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Tests various > 👩🏾‍🎓- Cardiac & Shock Test > Flashcards

👩🏾‍🎓- Cardiac & Shock Test Flashcards

1
Q

Arrhythmias can be affected by

A 
Disease states 
CAD and ACS 
Electrolyte imbalance 
Hypoxia 
Drugs/medications 
Trauma
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2
Q

Normal sinus rhythm

A

Rate: 60-100 bpm

Origin: SA node

Rhythm: P-P interval regular, R-R interval regular
P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike

PR Interval: 0.12-0.20 sec and constant from beat to beat

QRS Complex: 0.10 sec or less unless an intraventricular conduction delay

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3
Q

Sinus arrhythmia

A

Rate: Usually 60-100 bpm, but may be slower or faster

Origin: SA Node

Rhythm: Irregular, phasic with respiration; heart rate increases gradually during inspiration and decrease with expiration

P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike

PR Interval: 0.12-0.20 sec and constant from beat to beat

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4
Q

Sinus tachycardia

Origin, rate, pwave, Cause, symptoms, treatment

A

Origin: SA node

Rate: greater than 100bpm (in adults)

P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike. At very fast rates, differentiating a P wave from a T wave may be difficult.

Cause: activity, SNS stimulation, stress, pain, fever, anemia, hypoxia, hypotension, drugs, ACS, decreased CO, hypovolemia

Symptoms: likely asymptomatic, may experience palpitations, chest pain, fatigue, weakness, SOB, hypotension, anxiety

Treatment: determine and treat underlying cause

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5
Q

Sinus bradycardia

Origin, rate, pwave, Causes, symptoms, treatment

A

Origin: SA node

Rate: less than 60bpm/regular rhythm

P Waves: Positive (upright) in lead II, one precedes each QRS complex, P waves look alike

Cause: well conditioned athletes, vagal stimulation (vomiting/straining), ACS, heart block, hypoxemia, drugs

Symptoms: possibly asymptomatic, may experience syncope, dizziness, confusion, weakness, hypotension, diaphoresis, SOB, CP

Treatment: determine and treat underlying cause! May include atropine or external pacing

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6
Q

Premature atrial contractions PAC’s

Origin, rate, pwave, cause, symptoms, treatment

A

Origin: anywhere in the atria ; often seen with NSR

Rate: variable/irregular rhythm

P Waves: Premature (occurring earlier than the next expected sinus P wave), positive (upright) in lead II, one before each QRS complex, often differ in shape from sinus P waves; may be flattened, notched, pointed, biphasic, or lost in the preceding T wave

Causes: irritation to the atria including stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol or drugs; electrolyte imbalance, damage to cardiac muscle

Symptoms: usually asymptomatic; May feel palpitations

Treatment: usually treatment of the PAC is not necessary, treatment for underlying disorder is considered

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7
Q

Supraventricular tachycardia SVT

Origin, rate, pwave, cause, symptoms, treatment

A

Origin: anywhere in the atria

Rate: 140+ bpm/regular rhythm

P Wave: One positive (upright) P wave precedes each QRS complex in lead II; P waves differ in shape from sinus P waves; an isoelectric baseline is usually present between P waves.

Causes: irritation to the atria including stress, fatigue, anxiety, caffeine, nicotine, etc

Symptoms: may feel palpitations and anxiety, if prolonged may deteriorate into angina, decreased CO, shock

Treatment: may not be necessary unless SVT is sustained. Vagal maneuver may stop rhythm. If necessary antidysrhythmics to slow conduction or cardioversion

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8
Q

Risks factors for afib & aflutter

A

Risk factors- htn, dm, hf, ACS, pe, age, male, valve disease, alcohol abuse, cardiac surgery

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9
Q

Two important things to note about afib & aflutter

A

HR must be controlled or CO will rapidly decrease

Patient at very high risk for cardioembolic event - must be on anticoagulant

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10
Q

Afib & aflutter

Origin, rate, causes, symptoms, treatment

A

Origin: anywhere or everywhere in the atria

Rate: variable, if elevated must be controlled

Causes: age + risk factors

Symptoms: asymptomatic when rate is controlled; if rate is uncontrolled symptoms of HF rapidly develop

Treatment: antidysrhythmics to control rate or convert to NSR; anticoagulants to prevent thrombus formation; cardioversion if no thrombus seen; ablation; pacemaker placement; MAZE procedure

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11
Q

Symptoms of HF

A 
Fatigue 
Dizziness 
Activity intolerance 
Anxiety
Palpitations 
Hypotension
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12
Q

Junctional dysthymias

Origin, rate, pwave, causes, symptoms, treatment

A

Origin: AV node or junctional area

Rate: 40-60bpm/regular rhythm

Pwave: absent; inverted of present; one P wave before each QRS complex if present

Causes: unknown, damaged electrical path

Treatment: usually none

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13
Q

Premature ventricular contractions PVC

Origin, rate, pwave, cause, symptoms, treatment

A

Origin: ventricle, one or various sites

Rate: variable/irregular rhythm

P Wave: Usually absent or, with retrograde conduction to the atria, may appear after the QRS (usually upright in the ST segment or T wave)

