Heart Failure Flashcards

(77 cards)

1
Q

Mean Arterial Pressure

A

average pressure in the systemic circulation.

indicator of how much force needed to move blood around the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Intrathoracic Pressure & Venous return

A

Intrathoracic Pressure impedes venous return to the heart as it increases opposing pressure on veins and can occlude vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Systolic blood pressure

A

arterial blood pressure during ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diastolic blood pressure

A

arterial blood pressure during ventricular relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cardiac output

A

total volume of blood ejected from the left ventricle per minute

determined by: stroke volume x heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Stroke Volume

A

total volume of blood ejected from left ventricle per contraction

determined by preload, afterload, and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Frank-Starling Mechanism

A

states that within limits, increased preload (stretch) increases contractility.

this is due to the optimal arrangement of sarcomeres when stretched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Preload

A

wall tension placed on the ventricular at the end of diastolic filling.

determined by central venous volume
increased preload = increased stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Contractility

A

force of contraction during systole.

increases stroke volume independent of preload/afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Afterload

A

force heart has to work against during systolic contraction.

determined by peripheral vascular resistance and ventricular wall tension.
increased afterload = decreased stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

End Systolic Volume

A

blood volume remaining in ventricles after systole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

End Diastolic Volume

A

blood volume in ventricles at the end of diastolic filling.

end systolic volume + diastolic filling
determines preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Heart rate and Preload

A

Increased heart rate decreases amount of diastolic relaxation between contractions

Reduced end diastolic volume causes reduced preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Wall Tension & Wall Thickness

A

wall tension = opposing force of the wall of a blood vessel
wall thickness = diameter of the vessel wall

there is an inverse relationship between wall tension & wall thickness.
increased thickness = decreased tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Determinants of muscle contraction

A

Calcium
ATP
Oxygen
Na+/K+ pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Electrical Conduction System

A

SA Node –> AV Node (delayed) –> AV Bundle (delayed) –> Purkinje Fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Atrial Kick

A

during atrial contraction, the atria eject the remaining bit of blood from atrial chambers –> ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cardiac performance

A

affected by work demand of heart and ability of coronary perfusion to meet metabolic demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inotropy Factors

A

factors that alter muscle contraction

can be positive (promote contraction) or negative (inhibit contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Vasoconstrictors

A

Angiotensin II
Catecholamines (mainly norepinephrine)
ADH
Prostaglandins - released by arachidonic pathway
Serotonin - released by clotting platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vasodilators

A
Nitric Oxide - released by endothelial cells
Natriuretic Peptides 
Histamine - mast cells + basophils
Bradykinin
Ace-i
ARB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Common Causes of Heart Failure

A
Coronary Artery Disease
Hypertension
Myocardial Infarction
Dilated Cardiomyopathy
Valvular Heart Disease
Pulmonary disorders (Right-sided HF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ejection Fraction

A

percentage of blood ejected from the heart during systole

calculated by stroke volume / end diastolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Heart Failure EF

