Cardiovascular Pathophysiology Flashcards
1
Q
Risks factors of heart and cardiovascular disease
A
- Smoking
- Physical inactivity
- Obesity
- Suboptimal diet
- HTN
- Elevated serum total cholesterol: elevated low density lipoprotein or decreased high density lipoprotein
- Diabetes: family Hx (mother/father <60 years old with cardiovascular event)
- Age
- Gender: male risk is higher until females reach menopause then risk is equal
- Stress
- Anger and hostility
2
Q
Describe the difference between the Framingham risk score and the Reynolds risk score
A
- Framingham: estimation of 10 year cardiovascular disease risk
- Reynolds: Healthy and without diabetes it is designed to predict your risk of having a future heart attack, stroke, or other major heart disease in the next 10 years
3
Q
What are the major determinants of arterial blood pressure
A
- Cardiac output
- Total peripheral resistance
4
Q
What are the consequences of HTN
A
- Cerebral aneurysm or Hemorrhagic CVA (stroke)
- Retinopathy: arteriolar damage with micro aneurysms & rupture
- Persistent BP elevation
- Atherosclerosis
- Congestive heart failure, atherosclerosis, angina, and/or MI
- Nephrosclerosis and/or chronic renal failure
5
Q
Describe the relationship between stroke and atrial fibrillation
A
- A-fib remains a common & high risk condition for secondary ischemic stroke
- Clots often form in the L atrial appendage
- Anticoagulation is usually recommended if the patient has no contraindications
- Anticoagulation risk must be weighed with risk for hemorrhage and/or fall risk
- Heart rhythm monitoring for occult A-fib is usually recommended if no other cause of stroke is discovered
6
Q
What is atherosclerosis
A
- Fatty deposits (plaque) accumulate inside the artery wall causing blockage of blood flow
- Plaques are composed of lipid and thrombus
- Leads to progressive hardening & narrowing or abnormal dilation of the coronary, cerebral, & peripheral arteries
- Can occur throughout the body in large or small arteries based on disease process
7
Q
Possible consequences of atherosclerosis
A
- Partial occlusion of coronary arteries: angina pectoris (ischemic heart disease)
- Total occlusion of coronary arteries: MI
- Partial occlusion of carotid/cerebral arteries: transient ischemic attack
- Total occlusion of carotid/cerebral arteries: cerebrovascular accident (CVA/stroke)
- Occlusion in the aorta: aneurysm (occlusion, rupture and hemorrhage)
- Occlusion in the iliac arteries in the legs: peripheral vascular disease (gangrene and amputation)
8
Q
Describe what printzmetal (vasospastic angina) angina is
A
- Sclerotic arteries are prone to spasm
- Vasospastic angina occurs at rest (typically early morning) and is not associated with any preceding increase in myocardial oxygen demand
- Episodes of chest pain are associated with either transient ST segment elevation of 0.1 mV or depression of 0.1 mV
- Pain is relieved with nitroglycerin & other vasodilators
9
Q
What are the usual causes of death and immediate action necessary following a sudden cardiac arrest/death
A
- Ventricular tachycardia & ventricular fibrillation leading to cessation of cardiac output are usual causes of death
- Prompt delivery of bystander cardiopulmonary resuscitation with an automatic external defibrillator (AED) and entry into the emergency medical system is best chance of survival
10
Q
What is commotio cordis
A
- Abnormal heart rhythm (ventricular fibrillation) & cardiac arrest right after getting hit in the chest
- Most cases is caused by a baseball, hockey puck, or lacrosse ball hitting the L side of your chest
- Immediate CPR provides best chance of survival (~59% survival rate)
11
Q
Define angina
A
- Substernal pressure caused by an imbalance in the supply & demand of myocardial oxygen
- Can occur anywhere from the epigastric area to the jaw & is described as squeezing, tightness, or crushing
