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👩🏾‍🎓- 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
What does anaerobic metabolism cause
An increase in lactate lactic acidosis Normal range: 0-1.5
26
What are some things that increase cellular oxygen demand
Decrease hemoglobin Decrease O2 in body Decreased volume Pump problems
27
Motivation
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
28
SIRS symptoms
Systemic inflammatory response syndrome Overwhelming infection Symptoms- vasodilation, increased capillary permeability, microvascular clotting
29
SIRS criteria
2 or more of the following: WBC > 12000 or < 4000 or 10% bands Tachycardia Temperature > 100.4 or < 96.8 Tachypnea
30
List the 4 classifications of shock
Initial Compensatory (neural, endocrine, chemical) Progressive stage Refractory stage
31
Initial stage
The initial stage of shock is marked by hypoxia due to decreased deliver (DO2) to the cells.
32
Progressive stage
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
33
Refractory stage
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
34
Causes of cardiogenic shock
Number 1 cause: acute myocardial infarction Cardiomyopathy CHF Arrhythmia Papillary muscle rupture
35
Clinical symptoms of cardiogenic shock Neuro, respiratory, CV, GI, GU, skin
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
36
Cardiogenic shock diagnostics
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)
37
Brain natriuretic peptide
Hormone released by the ventricles in response to increased blood volume and blood pressure
38
What is the gold standard of cardiogenic shock treatment
Balloon pump Increase O2 supply, decrease O2 demand
39
Cardiogenic shock management
“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)
40
Cardiogenic shock HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
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
41
Obstructive shock Epidemiology, Pathophysiology
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
42
Saddle pe Diagnostic, s&s, treatment
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
43
Cardiac tamponade Diagnostic , s&s, treatment
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
44
Becks triad
Associated with cardiac tamponade 3 signs include: Low arterial blood pressure, JVD, distant muffled heart sounds (Muffled due to ⬆️ fluid)
45
Pulsus paradoxus
an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration.
46
Tension pneumothorax Diagnostic, s&s, treatment
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
47
Obstructive shock Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
HR ⬆️ BP ⬇️ Skin cold SVR ⬆️ CVP ⬆️ PAWP ⬆️ Loc
48
Causes of hypovolemia Hemorrhagic vs hypovolemic
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
49
Hypovolemic shock diagnostics
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
50
Lactate Acid Draw, range
Lactic acid is used to test for sepsis Draw- no turnicate because will ⬆️ anaerobic metabolism, put on ice Range- > 4 = death
51
Compensatory stage Neural, endocrine, chemical
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
52
Hypovolemic shock assessment Neuro, respiratory, skin, cv, Gu
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
53
Hypovolemic shock if bleeding
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
54
Hypovolemic shock medications- non bleeding patient
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
55
Hypovolemic shock Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
Hr ⬆️ BP ⬇️ Skin- cold SVR ⬆️ CVP ⬇️ due to dehydration PAWP ⬇️ Loc ⬇️ UOP ⬇️
56
Distributive shock
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
57
Anaphylactic shock Manifestations, management
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
58
Epinephrine administration in anaphylactic shock
.3 - .5 SQ/IM No IV can redo shot in 5-10min if no improvement
59
Neurogenic shock Epidemiology, pathophysiology, manifestations, treatment
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
60
Neurogenic HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
HR ⬇️ BP ⬇️ Skin- warm, flushed SVR ⬇️ CVP ⬇️ PAWP ⬇️ Loc ⬇️ UOP ⬇️ Treatment- IV fluids cautiously, drugs (atropine, norepinephrine, thrombolytics) transcutaneous pacing, ⬆️ hob
61
Anaphylactic HR, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
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
P wave
Atrial depolarization | Atrial systole
63
QRS complex
Ventricle depolarization | Ventricle systole
64
T wave
Ventricle repolarization | Ventricular diastole
65
SIRS , sepsis , severe sepsis , septic shock
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
What percentage of patients meet diagnostic criteria for SIRS on admission to hospital
68%
67
Severe sepsis Criteria
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
Septic shock
Severe sepsis + hypotension despite adequate fluid resuscitation OR initial lactate of 4 or greater
69
Treatment 3 hours of presentation with septic shock
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
When would you and would not administer crystalloid at a rapid rate ?
