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Cardiology > Cardio Test #1 > Flashcards

Cardio Test #1 Flashcards

1
Q

Coronary arteries

A

Left main LCA -> Circumflex and LAD

Right Main (RCA) -> RPA and Marginal

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2
Q

Left Coronary Arteries supply:

A

LDA: Supplies front and bottom of left ventricle and the front of the septum

Circumflex: Supplies left atrium and back and sides of left ventricle

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3
Q

Right Coronary Arteries supply:

A

Right atrium

Right ventricle

Bottom portion of both ventricles and back of the septum

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4
Q

Coronary artery lost, worry about?

A

LCA: immediate bypass - worse

RCA: worry about SA Node, may need a pacemaker

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5
Q

Common cardiac problems

A

Plumbing = ischemic heart dx, MI, acute coronary syndrome

Mechanical = CHF, restrictive and constrictive cardiomyopathies

Electrical = arrhythmias

Structural = Congenital or acquired abnormalities

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6
Q

PMI location

A

5-6th rib along mid-clavicular line

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7
Q

Pericarditis

A

Mostly viral

occurs in the pericardial cavity between 2 serous layers

Can also be idiopathic, autoimmune, or cancer

Think AI/CA w/ multiple incidents of pericarditis

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8
Q

Heart and Pericardial layers

Superficial to deep

A

Superficial fibrous pericardium

Deep 2-layer serous pericardium

-parietal and visceral

Epicardium (continuous w/ visceral serous pericardium

Myocardium

Endocardium (continuous w/ inside of heart and vessels)

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9
Q

Angina perctoris

A

Heart reporting a lack of oxygen

Cells are weakened

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10
Q

Myocardial infarction

A

Prolonged coronary blockage causes more cells to die the longer it stays there

Dead cells are replaced w/ noncontractile tissue

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11
Q

Cardiac muscle cells

A

1% have automaticity

intercalated disks/gap junctions allow contraction as a unit

fibrous insulator keeps electrical signls orderly

Longer refractory period to prevent tetany

Bulk of heart muscle is contractile muscle fibers

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12
Q

Autorhythmic cells

A

Unstable resting potential (-55 to -60)

Slow Na+ channels bring potential up to threshold (-40)

Once at threshold, Ca2+ channels burst open and initiate depolarization

Repolarization occurs once Ca2+ channels close and K+ channels open

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13
Q

Pacemaker potential

A

Slow opening of the Na2+ channels that makes cardiac muscle resting potenial so unstable

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14
Q

SA Node

A

In RA, just below SVC

60-100 bpm, PNS keeps it around 75

SNS and PNS innervated

If this is firing, will have a P wave (sinus rhythm)

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15
Q

AV Node

A

50 bpm

Less gap junctions = slower rate

Junctional rhythm (no P wave but normal QRS)

Delays the electrical impulse for 0.1 seconds to allow complete atrial contracion

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16
Q

Purkinje fibers

A

30 bpm

Escape, ventricular only rhythm

Widened QRS

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17
Q

Defective SA Node

A

ectopic focus or AV nodal pacing -> junctional rhythm

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18
Q

Defective AV Node

A

Partial/total block -> ventricular pacing

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19
Q

Extrinsic heart innervation

A

Medulla oblongata has cardioacceleratory (SNS) and cardioinhibitory (PNS) centers

SNS innervates SA, AV nodes, heart muscle, and coronary arteries

PNS innervates SA and AV nodes via vagus nerve

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20
Q

P wave and PR Interval durations

A

P wave: <0.12

PR Interval: 0.12-0.20

Gets long PR w/ heart blocks

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21
Q

QRS and QT Interval duration

A

QRS: <0.12

QT Interval: 0.34-0.43

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22
Q

Valve auscultation points

A

SL valves @ 2nd intercostal margin

AV valves @ 5th intercostal margin

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23
Q

Ventricular filling phase

A

Mid/late diastole

AVs open, SLs closed

80% blood passively flows into vent, 20% w/ atrial kick

EDV

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24
Q

Ventricular systole

A

Atria relax and ventricles contract

AV valves close, SL valves open when intravent>aorta pressure

Isovolumetric contraction until SL open

ESV

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25
Q

Isovolumetric relaxation

A

Early in diastole

Ventricals relax => T wave

Blood backflow closes SL valves -> diacrotic notch

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26
Q

Stroke Volume

A

EDV-ESV

Regulated by preload, contractibility, and afterload

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27
Q

Cardiac output

A

SV x HR

= volume of blood pumped by each ventricle in 1 minute

Max = 4-5X normal, or up to 35L/min (athletes)

