Ch. 1 Cardiology

Front 1

What is preload?

Back 1

Degree of tension (load) on ventricular muscle when it begins to contract.

End diastolic volume is primary determinant of preload.

Front 2

How does increased preload affect ventricular contraction?

Back 2

Makes contraction stronger (stretching of sacromeres allows for greater overlap of myosin and actin; Frank-Starling mechanism)

(Beyond a certain point causes less efficient ventricular contraction, i.e. CHF)

Front 3

Mean arterial blood pressure= ___ x ___

Back 3

MAP=TPR x CO

Front 4

CO= ___ x ___

Back 4

CO= SV x HR

Front 5

What's afterload?

Back 5

Pressure/resistance against which ventricles pump blood

High afterload decreases SV & CO)

Front 6

How does sympathetic nervous system promote arteriolar vasoconstriction?

Back 6

Stimulate alpha1 adrenergic receptors which increase calcium influx via Ca channels for smooth muscle contraction

Antihypertensives antagonize alpha1 receptors and/or arteriolar Ca channels

Front 7

When BP drops, arterial baroreceptors fire ____ (more/less) frequently.

Back 7

Less

This disinhibits sympathetic outflow. (When stretched, baroreceptors fire more to further inhibit sympathetics)

Front 8

Prazosin, terazosin, and doxazosin are all what kind of drugs?

Back 8

Antihypertensives

-osins antagonize alpha1 receptors to decrease vasoconstriction

Front 9

How do alpha1 antagonists cause orthostatic hypotension? Would there be an increase/decrease in heart rate?

Back 9

Can't compensate with baroreflex activation of sympathetics (alpha1 blocked so no vasoconstriction)

Heart rate can increase (reflex tachycardia) b/c mediated by beta receptors

Front 10

During ventricular systole, what is the source of intracellular Ca2+?

Back 10

1) AP causes influx of Ca from extracellular fluid
2) This Ca stimulates release of Ca from sarcoplasmic reticulum (Ca-induced Ca release)

(in skeletal muscles, AP just causes release of Ca from sarcoplasmic reticulum)

Front 11

What binds to troponin to expose myosin binding site?

Back 11

Ca

(force of contraction is proportional to intracellular Ca; Ca channel blockers decrease rate and contractility)

Front 12

How does sympathetic (beta adrenergic) stimulation of heart do the following?

1) increase contractility?

2) reduce time required for ventricular relaxation?

Back 12

1) Increase probability of Ca chan opening so more Ca influx

2) Stimulates Ca2+ uptake by ventricular sarcoplasmic reticulum (better filling in diastole)

Front 13

In phase 0 of the ventricular myocyte AP, what ion fluxes across the membrane?

Back 13

Na influx (membrane voltage rises sharply)

Front 14

In phase 1 of the ventricular myocyte AP, what ion(s) flux across the membrane?

Back 14

K+ (I to1), Cl- (I to2)

(small downward deflection)

Front 15

In phase 2 of the ventricular myocyte AP, what ion(s) flux across the membrane?

Back 15

Ca2+ influx, K+ efflux

(balance each other creating plateau)

Front 16

In phase 3 of the ventricular myocyte AP, what ion(s) flux across the membrane?

Back 16

K+ efflux

(rapid repolarization with unopposed K+ efflux)

Front 17

Which phase is the resting potential in a ventricular myocyte?

Back 17

Phase 4

Front 18

What is responsible for the drifting membrane potential in nodal cells?

Back 18

Nodal cells are more permeable to Na than cardiomyocytes

(Na comes in until reach threshold to activate slow Ca channels-->action potential)

Front 19

Which ion is responsible for fast upstroke of action potential in...

Cardiomyocyte?
Nodal cell?

Back 19

Myocyte: Na influx

Nodal cell: Ca (through slow Ca channels)

Front 20

How does sympathetic NS increase HR?

Back 20

Activate beta1 adrenergic receptors in nodal cells

(+ chronotropic effect by increasing influx of Na and decreasing efflux of K)

Front 21

Quinidine, procainamide

Drug type
Mech of action?

Back 21

Antiarrythmic (Class IA)

Inhibits Na & K channels
Prolongs QRS complex/QT interval
Prolongs effective refractory period

Front 22

Lidocaine

Drug type?
Mechanism of action?

Back 22

Class IA antiarrythmic

Inhibits Na channels
Shortens repolarization
Shorter QT interval

Front 23

What antiarrythmic can cause pulmonary fibrosis?

Back 23

Amiodarone

Front 24

Propranolol

Antiarrythmic type?
Mech of action?

Back 24

Antiarrythmic type 2

Increases PR interval, decreased automaticity in nodal cells-->fire less often)

Front 25

Amiodarone

Antiarrythmic type?
Mech of action?