Causes: aging, irritation of ventricles, ACS, HF, hypoxemia, electrolyte imbalance, stress, nicotine, caffeine, alcohol, infection , drugs

Symptoms: may be asymptomatic, palpitations, diminished pulses with “run” of PVCs

Treatment: none if infrequent or no history of CV disease

monitor this may be a warning sign for further V-Tach

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14
Q

Idioventricular Rhythm

Origin, rate, pwave, cause, symptoms, treatment

(Agonal heartbeats)

A

Origin: ventricles

Rate: less than 40bpm

P Waves: usually absent or, with retrograde conduction to the atria, may appear after the QRS (usually upright in the ST segment or T wave)

Causes: hypovolemia, hypoxia, acidosis, potassium disturbances, overdose, hypothermia, tension pneumothorax, PE, ACS, tamponade

Symptoms: unstable and likely in shock, hypotensive, diaphoretic, unresponsive

Treatment: PREARE FOR CPR THIS IS A DYING ❤️

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15
Q

Ventricular tachycardia

Origin, rate, pwave, cause, symptoms, treatment

A

Origin: ventricle, one site

Rate: >40bpm

Pwave: absent

Causes: ACS, cardiomyopathy, potassium imbalance, hypoxia, HF, drug overdose, shock

Symptoms: maybe asymptomatic or experience palpitations initially, anxiety, chest pain, unresponsive

Treatment: THIS IS A LETHAL RHYTHM
Stable vs unstable

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16
Q

Treatment for ventricle tachycardia

Stable vs unstable

A

Stable: O2, vagal maneuver, antidysrhythmics

Unstable: COR, ACLS protocol including defibrillation & antidysrhythmics

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17
Q

Pulseless electrical activity PEA

origin, rate, pwave, cause, symptoms, treatment

A

Origin: anywhere

Rate: variable; seen on monitor only- looks like sinus rhythm but NO PULSE IS PALPABLE

Pwave: present and uniform, one pwave before each QRS complex

Cause; hypovolemia, hypoxia, acidosis, potassium disturbances, overdose, hypothermia, tension pneumothorax, PE, ACS, tamponade

Symptoms: unresponsive

Treatment: INITIATE CPR

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18
Q

Ventricular asystole

Origin, rate, pwave, cause, symptoms, treatment

A

Origin: none

Rate: 0/UTD

Pwave: absent

Causes: ACS, cardiomyopathy, potassium imbalance, HF, drug overdose, shock

Symptoms: unresponsive, pulseless, apneic, no BP

Treatment: THIS PATIENT IS IN FULL ARREST
(CPR, acls protocol, epinephrine, atropine, airway management, transcutaneous pacing, resolution of cause of known)

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19
Q

First degree AV block

A

Impulses from SA are slow to conduct to AV

Monitor for bradycardia or progressive block

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20
Q

Second degree heart block type I (wenckebach)

A

PR interval: longer longer longer drop that’s the way you wenkebach

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21
Q

Normal lab values

A

RAP or CVP: 2-8

PAS: 20-30

PAD: 8-15

PAOP: 8-12

CO: 4-8

Cardiac Index: 2.5-5

SVR: 800-1200

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22
Q

How often should shock patients receive vital signs

A

Q 15mins VS until stable and cardiac/tele monitoring

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23
Q

Commonalities in shock

A

Hypoperfusion

Hypercoagulability

Activation of inflammatory response (SIRS)

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24
Q

Body generally uses about what percent of circulating oxygen off of hemoglobin

A

25%

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25
Q

What does anaerobic metabolism cause

A

An increase in lactate lactic acidosis

Normal range: 0-1.5

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26
Q

What are some things that increase cellular oxygen demand

A

Decrease hemoglobin
Decrease O2 in body
Decreased volume
Pump problems

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27
Q

Motivation

A

This is your LAST lecture test of your associates level nursing career. You have come to far to punk out now ! Study this material like your life depends on it, cuz well IT DOES ! With GOD by your side you can and will do this !

-amen

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28
Q

SIRS

symptoms

A

Systemic inflammatory response syndrome

Overwhelming infection

Symptoms- vasodilation, increased capillary permeability, microvascular clotting

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29
Q

SIRS criteria

A

2 or more of the following:

WBC > 12000 or < 4000 or 10% bands

Tachycardia

Temperature > 100.4 or < 96.8

Tachypnea

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30
Q

List the 4 classifications of shock

A

Initial

Compensatory (neural, endocrine, chemical)

Progressive stage

Refractory stage

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31
Q

Initial stage

A

The initial stage of shock is marked by hypoxia due to decreased deliver (DO2) to the cells.

