Exam 1

indicators of perfusion

• level of consciousness

• pulses

• skin color/temperature

• capillary refill time

• urine output

preload

filling pressures/volume (end diastolic volume). right heart → central venous pressure (CVP); left heart → pulmonary artery occlusion pressure (PAOP/PAW(edge)P)

lumens of pulmonary artery catheter

proximal, distal, thermistor, balloon inflation

measurements from pulmonary artery catheter (PA line)

• cardiac output

• SvO2

• pulmonary artery pressures - left heart preload (PAOP/PAWP)

measurements from central venous line

• pulmonary artery pressures - right heart preload (CVP)

• ScvO2

evaluating oxygenation

• oxygen delivery - CO, arterial oxygen content (Hgb, SaO2, PaO2)

• oxygen consumption/venous O2 saturation - normal is ~60-75%

SaO2

• percentage of hemoglobin that are carrying oxygen

• measured with pulse ox

• normal range >94%

PaO2

• partial pressure of oxygen dissolved in the blood (plasma)

• ABG

• normal range 80-100 mmHg

ScvO2 - central venous oxygen saturation

• amount of O2 in blood returning to heart after tissues have taken O2; reflective of upper body only - more commonly used

• measured with central venous catheter

• normal range 70-80%

SvO2 - mixed venous oxygen saturation

• amount of O2 in blood returning to heart after tissues have taken O2; true mixed-venous gas reflecting whole body

• measured with swan-ganz (pulmonary artery) catheter

• normal range 60-80%

P wave

• impulse from SA node through the atria

• atrial depolarization

• atrial contraction takes place milliseconds after depolarization

P-R interval

• time required for atrial depolarization

• atrial contraction

• .12-.20 sec

QRS complex

• impulse from bundle of HIS → to bundle branches → to Purkinje fibers

• ventricular depolarization

• also atrial repolarization (but this is not visible on ECG)

• <.10 sec

ST segment

ventricular contraction

T wave

ventricular repolarization

U wave

Purkinje fiber repolarization. rarely seen, may occur in cases of digoxin toxicity, hypokalemia

QT interval

• normal is less than or equal to 0.44 sec, danger over .50 seconds

• prolonged QT (ventricles take longer to recharge during beats) can cause dangerous arrhythmias

• can be due to congenital heart problems, electrolyte imbalances, or medication side effects

Regular Sinus Rhythm

• Rate: 60-100 bpm

• Rhythm: R - R =

• P waves: Upright, similar

• P-R: 0.12 - 0.20 sec & consistent

• qRs: 0.04 - 0.10 sec

• P:qRs: 1P:1qRs

Sinus Tachycardia

• Rate: >100

• Rhythm: R- R =

• P waves: Upright, similar

• P-R: 0.12 - 0.20 sec and consistent

• qRs: 0.04 - 0.10 sec

• P:qRs: 1p:1qRs

Sinus Bradycardia

• Rate: <60

• Rhythm: R- R =

• P waves: Upright, similar

• P-R: 0.12 - 0.20 sec and consistent

• qRs: 0.04 - 0.10 sec

• P:qRs: 1P:1qRs

• symptoms: syncope, change in mental status, hypotension, SOB, diaphoresis, chest pain

Premature Atrial Contractions (PAC)

• Rate: usually <100, dependent on underlying rhythm

• Rhythm: irregular

• P waves: early and upright, different from sinus

• P-R: 0.12 - 0.20 sec, different from sinus

• qRs: 0.04 - 0.10 sec

• P:qRs: = 1:1

• Causes: normal, excessive use of caffeine/tobacco/alcohol, CHF, myocardial ischemia or injury, hypokalemia, digoxin toxicity, COPD

Atrial Flutter

• Rate: atrial rate 250-350, ventricular rate 150 common

• Rhythm: atrial regular, ventricular regular or irregular

• P waves: not identifiable

• F waves: uniform (sawtooth or picket fence)

• PRI: not measurable

• qRs: 0.04-0.10 sec

• Causes: ischemic heart disease, hypoxia, acute MI, digoxin toxicity, mitral or tricuspid valve disease, PE

