MICHIGAN STATE UNIVERSITY: CARDIO EXAM 1
Lecture 1 and 2 (Cardiology Primer)
Orthopnea – Dyspnea that worsens immediately after lying down
Results from sudden increase in venous return
Paroxysmal Nocturnal Dyspnea – Dyspnea several hours after the pt lays down to
sleep
Results from central redistribution of fluids
Palpitations – sensation in which a person is aware of a irregular, hard or rapid
heartbeat
Angina – Symptomatic myocardial ischemia (may be an uncomfortable sensation
rather than pain)
Stable – Prompted by exertion or emotion and occurs in stable pattern
Unstable – Worsened in severity or frequency; new onset brought on by
minimal exertion
Echocardiography is useful for assessment of LV function and valvular heart
disease
NOT helpful for imaging of coronary arteries
Doppler Echocardiography
Useful for assessment of valvular stenosis or regurgitation
May help identify intracardiac shunts
Stress Nuclear Imaging
Isotopes (thallium) injected at peak exercise reveal myocardial blood flow
that is compared to resting
Stress Echocardiogram
LV function assessed at rest and exercise to reveal stress-induced
deterioration of regional LV function
Holtor Monitor – 24 hr device of 2-3 ECG leads to diagnose rhythm disturbances
Event Recorder – Can be worn up to 1 month to record rhythm during symptoms
Heart Cath – Visualize coronary anatomy, assess LV function, measure
intracardiac pressures
Coronary Artery Disease
Leading cause of death in US
Artherosclerosis of coronary arteries is major cause
, Progressive degenerative process that begins in childhood and manifests in
adulthood
Myocardial Ischemia
When oxygen supply does not meet demand
Angina pectoris is clinical manifestation
Acute Coronary Syndrome (ACS)
Unstable Angina
Chronic angina symptoms become more chronic and severe
New onset brought on by minimal exertion
Normal cardiac enzymes (CK-MB, troponin)
Non-ST elevation MI
Rupture of atherosclerotic plaque and subsequent intravascular
thrombosis
Flow limiting but not occlusive or only transiently occlusive
Symptoms of unstable angina
Cardiac enzymes increase, indicating myocardial necrosis
ST Elevation MI
Persistent complete occlusion of the involved coronary artery
Severe chest pain, nausea, vomiting, anxiety, dyspnea
Cardiac enzymes much higher than Non-STEMI
Cardiomyopathies
Dilated
LV dilation and systolic dysfunction
Viral, SLE, toxins, metabolic, or idiopathic
Hypertrophic
Marked thickening of ventricular myocardium, small LV cavity size,
and hyperdynamic LV func
Inherited disorder
Diastolic dysfunction
May result in syncope or sudden death due to outflow obstruction
Restrictive
Normal LV size and systolic function but impaired diastolic function
Idiopathic, infiltrative, scleroderma
Aortic Stenosis
Aortic leaflets fused, fibrosed, and/or calcified which limits valve opening
Progressive obstruction to LV flow causes a transvalvular pressure gradient
Compensatory hypertrophy develops
Triad of dyspnea, angina, and presyncope/syncope
, Mitral Stenosis
Pressure gradient increase leads to increase left atrium pressure and
enlargement
Atrial fibrillation is common
Heart Failure
Systolic
Heart is weakened and cannot effectively pump blood in systole
Impaired myocardial contractility
Pulmonary vascular congestion results from blood backing up
Primary mechanism of CHF in ischemic and dilated
cardiomyopathies
Diastolic
Impaired ventricular relaxation
Higher than normal LV pressure which is transmitted to pulmonary
system (dyspnea)
Primary mechanism of CHF in hypertensive, hypoertrophic, and
restrictive heart disease
Lecture 3 (Pharm Primer)
Nomenclature
ACE Inhibitors: –pril
DHP Calcium Channel Blockers: -dipine
Beta Blockers: -olol
Thiazide Diuretics: Contains “thiazide”
Angiotensin Receptor Blockers: -sartan
Alpha 1 Antagonists: -zosin
Nitrates: Contains nitrate
Class III Antiarrhythmia: -darone or –tilide
Statins: -statin