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32
Q

Progressive stage

A

The progressive stage is marked by the failure of compensatory mechanisms to maintain adequate blood pressure and circulating fluid volumes…losing the battle, needs life support/medical assistance or they will die-still reversible

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33
Q

Refractory stage

A

The refractory stage is marked by prolonged inadequate blood supply to the cells, resulting in cell death and multisystem organ failure…prepare patient and family for death

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34
Q

Causes of cardiogenic shock

A

Number 1 cause: acute myocardial infarction

Cardiomyopathy
CHF
Arrhythmia
Papillary muscle rupture

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35
Q

Clinical symptoms of cardiogenic shock

Neuro, respiratory, CV, GI, GU, skin

A

Neuro: Anxious, restless, eventually decreased LOC

Respiratory: Crackles, rales, increased O2 demand, decreased pulse ox, tachypnea

CV: Chest pain, delayed capillary refill, weak pulses, S3, S4, JVD

GI: Nausea, vomiting, decreased bowel sounds

GU: Decreased urine output

Skin: Pale, cold, clammy, mottled

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36
Q

Cardiogenic shock diagnostics

A

A good patient history

Cardiac Cath

Echocardiogram

Chest X-ray

Elevated myocardial tissue markers

Creatine Phosphokinase Myocardial bands (CPK-MB), Troponin

Brain natriuretic peptide (BNP)

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37
Q

Brain natriuretic peptide

A

Hormone released by the ventricles in response to increased blood volume and blood pressure

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38
Q

What is the gold standard of cardiogenic shock treatment

A

Balloon pump

Increase O2 supply, decrease O2 demand

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39
Q

Cardiogenic shock management

A

“Strengthen the pump”
Increase O2 supply decrease O2 demand
•Coronary intervention PCI/OHS- fix the problem
•Balloon pump –gold standard can be done before or after tx
•Impella just got FDA approval

  • Dobutamine, Primacor + inotropes decrease afterload however they increase oxygen demand can cause VT is some pts
  • IF BP can tolerate after load reducers, vasodilators (ACEI)
  • Careful with vasopressors, they increase SVR!
  • Diuretics usually, if fluids its cautiously and small boluses i.e. 250 over an hour (diuretics decrease preload)
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40
Q

Cardiogenic shock

HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment

A

HR ⬆️

BP ⬇️

Skin: cold

SVR ⬆️

CVP ⬆️

PAWP ⬆️

LOC ⬇️

Treatment: O2 100% nonrebreather, prepare for intubation, fluids uses cautiously, drugs (dopamine, norepinephrine, dobutamine, diuretics) morphine sulphate, rest

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41
Q

Obstructive shock

Epidemiology, Pathophysiology

A

Epidemiology - extra cardiac disorders such as cardiac tamponade, tension pneumothorax, saddle pe

Pathophysiology- there is a physical barrier obstructing the great vessels or heart itself. Barrier to ventricular filling or emptying. Heart can’t pump effectively

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42
Q

Saddle pe

Diagnostic, s&s, treatment

A

Diagnostic- RV strain on echo, CT angio, VQ scan, +ddimer, abg low pao2 and low paco2

S&s- pleurtic chest pain (worse on inspiration) dry cough, possible cough up blood, anxiety, apprehension

Treatment- thrombolytics, embolectomy

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43
Q

Cardiac tamponade

Diagnostic , s&s, treatment

A

Excessive air, fluid or blood collecting in the pericardial sac

Diagnostic- echocardiogram, X-ray

S&s- tachypnea, tachycardia, dyspnea, Low urine output, confusion, cold, clammy extremities, pulsus paradoxus

Beck’s triad

Treatment- fluid and inotropes while waiting for definitive treatment, pericardialcentesis

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44
Q

Becks triad

A

Associated with cardiac tamponade 3 signs include:

Low arterial blood pressure, JVD, distant muffled heart sounds

(Muffled due to ⬆️ fluid)

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45
Q

Pulsus paradoxus

A

an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration.

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46
Q

Tension pneumothorax

Diagnostic, s&s, treatment

A

Accumulation of air or blood in the pleural space

Diagnostics- CXR

S&s- sudden onset cp, chest tightness, SOB, tachycardia, tachypnea, cough, desaturation, severe dyspnea, JVD, narrowing pulse pressure, absent or diminished breath sounds, tracheal deviation toward unaffected side

Treatment- needle decompression, chest tube

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47
Q

Obstructive shock

Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment

A

HR ⬆️

BP ⬇️

Skin cold

SVR ⬆️

CVP ⬆️

PAWP ⬆️

Loc

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48
Q

Causes of hypovolemia

Hemorrhagic vs hypovolemic

A

Hemorrhagic- trauma, ruptured AAA/surgical, GI bleed, ectopic pregnancy

Hypovolemic- GI loss, burns, dehydration-poor intake, over use diuretics, third spacing, sirs (pancreatitis) DJA, hhnk, hhs

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49
Q

Hypovolemic shock diagnostics

A

Serum lactate

ABG (pH, base deficit)-fluid resuscitation

Metabolic studies (Chem 7, CMP)

CBC

H/H watch out for hemoconcentration

Coags (PT, PTT, INR)

