Perfusion NRS 325

perfusion definition

refers to blood flow through the circulatory system for optimal cellular activity

perfusion attributes

• central perfusion

• tissue perfusion

ischemia

a reduced blood flow and oxygen supply to the heart muscle, often caused by narrowed or blocked coronary arteries from plaque buildup

infarction 

a part of the heart muscle is dying because its blood supply is suddenly blocked, usually by a blood clot in a coronary artery

Anoxia

a complete lack of oxygen supply to the heart muscle

Hypoxia

low levels of oxygen in your body tissues

Hypoxemia

there is an abnormally low level of oxygen in the blood, which can lead to a lack of oxygen supply to the heart and other organs

Hydrostatic

the force exerted by blood pushing against the walls of the heart chambers and blood vessels

Oncotic

the force created by proteins, primarily albumin, within the heart's blood vessels that pulls water into the capillaries, counteracting the pressure that pushes fluid out

perfusion scope

excessive perfusion —> decreased perfusion

Normal Physiological Process: Central Perfusion

• Force of blood movement generated by cardiac output

• Requires adequate:

  •  Cardiac function

  •  Blood pressure

  •  Blood volume

Normal Physiological Process: Tissue or Local Perfusion

• Volume of blood that flows to target tissue

• Requires:

  •  Patent vessels

  •  Adequate hydrostatic pressure

  •  Capillary permeability

  •  Oncotic/colloidal pressure

Pulmonary Arteries

the only artery that carry oxygen-poor blood from the right side of the heart to your lungs

Remember: arteries usually go away 

preload def from class

• volume when ventricles are at rest

• volume to start off with 

pre load definition 

volume of blood in ventricles at end of diastole (end diastolic pressure)

pre load increase in

• hypervolemia

• regurgitation of cardiac valves

• heart failure

after load def from class

• how much pressure to push out

• how hard to push

after load definition 

resistance left ventricle must overcome to circulate blood

after load increases in

• hypertension

• vasoconstriction

An INCREASE in afterload means 

increase in cardiac workload

The equation of cardiac output

CO= SV x HR

Arterial End net filtration pressure 

• + 10 mm Hg

• fluid exit capillary

Mid capillary net filtration pressure

• 0 mm Hg

• no net movement of fluid

Venous end net filtration pressure

• -7 mmHg

• fluid re-enters capillary 

Risk Factors: Impaired Central Perfusion

• Occurs when cardiac output is inadequate.

• Reduced cardiac output results in a reduction of oxygenated blood reaching the body tissues

  •  If severe, associated with shock (hypoperfusion)

  •  If untreated, leads to ischemia, cell injury, and cell death

Risk Factors: Impaired Tissue Perfusion

• Associated with loss of vessel patency or permeability, or inadequate central perfusion

•  Results in impaired blood flow to the affected body tissue

  •  Leads to ischemia and, ultimately, cell death if uncorrected

TYPES OF individual risk factors

• age related change

• smoking

• obesity

• family history (genetics)

risk factor: age related change

Myocardial efficiency decreases, SA node decreases control, increased risk for left ventricular heart failure, blood vessel stiffening (resistance

risk factor: smoking

Vasoconstriction

risk factor: obesity

Relationship with chronic illness: Diabetes, hypertension, high cholesterol

risk factor: family history (genetics)

High cholesterol, atherosclerosis, history of chronic illness, history of hypertension

Common Diagnostic Tests

• CK-MB

• Troponin

• C-Reactive Protein

• Potassium (Serum)

• Serum lactate

• Cholesterol: HDL, LDL, Triglycerides

• Coagulation Labs

MORE Common Diagnostic Test

• Electrocardiogram (ECG/EKG)

• Cardiac stress tests

  • Exercise or pharmacological test

• Radiographic studies

  • Chest x-ray, ultrasound, arteriogram, echocardiogram

Basic EKG (parts of an EKG)

Note the normal waveforms and measurements:

•  P wave (atrial depolarization)

•  PR interval (slight atrial repolarization)

•  QRS (ventricular depolarization)

•  ST segment

•  T wave (Ventricular repolarization)

• This all happens in about 1 second!

P wave

atrial depolarization

PR interval

slight atrial repolarization

QRS

ventricular depolarization

T wave

Ventricular repolarization

Basic EKG Interpretation: 4 basic questions

• Rate – normal, brady, or tachy

• Rhythm – regular or irregular

• Is there a P for every QRS?