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28
Q

Cardiac reserve

A

CR = COmax - COresting

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29
Q

Vasodilating systems

A

PNS

Prostaglandins

ANP

Nitric Oxide

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30
Q

Vasoconstricting systems

A

SNS

Ca+

RAAS

Endothelin

Vasopressin

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31
Q

Ejection fraction (EF/LVEF)

A

measurement of ventricular systolic function

60% is normal

Measure via an echo or a cardiac cath

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32
Q

Preload

A

Cardiac muscle cell degree of stretch before contraction

Increased venous return stretches cells to optimal length in order to increase contraction force

Increased venous return via slow HR, exercise = more time to fill

Way to adjust EDV

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33
Q

Contractility

A

Contractile strength of a muscle cell

Independant of muscle stretch and EDV

Method of modifying EDV

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34
Q

Inotrope

A

Agent that alters the force/energy of muscular contractions

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35
Q

Chronotrophs

A

Agents that modify the heart rate

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36
Q

Afterload

A

Pressure to be overcome for ventricle ejection

HTN increases this = increases ESV = increases SV

Method of modifying ESV

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37
Q

Chronotrophic hormones

A

SNS -> norepinephrine which causes SA node to fire more rapidly and increases contractility

PNS -> acetylcholine which slows heart rate w/ no effect on contractility

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38
Q

Atrial reflex

A

Bainbridge reflex

SNS reflex w/ increased venous return

Atrial and carotid baroreceptors stretch and stimulate SA Node = increase in HR

Tachycardia decreases C.O. => heart doesnt have enough time to fill

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39
Q

Stroke volume modifiers

A

Increased preload = Increased SV

Increased afterload = Decreased SV

Increased contractibility = Decreased ESV = Increased SV

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40
Q

Chemical regulation of heart rate

A
  1. Hormones => Thyroxine increases HR, enhances NE and epi effects = increase in HR and contractility
  2. Intra/extracellular ion concentration must be maintained for normal heart function = arrhythmias from electrolyte imbalances
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41
Q

Drugs contraindicated w/ CHF

A

CCB = decreased heart contractility strength

BB = decreased heart rate and contractility

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42
Q

Perfusion assessment at bedside

A

Feel feet, check the urine output, and check BP

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43
Q

Primary HTN

A

Idiopathic, inherited, or genetic

Usually asymptomatic until end organ damage apparent

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44
Q

Secondary HTN

A

Caused by some other dx

-sleep apnea, thyroid, meds, illicit drugs

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45
Q

BP is dependent on:

A
  • Cardiac output
  • Peripheral vascular resistance
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46
Q

JNC 8

All age CKD w/ or w/o DM

A

BP goal < 140/90

All races:

First line: ACEI/ARB

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47
Q

JNC 8

All ages w/ DM w/o CKD

Age < 60yr

A

BP goal <140/90

Black: First line - Diuretic +/- CCB

Non-black: First line - Diuretic +/- ACEI/ARB/CCB

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48
Q

JNC 8

Age > 60yr

A

BP goal < 150/90

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49
Q

Pre-HTN

A

130-139/80-89

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50
Q

Symptoms of end organ damage

A

CHF

Cardiovascular disease

Cerebrovascular disease

Uremia

Microalbuminemia

Aortic dissection

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51
Q

Drugs that cause/worsen HTN

A

Oral contraceptives

Anabolic steroids

NSAIDS

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52
Q

Valves closed during ventricular diastole

A

Semi-lunar valves

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53
Q

Valves closed during ventricular systole

A

A-V valves

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54
Q

“Lubb” sound

A

S1

Created by mitral valve moving into LA w/ ventricular contraction and chordea tensing

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55
Q

“Dupp” sound

A

S2

When blood in the arteries flow back and depress the SL valves

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56
Q

S2 split

A

Occurs upon inspiration

A2 is usually louder and longer than P2 (higher pressure)

w/ inspiration, RA pressure increases -> increases RV ejection time -> P2 lasts longer