Antiarrhythmics
Na-B-K-Ca
Na: Sodium channel blocker Class I
B: Beta blocker Class II
K: Potassium channel blocker Class II
Ca: Calcium channel blocker Class IV
Physiologic Activity
Beta Blockers Block symp activation of beta receptors
, Slow HR and decrease force of contractility
Ca Channel DHP – peripheral vasodilation
Blockers NDHP – Blocks Ca channels on myocardial tissue decreases
HR and CO
Alpha1 Blocks NE effect on alpha receptors prevents vasoconstriction
Antagonist
Alpha2 Agonist “Shut off valve” to SNS tells body to stop secreting NE
Ex: Clonidine
ACE Inhibitor Inhibits conversion of Ang I to Ang II
Prevents Ang II induced release of aldosterone
Angiotensin Blocks Ang II from binding to receptor
Receptor Prevents Ang II induced release of aldosterone
Blockers
Renin Inhibitor Blocks RAAS at point of activation by inhibiting renin release
Ex: Aliskiren
Thiazide Increases excretion of sodium and water decreases edema
Diuretic Ex: Hydrochlorothiazide, metolazone
Loop Diuretic Decreases Na and Cl reabsorption in the loop of henle and distal
convoluted tubules
Water follows solute decreases fluid overload/edema
Ex: Furosemide
Potassium Blocks aldosterone from causing water retention
Sparing Ex: Spironolactone, eplerenone (AKA aldosterone antagonist)
Inhibits Na reabsorption at the distal convoluted tubule, decreasing
water reabsorption and increasing potassium retention
Ex: Triamterene, Amiloride
Direct Acting Directly relaxes vascular smooth muscle vasodilation
Vasodilator Ex: Hydralazine
Nitrates Directly relaxes vascular smooth muscle
Ranolazine Inhibits late phase action potential decreasing diastolic tension
and increases contractility
Digoxin Enhances cardiac contractility by inhibiting the Na/K ATPase
pump
Class I Na channel blockers slows conduction
Antiarrhyth.
Class II Same as beta blockers
Antiarrhyth.
Class III K channel blockers prolongs action potential
Antiarrhyth.
Class IV Same as NDHP Ca Channel Blockers
Antiarrhyth.
Lecture 1 and 2 (Cardiology Primer)
Orthopnea – Dyspnea that worsens immediately after lying down
Results from sudden increase in venous return
Paroxysmal Nocturnal Dyspnea – Dyspnea several hours after the pt lays down to
sleep
Results from central redistribution of fluids
Palpitations – sensation in which a person is aware of a irregular, hard or rapid
heartbeat
Angina – Symptomatic myocardial ischemia (may be an uncomfortable sensation
rather than pain)
Stable – Prompted by exertion or emotion and occurs in stable pattern
Unstable – Worsened in severity or frequency; new onset brought on by
minimal exertion
Echocardiography is useful for assessment of LV function and valvular heart
disease
NOT helpful for imaging of coronary arteries
Doppler Echocardiography
Useful for assessment of valvular stenosis or regurgitation
May help identify intracardiac shunts
Stress Nuclear Imaging
Isotopes (thallium) injected at peak exercise reveal myocardial blood flow
that is compared to resting
Stress Echocardiogram
LV function assessed at rest and exercise to reveal stress-induced
deterioration of regional LV function
Holtor Monitor – 24 hr device of 2-3 ECG leads to diagnose rhythm disturbances
Event Recorder – Can be worn up to 1 month to record rhythm during symptoms
Heart Cath – Visualize coronary anatomy, assess LV function, measure
intracardiac pressures
Coronary Artery Disease
Leading cause of death in US
Artherosclerosis of coronary arteries is major cause
, Progressive degenerative process that begins in childhood and manifests in
adulthood
Myocardial Ischemia
When oxygen supply does not meet demand
Angina pectoris is clinical manifestation
Acute Coronary Syndrome (ACS)
Unstable Angina
Chronic angina symptoms become more chronic and severe
New onset brought on by minimal exertion
Normal cardiac enzymes (CK-MB, troponin)
Non-ST elevation MI
Rupture of atherosclerotic plaque and subsequent intravascular