• Is the QRS normal or wide?

Normal Sinus

(Normal)

Sinus bradycardia

(rate is too slow)

sinus tachycardia

(rate is too fast)

atrial fibrilation

Irregular atrial signaling
(no P wave)

Decreased CO, increased risk of clotting

premature ventricular contraction 

Occasional irregular beat
(d/t ventricular signaling)

Ventricular Tachycardia

Can be sustained or nonsustained

Sustained = Emergency

Ventricular Fibrillation

No identifiable rhythm

Sustained = Emergency

Perfusion clinical management: Primary prevention 

• Smoking (causes vasoconstriction) and nicotine cessation

• Nutrition

• Exercise

Perfusion clinical management: Screening

˜Blood pressure screening

˜Lipid screening (HDL, LDL, Cholesterol, Triglycerides)

Perfusion Clinical Management: Collaborative Interventions

• Treatment strategies depend on underlying condition

• The most common strategies include:

  • Diet modification and smoking cessation

  • Increased activity (Cardiac reconditioning)

    • Inpatient

    • Immediately out-patient

    • Long term home management

    • Positioning

    • Activity level

  • Pharmacotherapy

Clinical Exemplars: Pregnancy and Fetal perfusion

• Increased blood volume, with decreased return

• Changes in hydrostatic pressure and blood pressure

• Problems with maternal perfusion can impact placental (fetal) perfusion

Perfusion Clinical Exemplars: Birth

• Monitor for signs of hemorrhage in birthing parent

Rapid changes in heart at birth

1. Assess newborns HR, BP, SpO2, heart sounds

2. Some transient cyanosis around mouth, hands, and feet is not uncommon in the first 3-4 days of life

Perfusion Clinical Exemplars: Infants and Children

Typically, perfusion problems
related to a congenital defect

Infants:

• Poor feeding

• Poor weight gain

• Failure to thrive

• Dusky color

Toddlers and children:

• Squatting and fatigue

• Developmental delay

• Failure to hit milestones

Clinical Exemplar: Infants

• Poor feeding

• Poor weight gain

• Failure to thrive

• Dusky color

Clinical Exemplar: Toddlers and children

• Squatting and fatigue

• Developmental delay

• Failure to hit milestones

Atrial Septal Defect

mixing of blood

Usually not detected till preschool years

What is an Atrial Septal Defect?

• there is a mixture of rich oxygenated and oxygenated blood due to a hole in the septum

• insufficient circulation and increased work load (Increase CO) 

Tetralogy of Fallot

4-5 defects

Infants develop hypoxia and cyanosis

What is the Tetralogy of Fallot?

• a hole in the ventricles 

• mixture of oxygenated and deoxygenated blood

• overriding aorta

Transposition of the Great Arteries

The pulmonary artery and the aorta are transposed

this is life threatening at birth.

What is Transposition of the Great Arteries?

• the heart is ONLY pumping DEOXYGENATED blood 

• PFO is what is keeping the baby alive 

  • allows a little bit of oxygen for the baby to survive

Clinical Exemplars: Adults

• Myocardium less efficient and less contractible

• SA Node decreases control

• Left ventricular slight hypertrophy

• Vessels become stiffer

Clinical Exemplars: Shock

Impaired tissue perfusion to the entire body

• Results in inadequate cellular oxygenation and life-threatening cellular dysfunction.

Clinical Exemplars: Types of Shock

• hypovolemic 

• cariogenic shock

• obstructive shock

• disruptive shock 

  • septic shock

  • neurogenic shock

  • anaphylactic shock

hypovolemic shock

• (Intravascular volume loss – absolute or relative)  

• hemorrhage= absolute and relative = fluid shift

Cardiogenic Shock

Pump failure

Obstructive Shock

Physical obstruction

Distributive shock

Systemic vasodilation

septic shock

infection

Neurogenic Shock

Spinal Cord Injury

Anaphylactic Shock

Widespread hypersensitivity AKA anaphylaxis

TYPES OF Clinical Exemplars: Classes of Shock

early, compensatory, decompensated, refractory

early class of shock

Something causes a decrease in Mean Arterial Pressure (MAP) – (This stage is rarely detected!)

compensatory class of shock

• Body starts to compensate for a lack of MAP.