12
Q
Symptoms of angina
A
- Pain is gradual and diffuse
- Pain accompanied by shortness of breath, nausea, & diaphoresis (sweating)
13
Q
What is the primary physiologic difference between unstable and chronic stable angina
A
- Absence of an increase in myocardial oxygen demand to provoke the syndrome
14
Q
What are the most common warning signs of heart attack
A
- Uncomfortable pressure, fullness, squeezing or pain in the center of the chest (prolonged)
- Pain that spreads to the throat, neck, back, jaw, shoulders, or arms
- Chest discomfort with lightheadedness, dizziness, sweating, pallor (unhealthy pale appearance), nausea, or shortness of breath
- Prolonged symptoms unrelieved by antacids, nitroglycerin, or rest
15
Q
Describe chronic stable angina
A
- Well established level of onset & is the result of not enough blood supply to meet the metabolic demand
- Usually can alleviate symptoms by reducing the intensity slightly or by taking sublingual nitroglycerin
- Metabolic demand = rate pressure product = Heart rate x Systolic BP
16
Q
Differentiate the different types/causes of chest pain
A
- Stable angina: tightness/pressure anywhere above the waist with exertion activity & diminishes with rest or nitroglycerin
- Unstable angina: chest discomfort that is accelerating in frequency or severity that may occur at rest but doesn’t result in myocardial necrosis
- Vasospastic angina (printzmetal): Chest discomfort with ST segment depression or elevation occurring at rest typically early morning
- Musculoskeletal chest wall pain: pain/discomfort that is increased with palpation over chest wall
- Pulmonary/Pleuritic: discomfort/pain sharp in nature that changes with breathing
- Bronchospasm: exertion ally related or induced by cold relieved by bronchodilator or stopping activity
- Vascular: sudden onset, constant, pleuritic pain with SOB
- Gastrointestinal: prolonged epigastric discomfort usually related to food intake; relieved by antacid
17
Q
What does CHEST PAIN stand for to indicate an acute coronary syndrome
A
- Chest pain
- High sensitivity
- Early care
- Share
- Testing
- Pathways
- Accompanying
- Identify
- Noncardiac
- Structured
18
Q
What is the preferred blood test for in evaluation of patients with chest pain
A
- Troponins
- Troponins may become elevated within 2-3 hours after myocardial injury
- High sensitivity cardiac Troponin reference range: women = <14; men = <22
19
Q
Vital signs recommendations to stop PT for acute coronary syndrome/MI patients
A
- Unable to comfortably speak
- RR >40
- Onset of S3 heart sound
- HR decrease >10 bpm
- SBP decrease >10 mmHg
- MAP increase >10 mmHg
- SpO2 <90% or a decrease ≥4%
- New onset or worsening of cardiac dysrhythmia
- Return of pre-MI angina like pain
20
Q
Vital signs for initiation of PT intervention for stable angina/ECG/down trending toponin
A
- RR <30 (able to speak comfortably)
- Resting HR <120 bpm
- MAP a minimum of 60 mmHg
- SpO2 >90%
- SBP <110 mmHg
21
Q
Diagnosis criteria for a non-STEMI
A
- Signs and symptoms of cardiac ischemia (chest pain or equivalent) and positive myocardial biomarkers (troponin)
- New pathologic Q wave on the ECG often does not develop
22
Q
Relationship between Q-wave and STEMI
A
- Patient with a STEMI develops a Q-wave on the ECG in the subsequent 24-48 hrs & previously was defined as Q-wave or transmural infarctions
23
Q
What is a NSTEMI
A
- Type of MI that happens when a part of your heart is not getting enough oxygen
- Usually occurs due to partial coronary artery blockage or blockage in a branch off of your main coronary artery
- Some electrical pattern changes visible but often not distinctive
24
Q
What clinical indications could require a percutaneous coronary intervention (PCI)
A
- Acute STEMI
- Non ST elevation acute coronary syndrome (NSTE-ACS)
- Unstable angina
- Stable angina
