Cardiac Function, Heart Failure, & Circulatory Shock (Ch. 27)-- Definition First Flashcards by Hannah Hinckley

Hypovolemic
- Acute blood loss (15% or more)
Cardiogenic
- Heart fails to pump sufficient amount of blood
Distributive (Normovolemic)
- Capacity of vascular compartment expands
  - Neurogenic
  - Anaphylactic
  - Septic

Types of Shock

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Left Ventricular Heart Failure

d/t– HTN (hypertrophy), Myocardial Ischemia (ventricular remodeling)

Diastolic failure
LVEF > 50% (normal)
⇣ LV Compliance → Abnormal diastolic relaxation → Pulmonary edema

S/S– Dyspnea w/ exertion, Fatigue

Treatment– None

Heart Failure with Preserved Ejection Fraction (HFpEF)

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Zone of hypoxic injury
- May progress to necrosis or return to normal
Zone of reversible ischemia
- May progress to necrosis or return to normal
Sudden severe chest pain
- Can radiate to neck, jack, arm, or epigastric region
Sending of impending doom → death
SOB
Weakness
N/V
Diaphoresis

Monitoring–

EKG
- Assess for rhythm changes
- Continuous monitoring
Vitals
O₂ levels
Lab work
- Troponin I
  - Most specific
  - Elevated 2-12 hrs. after damage
  - Remains elevated 2-4 wks.
- Creatinine Phosphokinase-MB (CPK-MB)
  - Not specific to the heart
  - Elevates w/i 4-8 hrs.
  - Peaks @ 24 hrs.

Myocardial Infarction Clinical Manifestations

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Infection of the inner surface of the heart

Microbial agents w/i valves & endocardium → Vegetation & destruction of cardiac tissue

High mortality rate
Staphylococcal infections
- Most common
Aortic & Mitral valves
- Most common
Acute
- Rapid onset
- Normal heart valves
Sub-acute
- Evolves slowly over months
- Underlying valve abnormality
- Life-threatening

d/t– Dental or surgical procedures, Illicit IV drug use, Valve or congenital abnormalities (⇡ risk)

Prevention– Prophylactic antibiotics (w/ dental or surgical procedure)

Infectious Endocarditis (IE)

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Widespread Type I Hypersensitivity reaction → Vasodilation & Hypovolemia

Treatment– Epinephrine → Vasoconstriction, Bronchodilation, ⇡ CO & Contractility, ⇣ Histamine

TOP PRIORITY: Maintain airway

Anaphylactic Shock

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Systemic Inflammatory Response System

Microvascular damage that causes clotting at all sites simultaneously

Inflammation → Endothelial injury → Clotting process repeats (steps 3-5) → All platelets & clotting factors used up → Uncontrolled bleeding

Disseminated Intravascular Coagulation (DIC)

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Life-threatening compression of the heart d/t accumulation of fluid w/i pericardial sac

Inflammation & pressure
Fluid displaces septum
- w/ inspiration
⇡ Intracardiac pressure
⇣ LV filling
⇣ SV
⇣ CO
Pulsus paradoxus
- 10 mmHg + decrease in SBP w/ inspiration

Cardiac Tamponade

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Volume ejected from ventricle w/ each beat

Stroke Volume (mL/beat)

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Short-term pericardial inflammation

< 2 weeks
Infectious or non-infectious

Acute Pericarditis

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Left Ventricular Heart Failure

d/t– Damage to myocardial tissue (MI, chronic HTN)

Systolic failure
LVEF < 40%
Dilation → ⇡ Preload → ⇣ Contractility
Ventricular remodeling d/t–
- ⇡ SANS
- ⇡ RAAS
- ⇡ Inflammatory mediators

Heart Failure with Reduced Ejection Fraction (HFrEF)

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Immune-mediated inflammatory response to group A streptococcal pharyngitis

Affects heart, skin, & connective tissue
Acute
- Inflammation of all 3 layers & valves
  - Epicardium
  - Myocardium
  - Endocardium
- History of streptococcal infection
  - Inflammatory lesions
Recurrent phase
- Continued effects
Chronic phase
- Permanent deformity of valves
- 10+ years after initial infection

Rheumatic Heart Disease/Rheumatic Fever

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Ascites
- Fluid w/i abdomen
Lower extremity edema
Dyspnea w/ exertion
Fatigue

Constrictive Pericarditis Clinical Manifestations

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⇡ Preload = ⇡ SV
- The further you stretch a rubberband, the harder it snaps back
Inotropy (⇡ SANS)
- ⇡ Contractility
  - Curve shifts up & L
Failure
- ⇣ Contractility
  - Curve shifts down & R