Severe sepsis- optional Hypotension, septic- required Cardiogenic- no rapid
71
Treatment within 6hrs of presentation with septic shock
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
How would you reassess fluid volume status
CVP
73
Hypoglycemia in a noninsulin receiving patient indicates what
Ominous sign of liver failure and gluconeogensis. Warrants emergency intervention and notification of the provider
74
What is something to remember about positioning and shock priorities
Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time
75
Sepsis HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
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
Tranexamic acid
An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients
77
Dopamine low dose, medium dose, high dose
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
Chronotropic drugs vs inotropic drugs
Inotropic drugs affect the force of cardiac contraction. Chronotropic drugs affect the heart rate.
79
In what shock state might lasix be appropriate
Cardiogenic
80
If a patient had a low CVP what might be an appropriate intervention
Fluids (NS or LR) Next vasopressor Next impella
81
If a patient had a low CVP what might be an appropriate intervention
Fluids (NS or LR) Next vasopressor Next impella
82
In what shock state might lasix be appropriate
Cardiogenic
83
Chronotropic drugs vs inotropic drugs
Inotropic drugs affect the force of cardiac contraction. Chronotropic drugs affect the heart rate.
84
Dopamine low dose, medium dose, high dose
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
Tranexamic acid
An antifibrinolytic Drug , has been shown to reduce blood loss in surgical patients
86
Sepsis HR, BP, skin, SVR, CVP, PAWP, LOC, UOP, treatment
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
What is something to remember about positioning and shock priorities
Don’t put patient in reverse trendeleburg or leave them flag for extended periods of time
88
Is heart failure ventricular or atrial failure
Ventricular failure
89
3 most common causes of HF and risk factors
Causes- hypertension , acute coronary syndrome , valve dysfunction Risk factors- CAD, age, HTN, obesity, diabetes, smoking, high cholesterol, African American
90
Cardiac output, stroke volume, ejection fraction
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
Normal range of ejection fraction
50-70%
92
What 4 things affect CO
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
Left sided systolic (contraction) failure
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
What is the hallmark sign of left sided systolic (contraction) failure
Decreased LV ejection fraction EF < 40%
95
Left sided diastolic (filling) failure
Impaired ability of ventricles to fill during diastole Usually the result of LV hypertrophy Characterized by pulmonary congestion Ejection fraction is normal
96
Systemic clinical manifestations of left HF Systolic, diastolic dysfunction
Systolic- lightheadedness, marginal BP, change in pulses, diaphoresis, pale color, nocturia Diastolic- exercise intolerance, S3 and S4 heart sounds
97
Pulmonary symptoms of left HF Systolic, diastolic dysfunction
Systolic- tachypnea, DOE, bibasilar crackles, respiratory acidosis Diastolic- orthopnea, DOE, bibasilar crackles, cough with frothy pink sputum, pulmonary edema, respiratory acidosis
98
Right heart failure may occur without LV dysfunction in presence of what ?
Pulmonary hypertension Right ventricular MI Pulmonary embolism COPD
99
What is right heart failure characterized by
Increased volume and pressure in the venous system and peripheral edema
100
Right heart failure clinical manifestations
Venous congestion Jugular vein distention Peripheral edema Hepatomegaly Splenomegaly Ascites Oliguria, nocturia Fatigue, weakness Low BP
101
A client’s heart disease has resulted in a reduction of stroke volume. Which compensatory mechanism is expected
Increased heart rate
102
Acute vs chronic HF
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
List 3 compensatory mechanisms of heart failure
Ventricular dilation and/or hypertrophy Increased sympathetic response RAAS responses lead to “remodeling”
104
Chronic HF clinical manifestations
Fatigue Dyspnea (paroxysmal nocturnal dyspnea) Tachycardia Chest pain Nocturia Dusky appearance Weight changes Edema Behavioral changes (restlessness, confusion, reduced attention span)
105
NYHA classifications of HF
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
Nursing assessment of HF patient
Auscuaybof heart and lungs Vitals JVD Edema Weight gain Ascites Mental status
107
How is HF diagnosed
Chest X-ray ,Ekg , Bnp levels , ABG’s , Echocardiogram, EF and PA pressure, Cardiac catheterization , ANP, thallium scanning, hemodynamic monitoring
108
HF treatment goals
Improve CO Reduce pulmonary and systemic congestion Improve gas exchange and oxygenation Prevent complications Educate patient and family about disease Maintain glycemic control
109
The nurses role in HF | How to prevent complications
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
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Normal values part II (HF)
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
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PCWP offers a more accurate reading on which type of patient
Patient with pulmonary hypertension | Pulmonary catheter wedge pressure
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PCWP treatment is too high or too low
Low- volume High- diuretics, dilators
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LVSW treatment if too high or too low
High- beta blockers Low- positive inotropes (Left ventricle stroke work)
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SVR treatment if too high or too low
High- dilators Low- vasopressors
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Preload treatment if too high or too low
High- diuretics , dilators Low- volume, arrhythmia control
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Afterload if treatment is too high or too low