Atrial Fibrillation

• Rate: atrial 400-700, ventricular 160-180 bpm

• Rhythm: atrial and ventricular irregular

• P waves: not identifiable

• f waves: may be seen

• P-R: unable to measure

• qRs: usually normal

• causes: ischemic heart disease, hypoxia, acute MI, digitalis toxicity, mitral or tricuspid disease

Ventricular Tachycardia (V-tach)

• rate: 180

• regularity: regular

• P wave: no

• P:QRS ratio and PR interval: n/a

• QRS width: .26

• causes: toxin, hypovolemia, hypoxia, hypothermia, toxins, cardiac tamponade, MI, PE, acidosis, K± issues

treatment for V-tach with a pulse

• treat cause

• anti-arryhthmic medications (amiodarone)

• cardioversion

treatment for pulseless V-tach

• initiate CPR

• defibrillation

• epinephrine, amiodarone

• address the cause

Polymorphic Ventricular Tachycardia (Torsade’s de Pointes)

• Rate: 270

• Regularity: Chaotic

• No P wave (so P:QRs ratio and PR interval n/a)

• QRS width: .20

• treatments: v-tach tx, magnesium

Ventricular Fibrillation

• rate: n/a

• regularity: chaotic

• no P wave, P:QRS ratio, PR interval, identifiable QRS width

• tx: initiate CPR, defibrillate immediately

• causes: hypovolemia, hypoxia, acidosis, hypo/hyperkalemia, hypoglycemia, hypothermia, toxins, cardiac tamponade, MI, PE

pulseless electrical activity (PEA)

• any viable rhythm without a pulse

• tx: initiate high quality CPR, epinephrine, repeat

H’s and T’s

potential reversible causes of cardiac arrest or PEA

H’s: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia

T’s: tension pneumothorax, tamponade (cardiac), toxins, thrombosis (pulmonary), thrombosis (cardiac)

defibrillation

• not synchronized - delivered at any time in cardiac cycle

• higher energy (electricity)

• indications - ventricular fibrillation, pulseless v-tach

cardioversion

• synchronized

• delivered on R wave

• lower energy (electricity)

• indications: atrial fibrillation (after anticoagulation), unstable tachyarrhythmias

epinephrine

• first line for pulseless rhythms

• 1mg q4min

amiodarone

• antiarrhythmic

• reduces heart rate

• drip used in tachyarrhythmias

atropine

• antimuscarinic anticholinergic

• increases heart rate

• used in bradycardias

• 1mg IVP

adenosine

• converts, stops or slows rhythms

• 6mg IVP

• prepare additional 12mg IVP if needed

sinus arrhythmia - has to have a greater than 10% variation on P-P waveform max and min cardiac cycle

• rate: 80

• regularity: irregular

• P-wave: yes

• P:QRS ratio: 1:1

• PR interval: 0.14

• QRS width: 0.06

treatment of sinus tachycardia

• distinguish whether symptomatic, compensating

• treat cause

• meds: beta blockers, CCBs

atrial fibrillation management

• anticoagulation: heparin infusion, oral anticoagulants

• rate control: sodium channel blockers, beta blockers, potassium channel blockers, nondihydropyridine CCBs, digoxin

• rhythm control: meds, cardiac ablation, cardioversion, pulmonary vein isolation (PVI) an/or ICD/PPM

factors influencing organ perfusion

• adequate oxygen availability - patent airway, adequate ventilation, adequate perfusion, respiratory assessment/ABG/SpO2

• oxygen movement - sufficient Hgb, CBC, H&H, contractility

• oxygen demand - is there an increased demand body is unable to meet, SvO2, ScvO2, lactate

• oxygen exchange - vascular tone (dilation/constriction), blood/fluid status, blood pressure (MAP)

stages of shock

• initial - initial insult, subtle changes in assessment/VS, beginning of cell damage

• compensatory - compensatory mechanisms begin, tachypnea/tachycardia, decreasING BP and urine output

• progressive - compensatory processes fail, blood shunted to vital organs

• refractory - prolonged tissue hypoperfusion, multi-system organ failure, irreversible