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57
Q

High frequency heart sounds and stethescope use

A

S1

S2 (plus split)

aortic regurgitation - hardest to hear

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58
Q

Low frequency heart sounds and stethescope use

A

S3

S4

Mitral diastolic murmur

Best to hear S3 and S4 @ the apex in left lateral position

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59
Q

S3

A

Normal in kids

Rapid filling of the ventricles - compliant in kids, dilated in elderly w/ AV valve distention - valve distention makes the sound

1,3,2

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60
Q

S4

A

Abnormal in all

Atrial contraction in the presence of a non-compliant ventricle

4,1,2

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61
Q

Acyanotic CHD

A

“pink babies”

Left to right cardiac shunt

Atrial septal defect (ASD)

Ventricular septal defect (VSD)

Patent Ductus Arteriosus (PDA)

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62
Q

Cyanotic CHD

A

“blue babies”

Right to left cardiac shunts

Tetralogy of Fallot

Transposition of the Great Arteries

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63
Q

Obstructive CHD

A

Narrowing structures

Right side: Pulmonic valve stenosis (PVS)

Left side: Coarctation of the Aorta

-Congenital aortic stenosis (AS)

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64
Q

Umbilical cord makeup

A

2 arteries (away from heart)

1 vein (towards heart)

Here, the arteries carry unoxygenated blood to mom while vein takes oxygenated blood to baby

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65
Q

Prostaglandin inhibitors

A

Ibuprofen

NSAIDS

If taken during pregnancy, may interfere w/ fetal circulation (ibuprofen is Class D in 3rd trimester)

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66
Q

Atrial septal defect

A

Ostium primum @ bottom atrias most common

Widely split and fixed S2 over P w/ a systolic ejection murmur and RV heave felt @ lower left sternal border

Dx: TTE

Tx: surgical percutaneous repair @ 1-3 yrs

Can be earlier in kids w/ CHF

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67
Q

Ventricular septal defect

A

Most common CHD, usually membranous

If small, the child may lack sx and require no intervention - may have a harsh holosystolic murmur

If large, child will present w/ CHF in 1-6 mo, failure to thrive (cant breathe to eat)

Dx: CXR, EKG, TTE

Tx: ACEI, Diuretic, trans-catheter close

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68
Q

Patent Ductus Arteriousus

A

Common in preterm - give Inodmethacin to close

Overloads lungs, causes pulmonary HTN and L side failure

Usually asx w/ continuous rough machinery murmur @ L sternal border

Dx: TTE

Tx: Indomethacin, cardiac catheter, or surgical ligation to close

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69
Q

Teratology of Fallot components

A
  1. VSD ( ventricular septal defect)
  2. Pulmonary artery obstruction/stenosis
  3. Overriding aorta
  4. RVH (right ventricular hypertrophy)
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70
Q

Teratology of Fallot presentation

A

May not come out blue, happens when PDA closes

Cyanotic, fatigue/dyspnea on exertion, harsh systolic ejection murmur

Tet spell - crying/pooping => increased systolic pressure => no blood flow => turn blue/limp, pass out

71
Q

Teratology of Fallot diagnosis and treatment

A

Boot-shaped heart on CXR, TTE and Echo to confirm

Tx: prostaglandins to open PDA, Temporary Blalock-Taussig shunt between L subclavian and pulm-artery

Total surgical repair

72
Q

Transposition of the Great Arteries

A

Babies COME OUT BLUE unless w/ other CHD defects

-issues once the foramen ovale closes

Dx: Egg on a string CXR, TTE for confirmation

Tx: prostaglandins/Rashkind balloon to open foramen ovale

Arterial switch surgery @ 4-7 days post-birth

73
Q

Pulmonic valve stenosis

A

Prevent blood flow to lungs

Asx to cyanotic @ birth, rough ejection systolic murmur and click

Can get RV failure

Dx: echo, cath

Tx: balloon valvuloplasty or surgical repair

74
Q

Coarctation of the Aorta

A

Narrowing @ juxtaductal aorta, associated w/ Turner’s syndrome

presents @ 4-10 days old, bounding upper limb pulses w/ absent femoral pulse and blowing systolic murmur

Dx: CXR (rib notches), echo

Tx: Prostaglandins, balloon angioplasty, surgical repair

75
Q

Congenital aortic stenosis

A

asx until severe, can make it to 3rd-5th decade before heart failure

Dx: CXR, EKG, echo

Tx: cardiac cath, Ross procedure

76
Q

Cardiac biomarkers

A

AKA cardiac enzymes

Troponin

CK-MB

Myoglobin

77
Q

Lab tests for CV risk assessment

A

hs-CRP

homocystine

78
Q

What makes a cardiac biomarker unnescessary?