Back 25

Type 3

Inhibits K channels

(can cause pulmonary fibrosis)

Front 26

Verapamil, diltiazem

Drug type?
Mechanism of action?

Back 26

Type 4 antiarrythmic

Inhibit Ca channels (increase PR interval, decrease automaticity in nodal cells)

Front 27

Type 1 (A, B, C) antiarrhythmic drugs all inhibit ___ channels

Back 27

Na+

Front 28

What are 4 classes of drugs that could be used to treat HT?

Back 28

1) Diuretics
2) ACE inhibitors (inhibit RAAS effects) (or ATII receptor blockers, losartan)
3) Vasodilators (i.e. direct action, Ca-chan blockers)
4) Sympatholytics (beta-blockers, alpha1 blockers, etc.)

Front 29

Caution should be used when prescribing beta blockers in which types of patients?

Back 29

1) Asthma (other COPD)
2) Peripheral artery disease (beta2 maintains vasodilation)
3) First degree ventricular heart block

Front 30

How do beta blockers decrease BP? (2 ways)

Back 30

1) beta1 adrenergic blockade decreases HR and contractility
2) Blocking beta1&2 receptors decreases RAAS

Front 31

Which beta blockers (3) are more cardioselective?

Back 31

Atenolol, esmolol, metoprolol

(more specific to beta1)

Front 32

What is best to treat HT in diabetics?

Back 32

ACE inhibitors

(cause vasodilation of efferent arterioles in kidney)

Front 33

Why could it be bad to give beta blockers to treat HT in diabetics?

Back 33

1) Can mask signs of hypoglycemia (except sweating which is innervated by sympathetic cholinergic, not sympathetic adrenergic)
2) Can antagonize gluconeogenesis/glycogenolysis
3) Exacerbate claudication from peripheral artery disease

Front 34

What drug class can cause a dry cough? Why?

Back 34

ACE-inhibitors (lisinopril, other -prils)

Inhibit angiotensin converting enzyme which also breaks down bradykinin (activates nocireceptors in air ways)

Front 35

Losartan, valsartan

Drug class?
Mech of action?

Back 35

Antihypertensive

Antiotensin II receptor blockers; stops effects of ATII (systemic vasoconstriction, increased thirst, vasoconstrict EA in kidney, aldosterone)

Good to use in people who develop cough from ACE inhibitors

Front 36

Captopril, lisonopril, quinapril

Drug class?
Mech of action?

Back 36

Anti-HT

ACE inhibitors (decreases ATII, decrease peripheral resistance, aldosterone secretion, etc.)

Front 37

Hydralazine

Drug class?
Mech of action?
SE?

Back 37

Anti-HT

Arterial vasodilator

Lupus-like syndrome

Front 38

Methyldopa, clonidine

Drug class?
Mech of action?

Back 38

Anti-HT

alpha2 receptor agonists (vasodilation)

Front 39

Atenolol, esmolol, metoprolol

Drug class?
Mech of action?
SE?

Back 39

Anti-HT

SELECTIVE beta1 receptor blockers (negative chronotropic/ionotropic effects to reduce cardiac output)

AV block, bradycardia, sex dysfunction, bronchospasm (though less likely than propranolol)

Front 40

Prazosin, terazosin, doxazosin

Drug class?
Mech of action?
SE?

Back 40

Anti-HT

Alpha1 antagonist

Postural hypotension (but still have beta1 mediated reflex tachycardia)

Front 41

Labetalol, carvedilol

Drug class?
Mech of action?

Back 41

Anti-HT

Alpha1 and beta blockers

(-lol = alpha1+ beta blocker; -olol = beta blocker)

Front 42

Diltiazem, verapamil

Drug class?
Mech of action?

Back 42

Anti-HT

Ca-chan blockers (decrease peripheral resistance, decrease cardiac output)

**Nondihydropurine (dihydropurine is more specific for vascular smooth muscle than heart)

Front 43

Amplodipine, nifedipine

Drug class?
Mech of action?

Back 43

Anti-HT

Ca-chan blocker (dihydropurine); decreased peripheral resistance (smooth muscle relax)

(-Pines are more for Peripheral resistance; diltiazem/verapamil are also Ca chan blockers but decrease cardiac output as well as decreasing peripheral resistance)

(dihydropurine is more specific for vascular smooth muscle than heart)

Front 44

Hydrochlorothiazide

Drug class?
Mech of action?
SE?

Back 44

Thiazide diuretic (anti-HT)

Inhibit Na/water resorption in distal convoluted tubule

SE: Hypokalemia, hyperglycemia, hyperuricemia

Front 45

Furosemide, bumentanide

Drug class?
Mech of action?
SE?

Back 45

Loop diuretic (Anti-HT)

Inhibit Na/K/2Cl pump in thick ascending loop of Henle

Hypokalemia, hyperuricemia, hyperglycemia, ototoxicity (w/aminoglycosides)

Front 46

Spirinolactone

Drug class?
Mech of action?
SE?