DIC - disseminated intravascular coagulopathy

overwhelming inflammatory response leads to excessive clotting, which exhausts clotting factors and this depletion leads to excessive bleeding

DIC labs

• elevated d-dimer r/t clots

• decreasing clotting factors (platelets, fibrinogen)

• increased clotting times (PTT, INR)

• increased fibrin degradation products

DIC treatment

• supportive care: optimize oxygenation, pH, electrolytes

• treat cause

• volume replacement and replacement of clotting factors

• bleeding precautions

MODS: multiple organ dysfunction syndrome

• decreased oxygen delivery to organs + increased oxygen demand + poor oxygen utilization

• organ dysfunction leads to organ death

• lungs and kidneys usually first

• 40% mortality w lung involvement, 80-90% mortality once 3 organs are involved

• identification: depends on system failing, i.e. respiratory failure, anuria, absent bowel sounds

• tx: supportive care, treatment of cause

assessment findings - initial stage of shock

• subtle changes to baseline, or no change at all

• may see lactate this early

assessment findings - compensatory stage of shock

• subtle mental status change (restlessness, confusion)

• tachycardia

• weak pulses

• decreasing BP, narrowing pulse pressure

• tachypnea - respiratory alkalosis

• decreasing urine output

• cool, moist skin

assessment findings - progressive stage of shock

• lethargy or coma

• hypotension

• dysrhythmias

• anuria

• absent bowel sounds

• metabolic/respiratory acidosis (or both)

• cold extremities

• weak/absent pulses

assessment findings: refractory stage of shock

• coma

• hepatic, renal failure

• peripheral ischemia and necrosis

obstructive shock

obstruction to ventricular filling and/or emptying, decreasing cardiac output. independent of other mechanisms

obstructive shock - causes that impair filling

• tension pneumothorax: disruption in thoracic pressure presses on the heart. cardinal signs = decreased breath sounds on one side, tracheal deviation. tx with needle decompression

• cardiac tamponade: fluid around the heart presses on the heart. cardinal signs = muffled heart sounds, JVD, hypotension with narrow pulse pressure (Beck’s triad). tx w pericardiocentesis

obstructive shock - causes that impair emptying

• pulmonary embolism: clot in the lung blocking blood flow into pulmonary vasculature. cardinal signs: sudden shortness of breath, hemoptysis. tx w thrombolytic, thrombectomy

hemodynamic findings of obstructive shock

• HR: ↑ r/t compensation

• BP: ↓ r/t deficient CO

• preload: ↑ OR ↓ (dependent on variables)

• afterload/SVR: ↑ r/t compensation

• contractility: no change

hypovolemic shock

inadequate vascular volume resulting in inadequate CO

hypovolemic shock causes

fluid loss dt vomiting/diarrhea, dehydration, blood loss, internal bleeding

clinical manifestations of hypovolemic shock

hypotension, tachycardia, change in mental status, pale/cool/clammy skin, weak pulses, prolonged capillary refill, decreased urine output

hemodynamic findings of hypovolemic shock

HR: ↑ r/t compensation

BP: ↓ r/t deficient intravascular volume

preload: ↓ r/t deficient intravascular volume

afterload/SVR: ↑ r/t compensation

contractility: ↑ r/t compensation

diagnostic findings for hypovolemic shock:

• SpO2, PaO2, ScO2: Normal until late stages (pt still oxygenating, all hgb still carrying O2)

• pH: High during compensatory stage (hyperventilation), low when body shifts to anaerobic metabolism

• PaCO2: Low in compensatory stage (hyperventilation), high in late stages if pt develops respiratory distress

• Lactate: Elevated when pt transitions to anaerobic metabolism

• Hemoglobin: Low with blood loss

• BUN: High in dehydration

• Creatinine: High in kidney injury

anaphylactic shock

distributive shock caused by extreme hypersensitivity reaction to an allergen

anaphylactic shock pathophysiology

exposure to allergen → histamine response → venous dilation, increased capillary permeability, smooth muscle contraction → airway compromise, angioedema, profound hypotension

clinical manifestations of anaphylactic shock

• airway compromise: SOB, tachypnea, wheezing, stridor, cyanosis, mental status change