Frank-Starling Mechanism

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Mitral valve stenosis (narrowing)
Rheumatic carditis
Polyarthritis
- Most common
Skin lesions

Rheumatic Heart Disease Clinical Manifestations

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Proportion of blood pumped out of ventricle with each beat

Measured w/ echocardiogram

LVEF (%) = (SV/EDV)100

LVEF= Left ventricular ejection fraction (normal 55-75%)

SV= Stroke volume

EDV= End diastolic volume

Ejection Fraction (EF)

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Neurohumoral compensatory mechanism of HF

Diuresis & Natriuresis (⇡ GFR) → ⇣ Fluid volume → ⇣ Workload of the heart

Inhibit SANS, RAAS, ADH/Vasopressin, & CNS thirst/salt appetite signaling

Atrial natriuretic peptide (ANP)
- Released from atrium
  - d/t atrial stretch, pressure, or fluid overload
B-type natriuretic peptide (BNP)
- Released from ventricles
  - d/t increased ventricular pressure or fluid overload
  - Measured clinically

Natriuretic Peptides

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Goal: Control compensatory mechanisms

First-line HFrEF treatment
- Diuretics
  - ⇣ Blood volume
- ACE-Is
  - ⇣ RAAS
- Beta-Blockers
  - ⇣ SANS

Heart Failure Pharmacological Treatments

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Imbalance → Ischemia, Angina, MI, or sudden death

Supply
- Determinants:
  - Perfusion of blood to capillaries
    - O₂-carrying capacity of blood
      - Hgb levels
Demand
- ⇡ LV contractility → ⇡ O₂demand
  - Systole
- ⇡ HR → ⇡ O₂demands & ⇣ Blood flow d/t ⇣ Filling time
- ⇡ LV pressure → ⇡ O₂ demand & Coronary artery pressure
  - d/t ⇡ Preload
  - Water balloon effect

Myocardial Oxygen Supply & Demand

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Life-threatening complication of shock

Progressive dysfunction of two or more organ systems

d/t– Uncontrolled inflammatory response to severe injury/illness (sepsis, trauma, burns, major surgery…)

Manifestations
- Dysfunction of–
  - Respiratory organs
  - Liver
  - Kidneys
  - GI organs
  - Heart failure

Interventions– Support affected organs

Multiple Organ Dysfunction System (MODS)

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Coronary blood flow doesn’t meet metabolic demands of heart

1st– Stable angina

2nd– Unstable angina → ACS

Prolonged– MI (STEMI or non-STEMI)

Myocardial Ischemia

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Dilated LV w/ thin walls (“floppy”) → ⇣ Contractility → ⇡ Preload → Systolic dysfunction & HF

d/t– DM, MI, Alcoholism, Hyperthyroidism

Dilated (Congestive) Cardiomyopathy

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Acute Lung Injury (ALI)/Acute Respiratory Distress Syndrome (ARDS)
- Sudden onset of profound dyspnea
- Hypoxemia refractory to supplemental O₂
- Potentially fatal
Acute Kidney Injury (AKI)
- ⇣ Renal perfusion
Disseminated Intravascular Coagulation (DIC)
Multiple Organ Dysfunction Syndrome (MODS)

Complications of Shock

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Chest pain
- ⇡ w/ breathing, coughing, swallowing, & positional changes
- ⇣ w/ sitting upright & leaning forward
Pericardial friction rub
EKG changes
⇣ CRP
- C-reactive protein
⇣ ESR
- Erythrocyte sedimentation rate

Treatment– NSAIDs, Antimicrobials

Acute Pericarditis Clinical Manifestations

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Acute loss of blood volume (600-900 mLs)

d/t– Hemorrhage, Burns (⇣ plasma), Loss of GI fluid (N/V)

Compensation
- ⇡ SANS
- ⇡ RAAS
- ⇡ ADH/Vasopressin
Nursing interventions
- STOP blood loss
- Replace lost volume

Hypovolemic Shock

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**Heart fails to pump** adequate amount of blood to **meet O₂ demands** d/t-- MI w/ LV failure * **⇣ CO** * Tissue hypoxia * **Normal vascular volume** * Compensatory mechanisms * **WORSEN** situation * ⇡ SANS * **⇡ HR** * **⇡ Preload** * ⇡ RAAS * **⇡ Blood volume** * ⇡ ADH/Vasopressin * **⇡ Blood volume**