A

Pt w/ ischemic chest pain and ST elevation => MI

79
Q

Troponin

A

Highly specific, fairly reliable - used for Dx of MI

Rises in 2-6 hours, peask @ 12-16 hours, remains elevated for 10 days - 2 wks

Measure @ presentation, repeat @ 3-6 hours, may repeat after 6 hrs if initially normal, EKG changes, or high-risk pt

80
Q

Creatine Kinase (CK)

A

CK-MB may help support Troponin - MI Dx

Rises @ 4-6 hrs, peaks @ 24 hrs, normalized in 48-72 hrs

Less reliable than troponin

81
Q

Myoglobin

A

Found in skeletal and cardiac muscle, not cardioselective

rises @ 2-4 hrs, peaks @ 6-12 hrs, normalizes in 24-36 hrs

82
Q

hs-CRP

A

Stronger predictor of heart disease and stroke than LDL

Use for primary/secondary prevention, not acutely

May help motivate pt to lower risk factors

83
Q

Homocystine

A

Byproduct of meat protein

Does not change treatment

May be linked to CVD if B supplements don’t improve outcomes

84
Q

Brain naturetic peptide (BNP)

A

Produced by heart in response to myocardial stretch

Triggers Na+/water excretion

May help differentiate CHF from lung disease

85
Q

Suspected arrhythmias workup

A

Holter monitor

Event monitor

Electrophysiology Studies (EPS)

Good for syncope, A-fib, palpitations, dizziness, bradycardia

86
Q

Interventions for arrhythmias/systolic heart failure

A

Pacemaker

Defibrillator

Advanced heart failure therapy:

  • Bi-ventricular pacing
  • LVAD
87
Q

Pacemaker

A

Only treatment for bradyarrhythmias

provide electrical stimuli to cause cardiace contraction when intrinsic activity is slow/absent

88
Q

Types of pacemakers

A

External/Transcutaneous

Permenent

Biventricular

ICD

89
Q

External pacemaker

A

Used in emergencies - short term until permenant therapy applied

Pacing pads on front and back of pts chest

Recommended for stabilization of heodynamically significant bradycardia

90
Q

Single lead or Dual chamber pacemaker indications

A

Single lead paces in ventricle

-for a BBB, or backup pacemaker

Dual chamber can pace in atrium or ventricle

-typical type, AV node must be intact

91
Q

Pacemaker indications

A

Sick sinus syndrome

3rd degree block

Prolonged QT syndrome

A-fib w/ slow ventricular response

92
Q

Pacemaker rate

A

Pacemaker checks seconds between beats, not bpm

May have recording of HR slower than 60, but unless pt is having sx, they are fine

93
Q

Single chamber pacemaker EKG

A

No P wave

Wide QRS that is really just a QS

Can’t assess ST abnormalities w/ a pacemaker or BBB

94
Q

Pacemaker syndrome

A

Pt feels worse or CHF symptoms worse

Loss of atrioventricular synchrony causes this

95
Q

Biventricular pacing

A

Adds a 3rd lead to Left ventricle

Reserved for advanced heart failure

Get synchronized ventricular pumping to increase EF

96
Q

ICD Therapy

A

Pacing, cardioversion, and defibrillation abilities

Used w/ previous MI, cardiomyopathy

Used to prevent sudden cardiac death

97
Q

LVAD

A

Left ventricular assist device

For severe systolic heart failure, bridge/pallative alternative to transplant

98
Q

Balloon Angioplasty

A

Balloon infalted to compress plaque

Very high restenosis rate

99
Q

Angioplasty/Stent placement Post OP

A

ASA for life

P2Y12 inhibitor w/ stent placement for at least 12 months

100
Q

CABG

A

Coronary artery bypass graft

Reserved for multicoronary vessel disease

Arteries have the highest success rate

Post-op A-fib is common - myocardium is irritated and inflamed

101
Q

Contraindications to stress testing

A

Acute MI

Unstable angina

Acute pericarditis

Acute systemic illness

Severe aortic stenosis

CHF exacerbation

Severe HTN

Uncontrolled arrhythmias

102
Q

Exercise EKG positive test criteria

A

Can only rule in/out ischemia

Horizontal/downsloping 1 mm ST depression 0.08 s after J point in 3 continuous leads

