinical uses of cardiac glycosides
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CHF (increase contractility)
Atrial fibrillation (decrease conduction at AV node and depression of SA node) |
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Name 6 toxicities of cardiac glycosides
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Increased PR
Decreased QT Scooping of ST segment T-wave inversion of ECG Increased parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision Arrhythmia |
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What increases toxicities of digoxin?
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Renal failure (decreased excretion)
Hypokalemia (digoxin competes with K+ at its binding site in Na/K ATPase so decreased K --> increased digoxin binding --> increased digoxin effect) Quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites) |
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What is the antidote for cardiac glycoside toxicity?
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Slowly normalize K+
Lidocaine Cardiac pacer Anti-dig Fab fragments Mg2+ |
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What do antiarrhythmics - Na channels blockers (class I) do?
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Local anesthetics
Slow or block conduction (especially in depolarized cells) Decrease slope of phase 4 depolarization and increase threshold for firing in abnormal pacemaker cells Are state dependent (selectively depress tissue that is frequently depolarized) |
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Name 3 Class IA antiarrhythmics
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Quinidine
Procainamide Disopyramide |
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How Class IA antiarrhythmics work?
What kind of arrhythmias do they affect? |
Increase AP duration
Increase effective refractory period Increase QT interval Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia |
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What are the toxicities of Class IA antiarrhythmics?
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Quinidine (cinchonism - headache, tinnitus; thrombocytopenia; torsades de pointes due to increase QT interval)
Procainamide (reversible SLE-like syndrome) |
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Name 3 Class IB antiarrhythmics
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Lidocaine
Mexiletine Tocainide |
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How do Class IB antiarrhythmics work?
What kind of arrhythmias do they affect? |
Decrease AP duration
Affect ischemic or depolarized Purkinje and ventricular tissue Useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias |
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Name 3 Class IC antiarrhythmics
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Flecainide
Encainide Propafenone |
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How do Class IC antiarrhythmics work?
What kind of arrhythmias do they affect? |
No effect on AP duration
Useful in V-tachs that profress to VF and in intractable SVT Usually used only as last resort in refractory tachyarrhythmias For patients without structural abnormalities |
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What is the toxicity of Class IC antiarrhythmics?
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Proarrhythmic, especially post-MI (contraindicated)
Significantly prolongs refractory period in AV node |
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How does hyperkalemia affect antiarrhythmics?
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Causes increased toxicity for Class IA, IB, IC
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Draw the effect on action potential of antiarrhythmic Class IA, IB, IC drugs
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P. 276
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What are Class II antiarrhythmics?
Name 5 |
Beta-blockers
Propranolol, esmolol (very short acting), metoprolol, atenolol, timolol |
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What is the mechanism of Class II antiarrhythmics?
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Decrease cAMP, decrease Ca currents
Suppress abnormal pacemakers by decreasing slope of phase 4 AV node particularly sensitive - increase PR interval |
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What are 6 toxicities of Class II antiarrhythmics?
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Impotence
Exacerbation of asthma Cardiovascular effects (bradycardia, AV block, CHF) CNS effects (sedation, sleep alterations) May mask the signs of hypoglycemia Metoprolol can cause dyslipidemia |
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What are Class III antiarrhythmics?
Name 3 |
K+ channel blockers
Sotalol Ibutilide Amiodarone |
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What is the mechanism of Class III antiarrhythmics?
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Increases AP duration
Increases ERP Used when other antiarrhythmics fail Increases QT interval |
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Name 2 toxicities of sotalol
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Torsades de pointes
Excessive beta block |
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Name a toxicity of ibutilide
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Torsades de pointes
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Name 2 toxicities of bretylium
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New arrhythmias
Hypotension |
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Name 9 toxicities of amiodarone
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Pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF), hypothyroidism/hyperthyroidism
**Check PFTs, LFTs, and TFTs when using amiodarone |
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Draw the cardiac action potential and antiarrhythmic Class III effects
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P. 277
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What are Class IV antiarrhythmics?
Name 2 |
Ca channel blockers
Verapamil Diltiazem |
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What is the mechanism of Class IV antiarrhythmics?
When are they used? |
Primarily affect AV nodal cells
Decrease conduction velocity Increase ERP Increase PR interval Used in prevention of nodal arrhythmias (ex. SVT) |
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Name 4 toxicities of Class IV antiarrhythmics
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Constipation
Flushing Edema CV effects (CHF, AV block, sinus node depression) |
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Draw the cardiac action potential and antiarrhythmic Class IV effects
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P. 278
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Name 3 older antiarrhythmics
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Adenosine
K+ Mg2+ |
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How does adenosine work as an antiarrhythmic?
When is it used? 3 toxicities |
Increases K+ out of cells --> hyperpolarizing the cells and decreasing Ica
Drug of choice in diagnosing/abolishing AV nodal arrhythmias Very short acting (15 sec) Toxicity: Flushing, hypotension, chest pain |
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How does K+ work as an antiarrhythmic?
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Depresses ectopic pacemakers in hypokalemia (ex. digoxin toxicity)
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How does Mg2+ work as an antiarrhythmic?
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Effective in torsades de pointes and digoxin toxicity
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