May need CT angio, nuclear med, endo IR - stop bleeding

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50
Q

Lactate Acid

Draw, range

A

Lactic acid is used to test for sepsis

Draw- no turnicate because will ⬆️ anaerobic metabolism, put on ice

Range-
> 4 = death

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51
Q

Compensatory stage

Neural, endocrine, chemical

A

Body initiated compensatory mechanisms in an effort to maintain adequate volume, CO and blood flow to the tissues

Neural compensation- characterized by the detection of hypotension by barorecptors in the carotid sinus and aortic arch that results in the stimulation of the sympathetic nervous system and the release of catecholamines epinephrine and norepinephrine from the adrenal medulla

Endocrine compensation- or hormonal mechanisms that exert control over BP, include: angiotensin II, epinephrine and norepinephrine, aldosterone, and adh. Angiotensin II creates in response to ⬇️ BP is an end product of series of events

Chemical compensation- is produced through the reaction of chemoreceptors in the aorta and carotid arteries that are stimulated by low oxygen levels

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52
Q

Hypovolemic shock assessment

Neuro, respiratory, skin, cv, Gu

A

Neuro- ams, lethargy, unresponsive

Respiratory- rapid and deep respirations may become deep and labored as they deteriorate

Skin- cool, clammy

CV- pulse weak, threats, tachycardia then hypotension

GU- decreased urine output, urine is dark and concentrated

If invasive hemodynamic monitoring ⬇️ CVP, PCWP, CO and ⬆️ SVR

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53
Q

Hypovolemic shock if bleeding

A

Stop the bleeding

If bleeding nothing replaces blood (over treatment with NS/LR May make acidosis and coagulopathy worse)

Correct coagulopathy

Warm the patient

Monitor trends should be improving

Watch out for banked blood- potassium, 2,3 dpg, hypothermia, transfusion reactions

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54
Q

Hypovolemic shock medications- non bleeding patient

A

Volume resuscitation NS or LR

Colloids use in caution- SIRS

Add vsopressors only after fluid resuscitation initiated (don’t squeeze an empty tank)

Beware of dopamine , may ⬆️ HR

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55
Q

Hypovolemic shock

Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment

A

Hr ⬆️

BP ⬇️

Skin- cold

SVR ⬆️

CVP ⬇️ due to dehydration

PAWP ⬇️

Loc ⬇️

UOP ⬇️

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56
Q

Distributive shock

A

Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone-fluid in the wrong space

Caused by loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, capillary leak

Blood volume distributed to interstitial tissues where it can’t circulate, deliver oxygen

Anaphylaxis, neurogenic, septic

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57
Q

Anaphylactic shock

Manifestations, management

A

Allergic reaction causing a release of histamine- resulting in widespread venous dilation, increased capillary permeability, and smooth muscle contraction

Vasodilation, ⬇️ venous return

Manifestations- early uticarial, redness. Airway compromise include sob, tachypnea, angioedema, wheezing, stridor, cyanosis and confusion due to hypoxia, hypotension

Management- treatment priorities include immediately removing the trigger, emergency airway management, antihistamines (benadryl), h2 blockers (Pepcid, zantac) corticosteroids, epinephrine SC (not IV) NS bolus if hypotension develops

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58
Q

Epinephrine administration in anaphylactic shock

A

.3 - .5 SQ/IM

No IV can redo shot in 5-10min if no improvement

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59
Q

Neurogenic shock

Epidemiology, pathophysiology, manifestations, treatment

A

Epidemiology- disruption of the sympathetic nervous system , spinal cord injury above T6

Pathophysiology- hypotension, bradycardia, hypothermia

Manifestations- skin is warm, dry and flushed due to systemic vasodilation. ⬇️ CO, CVP, PAOP, SVR

** different from other forms of shock **

Management- fluid administration, vasopressors, MAP 85-90 prevent secondary injury, watch for cord spread, temperature management, bowel and bladder protocols, may need airway/pacemaker assistance

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60
Q

Neurogenic

HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment

A

HR ⬇️

BP ⬇️

Skin- warm, flushed

SVR ⬇️

CVP ⬇️

PAWP ⬇️

Loc ⬇️

UOP ⬇️

Treatment- IV fluids cautiously, drugs (atropine, norepinephrine, thrombolytics) transcutaneous pacing, ⬆️ hob

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61
Q

Anaphylactic

HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment

A

HR ⬆️ with weak pulses

BP ⬇️

Skin- urticaria, angioedema, pale, cold

SVR ⬇️ due to systemic vasodilation

CVP ⬇️

PAWP ⬇️

Loc- sob, wheezing

UOP ⬇️

Treatment- remove trigger, O2 100% nonrebreather, IV fluids, drugs (epinephrine 0.3-0.5mg May repeat q 5-10mins, antihistamines, corticosteroids, bronchodilators)