103
Q

Exercise EKG immediately admit if:

A

BP drops as exercise increase

>2mm ST depression

Downsloping ST depression

ST depression or sx < 6min into test or HR <70% predicted

ST depression doesnt not resolve quickly in recovery

104
Q

Stress imaging indications

A

Abnormal Resting EKG

Confirm exercise EKG results

Localize region of ischemia

Distinguish ischemia from MI

Assess revascularization post-stent

Evaluate prognosis

105
Q

Myocardial perfusion scintigraphy w/ SPECT

A

AKA radionuclide imaging/nuclear stress test

Measure myocardial uptake of radionuclide tracer to determine dead spots

Take nuclear images before and after stress (exercise or pharmacologic)

Look for wall motion abnormalities

106
Q

Stress Echocardiography

A

Evaluate Left ventricle for wall abnormalities

Only gives information about presence/absence of ishcemia

Good for CAD, not good for LBBB or previous wall motion abnormalities

107
Q

MUGA scan

A

Most precise way to measure ejection fraction

Multi-gated axquisition scan

Radionuclide tracers to image left ventrical wall motion and calculate ejection fraction

Use for cancer pts on cardiotoxic drugs

108
Q

Cardiac CT

A

Imaging blood flow through coronaries

Trying to avoid heart cath in no risk pts w/ abnormal stress test

-Have to cath if you find a lesion

EBCT - electron beam

correlates w/ stenosis likelihood - cannot determine degree

109
Q

What test if the pt has a LBB, pacemaker, or afib?

A

Nuclear scan, w/ either exercise or pharmacologic stress

110
Q

Test for pt w/ known LV wall abnormalities?

A

Stress echo w/ exercise/pharmacologic stress

111
Q

Stable angina

A

Predictable, pt knows their limitations

Fixed atherosclerotic plaque which can cause symptoms if pt increases workload and oxygen supply is reduced

Relieved by rest/nitrates

Long-standing >1-2 months

112
Q

Unstable angina

A

Plaque rupture w/ thrombus

Arterial dissection also occurs at site of rupture

MI is impending if it hasn’t already occurred

Chest pain @ rest

New onset/worsening angina w/ a change in pattern

113
Q

History of Angina must contain

A
  1. Precipitating and alleviating factors
  2. Characteristics of discomfort
  3. Location and radiation
  4. Duration - of this episode and all incidences
  5. Effects of nitro (if the pt has it prescribed)
114
Q

Typical angina criteria

A

Substernal pain

Provoked by stress or exertion

Relieved by rest or nitro

115
Q

Class 1 angina

A

Asymptomatic

116
Q

Class 2 angina

A

Mild exercise limitations

Symptoms w/ ordinary exertion

117
Q

Class 3

A

Moderate exercise limitations

Symptoms w/ minimal exertion

118
Q

Class 4

A

Severe activity limitation

Symptoms at rest

119
Q

Angina physical exam

A

Look for Levine’s sign

Diaphoresis

S4(decreased LV compliance)/S3 (decreased systolic function)

Mitral regurge systolic murmur

Paradoxically split S2 (LV is not working, occurs w/ expiration)

120
Q

Stable angina labs

A

Look for precipitating cause

  • CBC (check for anemia)
  • TSH
  • Check lipids and A1C
  • Update BMP
121
Q

Unstable angina labs

A

Troponin

CBC

TSH

Lipids/A1C

CMP

122
Q

Ischemia on EKG

A

New bundle branch block

T wave inversion/depression/flattening

ST depression/elevation

(new) Q waves

Changes from previous EKG?