Cardiogenic Shock

Dysfunction **@ any valve → Heart Failure** (HF) * **Stenosis** * Narrowing/stiffness of valve * Impaired valvular opening * **⇡ Resistance** → ⇡ Myocardial work & ⇡ Heart chamber volume * **Incompetent/Regurgitant Valve** * “Floppy” * Impaired valvular closing * **Backflow** of blood

Valvular Heart Disease

**⇡ Afterload → Hypertrophy of myocytes** to compensate for ⇡ workload Diastolic dysfunction → Systolic dysfunction d/t-- **HTN, Aortic stenosis** (Narrowing of aortic opening)

Hypertensive (Valvular) Hypertrophic Cardiomyopathy

Assessment of coronary blood flow & perfusion * Done under **x-ray** * **Invasive, sterile procedure** * Catheter placed in **femoral or brachial artery or vein** * Assess blood flow through the heart * **Angioplasty** * Inflate balloon → Improved blood flow through arteries * **Stent** * Metal mesh coil keeps arteries open * Heart tissue biopsy * Fractional flow reserve * Measurement of arterial blockage * Intravascular ultrasound (IVUS) * Blood vessel lumen measurement

Cardiac Catheterization

* **Unpredictable chest pain unrelieved** w/ rest & nitroglycerin * Occurs @ rest & w/ exertion * **Ruptured** atherosclerotic plaque * **Reversible MI** * Forewarning * **Return of perfusion** before significant necrosis occurs * Transient episodes @ site of plaque damage * **Thrombotic vessel occlusion** * **Vasoconstriction**

Unstable Angina

* Non-Invasive * **Chest x-ray** * Fluid congestion * White cotton candy-like appearance * **Echocardiogram** * Elevated filling pressures * Invasive * R heart or pulmonary artery **catheterization**

Objective Evidence of Cardiogenic Systemic or Pulmonary Congestion

* Impaired **contractility** * **Deprivation of myocardial O₂ & nutrients** * Mismatch b/w supply & demand * Leads to **CAD**

Atherosclerosis

Clinical syndrome d/t **structural or functional cardiac abnormality;** End result of many clinical disease states (no single S/S) Corroborated by: * **⇡ Natriuretic peptide levels** * and/or **Objective evidence of cardiogenic pulmonary or systemic congestion** **Ventricle** is either **too weak** (dilation) **or too stiff** (stenosis) to pump blood d/t-- **Ischemic heart disease** (post-MI) and/or **HTN** → **Hypertrophy** and/or **Dilation** Risk factors-- * Age * Obesity * DM * **Renal failure** * **Valvular heart disease** * **Cardiomyopathies** * **Congenital heart disease** * Myocarditis * Excessive alcohol intake

Heart Failure

Assessment of coronary blood flow & perfusion * Measure of **electrical conduction through the heart** * Impacted by * **Temperature** * **Stress** * Full * 12 leads * Monitor * 3-5 leads

Electrocardiogram

* Pressure/Volume * **@ end of diastole** * on **LV wall** prior to contraction * Determinants * **End systolic volume** * **Venous return** * Increases w/ * **⇣ Contractility** * **⇡ Plasma volume**

Preload (End Diastolic Volume)

**Prolonged ischemia** causes irreversible damage to the heart muscle **(myocyte necrosis)** * Myocyte **injury → death** * Structural & functional changes of cardiomyocytes (permanent cells) * Adverse myocardial **remodeling** * **Fibrosis of myocardium**

Myocardial Infarction

**Pulmonary** vascular congestion & **⇣ CO** Left = Lungs **⇡ Pulmonary** hydrostatic pressure → **Pulmonary edema & Dyspnea** * **Exertional dyspnea** * SOB w/ activity * **Orthopnea** * SOB while laying flat * **Paroxysmal nocturnal dyspnea** * Sudden SOB while sleeping * **Fatigue & weakness** * Especially w/ exertion * **Pulmonary edema** * Cough * **Crackles** * **Wheezes** * **Sputum** * Blood-tinged * **Frothy** * Tachypnea * Confusion * Tachycardia * Cyanosis * Restlessness

Left Heart Failure Clinical Manifestations

* Stenosis * Incomplete **opening of MV** during diastole → **LA distention/dilation** & Impaired LV filling → ⇡ **Pressure** w/i pulmonary venous system → **Pulmonary edema** * Regurgitation d/t MV prolapse * Incomplete **closure of MV → Backflow** into LA (systole) **→** LA distention/dilation & **⇣ LV SV** → LV Hypertrophy → **LV HF**