- Anginal equivalent (dyspnea, arrhythmia, dizziness or syncope)
- High risk stress test findings
- Critical coronary artery stenosis is indicated fro PCI but no for coronary artery bypass surgery (CABG)
25
Q
Absolute contraindications for Fibrinolysis use in ST elevation MI
A
- Any prior ICH
- Known structural cerebral vascular lesion
- Known malignant intracranial neoplasm
- Ischemic stroke with 3 months except acute ischemic stroke within 3 hours
- Suspected aortic dissection
- Active bleeding or bleeding diathesis (excluding menses)
- Significant closed head or facial trauma within 3 months
26
Q
Criteria for Type 1 MI
A
- Symptoms of acute myocardial ischemia
- New ischemic ECG changes
- Development of pathological Q-waves
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
- Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy
27
Q
What is a Type 1 MI
A
- Plaque rupture/erosion with occlusive thrombus
- Plaque rupture/thrombus with non-occlusive thrombus
28
Q
Criteria of Type 2 MI
A
- Symptoms of acute myocardial ischemia
- New ischemic ECG changes
- Development of pathological Q-waves
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
29
Q
What is a Type 2 MI
A
- Atherosclerosis & oxygen supply/demand imbalance
- Vasospasm or coronary microvascular dysfunction
- Non-atherosclerotic coronary dissection
- Oxygen supply/demand imbalance alone
30
Q
What is a Type 3 MI
A
- AKA sudden cardiac death
- Ventricular tachycardia & ventricular fibrillation leading to cessation of cardiac output
- Irreversible brain damage starts within 4-6 min from a lack of blood flow to the brain
- Prompt delivery of bystander resuscitation with AED & entry into the emergency medical system is their best chance of survival
31
Q
Any 1 of the following criteria meets the diagnosis for prior or silent/unrecognized MI
A
- Pathological Q-waves with or without symptoms in the absence of non-ischemic causes
- Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology
- Pathological findings of a prior MI
32
Q
Criteria for Type 4a MI
A
- New ischemic ECG changes
- Development of new pathological Q-waves
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
- Angiographic findings consistent with a procedural flow-limiting complication such as coronary dissection, occlusion of a major epicardial artery or a side branch occlusion/thrombus, disruption of collateral flow, or distal embolization
33
Q
What is a Type 4b MI
A
- Stent/scaffold thrombus associated with percutaneous coronary intervention
- Acute = 0-24 hrs
- Subacute = >24 hrs to 30 days
- Late = >30 days to 1 yr
- Very late = >1 yr after stent/scaffold implantation
34
Q
What is a Type 4c MI
A
- Restenosis associated with percutaneous coronary intervention
- In-stent restenosis or restenosis following balloon angioplasty in the infarct territory
- Defined as focal or diffuse restenosis or a complex lesion associated with a rise and/or fall of cTn values
35
Q
Criteria for a Type 5 MI
A
- Happens after a CABG surgery
- Development of new pathological Q-waves
- Angiographic documented new graft occlusion or new native coronary artery occlusion
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
36
Q
Wells Score/Criteria for DVT
A
- Active CA (ongoing tx, within last 6mo, or palliative)
- Paralysis, paresis, or recent plaster immobilization of LE
- Recently bedridden for ≥3 days or major surgery within 12 wks requiring general/regional anesthesia
- Localized tenderness along distribution of deep venous system
- Entire leg swollen
- Calf swelling at least 3cm larger than asymptomatic side
- Pitting edema confined to symptomatic leg
- Collateral superficial veins (nonvaricose)
- Previously documented DVT
- Alternative diagnosis at least as likely as DVT (-2 points from score)
- DVT likely = ≥2 points
- DVT unlikely = <2 points
37
Q
What is the Constans criteria for DVT in UE
A
- CVC or pacemaker