123
Q

Chronic stable anigna cath indications

A

Worsening symptoms

Persistent limiting angina w/ maximal medication

Stress test indicates high risk

Hx aortic valve disease -> check to see if cause is valve disease or ischemia

124
Q

Chronic stable angina meds and treatment goal

A

Nitrates

BB

CCB

Na-channel blocker

Antiplatelet agents

GOAL: prevent chest pain

125
Q

Ranolazine

A

Specialist-only, last resort medication

Blocks sodium channel into myocyte during repolarization

->decreased ICF Na+ => decreased ventricular tension => decreased myocardial oxygen consumption

Lots of DI, Can cause QT prolongation

126
Q

Chronic angina pt other medications

A

ASA/P2Y12I

Statin - decrease chances of plaque rupture

127
Q

Coronary vasospasm/Prinzmetal’s angina/Variant angina

A

Chest pain that lacks usualy precipitating facors

ST elevation w/ episodes, cyclical pain pattern over months

Tx: CCB, long and short term nitrates to prevent

Avoid BB, they may provoke spasm (angiogram may as well)

128
Q

CABG grafts and ACS

A

Worry about 10 year mark of CABG - think that lesion is in vein graft, not in new coronary vessel

129
Q

Myocardial infarction definition

A

Elevated Troponin/CK-MB

+ (at least one)

  • ischemic symptoms
  • Ischemic EKG chances
  • new Q waves
  • Imaging shows new wall motion abnormality

if not an MI = unstable angina

130
Q

EKG criteria for NSTEMI

A

New horizontal or downsloping ST depression

> 0.5 mm in 2 contiguous leads

+/- T wave inversions

131
Q

EKG criteria for STEMI

A

ST elevation of > 1mm at J point in 2 contiguous leads

ST elevation >2mm (men) or > 1.5 mm (women) in V2, V3

132
Q

Distingush Unstable angina from STEMI/NSTEMI

A

Cardiac enzymes will be normal w/ UA

133
Q

Medical therapy for unstable angina and NSTEMI

A

To relieve pain and decrease myocardial O2 consumption:

  • Oxygen - only if they’re hypoxic (worse outcomes if not)
  • Nitro
  • Morphine
  • BB - CI if HOTN, bradycardia, or CHF exacerbation

Also add on antiplatelet and anticoagulation therapy

134
Q

NSTEMI antiplatet therapy

A

ASA 325 mg chewed

+ P2Y12 blocker*

*Check w/ cardiologist first*

135
Q

Unstable angina anticoagulation

A

Enoxaparin (Lovenox) - 1 mg/kg SQ q12hrs

136
Q

NSTEMI anticoagulation

A

Put them on Heparin (UFH)

Lovenox cause too much bleeding when combined w/ plavix

May also want to add GPIIB/IIIA inhibitor for high-risk

137
Q

Cocaine-associated MI

A

Managed similar to all other ACS except:

Give benzodiazepines early

Do no use BB - can cause further vasospasm

138
Q

STEMI Medical therapy

A

O2, nitro, morphine, BB

Antiplatelet therapy, anticoagulation

+ go straight for PCI or get fibrinolytic therapy

139
Q

STEMI Reperfusion therapy

A

1st line: PCI w/in 90-120 mins

2nd line: fibrinolytics IF

  • PCI not available w/in 90-120 mins
  • Symptoms have occured for <12 hrs
  • No contraindications
140
Q

STEMI anticoagulation therapy

A

A. Unfractionated heparin - undergoing PCI who got fibrinolysis

B. Bivalrudin + GPIIB/IIIA inhibitor

C. LMWH (lovenox) - small loading dose then SQ

-no antidote to lovenox, can’t take it back

141
Q

Absolute fibrinolytic contraindications

A

Any intracranial hemorrhage

Ischemic stroke w/in 3 months

Cerebral vascular malformation

Bleeding disorder/acting bleeding

Closed head injury/facial trauma in last 3 months

142
Q

Relative fibrinolytic contraindications

A

Severe uncontrolled HTN

Ischemic stroke > 3months ago

Dementia/any known intracranial dx

Traumatic/prolonged CPR

Pregnancy

Major surgery w/in 3 weeks

Internal bleeding/active peptic ulcer

143
Q

Systolic blood pressure

A

Force the blood exerts on the artery walls as the heart contracts to pump out blood

144
Q

Diastolic blood pressure

A

Force as the heart relaxes to allow blood frlow into the heart

145
Q

Mean arterial pressure

A

Determined by cardiac output, systemic resistance, and central venous pressure

MAP = (COxSVR) - CRP

146
Q

Arterial pulse pressure

A

Difference between systolic and diastolic readings during ejection

-indicator of vessel wall stiffness and inflammation

147
Q

Peripheral vascular resistance (PVR)

A

Defines the resistance to flow that must be overcome by the heart in order for blood to flow through the circulatory system

148
Q

Systemic vascular resistance (SVR)