Back 46

Potassium sparing diuretic (Anti-HT)

Blocks action of aldosterone

Hyperkalemia

Front 47

Why might cardiac ischemia be "silent" in people with heart transplants or DM?

Back 47

Visceral cardiac pain is sensed by sympathetic fibers

(autonomic neuropathy in DM)

Front 48

Stable vs. unstable vs. variant angina

Back 48

Stable=constant, predicatable level of exertion elicits pain

Unstable=chest pain in new setting (indicates change in coronary atheromatous plaque; could be impending MI)

Variant=Prinzmetal's/vasospastic angina; coronary arteries spasm

Front 49

How can angina occur without coronary atherosclerosis?

Back 49

Prinzmetal's angina

(due to vasospasm of coronary arteries; pain more likely at rest or in morning)

(Severe anemia or rarely pheo could trigger CA spasm)

Front 50

Less time in _______ can cause less perfusion of myocardium.

Back 50

Diastole

(tachycardia, low diastolic perfusion pressure and resistance in coronary arteries can decrease myocardial perfusion)

Front 51

How does nitroglycerin treat angina?

Back 51

Converted to nitric oxide in endothelial cells to...

1) MAIN EFFECT: peripheral venous dilation (decrease preload so less contractility, wall tension)
2) Arteriolar dilation (decrease afterload)
3) Vasodilate coronary arteries (relieve spasm)

Front 52

Dobutamine

Back 52

Synthetic catecholamine used to simulate stress of exercise in people in whom an exercise stress test is contraindicated

Front 53

In a patient with complete occlusion of a coronary artery resulting in transmural infarction...

...what would be abnormal on ECG?
...what's the treatment?

Back 53

ST segment elevation (STEMI)

Angioplasty (stent), thrombolytics

Front 54

Treatment for STEMI vs. NSTEMI

Back 54

STEMI: angioplasty+stent, thrombolytics (this is a occlusive thrombus)

NSTEMI: anti-platelet, anticoag, stent high risk (this is an unstable plaque with aggregation of platelets so don't use thrombolytics)

Front 55

What drugs should be given post-MI?

Back 55

1) Statins
2) Aspirin, clopidogrel
3) Beta-blockers
4) ACE-inhibitor

Front 56

Dressler's syndrome

Back 56

Autoimmune (probably) pericarditis that develops 2-10 weeks after an MI

(suspect pericarditis if you hear a friction rub)

Front 57

What is sudden cardiac death and why are people who have had MIs predisposed to it?

Back 57

Death within 1 hr of symptoms (usually lethal arrythmia)

MIs leave scar tissue that deosn't conduct normally leading to arrythmia

Front 58

What are 2 sensitive indicators (cardiac muscle enzyme) of MI?

Back 58

1) Creatine kinase myocardial band (CK-MB)
2) Cardiac specific troponins (cardiac troponin T, cardiac troponin I)

Front 59

What are the 2 broad types of heart failure?

Back 59

Systolic (pump failure)
Diastolic (filling failure)

Front 60

Systolic vs. diastolic heart failure

Which has preserved EF?
Which is more common?
Which is more treatable?

Back 60

Which has preserved EF? Diastolic (insufficient filling, not ejection; EF=SV/EDV)
Which is more common? Systolic
Which is more treatable? Systolic

Features of each may overlap

Front 61

EF= ___ x ___

Back 61

EF= SV x EDV

Usually 55-70%

Front 62

What can cause heart failure?

Back 62

Any diseases that impairs cardiac function. Etiologies of systolic/diastolic HF overlap.

1) Valvular disease (i.e. AS)
2) Ischemic heart disease
3) Intrinsic myocardial disease (congenital cardiomyopathy)
4) Long-standing HT
5) High-output HF (inability of heart to maintain elevated CO in a pathologic situation (sepsis, severe anemia, etc.) that demands it)

Front 63

Would sympathetic activity be increased/decreased in a patient with HF? Is this good or bad?

Back 63

Sympathetic activity is increased

Pros: increased contractility so increase CO; vasoconstriction helps maintain adequate MAP/perfusion (MAP=CO x TPR)

Cons: reduced time in diastole (ischemia); less diastole=less filling=less CO=vicious cycle

Front 64

How does remodelling/hypertrophy differ in...

a volume overloaded heart?

a pressure overloaded heart?

Back 64

Volume over load (HF, etc.)
-Sarcomeres added in series
-Expand chamber volume (eccentric hypertrophy)

Pressure overload (AS, HT, etc.)
-Sarcomeres added in parallel (concentric hypertrophy); reduces stress on each sarcomere
-Thicker wall; reduced ventricular compliance

Both can exacerbate ischemia as blood supply doesn't increase proportionately to hypertrophy of muscle

Front 65

What are 3 ways the heart compensates in HF? What is the goal?