62
Q

P wave

A

Atrial depolarization

Atrial systole

63
Q

QRS complex

A

Ventricle depolarization

Ventricle systole

64
Q

T wave

A

Ventricle repolarization

Ventricular diastole

65
Q

SIRS , sepsis , severe sepsis , septic shock

A

SIRS- temp > 38’c or <36’c, HR >90, RR >20 or PaCO2 < 32, wbc >1200 or <4000 or >10% bands

Sepsis- SIRS + infection

Severe sepsis- sepsis + end organ damage

Septic shock- severe sepsis + hypotension

66
Q

What percentage of patients meet diagnostic criteria for SIRS on admission to hospital

A

68%

67
Q

Severe sepsis

Criteria

A

Sepsis + organ dysfunction (one of the following criteria):

Lactate > 4
Oliguria < 0.5 ml/kg/hr
Thrombocytopenia < 100,000
Coagulopathy: INR > 1.5 
Creatinine > 2 
Bilirubin > 2
68
Q

Septic shock

A

Severe sepsis + hypotension despite adequate fluid resuscitation OR initial lactate of 4 or greater

69
Q

Treatment 3 hours of presentation with septic shock

A

Measure lactate level

Obtain 2 blood cultures from 2 different sites (prior to administrating antibiotics)

Administer broad-spectrum antibiotics

Administer 30 ml/kg of crystalloid if patient hypotensive or lactate level at least 4 mg/dL

70
Q

When would you and would not administer crystalloid at a rapid rate ?

A

Severe sepsis- optional

Hypotension, septic- required

Cardiogenic- no rapid

71
Q

Treatment within 6hrs of presentation with septic shock

A

Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure >65 mmHg

Persistent hypotension after initial fluid administration OR initial lactate was >4 reassess volume status and tissue perfusion and document findings

Remeasure lactate within 6hrs if initial lactate elevated >2

72
Q

How would you reassess fluid volume status

A

CVP

73
Q

Hypoglycemia in a noninsulin receiving patient indicates what

A

Ominous sign of liver failure and gluconeogensis. Warrants emergency intervention and notification of the provider

74
Q

What is something to remember about positioning and shock priorities

A

Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time

75
Q

Sepsis

HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment

A

HR ⬆️ bounding pulses

BP ⬇️

Skin- warm, flushed, fever (then changes to cold)

SVR ⬇️

CVP ⬇️

PAWP ⬇️

Loc ⬇️

UOP ⬇️

Treatment- meticulous handwashing, O2, prepare for intubation, mouth care, blood cultures, IV fluids, drugs (antibiotics, dopamine, norepinephrine)

76
Q

Tranexamic acid

A

An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients

77
Q

Dopamine low dose, medium dose, high dose

A

Low dose 1-5 mcg/kg/min (⬆️ CO, contractility, renal flow)

Medium dose 5-15 (dose the same as low)

High dose 20-50 (vasoconstrict, severe ⬆️ BP, causes tachy arrythmias)

78
Q

Chronotropic drugs vs inotropic drugs

A

Inotropic drugs affect the force of cardiac contraction.

Chronotropic drugs affect the heart rate.

79
Q

In what shock state might lasix be appropriate

A

Cardiogenic

80
Q

If a patient had a low CVP what might be an appropriate intervention

A

Fluids (NS or LR)

Next vasopressor

Next impella

81
Q

If a patient had a low CVP what might be an appropriate intervention

A

Fluids (NS or LR)

Next vasopressor

Next impella

82
Q

In what shock state might lasix be appropriate

A

Cardiogenic

83
Q

Chronotropic drugs vs inotropic drugs

A

Inotropic drugs affect the force of cardiac contraction.

Chronotropic drugs affect the heart rate.

84
Q

Dopamine low dose, medium dose, high dose

A

Low dose 1-5 mcg/kg/min (⬆️ CO, contractility, renal flow)

Medium dose 5-15 (dose the same as low)

High dose 20-50 (vasoconstrict, severe ⬆️ BP, causes tachy arrythmias)

85
Q

Tranexamic acid

A

An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients

86
Q

Sepsis

HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment

A

HR ⬆️ bounding pulses

BP ⬇️

Skin- warm, flushed, fever (then changes to cold)

SVR ⬇️

CVP ⬇️

PAWP ⬇️

Loc ⬇️

UOP ⬇️

Treatment- meticulous handwashing, O2, prepare for intubation, mouth care, blood cultures, IV fluids, drugs (antibiotics, dopamine, norepinephrine)

87
Q

What is something to remember about positioning and shock priorities

A

Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time

88
Q

Is heart failure ventricular or atrial failure

A

Ventricular failure

89
Q

3 most common causes of HF and risk factors

A

Causes- hypertension , acute coronary syndrome , valve dysfunction

Risk factors- CAD, age, HTN, obesity, diabetes, smoking, high cholesterol, African American

90
Q

Cardiac output, stroke volume, ejection fraction

A

Cardiac output- amount of blood the heart pumps per minute

Stroke volume- amount of blood the heart pumps per beat

Ejection fraction- percentage of blood ejected from left ventricle with each beat