A

equal to or under 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Heart Failure Definition
functional or structural impairment of the heart causing inadequate cardiac output to meet metabolic demand caused by heart not pumping properly or filling properly
26
HF Compensatory Mechanisms
``` Frank-Starling Law --> increased preload SNS activation RAAS activation Natriuretic peptides Myocardial remodeling ```
27
Pathology of Ventricular Hypertrophy
initially is effective as a compensatory mechanism. concentric hypertrophy over time decreases contractility due to arrangement of sarcomeres + reduces ventricular lumen increased wall thickness = decreased wall tension therefore reducing contractility and increases metabolic demand of heart
28
Angiotensin II functions
``` vasoconstrictor stimulates adrenal medulla to rls aldosterone stimulates PPG to rls ADH stimulates rls of norepinephrine increase thirst response ```
29
Aldosterone functions
Increase sodium reabsorption --> increase water retention Increase potassium excretion stimulate fibroblast activity in myocardium
30
Antidiuretic Hormone functions
aka vasopressin increases water reabsorption vasoconstrictor
31
Natriuretic Peptides
ANP --> rls by atrial cells BNP --> rls by ventricular cells. biomarker for heart failure released in response to stretch promote excretion of sodium and water vasodilator
32
Types of Heart Failure
``` Right-side vs. Left-side Diastolic vs. Systolic Reduced Ejection Fraction vs. Preserved Ejection Fraction Acute vs. Chronic Biventricular ```
33
S/S of Left Sided HF
``` Wet cough Reduced ejection fraction Hemoptysis SOB Dizziness, light-headedness Fatigue - gets worse throughout day Hypoxemia --> hypoxic tissue injury Orthopnea Proxysmal Nocturnal Dyspnea Inspiratory crackles ```
34
S/S of Right Sided HF
``` Distended Jugular Vein Peripheral edema Upper abdominal pain Hepatomegaly, splenomegaly Reduced appetite Nocturia ```
35
Normal BNP levels
<100 pg/Ml
36
Normal EF
>50%
37
Pleural Effusion
fluid build in in the pleural cavity
38
Calcium Efflux mechanisms
1) Active calcium pump (req ATP) | 2) Sodium-calcium exchanger
39
Medication classes used for heart failure
Diuretics Ace-i Angiotensin II Receptor Blockers (ARB) Cardiac Glycosides
40
Spironolactone
potassium sparing diuretic onset: unknown peak: 2-3 days duration: 2-3 days
41
Spironolactone mechanism
competitive antagonist blocks aldosterone receptors on the distal convoluted tubule prevents reabsorption of sodium while saving potassium and hydrogen ions
42
Captopril
``` ace inhibitor side fx: chronic dry cough onset: 15-60 min peak: 60-90 min duration: 6-12 hours ```
43
Captopril mechanism
antagonist? inhibits ACE-i activity thereby preventing the conversion of angiotensin I to angiotensin II promotes vasodilation, decreased sodium reabsorption, decreased release of aldosterone
44
Angiotensin II effects
major vasoconstrictor -> increases blood pressure promotes release of ADH from PGH promotes release of aldosterone from adrenal medulla increase sodium reabsorption in the kidneys increases thirst sensation decreases baroreceptor sensitivity
45
Losartan
``` angiotensin II receptor blocker used when ACE-i are contraindicated onset: 6 hours peak: 3-4 weeks duration: 24 hours ```
46
Losartan Mechanism
prevents angiotensin II from binding to receptors on smooth muscle --> promotes vasodilation lowers blood pressure
47
Bisoprolol
selective beta-1 blocker onset: 1-4 hours peak: 2-4 hours duration: 24 hours
48
Andrenergic receptors
cell membrane receptors that bind with catecholamines
49
Beta-1 Receptor Locations
heart kidneys fat cells
50
Bisoprolol Mechanism
prevents epinephrine from binding with beta-1 receptors on the myocardium reduces contractility, decreases heart rate, promote diastolic filling, reduce O2 demand reduces cardiac output (decrease work of heart) decreases renin production by juxtaglomerular cells
51
Digoxin
``` cardiac glycoside requires a loading dose onset: 50min-2 hours peak: 2-6 hours duration: 2-4 days ```
52
Digoxin mechanism
beta-1 agonist inhibits the sodium-potassium pump, increasing sodium --> increasing intracellular calcium promotes increased contractility --> increased cardiac output increases refractory period at sa/av nodes --> decreased heart rate
53
Inotropy
agent that affects the force of muscular contractions. can be positive or negative positive = increase contraction negative = decrease contraction
54
Positive inotropic agents
Digoxin | Calcium
55
BNP
``` brain natriuretic peptide released from ventricular cells in response to overstretching biomarker of heart failure <100 = normal >400 = heart failure likely ```
56
Normal hemoglobin levels for women
117-155 g/L
57
Normal hemoglobin levels in men
140-173 g/L
58
Heart Failure Treatment
``` fluid restrictions (1.5 L/day) daily weigh-ins restrict salt restrict fatty food exercise with rest periods medication tertiary prevention ```
59
Recommended Salt for HF Patients
2000 mg/day
60
Recommended activity levels
30 min of moderate activity daily
61
Acute cardiac symptoms
chest pain shortness of breath dizziness/light-headedness
62
HF Weight guidelines
no more than 4 lbs in 2 days or 5 lbs in 1 week
63
Aim of Heart Failure Medication Treatment
Increase preload Increase contractility Decrease remodeling Decrease afterload
64
Which kidney cell produces renin
juxtaglomerular cells
65
First Line HF treatment
``` vasodilators (ACE-i, BNP, ARB) diuretics b-1 antagonists diuretics HCN blockers ```
66
Second Line HF treatment
``` Cardiotonic agents (digoxin) positive inotropic agents ```
67
Calcium efflux
sodium-calcium exchanger (3 Na+ for 1 Ca++) exchange depends on voltage of plasma membrane positive = more calcium ENTERS cell negative = more calcium EXITS cell
68
Proxysmal nocturnal dyspnea
SOB that occurs during sleeping due to fluid accumulation in lungs --> wakes up the patient
69
HF Diagnostics
``` Blood tests - check for BNP levels Chest Xray - look at heart size ECG Exercise stress test Angiogram Echo - measures EF ```
70
5 Areas of HF
``` Coronary (Perfusion) Valvular Percardium Myocardium Electrical ```
71
Types of cyanosis
Central | Peripheral
72
Central cyanosis
caused by hypoxemia | decreased O2 in arterial blood
73
Peripheral cyanosis
caused by tissue consumption of O2 | reduced cardiac output, vasoconstriction
74
Types of cardiomyopathies
dilated hypertrophy restrictive
75
Dilated cardiomyopathy
all four heart chambers dilate impacts systolic and diastolic function ventricle walls thin --> decreased contractility diluted lumen --> excessive preload
76
Hypertrophic cardiomyopathy
concentric hypertrophy --> narrows lumen impairs contractility due to overcrowding of sarcomeres decreases diastolic filling due to narrow ventricular lumen
77
Restrictive cardiomyopathy
fluid in pericardium/fibrosis decreases cardiac compliance | impairs diastolic filling