Back 65

1) Increase sympathetic activity
2) Fluid retention
3) Myocardial hypertrophy

Goal: increase CO with these compensatory mechanism

These adaptive responses become maladaptive if prolonged leading decompensation (can't restore adequate CO via these mechanisms) and eventually death.

Front 66

Why are beta blockers helpful in HF? (3 reasons)

Back 66

1) Inhibit sympathetic effects: -Decrease beta1 mediated increase in contractility/HR=decrease SV and venous return=decrease O2 need
-Decrease peripheral vasoconstriction
2) Decrease renin secretion (less fluid retained)
3) Interfere with remodeling

Front 67

What does digitalis do? Does it improve mortality in HF?

Back 67

Inhibits Na/K pump which drives the Na-Ca exchanger, so more Ca stays in cell=increased contractility

(+ionotropic, - chronotropic, increased EF)

Improves cardiac performance and quality of life in HF, but not life expectancy.

Front 68

Name 3 drugs used to treat HF

Back 68

1) Digitalis: cardiac glycoside (+ionotropic, - chronotropic, increased EF)
2) Metoprolol: beta blocker (- ion, - chrono; decreased MVO2 demand)
3) ACE inhibitors/ATII receptor antagonists (decrease fluid retention, decrease peripheral vasoconstrict)

#2 & #3 increase life expectancy, #1 doesn't

Front 69

How can aortic stenosis cause dyspnea/pulmonary edema?

Back 69

-Elevated afterload causes concentric hypertrophy.
-Thickened myocardium is less compliant and requires increased filling pressure predisposing to these conditions.

Front 70

In aortic stenosis, is more time spent in isotonic or isovolemic contraction?

Back 70

Isovolemic (need more pressure build up before aortic valve opens)

Isotonic ejection phase is shorter

Front 71

In aortic stenosis, is more time spent in systole or diastole?

Back 71

Systole

(less coronary perfusion)

Front 72

How does aortic stenosis affect coronary perfusion?

Back 72

1) Less time in diastole
2) Aortic pressure is reduced

Both decrease perfusion

Front 73

Why is atrial fibrillation particularly dangerous in a patient with aortic stenosis?

Back 73

AS has impaired ventricular filling due to hypertrophy and needs the "atrial kick" in diastole to maintain CO.

In a normal person, the atrial systole doesn't contribute a big % of CO. Also, a fib can lead to embolic stroke.

Front 74

What's a lipoprotein?

Back 74

Macromolecular structures with inner core of cholesterol esters/triglycerides and outer core of apoproteins, phospholipids, unesterified free cholesterol.

Ex: Chylomicrons, VLDL, LDL, HDL

Front 75

Where are lipoproteins made?

Back 75

Chylomicrons: synthesized in intestinal enterocytes

VLDLS: made in liver

IDL/HDL/LDL: formed in circulation via VLDL catabolism

Front 76

What are chylomicrons for?

Back 76

Deliver dietary triglycerides to adipose, skeletal/cardiac muscle (VLDL delivers triglycerides made in liver)

Then cholesterol rich chylomicron remnants are taken up by liver

Front 77

What delivers cholesterol to cells throughout body?

How is this molecule removed from blood?

Back 77

LDL

Internalization via LDL receptor (liver)

Front 78

What returns excess cholesterol from cells to the liver for biliary secretion?

Back 78

HDL

Front 79

How do -statins work?

Back 79

Inhibit hepatic synthesis of cholesterol by inhibiting the rate liming enzyme (3-hydroxy-3-methylglutaryl coenzyme A reductase)

(Potent for decreasing LDL, a little increase in HDL)

Front 80

Using statins with ______ can increase risk for myositis and liver damage.

Back 80

fibrates

(fibrates, like gemifrozil & fenofibrate, decrease triglycerides)

Front 81

What enzymatic mechanism clears triglycerides from circulation?

Back 81

Lipoprotein lipase (luminal surface of capillary endothelial cells) releases fatty acids from triglycerides in chylomicrons/VLDL

Front 82

How do fibrates work?

Back 82

Increase lipoprotein lipase activity=decrease triglycerides

Front 83

How can you increase HDL?

Back 83

Niacin, exercise

Front 84

What are bile sequestering resins used for?

Back 84

Cholestyramine, colestipol, and other bile sequestering resins decrease LDL.

They prevent reuptake of bile acids in terminal ileum so the liver has to use more cholesterol to make more (can result in fat/vitamin malabsorption).

Front 85

Abetalipoproteinemia

Back 85

Genetic disorder chracterized by absence of apolipoprotein B (enterocytes can't assimilate triglycerols into chylomicrons)

-Lipid vacuoles in enterocytes
-Few to no chylomicrons in circulation