91
Q

Normal range of ejection fraction

A

50-70%

92
Q

What 4 things affect CO

A

Preload- volume of blood in LV at the end of diastole

Afterload- (SVR) resistance heart must overcome to pump blood

Myocardial contractility

Heart rate

93
Q

Left sided systolic (contraction) failure

A

Left ventricle has reduced function

  • Can’t generate enough pressure
  • Can’t eject end diastolic volume
  • LV muscle overworks
  • LV enlarges leading to hypertrophy
94
Q

What is the hallmark sign of left sided systolic (contraction) failure

A

Decreased LV ejection fraction

EF < 40%

95
Q

Left sided diastolic (filling) failure

A

Impaired ability of ventricles to fill during diastole

Usually the result of LV hypertrophy

Characterized by pulmonary congestion

Ejection fraction is normal

96
Q

Systemic clinical manifestations of left HF

Systolic, diastolic dysfunction

A

Systolic- lightheadedness, marginal BP, change in pulses, diaphoresis, pale color, nocturia

Diastolic- exercise intolerance, S3 and S4 heart sounds

97
Q

Pulmonary symptoms of left HF

Systolic, diastolic dysfunction

A

Systolic- tachypnea, DOE, bibasilar crackles, respiratory acidosis

Diastolic- orthopnea, DOE, bibasilar crackles, cough with frothy pink sputum, pulmonary edema, respiratory acidosis

98
Q

Right heart failure may occur without LV dysfunction in presence of what ?

A

Pulmonary hypertension

Right ventricular MI

Pulmonary embolism

COPD

99
Q

What is right heart failure characterized by

A

Increased volume and pressure in the venous system and peripheral edema

100
Q

Right heart failure clinical manifestations

A

Venous congestion

Jugular vein distention

Peripheral edema

Hepatomegaly

Splenomegaly

Ascites

Oliguria, nocturia

Fatigue, weakness

Low BP

101
Q

A client’s heart disease has resulted in a reduction of stroke volume. Which compensatory mechanism is expected

A

Increased heart rate

102
Q

Acute vs chronic HF

A

Acute HF- heart is overwhelmed by abrupt alteration in cardiac function and unable to bring compensatory mechanisms into play

Chronic HF- compensatory mechanisms have time to partially or completely restore cardiac function

103
Q

List 3 compensatory mechanisms of heart failure

A

Ventricular dilation and/or hypertrophy

Increased sympathetic response

RAAS responses lead to “remodeling”

104
Q

Chronic HF clinical manifestations

A

Fatigue

Dyspnea (paroxysmal nocturnal dyspnea)

Tachycardia

Chest pain

Nocturia

Dusky appearance

Weight changes

Edema

Behavioral changes (restlessness, confusion, reduced attention span)

105
Q

NYHA classifications of HF

A

Based on tolerance to physical activity

Class I: no limitations

Class II: slight limitation / mild symptoms with ordinary activities

Class III: marked limitation / marked limitation with physical activity but comfortable at rest

Class IV: inability to carry out any physical activity without discomfort / severe limitation and distress with physical activity or at rest

106
Q

Nursing assessment of HF patient

A

Auscuaybof heart and lungs

Vitals

JVD

Edema

Weight gain

Ascites

Mental status

107
Q

How is HF diagnosed

A

Chest X-ray ,Ekg , Bnp levels , ABG’s , Echocardiogram, EF and PA pressure, Cardiac catheterization , ANP, thallium scanning, hemodynamic monitoring

108
Q

HF treatment goals

A

Improve CO

Reduce pulmonary and systemic congestion

Improve gas exchange and oxygenation

Prevent complications

Educate patient and family about disease

Maintain glycemic control

109
Q

The nurses role in HF

How to prevent complications

A

Providing oxygen and rest

Controlling heart rate and BP

Daily weights

Monitoring I&O

Monitoring drug effects

Education about activity

Education about diet and fluid restrictions

Education about home care

110
Q

Normal values part II (HF)

A

RAP or CVP: 2-6

PAP: 20-30/8-15

PCWP: 6-12

CO HR x SV: 4-8

SV HR x CO: 20-60

SVR ((MAP - RAP)*80)/CO): 900-1200

PVR ((PAP-PCW)*80/CO): 100-200

MAP (SBP + 2DBP)/3: needs to be > 60

111
Q

PCWP offers a more accurate reading on which type of patient

A

Patient with pulmonary hypertension

Pulmonary catheter wedge pressure

112
Q

PCWP treatment is too high or too low

A

Low- volume

High- diuretics, dilators

113
Q

LVSW treatment if too high or too low

A

High- beta blockers

Low- positive inotropes

(Left ventricle stroke work)

114
Q

SVR treatment if too high or too low

A

High- dilators

Low- vasopressors

115
Q

Preload treatment if too high or too low

A

High- diuretics , dilators

Low- volume, arrhythmia control

116
Q

Afterload if treatment is too high or too low

A

High- dilators, IABP

Low- vasopressors, IABP

117
Q

Pharmacological management of HF

A

Primary goals of therapy:

  • improve contractility = ⬆️ perfusion to maintain CO
  • optimize heart rate
  • reduce preload
  • reduce afterload
  • most HF patients will be on a combination of drugs to meet goals*
118
Q

Types of drugs that optimize heart ❤️ rate

A

Positive inotropes

Antidysrhythmics

Beta blockers

119
Q

Types of drugs that ⬇️ afterload

Acute care

A

Ace inhibitors , ARB’s

Acute care- nitrates, b type natriuretic peptides

120
Q

Types of drugs that improve contractility

Acute care

A

Positive inotropes , beta blockers

Acute care- dopamine, dobutamine, b type natriuretic peptide

121
Q

Drugs that ⬇️ preload

Acute care

A

Diuretics, ace inhibitors, arbs

Acute care- nitrates, morphine

122
Q

Example of inotropic and human b-type natriuretic peptide drugs to treat HF

A

Inotropes- digoxin, dobutamine, dopamine

B type natriuretic peptide- natrecor, primacor

123
Q

Cardiac glycosides and inotropic agents are used to treat HF and arterial dysrhythmias how

A

Work through

Positive inotropic action- increase force of contraction

Negative chronotropic action- decrease heart rate

Negative dromotropic action- decrease speed of conduction

124
Q

Digoxin

Route, Half life, therapeutic range, contraindications, toxicity, antidote

A

Route- maybe given PO or IV

Half life- very long 30 to 40hrs

Therapeutic range- 0.5-2.0

Contraindications- DO NOT GIVE with ventricular dysrhythmias, 2nd or 3rd Degree HB

Monitor closely for hypokalemia

Toxicity- bardaycardia, blurry vision, yellow halos, diplopia, GI distress, drowsiness, confusion, heart block, dysrhythmias

Antidote- digibind

125
Q

Beta blockers

Use, action, monitor for

A

Used to treat chronic HF, hypertension, dysrhythmias and ACS

Works through- interference with the RAAS to lower BP through vasodilation, lowers HR through sympathetic response

Monitor closely for coughing

126
Q

Metoprolol

Route, contraindications, Monitor for, patient education

A

Cardioselective B1

Maybe given PO or IV

DO NOT give in presence of heart block or bradycardia

Monitor closely for- bradycardia, hypotension, orthostatic hypotension, heart block, cough, rebound hypertension

Patient education- BP & HR monitoring, avoid orthostatic hypotension, risk of hypoglycemia, caution with OTC preparations, sexual side effects, don’t skip doses, lifestyle changes

127
Q

Ace inhibitor: lisinopril / arb: losartan

Action, contraindications, Monitor for, patient education

A

Action- both interfere with RAAS to lower BP through vasodilation

DO NOT take with potassium sparing diuretics

Monitor closely for- hypotension, orthostatic hypotension, rebound hypertension, reflex tachycardia, renal Function, ANGIOEDEMA

Patient education- BP monitoring, avoid orthostatic hypotension, caution with OTC preparations, sexual side effects, pregnancy risk, don’t skip doses, lifestyle changes, dry cough is likely

128
Q

How do diuretics work

A

Reduce preload & afterload by lowering BP and/or removing excess fluid

Work by inhibiting the reabsorption of sodium

129
Q

Furosemide

Excretes, contraindications, Monitor for, patient education

A

Water, Na, K, Ca & Mg are lost

Very potent, only use if less potent diuretics don’t work

Highly protein bound

DO NOT give with another loop diuretic

Monitor closely for- hypokalemia, electrolyte imbalance, hypotension, digitalis toxicity, hyperglycemia, renal Function, dehydration, I&O, falls

Patient education- take exactly as prescribed, potassium supplement, fluid restrictions, daily weight, monitor BP , monitor glucose levels

130
Q

Hydrochlorothiazide

Excretes, contraindications, Monitor for, patient education

A

Water, Na, K, Mg, chloride are excreted, Ca is retained

More effective at lowering BP than fluid elimination

Not used in patients with renal dysfunction

Monitor closely for- hypotension, hypercalcemia, hypokalemia, electrolyte imbalance, digitalis toxicity, lithium toxicity, hyperglycemia, renal function, I&O

Patient education- take in morning, fluid restriction, monitor BP , monitor glucose levels

131
Q

Spironolactone

Excretes, contraindications, Monitor for, patient education

A

Water and Na are excreted, K is retained

Least effective at removing excess fluid, often prescribed in combination with other diuretics

SHOULD NOT be given with acei’s or arb’s

Monitor for- hyperkalemia, electrolyte imbalance, renal function, hypotension, I&O

Patient education- take in morning, fluid intake, BP monitoring, daily weight

132
Q

How does an IABP work

A

Inflates during diastole= ⬆️ contractility in aorta (t wave)

Deflates during systole= creates pressure to pull blood from left ventricle

133
Q

Mitral valve stenosis

A

Valve doesn’t open completely

Results in ⬇️ blood flow from LA to LV, leads to pulmonary congestion and right side HF