• Changes to HR, BP, peripheral perfusion, mental status noted

decompensated class of shock

• Body no longer compensating for lack of perfusion

• Notable changes in assessment indicating WORSENING perfusion

refractory class of shock

• Irreversible. Results in death of cells, tissues, organs

Clinical Exemplars: Atherosclerosis, Angina

Notice:

• What does Atherosclerosis do to perfusion?

• What is the difference between: Stable and Unstable angina

• What does ST-Segment elevation look like on an ECG?

• What does Atherosclerosis do to perfusion?

blocking or decrease flow to tissues and/organs by narrowing or hardening the arteries

Angina

chest pain 

stable angina

• has a regular pattern 

• rest and medications usually help

unstable angina

• random pattern

• pain usually doesn’t go away with medications

what does ST-segment elevation look like on an ECG?

• ST raised in baseline

• plaque in the coronaries

• ischemia or infraction 

Pharmacotherapy: Impaired Perfusion

• RAAS suppressants
  (ACEIs and ARBs)

• Adrenergic antagonists
  (beta and alpha)

• Calcium channel blockers

• Organic nitrates

• Digoxin

• Statins

Vasopressors

• Cause vasoconstriction to increase blood pressure

• Used in certain types of shock, critical care settings

RAAS Suppressants: ACE-I & ARBS

Angiotensin-Converting Enzyme Inhibitors (ACEIs) “prils”

• enalapril

• lisinopril

˜

Angiotensin II Receptor Blockers (ARBs) “sartans”

• Losartan

• Valsartan

Treatment of:

• High Blood pressure

• Heart Failure symptoms
  (excess fluid volume)

• Reduce risk of MI, stroke

• Slow progression of diabetic
  nephropathy

Angiotensin-Converting Enzyme Inhibitors (ACEIs) “prils”

• enalapril

• lisinopril

Angiotensin II Receptor Blockers (ARBs) “sartans”

• Losartan

• Valsartan

Types of treatment for RAAS Suppressants: ACE-I & ARBS

• High Blood pressure

• Heart Failure symptoms
  (excess fluid volume)

• Reduce risk of MI, stroke

• Slow progression of diabetic
  nephropathy

RAAS Suppressants: ACE-I & ARBS —> Assessment

Is the med appropriate?

• Assess blood pressure / Cardiac Assessment

• Treat High Blood pressure

• Treat Heart Failure symptoms (excess fluid volume)

• Reduce risk of MI, stroke

• Slow progression of diabetic nephropathy

RAAS Suppressants: ACE-I & ARBS —> Caution 

Contraindicated in: Pregnancy; history of angioedema; renal artery stenosis

RAAS Suppressants: ACE-I & ARBS —> Effects

dehydration 

RAAS Suppressants: ACE-I & ARBS —> Implementation/Patient teaching

Drug interactions:

Concurrent use of drugs that lower BP can cause exaggerated hypotension

Concurrent use of potassium-sparing diuretics and potassium supplements can cause exaggerated hyperkalemia

Concurrent use of lithium may result in lithium toxicity

Concurrent use of NSAIDs may reduce effectiveness of ACE inhibitor

RAAS Suppressants: ACE-I & ARBS —> Evaluation 

Did it work?

Consider why was this patient taking the med?

HTN: BP is lower

CHF: less symptoms of fluid volume overload

Diabetic Nephropathy: is kidney function better?

TYPES OF RAAS Suppressants: Planning, Implementation

• 1st dose

• cough

• hyperkalemia

• Angioedema

RAAS Suppressants:
Planning, Implementation —> 1st dose hypertension

ACEI: Yes

ARB: No

Nursing Interventions: Monitor, ensure safety

RAAS Suppressants:
Planning, Implementation —> Cough

ACEI: Yes

ARB: No

Nursing interventions: Monitor, Problem?

RAAS Suppressants:
Planning, Implementation —> Hyperkalemia

ACEI: Yes

ARB: Yes

Nursing Interventions: Avoid with other meds that raise K+, and salt substitutes

RAAS Suppressants:
Planning, Implementation —> Angioedema

ACEI: Rare 

ARB: Even more rare

Nursing Interventions: Monitor Emergency!!

SNS Activation stimulates

alpha and beta receptors

Beta Blockers – “olol’s”

Non-cardioselective (Block beta 1 AND 2)

• Propranolol

Cardioselective (Block beta 1 only)

• Metoproplol

Treatment of:

• High blood pressure

• Heart failure symptoms

• Angina pectoris

• Dysrhythmias (which type?)

Non-cardioselective (Block beta 1 AND 2)

Propranolol