Mitral Valve Disorders

Known or suspected infection → **Overactivation of inflammatory response** * Systemic **inflammatory** response syndrome **S/S** * **Fever** * **Tachycardia** * **Leukocytosis** * **Altered mental status** * **Hyperglycemia** * SEVERE * **Organ dysfunction** * **Tissue hypoxia** * SHOCK * **Hypotension** * Even w/ fluid replacement * ⇡ Risk of mortality

Sepsis

* Venricular assist device * **LVAD**/bi-VAD * Internal device * **Takes over work of LV** * ⇡ Survival rates * Bridge gap to transplant * High maintainence * Infection & blood clot risk * Heart transplantation * Survival rate * 85% after one year * 65% after 5 years * **Low donor availability**

Advanced Therapy in End-Stage HF

* **Dilated** * Congestive * **Hypertrophic** * Obstructive * Hypertensive (Valvular)

Types of Cardiomyopathies

**Acute failure of circulatory system** to supply **peripheral tissues and organs** with adequate blood supply **resulting in cellular hypoxia** * **⇣ O2 & Nutrients** * **⇡ Waste** * Impaired cellular metabolism * Aerobic → **Anaerobic** * Release of **inflammatory mediators**

Circulatory Shock

* **Frank-Starling mechanism** * SANS * RAAS * Natriuretic peptides * Myocardial hypertrophy → Remodeling

Compensatory Mechanisms of the Heart

* Pharmacologic therapy * **ASA** (chewed) * ⇣ Platelet aggregation * **Morphine** * Pain * Vasodilation * **Sublingual Nitroglycerin (MONA)** * Vasodilation * Supplemental O2 * Active STEMI (EKG verfied) * Percutaneous coronary intervention **(PCI)**-- w/i 60 min. * **Cath lab** * Coronary artery bypass graft **(CABG)** * Fibrinolysis-- w/i 30 min. * Tissue plasminogen activator **(tPA)** * **“Clot buster”** * If no cath lab

MI Treatment (STEMI)

**Occlusion or stenosis of coronary arteries** → **Imbalance** b/w coronary blood **supply** and myocardial O₂ & nutrient **demand** d/t-- Atherosclerosis (most common)

Coronary Artery Disease (CAD)

Amount of blood ejected in **one minute (4-6 L)** ## Footnote **CO = SV x HR**

Cardiac Output (mL/min)

* **Can and do coexist** * **HFpEF** * **Diastolic** failure * Dilation → **⇣ Preload** * Preserved ejection fraction * **LVEF \> 50%** * **HFrEF** * **Systolic** failure * **⇣ Contractility** * Reduced ejection fraction * **LVEF \< 40%**

Types of Left Ventricular Heart Failure

The extent of necrosis determines EKG tracing differences * **STEMI** * **ST-segment elevation** * **Full necrosis** of one area * Blocked conduction * “Tombstone” = **MI** * **Non-STEMI** * Non-ST segment elevation * **ST-segment** **depression** * **Partial necrosis** * **⇣** Conduction * OR **T inversion** * May indicate **ischemia** * Does not always = MI

Myocardial Infarction Types

* **Predictable** **chest pain relieved** w/ rest & nitroglycerin * **Fixed** atherosclerotic plaque * Narrow/partially occluded vessel * @ Rest, supply = demand * **Exertion →** chest pain * Vasoconstriction → Mismatch b/w supply and demand

Stable Angina

**Decreased SANS** control of blood vessel tone **Increased PANS** activity d/t-- **Neurologic** injury (**vasomotor center** defect-- brain stem injury or anesthesia; **sympathetic outflow** defect-- spinal cord injury) * **Massive vasodilation** * **⇣** Vascular tone

Neurogenic Shock

* Fatigue & weakness * **⇣ CO** * Cognitive impairment * **d/t ⇣ brain perfusion** * Confusion * Memory loss * Restlessness * Anxiety * Insomnia * Cachexia & malnutrition * **Ascites & tissue wasting w/ end-stage HF** * **⇣** food intake d/t depression, illness, GI congestion * Sudden cardiac death * **d/t ventricular tachycardia or fibrillation**

Heart Failure Clinical Manifestations

* **Force** * **LV must generate** to eject blood into aorta * **@ beginning of systole** * “Load” against which heart must pump * Determinants * **PVR** * ⇡ BP = ⇡ CO & ⇡ PVR * Increased w/ * **⇡ PVR** * **HTN**

Afterload

**Systemic** circulatory pressures & **⇣ CO;** Inbility of RV to **provide adequate blood flow to pulmonary circulation** d/t-- L HF, **Pulmonary HTN** (hypoxic pulmonary disease) Right = Rest of the body **⇡ Peripheral** hydrostatic pressure → **Edema & Third spacing** * **JVD** * **Edema** * **Peripheral** * **Dependent** * **Hepatosplenomegaly** * GI distress * Anorexia * **Ascites** * **Weight gain**