High- dilators, IABP Low- vasopressors, IABP
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Pharmacological management of HF
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*
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Types of drugs that optimize heart ❤️ rate
Positive inotropes Antidysrhythmics Beta blockers
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Types of drugs that ⬇️ afterload Acute care
Ace inhibitors , ARB’s Acute care- nitrates, b type natriuretic peptides
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Types of drugs that improve contractility Acute care
Positive inotropes , beta blockers Acute care- dopamine, dobutamine, b type natriuretic peptide
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Drugs that ⬇️ preload Acute care
Diuretics, ace inhibitors, arbs Acute care- nitrates, morphine
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Example of inotropic and human b-type natriuretic peptide drugs to treat HF
Inotropes- digoxin, dobutamine, dopamine B type natriuretic peptide- natrecor, primacor
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Cardiac glycosides and inotropic agents are used to treat HF and arterial dysrhythmias how
Work through Positive inotropic action- increase force of contraction Negative chronotropic action- decrease heart rate Negative dromotropic action- decrease speed of conduction
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Digoxin Route, Half life, therapeutic range, contraindications, toxicity, antidote
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
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Beta blockers Use, action, monitor for
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
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Metoprolol Route, contraindications, Monitor for, patient education
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
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Ace inhibitor: lisinopril / arb: losartan Action, contraindications, Monitor for, patient education
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
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How do diuretics work
Reduce preload & afterload by lowering BP and/or removing excess fluid Work by inhibiting the reabsorption of sodium
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Furosemide Excretes, contraindications, Monitor for, patient education
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
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Hydrochlorothiazide Excretes, contraindications, Monitor for, patient education
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
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Spironolactone Excretes, contraindications, Monitor for, patient education
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
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How does an IABP work
Inflates during diastole= ⬆️ contractility in aorta (t wave) Deflates during systole= creates pressure to pull blood from left ventricle
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Mitral valve stenosis
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
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Mitral valve regurgitation
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
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Mitral valve is opened/closed during what
Open during diastole Closed during systole
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Aortic valve is opened/closed during what
Closed during diastole Open during systole
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Mitral valve prolapse
Valve prolapses into LA during systole (when it should be closed)
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Mitral valve prolapse
Valve prolapses into LA during systole (when it should be closed)
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Aortic valve is opened/closed during what
Closed during diastole Open during systole
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Mitral valve is opened/closed during what
Open during diastole Closed during systole
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Mitral valve regurgitation
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
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Mitral valve stenosis
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
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Infective endocarditis Risk factors, symptoms, complications
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
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Janeway’s lesions
Irregular, erythematous, flat, painless macular on the palms of hands and soles of feet. Associated with infective endocarditis
145
Rheumatic carditis Symptoms & complications
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)
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Pericarditis Risk factors & causes, symptoms & complications
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!
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Dilated cardiomyopathy Cause, treatment
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
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Hypertrophic cardiomyopathy S&s, treatment
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
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Restrictive cardiomyopathy s&s, treatment
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)
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Heart transplant Criteria, complications
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
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Hypovolemic shock Hr, BP, skin, SVR, CVP, PAWP, loc, UOP, treatment
Hr ⬆️ BP ⬇️ Skin- cold SVR ⬆️ CVP ⬇️ due to dehydration PAWP ⬇️ Loc ⬇️ UOP ⬇️ Treatment- O2 100% nonrebreather, 2 IV’s, fluid NS or LR

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