Cardiac Function, Heart Failure, & Circulatory Shock (Ch. 27)-- Term First Flashcards
Exam 2
Coronary Artery Disease (CAD)
Occlusion or stenosis of coronary arteries → Imbalance b/w coronary blood supply and myocardial O2 & nutrient demand
d/t– Atherosclerosis (most common)
Heart Failure Clinical Manifestations
- Fatigue & weakness
- ⇣ CO
- Cognitive impairment
-
d/t ⇣ brain perfusion
- Confusion
- Memory loss
- Restlessness
- Anxiety
- Insomnia
-
d/t ⇣ brain perfusion
- Cachexia & malnutrition
-
Ascites & tissue wasting w/ end-stage HF
- ⇣ food intake d/t depression, illness, GI congestion
-
Ascites & tissue wasting w/ end-stage HF
- Sudden cardiac death
- d/t ventricular tachycardia or fibrillation
Constrictive Pericarditis Clinical Manifestations
-
Ascites
- Fluid w/i abdomen
- Lower extremity edema
- Dyspnea w/ exertion
- Fatigue
Frank-Starling Mechanism
-
⇡ Preload = ⇡ SV
- The further you stretch a rubberband, the harder it snaps back
- Inotropy (⇡ SANS)
-
⇡ Contractility
- Curve shifts up & L
-
⇡ Contractility
- Failure
- ⇣ Contractility
- Curve shifts down & R
- ⇣ Contractility
Cardiomyopathies
Inappropriate ventricular hypertrophy or dilation
d/t– Genetics, Ischemia, MI (ventricular remodeling), Idiopathic
Acute Pericarditis
Short-term pericardial inflammation
- < 2 weeks
- Infectious or non-infectious
Contractility
Ability of myocardial tissue to contract
⇣ d/t– MI (most common), ⇣ O2 supply
MI Treatment (STEMI)
- Pharmacologic therapy
-
ASA (chewed)
- ⇣ Platelet aggregation
-
Morphine
- Pain
- Vasodilation
-
Sublingual Nitroglycerin (MONA)
- Vasodilation
-
ASA (chewed)
- 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
- Tissue plasminogen activator (tPA)
- Percutaneous coronary intervention (PCI)– w/i 60 min.
Constrictive Pericarditis
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
Pericardial Effusion
Accumulation of fluid in pericardial cavity → Cardiac tamponade
d/t– Inflammation or infection (CA, cardiac surgery, trauma…)
Treatment– Removal of fluid, Percardiocentesis (needle aspiration)
Ejection Fraction (EF)
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
Shock Response
-
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
-
⇡ Angiotensin II
-
⇡ SANS
Objective Evidence of Cardiogenic Systemic or Pulmonary Congestion
- Non-Invasive
-
Chest x-ray
- Fluid congestion
- White cotton candy-like appearance
- Fluid congestion
-
Echocardiogram
- Elevated filling pressures
-
Chest x-ray
- Invasive
- R heart or pulmonary artery catheterization
Myocardial Infarction
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
- Adverse myocardial remodeling
Natriuretic Peptides
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
- Released from atrium
- B-type natriuretic peptide (BNP)
- Released from ventricles
- d/t increased ventricular pressure or fluid overload
- Measured clinically
- Released from ventricles
Myocardial Infarction Types
The extent of necrosis determines EKG tracing differences
-
STEMI
-
ST-segment elevation
-
Full necrosis of one area
- Blocked conduction
- “Tombstone” = MI
-
Full necrosis of one area
-
ST-segment elevation
-
Non-STEMI
- Non-ST segment elevation
-
ST-segment depression
-
Partial necrosis
- ⇣ Conduction
-
Partial necrosis
- OR T inversion
-
ST-segment depression
- May indicate ischemia
- Does not always = MI
- Non-ST segment elevation
Cardiac Catheterization
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
Atherosclerosis
- Impaired contractility
-
Deprivation of myocardial O2 & nutrients
- Mismatch b/w supply & demand
- Leads to CAD
Types of Shock
-
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
- Capacity of vascular compartment expands
Rheumatic Heart Disease Clinical Manifestations
- Mitral valve stenosis (narrowing)
- Rheumatic carditis
-
Polyarthritis
- Most common
- Skin lesions
Myocardial Ischemia
Coronary blood flow doesn’t meet metabolic demands of heart
1st– Stable angina
2nd– Unstable angina → ACS
Prolonged– MI (STEMI or non-STEMI)
Acute Coronary Syndrome