• vasodilation and capillary leak → “relative hypovolemia”: hypotension, tachycardia, cool/pale skin, weak pulses, peripheral edema

• hypersensitivity reaction: angioedema, flushing, uticaria, rash

hemodynamic findings of anaphylactic shock

• HR: ↑ r/t compensation

• BP: ↓ r/t vasodilation, capillary leak

• preload: ↓ r/t decreased venous return

• afterload/SVR: ↓ r/t vasodilation

• contractility: ↓ r/t coronary hypoperfusion, damage

treatment of anaphylactic shock

• remove allergen first

• administer epinephrine IM second

• rescue: oxygenation - apply oxygen via NRB, prep for advanced airway) cardiovascular - IV fluids (need IV access)

• ongoing: antihistamines, corticosteroids to shorten/calm anaphylactic rxn and decrease airway swelling, bronchodilators to relieve bronchoconstriction

neurogenic shock pathophysiology

injury to nervous system d/t by spinal cord or brain injury causes:

• sympathetic disruption - loss of vascular tone (SVR) → vasodilation, decreased venous return, relative hypovolemia

• unopposed parasympathetic response - bradycardia → low CO d/t low HR/SV, loss of compensatory tachycardia

• hypotension, hypoperfsuion of tissues, anaerobic metabolism

neurogenic shock clinical manifestations

• warm, dry, flushed skin r/t vasodilation

• hypotension r/t decreased vascular tone (SVR)

• bradycardia r/t unopposed parasympathetic activiy

• ↓ venous return - ↓ SV, CVP

• ↓ CO r/t bradycardia, ↓ SV

• LOC changes r/t acidosis, hypoperfusion

• elevated lactate, metabolic acidosis r/t anaerobic metabolism from ↓ perfusion

medical management of neurogenic shock

• priority is maintain vital functions → rescue. tx hypotension = fluid administration, vasopressor infusion; tx bradycardia = atropine, pacing; tx respiratory compromise = intubation w mechanical ventilation

• definitive: tx for cause

• serial labs: lactate, ABG

septic shock

shock caused by body’s uncontrolled response to infection. insult (infection) → localized inflammation becomes systemic → distributive shock. leading cause of in-hospital deaths in the U.S.

septic shock pathophysiology

• local response to infection = ↑ capillary permeability, mobilization of macrophages/neutrophils, formation of fibrin mesh

• systemic (septic response) = systemic ↑ capillary permeability - vasodilation, capillary leak, relative hypovolemia, ↓ venous return and CO; hypercoagulation - septic emboli, DIC

clinical manifestations of early sepsis - hyperdynamic/”warm”

• fever

• tachycardia

• bounding pulses

• warm, flushed skin

• decreasing BP and urine output

• confusion/restlessness

• increased CO

clinical manifestations of late sepsis - hypodynamic/”cold”

• cool, pale skin

• weak, thready pulses

• hypothermia (very late)

• decreased CO

hemodynamic findings for septic shock

• HR: ↑ r/t compensation

• BP: ↓ r/t decreased venous return

• Preload: ↓ r/t decreased venous return

• Afterload/SVR: ↓ r/t vasodilation

• Contractility: ↑ in early/hyperdynamic stage r/t compensation

diagnostic findings for septic shock

• ABG: respiratory alkalosis early, metabolic acidosis later

• lactate: ↑ r/t anaerobic metabolism

• leukocytes: ↑ r/t infectious process

• cultures: + based on organism

• clotting studies: ↓ in clotting factors (platelets, fibrin), ↑ clotting time (PTT, INR)

• organ function: renal (creatinine), hepatic (AST/ALT) ↑ as organ dysfunction progresses

SCCM sepsis guidelines (hour-1 bundle)

1. measure lactate level

2. obtain blood cultures before administering antibiotics

3. administer broad spectrum antibiotics

4. begin rapid admin of 30mL/kg crystalloid for hypotension or lactate greater than or equal to 4 mmol/L