A

Resistance offered by the peripheral circulation

149
Q

Arterial baroreceptors

A

Carotid sinus and aortic arch

-inhibit SNS w/ arterial wall stretching to regulate arterial pressure

150
Q

Arterial chemoreceptors

A

In the carotid bodies and aortic arch

Sense the O2, CO2, and H+ concentrations in blood

Communicate w/ vasomotor center to induce widespread vasoconstriction

151
Q

SNS neurotransmitter

A

Norepinephrine -> Adrenergic

Works on both alpha and beta adrenergic receptors

alpha = vasoconstriction

beta = vasodilation

152
Q

PNS neurotransmitter

A

Acetylcholine -> Cholinergic receptors

153
Q

Ischemic response

Cushings reflex

A

Ischemic = increased flow causes cerebral HTN

Cushings = peripheral vasocostriction w/ increased cardiac output causes cerebral edema

154
Q

Increases in PVR

A

May be caused by an increase in intracerllular calcium which causes structural arteriol changes => increased in resistance

This may explain why CCB work so well

155
Q

Aldosterone functions

A

Causes the kidney to retain salt and water and secrete potassium

156
Q

Angiotensin II functions

A

Induces widespread vasoconstriction

Induces aldosterone release from the kidney

Enhances SNS function w/ NE reuptake inhibition

Released vasopressin from pituitary - antidiuretic

Stimulates brain thirst center

157
Q

Renin

A

Released from Juxtaglomerular cells in afferent arteriole

158
Q

Macula densa cells

A

In distal tubules

Sense sodium and chloride ions in tubular fluids

Control renin release

159
Q

Natiuretic peptides

A

Also regulate RAAS

Peptides (ANP, BNP) released from heart in response to atrial distention

Vasodilate

Increase GFR for sodium and water excretion

POTASSIUM SPARING

160
Q

Nitric oxide

A

Vasodilator - affects smooth muscle

161
Q

Endothelin

A

Vasoconstrictor - activates renin, intracellular calcium release, to produce a sodium-sensitive rise in blood pressure

162
Q

Bradykinin

A

Vasodilator - released by ACEI

ACE inhibits bradykinin release

This is what causes the ACEI dry cough

163
Q

Isolated systolic hypertention

A

Elevated systolic pressure w/ normal diastolic

Pt is at danger for heart/stroke events

Often develop LVH

Due to elevated pulse pressure

164
Q

Renovascular HTN

A

Renal artery stenosis

Fibromuscular dysplasia

Most common

Tx w/ stents

AVOID ACEI

165
Q

Adrenal caused HTN

A

Hyperaldosteronism

Pheochromocytoma

166
Q

Primary Hyperaldosteronism

A

Benign adrenal gland secretes aldosterone -> pressure issues

Can be unilateral or bilateral

Renin is low w/ high serum aldosterone

Tx: Resect tumor, Spironolactone and diuretics if hyperplasia

167
Q

Spironolactone

A

Aldosterone antagonist

Treatment for Adrenal hyperplasia

168
Q

Pheochromocytoma

A

Over abundance of NE and epi in a episodic release pattern

Resect tumor w/ alpha and beta blockage pre-op in case of “spills”

Or Phenoxybenzamine (alpha blocker) if unresectable

24 UA for Dx - check for cetecholamines and meninephrines (byproducts)

169
Q

HTN labs

A

CMP - potassium, glucose, electrolyte levels

Fasting lipid

U/A

CBC - hematocrit

EKG

Echo

170
Q

Long-term HTN treatment goals

A

Controll CV risk factors

Reduce HTN-induced mortality

171
Q

Hypertensive crisis

A

Sudden increase in BP

Urgent and Emergency types

Usually occur in pts w/ existing/poorly controlled HTN

Also rebound HTN

172
Q

Hypertensive crisis staging

A

Fundoscopic exam

CMP (kidney function)

CBC

U/A

173
Q

Urgent Hypertensive crisis

A

No end-organ damage

Lower BP over 1-2 days w/:

Captopril/Amlodipene/Clonidine

174
Q

Emergent Hypertensive crisis

A

Organ damage is apparent/impending

Admit, lower BP carefully but efficiently - 10mmHg/6 hrs

Nitroprusside - low and slow

Nitroglycerin/Fenoldopam/Lebetalol/Hydralazine also work

Fedoldopam is good w/ renal failure

Cardiology (7 decks)

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