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
Types of Heart Failure
- Can lead to each other
-
Left ventricular failure
- HFpEF
- HFrEF
- Right ventricular failure
- Both ventricles fail
Electrocardiogram
Assessment of coronary blood flow & perfusion
- Measure of electrical conduction through the heart
- Impacted by
- Temperature
- Stress
- Full
- 12 leads
- Monitor
- 3-5 leads
Stroke Volume (mL/beat)
Volume ejected from ventricle w/ each beat
Aortic Valve Disorders
- Stenosis
- ⇡ Afterload → LV Hypertrophy → HF
- Regurgitation
- ⇡ Preload → ⇡ Size/Dilation of LV → ⇡ SV → HF
Cardiogenic Shock
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
Acute Pericarditis Clinical Manifestations
-
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
Hypertrophic (Obstructive) Cardiomyopathy
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
Afterload
-
Force
-
LV must generate to eject blood into aorta
- @ beginning of systole
- “Load” against which heart must pump
-
LV must generate to eject blood into aorta
- Determinants
-
PVR
- ⇡ BP = ⇡ CO & ⇡ PVR
-
PVR
- Increased w/
- ⇡ PVR
- HTN
Complications of Shock
- 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)
Control of Coronary Blood Flow
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
-
SANS
-
Myocardial metabolic factors
- Driven by O2 demands
- Protective factors
-
Adenosine
- Vasodilation → ⇡ Blood flow
-
Nitric oxide
- Vasodilation
-
Adenosine
Circulatory Shock
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
RAAS
- ⇡ Blood volume
- ⇡ BP
- ⇡ PVR
- ⇡ Preload
- ⇡ CO
Multiple Organ Dysfunction System (MODS)
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
- Dysfunction of–
Interventions– Support affected organs
Sepsis
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
-
Hypotension
Infectious Endocarditis (IE)
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)
Myocardial Infarction
Myocardial tissue necrosis d/t impaired coronary blood flow
Coronary occlusion → Necrosis in 10 seconds w/o O2
Compensatory Mechanisms of the Heart
- Frank-Starling mechanism
- SANS
- RAAS
- Natriuretic peptides
- Myocardial hypertrophy → Remodeling
Advanced Therapy in End-Stage HF
- 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
-
LVAD/bi-VAD
- Heart transplantation
- Survival rate
- 85% after one year
- 65% after 5 years
- Low donor availability
- Survival rate
Echocardiogram
Measure of coronary blood flow & perfusion
- Assessment of structure & function of the heart
-
Ultrasound
- Valves
- Septal movement & volume
- Measurements
-
Ultrasound
Right Heart Failure Clinical Manifestations
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
Types of Left Ventricular Heart Failure
- Can and do coexist
-
HFpEF
-
Diastolic failure
- Dilation → ⇣ Preload
- Preserved ejection fraction
- LVEF > 50%
-
Diastolic failure
-
HFrEF
-
Systolic failure
- ⇣ Contractility
-
Systolic failure
- Reduced ejection fraction
- LVEF < 40%
Cardiac Tamponade
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
Rheumatic Heart Disease/Rheumatic Fever
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
- Inflammation of all 3 layers & valves
- Recurrent phase
- Continued effects
- Chronic phase
- Permanent deformity of valves
- 10+ years after initial infection
Factors Affecting Stroke Volume (SV)
- Preload
- Afterload
- Contractility
Types of Cardiomyopathies
-
Dilated
- Congestive
-
Hypertrophic
- Obstructive
- Hypertensive (Valvular)
Heart Failure with Preserved Ejection Fraction (HFpEF)
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
Neurogenic Shock
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
Stable Angina
- 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
- Narrow/partially occluded vessel
Heart Failure with Reduced Ejection Fraction (HFrEF)
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
Mitral Valve Disorders
- 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
Myocardial Infarction Clinical Manifestations
-
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.