5. apply vasopressors if hypotensive during or after fluid resuscitation to maintain a mean arterial pressure greater than or equal to 65mmHg

cardiogenic shock pathophysiology

decreased oxygen supply to heart muscle, anaerobic metabolism → lactic acidosis

decreased heart contractility → decrease in CO

cardiogenic shock risk factors

• co-morbidities: decompensated HF

• trauma: blunt chest trauma

• post-surgery: CABG

• direct tissue injury: STEMI

cardiogenic shock clinical manifestations

• hemodynamics: CO and SV ↓

• ↓ LOC/altered mental status

• SOB

• tachycardia, tachypnea

• hypotension (narrowed pulse pressure - compensatory vasoconstriction maintains diastolic pressure while systolic pressure fails dt ↓ SV)

• diaphoresis, pallor

• N/V

cardiogenic shock diagnostics

• diagnostic testing: CXR, echocardiogram, ECG, coronary angiography

• laboratory testing: troponin, BNP; ABG/VBG, lactate, CMP

medications for cardiogenic shock

• vasoactive (i.e. norepinephrine) - increase MAP and perfusion

• inotropes (i.e. dobutamine) - increase contractility and CO

• diuretics (i.e. furosemide) - decrease preload and fluid overload

surgical and supportive management for cardiogenic shock

• mechanical circulatory support (MCS)

  • intra-aortic balloon pump (increases coronary perfusion by improving filling and decreasing afterload - balloon inflates during diastole and deflates during systole)

  • ventricular assist device - implantable

  • extracorporeal membrane oxygenation

• heart transplant (rare)

pathophysiology of MI

vessel wall injury → atherosclerotic plaque build-up → obstruction of oxygen-rich blood flow through coronary vessels → plaque rupture and thrombosis

progression of vessel plaque build-up

plaque disruption and thrombus formation causes unstable angina → thrombus grows and causes partial occlusion (NSTEMI) → thrombus continues to grow and causes complete occlusion (STEMI)

typical clinical manifestations of MI

• sternal chest pain

• shoulder and arm pain

• anxiety, impending doom

non-typical clinical manifestations of MI

• dizziness, lightheadedness

• N/V

• indigestion

• fatigue

• radiation to neck/jaw/back

• more common in women

diagnostic tests

• lab tests: troponin I (highly sensitive to cardiac tissue), creatinine kinase, CK-MB/LDH (cardiac and tissue biomarkers used to detect damage), BMP/CBC/BNP/Lipid profile

• diagnostic tests: 12 lead ECG, cardiac angiography (left heart catheterization)

ischemic changes in MI ECG

infarction - ST elevation in MI ECG. lasts mins to hours

Q wave in MI ECG. up to 12 hours

ST elevation with T wave inversion in MI ECG. can persist for 2-5 days

treatment goals of medical management of MI

• maximize oxygenation

• control pain

• dilate coronary arteries

• prevent clots

• decrease myocardial workload

percutaneous coronary intervention

type of reperfusion therapy, performed in cath lab, minimally invasive procedure used to open clogged coronary arteries and restore blood flow to the heart

medications given during MI

• morphine for pain

• oxygen

• nitroglycerin

• aspirin - ASA (325mg)

medication given after MI

• daily aspirin - ASA (81mg)

• beta blockers

• lipid lowering medications (i.e. Statins)

• Antiplatelets (i.e. Clopidogrel)

• ACE-Is or ARBs

coronary artery bypass graft (CABG)

surgical procedure used to treat severe coronary artery disease by creating new pathways (detours) for blood and oxygen to bypass blocked or narrowed arteries feeding the heart muscle.

• single bypass = one artery or vein is used to bypass a single blocked vessel

• double bypass = two grafts are placed to bypass two blocked vessels

• …and so on to triple, quadruple, etc

complications of CABG

• arrhythmias

• bleeding

• infection

• organ failure

• cardiac tamponade (Beck’s triad: JVD, muffled heart sounds, hypotension)

quadruple therapy for meds after MI

• beta blocker

• statin

• ASA

• ACE or ARB

saccular aneurysm

pseudoaneurysm - 1-2 layers involved

fusiform aneurysm - bulging of entire artery

aneurysm pathophysiology

media layer of artery is weakened → intima layer of artery is stretched → artery widens, tension increases, widening continues

50% widening is diagnostic, can stretch as wide as 2x diameter

aneurysm types