- Localized pain
- Unilateral swelling
- Alternative diagnosis likely (-1 point from score)
- DVT UE likely = ≥2 points
- DVT UE unlikely = ≤1 point
38
Q
What is the Geneva clinical prediction rule for pulmonary embolism (PE)
A
- Age >65 y/o
- Previous DVT or PE
- Surgery within 1mo
- Active malignant condition
- Unilateral lower limb pain
- Hemoptysis
- Heart Rate ≥95 bpm
- Pain on lower limb deep venous palpation & unilateral edema
39
Q
Based on the medication given for a DVT/PE how long after administration is it safe to mobilize
A
- LMWH: 3-5 hrs check with medical team; >5hrs mobilize
- Fondaparinux: 2-3hrs check with medical team; >3hrs mobilize
- UFH: >24hrs check with medical team
- DOAC: 2-3hrs check with medical team; >3hrs mobilize
40
Q
Criteria for HAS-BLED bleeding risk with anti-coagulation therapy
A
- HTN uncontrolled: >160 mmHg systolic
- Abnormal renal failure: dialysis, transplant, Cr >2.26 mg/dL or >200 umol/L
- Abnormal liver function: cirrhosis or bilirubin
- Stroke: prior Hx of stroke
- Bleeding: prior major bleeding or predisposition to bleeding
- Labile INR: (unstable/high INR) time in therapeutic range <60%
- Elderly: age >65 y/o
- Drug or alcohol usage history (≥8 drinks/wk)
- Guidelines advise stopping anticoagulation if the HAS-BLED score is ≥4 and cannot be modified
41
Q
Describe how HTN, CAD, or Cardiac dysrhythmias can cause congestive heart failure
A
- HTN: increased arterial pressure leads to L ventricular hypertrophy & increased energy expenditure
- CAD (myocardial ischemia): dysfunction of L/R ventricle as result of injury, scar formation & decreased contractility may occur as well as reduced relaxation
- Cardiac dysrhythmias: extremely rapid or slow cardiac arrhythmias impair the functioning ventricles
42
Q
Describe how renal insufficiency, cardiomyopathy, or heart valve abnormality can cause congestive heart failure
A
- Renal insufficiency: causes fluid overload
- Cardiomyopathy: contraction/relaxation or myocardial muscle fibers are impaired
- Heart valve abnormality: valvular stenosis or incompetent valves cause myocardial hypertrophy & a decrease in ventricular distensibility with mild diastolic dysfunction
43
Q
Describe how pericardial effusion, pulmonary HTN, or pulmonary embolism can cause congestive heart failure
A
- Pericardial effusion: injury to pericardium leads to pericarditis & progress to peripheral effusion & cardiac compression as fluid fills the pericardial sac
- Pulmonary HTN: elevated pressures in pulmonary artery leads to increased after load for R ventricle & overtime to R ventricular failure
- Pulmonary embolism: severe hypoxemia may result from embolism blocking a mod-large amount of lung increasing pulmonary artery pressures
44
Q
Describe how SCI or age related changes can cause congestive heart failure
A
- SCI: transaction of the cervical spinal cord prevents the sympathetic driven changes necessary to maintain cardiac performance
- Age related changes: decrease in cardiac output by altered contraction/relaxation of cardiac muscle
45
Q
What are the references ranges for BNP and pro-BNP
A
- Substance made by the heart & used in the diagnosis/stratification of patients with heart failure
- BNP <100
- Pro-BNP <300
- BNP >400: heart failure is likely
46
Q
Common drugs that cause orthostatic hypotension
A
- Diuretics
- Alpha Adrenoceptor Blockers for benign prostatic hypertrophy
- Beta blockers (-lol’s)
- ACE inhibitors (-pril)
- Calcium channel blockers (-pine/-azem)
- Angiotensin II receptor blockers (-tan)
- Insulin, Levodopa, & Tricyclic antidepressants
47
Q
Describe the relationship between CHF and pulmonary HTN
A
- Pulmonary HTN = mean pulmonary artery pressure ≥20 mmHg
- A damaged or failing L heart can also lead to Pulmonary HTN as elevated L sided filling pressures bc of a weakened L ventricle beginning to passively back up into the pulmonary system increasing pressures in the pulmonary circulation