-
Troponin I
Heart Failure
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
Preload (End Diastolic Volume)
- Pressure/Volume
- @ end of diastole
- on LV wall prior to contraction
- Determinants
- End systolic volume
- Venous return
- Increases w/
- ⇣ Contractility
- ⇡ Plasma volume
Unstable Angina
-
Unpredictable chest pain unrelieved w/ rest & nitroglycerin
- Occurs @ rest & w/ exertion
-
Ruptured atherosclerotic plaque
-
Reversible MI
- Forewarning
- Return of perfusion before significant necrosis occurs
-
Reversible MI
- Transient episodes @ site of plaque damage
- Thrombotic vessel occlusion
- Vasoconstriction
Valvular Heart Disease
Dysfunction @ any valve → Heart Failure (HF)
-
Stenosis
- Narrowing/stiffness of valve
- Impaired valvular opening
- ⇡ Resistance → ⇡ Myocardial work & ⇡ Heart chamber volume
- Narrowing/stiffness of valve
-
Incompetent/Regurgitant Valve
- “Floppy”
- Impaired valvular closing
- Backflow of blood
- “Floppy”
Infectious Endocarditis Clinical Manifestations
-
S/S of systemic infection
- Fever
- ⇡ WBCs
- Chills
- Diaphoresis
- Heart murmur
Hypovolemic Shock
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
Hypertensive (Valvular) Hypertrophic Cardiomyopathy
⇡ Afterload → Hypertrophy of myocytes to compensate for ⇡ workload
Diastolic dysfunction → Systolic dysfunction
d/t– HTN, Aortic stenosis (Narrowing of aortic opening)
Disseminated Intravascular Coagulation (DIC)
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
Myocardial Oxygen Supply & Demand
Imbalance → Ischemia, Angina, MI, or sudden death
-
Supply
- Determinants:
-
Perfusion of blood to capillaries
- O2-carrying capacity of blood
- Hgb levels
- O2-carrying capacity of blood
-
Perfusion of blood to capillaries
- Determinants:
-
Demand
-
⇡ LV contractility → ⇡ O2 demand
- Systole
- ⇡ HR → ⇡ O2 demands & ⇣ Blood flow d/t ⇣ Filling time
-
⇡ LV pressure → ⇡ O2 demand & Coronary artery pressure
- d/t ⇡ Preload
- Water balloon effect
-
⇡ LV contractility → ⇡ O2 demand
Cardiac Output (mL/min)
Amount of blood ejected in one minute (4-6 L)
CO = SV x HR
Left Heart Failure Clinical Manifestations
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
Heart Failure Pharmacological Treatments
Goal: Control compensatory mechanisms
- First-line HFrEF treatment
-
Diuretics
- ⇣ Blood volume
-
ACE-Is
- ⇣ RAAS
-
Beta-Blockers
- ⇣ SANS
-
Diuretics
Heart Failure Clinical Manifestation
- 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
Dilated (Congestive) Cardiomyopathy
Dilated LV w/ thin walls (“floppy”) → ⇣ Contractility → ⇡ Preload → Systolic dysfunction & HF
d/t– DM, MI, Alcoholism, Hyperthyroidism
Anaphylactic Shock
Widespread Type I Hypersensitivity reaction → Vasodilation & Hypovolemia
Treatment– Epinephrine → Vasoconstriction, Bronchodilation, ⇡ CO & Contractility, ⇣ Histamine
TOP PRIORITY: Maintain airway