thrombosis
Flow limiting but not occlusive or only transiently occlusive
Symptoms of unstable angina
Cardiac enzymes increase, indicating myocardial necrosis
ST Elevation MI
Persistent complete occlusion of the involved coronary artery
Severe chest pain, nausea, vomiting, anxiety, dyspnea
Cardiac enzymes much higher than Non-STEMI
Cardiomyopathies
Dilated
LV dilation and systolic dysfunction
Viral, SLE, toxins, metabolic, or idiopathic
Hypertrophic
Marked thickening of ventricular myocardium, small LV cavity size,
and hyperdynamic LV func
Inherited disorder
Diastolic dysfunction
May result in syncope or sudden death due to outflow obstruction
Restrictive
Normal LV size and systolic function but impaired diastolic function
Idiopathic, infiltrative, scleroderma
Aortic Stenosis
Aortic leaflets fused, fibrosed, and/or calcified which limits valve opening
Progressive obstruction to LV flow causes a transvalvular pressure gradient
Compensatory hypertrophy develops
Triad of dyspnea, angina, and presyncope/syncope
, Mitral Stenosis
Pressure gradient increase leads to increase left atrium pressure and
enlargement
Atrial fibrillation is common
Heart Failure
Systolic
Heart is weakened and cannot effectively pump blood in systole
Impaired myocardial contractility
Pulmonary vascular congestion results from blood backing up
Primary mechanism of CHF in ischemic and dilated
cardiomyopathies
Diastolic
Impaired ventricular relaxation
Higher than normal LV pressure which is transmitted to pulmonary
system (dyspnea)
Primary mechanism of CHF in hypertensive, hypoertrophic, and
restrictive heart disease
Lecture 3 (Pharm Primer)
Nomenclature
ACE Inhibitors: –pril
DHP Calcium Channel Blockers: -dipine
Beta Blockers: -olol
Thiazide Diuretics: Contains “thiazide”
Angiotensin Receptor Blockers: -sartan
Alpha 1 Antagonists: -zosin
Nitrates: Contains nitrate
Class III Antiarrhythmia: -darone or –tilide
Statins: -statin
Antiarrhythmics
Na-B-K-Ca
Na: Sodium channel blocker Class I
B: Beta blocker Class II
K: Potassium channel blocker Class II
Ca: Calcium channel blocker Class IV
Physiologic Activity
Beta Blockers Block symp activation of beta receptors
, Slow HR and decrease force of contractility
Ca Channel DHP – peripheral vasodilation
Blockers NDHP – Blocks Ca channels on myocardial tissue decreases
HR and CO
Alpha1 Blocks NE effect on alpha receptors prevents vasoconstriction
Antagonist
Alpha2 Agonist “Shut off valve” to SNS tells body to stop secreting NE
Ex: Clonidine
ACE Inhibitor Inhibits conversion of Ang I to Ang II
Prevents Ang II induced release of aldosterone
Angiotensin Blocks Ang II from binding to receptor
Receptor Prevents Ang II induced release of aldosterone
Blockers
Renin Inhibitor Blocks RAAS at point of activation by inhibiting renin release
Ex: Aliskiren
Thiazide Increases excretion of sodium and water decreases edema
Diuretic Ex: Hydrochlorothiazide, metolazone
Loop Diuretic Decreases Na and Cl reabsorption in the loop of henle and distal
convoluted tubules
Water follows solute decreases fluid overload/edema
Ex: Furosemide
Potassium Blocks aldosterone from causing water retention
Sparing Ex: Spironolactone, eplerenone (AKA aldosterone antagonist)
Inhibits Na reabsorption at the distal convoluted tubule, decreasing
water reabsorption and increasing potassium retention
Ex: Triamterene, Amiloride
Direct Acting Directly relaxes vascular smooth muscle vasodilation
Vasodilator Ex: Hydralazine
Nitrates Directly relaxes vascular smooth muscle
Ranolazine Inhibits late phase action potential decreasing diastolic tension
and increases contractility
Digoxin Enhances cardiac contractility by inhibiting the Na/K ATPase
pump
Class I Na channel blockers slows conduction
Antiarrhyth.
Class II Same as beta blockers
Antiarrhyth.
Class III K channel blockers prolongs action potential
Antiarrhyth.
Class IV Same as NDHP Ca Channel Blockers
Antiarrhyth.