48
Q
What are the signs and symptoms of CHF
A
- Dyspnea (difficult/labored breathing)
- Tachypnea
- Paroxysmal nocturnal dyspnea
- Orthopnea (SOB when lying flat)
- Peripheral edema
- Cold, pale, & possibly cyanotic extremities
- Weight gain
- Hepatomegaly (enlargement of liver)
- Jugular venous distention (act of swelling)
- Rales (crackles)
- Tubular breath sounds & consolidation
- Prescience of an S3 heart sound
- Sinus tachycardia
- Decreased exercise tolerance or physical work capacity
49
Q
Describe the differences b/w HFrEF and HFpEF
A
- HFrEF (HF with reduced ejection fraction): result of low cardiac output at rest or during exertion, systolic dysfunction, resting ejection fraction <40%, impaired contraction of ventricles during systole causing a low stroke volume
- HFpEF (HF with preserved ejection fraction): impaired relaxation of L ventricle & passive L ventricle compliance resulting in stiffness & increased diastolic pressures, resting EF ≥50%
50
Q
Describe the classes of HF
A
- Class I: no limitation in physical activity, no fatigue, palpitations, or dyspnea due to ordinary physical activity
- Class II: slight limitation in PA; fatigue, palpitations, or dyspnea caused by ordinary PA
- Class III: marked limitation of PA, less than ordinary PA cases fatigue, palpitations, or dyspnea
- Class IV: symptoms at rest; unable to do any PA without symptomology
51
Q
Comorbidities that impact patients with CHF
A
- COPD
- Anemia
- Diabetes
- Renal dysfunction
- Sleep disordered breathing
- Obesity
52
Q
Symptoms that may indicate an adjustment in medications & therefore warrants communication with the physician in CHF patients
A
- Weight gain of 2-3 lbs in 24hrs
- Increased cough
- Peripheral edema
- Increase in shortness of breath with activity
- Orthopnea: increase in the number of pillows needed
53
Q
Symptoms that indicate overt decompensation & an immediate visit to the emergency department or physician office in patients with CHF
A
- Shortness of breath at rest
- Unrelieved chest pain
- wheezing or chest tightness at rest
- Paroxysmal nocturnal dyspnea: requiring to sit in chair to sleep
- Weight gain or loss of more than 5lbs in 3 days
- Confusion
54
Q
What is dilated cardiomyopathy
A
- Dysfunction of myocardial mitochondria leads to a lack of energy necessary for proper cardiac function causing the heart to be a less effective pump
- Ineffective pumping increases L ventricular end diastolic volume & pressure which dilate the L ventricle
- LV is unable to contract/relax properly in response to increased workload preventing myocardial hypertrophy but producing ineffective systolic function
55
Q
What is hypertrophic cardiomyopathy
A
- Diastolic dysfunction impairs filling of ventricles during diastole
- Increase in L ventricular end diastolic pressure & eventually L arterial, pulmonary artery, & pulmonary capillary pressures leading to a hyper contractile LV
- High risk of sudden cardiac death
56
Q
What is restrictive cardiomyopathy
A
- Cardiomyopathy of diastolic dysfunction & frequently unimpaired contractile functiion
57
Q
What is Takotsubo cardiomyopathy (AKA broken heart syndrome)
A
- Condition is usually the result of severe emotional or physical stress such as a sudden illness, loss of a loved one, serious accident, or a natural disaster such as an earthquake
- Most common in women ages 58-75 y/o
- Most people recover with no long-term heart damage
58
Q
what causes valvular stenosis
A
- Blocked valves
- Calcifications
59
Q
Symptoms of a heart valve disease
A
- Pain, tightness, or pressure in the chest
- Lightheadedness or dizziness
- Shortness of breath
- Rapid fluttering heartbeat
- Fainting
- Difficulty sleeping or sitting up
- Swollen ankles or feet
- Difficulty walking short distances
- Not engaging in activities you once did