Right Heart Failure Clinical Manifestations

Measure of coronary blood flow & perfusion * Assessment of **structure & function of the heart** * **Ultrasound** * Valves * Septal movement & volume * Measurements

Echocardiogram

* **Anaerobic** metabolism * **Lactic acid** accumulation * ⇣ ATP → **Na⁺/K⁺ ATPase pump failure** * **⇡** Membrane permeability **→ Cell swells & bursts** * **Compensatory** mechanisms **(Short-term)** * **⇡ SANS** * ⇡ HR * Vasoconstriction * ⇡ Renin * **⇡ Angiotensin II** * Vasoconstriction * ⇡ Blood volume * **⇡ Aldosterone** * ⇡ Blood volume

Shock Response

* ⇡ Blood volume * ⇡ BP * ⇡ PVR * ⇡ Preload * ⇡ CO

RAAS

**Sudden coronary obstruction** d/t thrombosis formation b/c of an **unstable lesion** d/t-- **Unstable angina**, MI (STEMI or non-STEMI) * Complications * **Dysrhythmias** * **CHF** * **Sudden death**

Acute Coronary Syndrome

Development of a **constrictive membrane** around the heart * **Scar tissue b/w visceral & parietal layers** * Fixed CO * Regardless of contractility d/t-- Chronic inflammation, Cardiac surgery Infection & Removal of pericardial sac → Remodeling

Constrictive Pericarditis

Inappropriate **ventricular hypertrophy** or dilation d/t-- **Genetics, Ischemia, MI** (ventricular remodeling), Idiopathic

Cardiomyopathies

Thickening of septal wall/**⇣ LV chamber size** → **⇣ Outflow from LV → ⇣** Compliance & **⇣ SV** **⇣** Ventricular relaxation & **⇣** Compliance → **Impaired diastole** * Most common inherited heart defect * **Autosomal dominant** * 1:500 * Cause of **sudden cardiac death in young athletes**

Hypertrophic (Obstructive) Cardiomyopathy

* Stenosis * **⇡ Afterload → LV Hypertrophy** → HF * Regurgitation * **⇡ Preload → ⇡ Size/Dilation of LV → ⇡ SV** → HF

Aortic Valve Disorders

**Myocardial tissue necrosis** d/t impaired coronary blood flow Coronary occlusion → Necrosis in **10 seconds** w/o O₂

Myocardial Infarction

* **Preload** * **Afterload** * **Contractility**

Factors Affecting Stroke Volume (SV)

* Dyspnea * **Orthopnea** * SOB when laying down * **Paroxysmal nocturnal dyspnea** * Wake up d/t SOB * ⇣ Exercise tolerance * Fatigue * Edema * **Bendopnea** * SOB w/ bending over * **JVD** * S3 (Third heart sound) * **Cardiomegaly** * **Hepatojugular reflex** * JVD w/ pressure on the liver

Heart Failure Clinical Manifestation

Ability of **myocardial** tissue to **contract** **⇣** d/t-- **MI** (most common), **⇣ O₂ supply**

Contractility

Accumulation of fluid in pericardial cavity → **Cardiac tamponade** (compression/pressure) & **Pulsus paradoxus** (exaggeration drop in BP w/ inhalation) d/t-- Inflammation or infection (CA, cardiac surgery, trauma…) Treatment-- Removal of fluid, **Percardiocentesis** (needle aspiration)

Pericardial Effusion

* **S/S of systemic infection** * Fever * ⇡ WBCs * Chills * Diaphoresis * **Heart murmur**

Infectious Endocarditis Clinical Manifestations

Dysfunction = **Coronary Artery Disease** (CAD) * **Physical** factors * Aortic bp * **Systole** = Contraction/Pushing * Coronary arteries compress * **Diastole** = Relaxation/Filling * Perfusion of the heart * **Neural** factors * **SANS** * ⇡ Flow * **PANS** * **⇣** Flow * Changes in HR, contractility, & bp * **Myocardial metabolic** factors * Driven by **O₂ demands** * Protective factors * **Adenosine** * Vasodilation → ⇡ Blood flow * **Nitric oxide** * Vasodilation

Control of Coronary Blood Flow

* Can lead to each other * **Left ventricular failure** * HFpEF * HFrEF * **Right ventricular failure** * **Both ventricles fail**

Types of Heart Failure

Cardiac Function, Heart Failure, & Circulatory Shock (Ch. 27)-- Definition First Flashcards

Exam 2