Fatigue, DOE, orthopnea, NVD, hepatomegaly, edema afib

Rumbling apical DIASTOLIC murmur

Low pitch, loud sound heard best with bell of stethoscope

134
Q

Mitral valve regurgitation

A

Valve doesn’t close completely

(flappy doors, won’t stay closed)

Results in blood ejected from LV into LA during systole (returns during diastole), leads to increased volume in LV and left side HF

High pitched SYSTOLIC murmur at apex heard best with diaphragm of stethoscope

fatigue, DOE, orthopnea, afib, NVD, edema

135
Q

Mitral valve is opened/closed during what

A

Open during diastole

Closed during systole

136
Q

Aortic valve is opened/closed during what

A

Closed during diastole

Open during systole

137
Q

Mitral valve prolapse

A

Valve prolapses into LA during systole (when it should be closed)

138
Q

Mitral valve prolapse

A

Valve prolapses into LA during systole (when it should be closed)

139
Q

Aortic valve is opened/closed during what

A

Closed during diastole

Open during systole

140
Q

Mitral valve is opened/closed during what

A

Open during diastole

Closed during systole

141
Q

Mitral valve regurgitation

A

Valve doesn’t close completely

(flappy doors, won’t stay closed)

Results in blood ejected from LV into LA during systole (returns during diastole), leads to increased volume in LV and left side HF

High pitched SYSTOLIC murmur at apex heard best with diaphragm of stethoscope

fatigue, DOE, orthopnea, afib, NVD, edema

142
Q

Mitral valve stenosis

A

Valve doesn’t open completely

Results in ⬇️ blood flow from LA to LV, leads to pulmonary congestion and right side HF

Fatigue, DOE, orthopnea, NVD, hepatomegaly, edema afib

Rumbling apical DIASTOLIC murmur

Low pitch, loud sound heard best with bell of stethoscope

143
Q

Infective endocarditis

Risk factors, symptoms, complications

A

Infection of inner lining of heart or valves, most commonly strep/staph

Risk factors- structural cardiac defects, systemic infection, valve replacement, IV drug use, poor oral health

Symptoms & complications- HF, vegetation on valve, valve dysfunction, new or changing murmur, arterial embolization, splenic rupture, petechia, janeways lesions

144
Q

Janeway’s lesions

A

Irregular, erythematous, flat, painless macular on the palms of hands and soles of feet.

Associated with infective endocarditis

145
Q

Rheumatic carditis

Symptoms & complications

A

Inflammatory response following group A beta-hemolytic strep upper respiratory infections

Symptoms & complications- Aschoff bodies that develop scar tissue, cardiomegaly, new or changing murmur, pericardial rub, valve dysfunction, HF, tachycardia, EKG changes

PREVENTION IS KEY !
(once damage is done it is often irreversible)

146
Q

Pericarditis

Risk factors & causes, symptoms & complications

A

Inflammation of or fluid accumulation in the pericardial sac

Risk factors & common causes- malignancy, infection, MI, cardiac surgery, connective tissue disorder, renal failure

Symptoms & complications- CP, pericardial rub, LHF in acute phase, RHF in chronic phase, fatigue, elevated WBC’s, EKG changes/afib, pericardial effusion, CARDIAC TAMPONADE!

147
Q

Dilated cardiomyopathy

Cause, treatment

A

Chronic disease involving damage to cardiac muscle

Often causes by alcohol abuse, chemotherapy, infection, inflammation, inadequate nutrition

Ventricles are enlarged but wall thickness is normal, results in ⬇️ cardiac output, ⬆️ size of chambers, systolic dysfunction, fatigue, weakness, S3 and S4, signs of LHF

Treatment- inotropes, antidysrhythmics, heart transplant

148
Q

Hypertrophic cardiomyopathy

S&s, treatment

A

Chambers are reduced, muscle is thickened

S&s- diastolic dysfunction, mitral regurgitation, syncope as cardiac output can’t increase with increased demand, dyspnea, angina, S4, sudden death common, HF S&s

Treatment- b blockers, Ca channel blockers, ablation, NO INOTROPES NO DILATORS

149
Q

Restrictive cardiomyopathy

s&s, treatment

A

Ventricular wall rigidity

s&s- diastolic dysfunction, low cardiac output, orthopnea, venous enforcement

Treatment- remove fluid, low Na diet, improve pump
(transplant may be only treatment for late stage disease)

150
Q

Heart transplant

Criteria, complications

A

Criteria- life < 1yr, < 65, normal PVR, no infection, psychosocial, no abuse

Bicaval vs orthotopic (2 p waves)

Debervation (only isuprel) - atropine won’t work

Complications- infection, tamponade, rejection

151
Q

Hypovolemic shock

Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment

A

Hr ⬆️

BP ⬇️

Skin- cold

SVR ⬆️

CVP ⬇️ due to dehydration

PAWP ⬇️

Loc ⬇️

UOP ⬇️

Treatment- O2 100% nonrebreather, 2 IV’s, fluid NS or LR

Tests various (20 decks)

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